cancer risk essay

Essay on Cancer for Students and Children

500+ words essay on cancer.

Cancer might just be one of the most feared and dreaded diseases. Globally, cancer is responsible for the death of nearly 9.5 million people in 2018. It is the second leading cause of death as per the world health organization. As per studies, in India, we see 1300 deaths due to cancer every day. These statistics are truly astonishing and scary. In the recent few decades, the number of cancer has been increasingly on the rise. So let us take a look at the meaning, causes, and types of cancer in this essay on cancer.

Cancer comes in many forms and types. Cancer is the collective name given to the disease where certain cells of the person’s body start dividing continuously, refusing to stop. These extra cells form when none are needed and they spread into the surrounding tissues and can even form malignant tumors. Cells may break away from such tumors and go and form tumors in other places of the patient’s body.

Types of Cancers

As we know, cancer can actually affect any part or organ of the human body. We all have come across various types of cancer – lung, blood, pancreas, stomach, skin, and so many others. Biologically, however, cancer can be divided into five types specifically – carcinoma, sarcoma, melanoma, lymphoma, leukemia.

Among these, carcinomas are the most diagnosed type. These cancers originate in organs or glands such as lungs, stomach, pancreas, breast, etc. Leukemia is the cancer of the blood, and this does not form any tumors. Sarcomas start in the muscles, bones, tissues or other connective tissues of the body. Lymphomas are the cancer of the white blood cells, i.e. the lymphocytes. And finally, melanoma is when cancer arises in the pigment of the skin.

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Causes of Cancer

In most cases, we can never attribute the cause of any cancer to one single factor. The main thing that causes cancer is a substance we know as carcinogens. But how these develop or enters a person’s body will depend on many factors. We can divide the main factors into the following types – biological factors, physical factors, and lifestyle-related factors.

Biological factors involve internal factors such as age, gender, genes, hereditary factors, blood type, skin type, etc. Physical factors refer to environmental exposure of any king to say X-rays, gamma rays, etc. Ad finally lifestyle-related factors refer to substances that introduced carcinogens into our body. These include tobacco, UV radiation, alcohol. smoke, etc. Next, in this essay on cancer lets learn about how we can treat cancer.

Treatment of Cancer

Early diagnosis and immediate medical care in cancer are of utmost importance. When diagnosed in the early stages, then the treatment becomes easier and has more chances of success. The three most common treatment plans are either surgery, radiation therapy or chemotherapy.

If there is a benign tumor, then surgery is performed to remove the mass from the body, hence removing cancer from the body. In radiation therapy, we use radiation (rays) to specially target and kill the cancer cells. Chemotherapy is similar, where we inject the patient with drugs that target and kill the cancer cells. All treatment plans, however, have various side-effects. And aftercare is one of the most important aspects of cancer treatment.

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Diet, nutrition, and cancer risk: what do we know and what is the way forward?

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• Diet, nutrition, and cancer risk: what do we know and what is the way forward? - March 11, 2020
• Timothy J Key , deputy director 1 ,
• Kathryn E Bradbury , senior research fellow 2 ,
• Aurora Perez-Cornago , senior nutritional epidemiologist 1 ,
• Rashmi Sinha , senior investigator 3 ,
• Konstantinos K Tsilidis , assistant professor of epidemiology 4 5 ,
• Shoichiro Tsugane , director 6
• 1 Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK
• 2 National Institute for Health Innovation, School of Population Health, University of Auckland, Auckland, New Zealand
• 3 Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
• 4 Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece
• 5 Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
• 6 Center for Public Health Sciences, National Cancer Center, Tokyo, Japan
• Correspondence to: TJ Key tim.key{at}ndph.ox.ac.uk

Timothy J Key and colleagues describe the evidence linking diet and nutrition to cancer risk, concluding that obesity and alcohol are the most important factors

Scientists have suspected for decades that nutrition has an important influence on the risk of developing cancer. Epidemiological studies as early as the 1960s showed that cancer rates varied widely between populations and that cancer rates in migrants moving from low to high risk countries could rise to equal or sometimes exceed the rates in the host population. 1 2 These observations implied the existence of important environmental causes of cancer, and other studies showed strong correlations between many types of cancer and dietary factors; for example, countries with high intakes of meat had high rates of colorectal cancer. 3 Furthermore, experiments in animals showed that cancer rates could be altered by manipulating diet, with compelling evidence that restricting energy intake causes a general reduction in cancer development. 4 5

Cancer is predicted to be the leading cause of death in every country of the world by the end of this century. 6 Although dietary factors are thought to be important in determining the risk of developing cancer, establishing the exact effects of diet on cancer risk has proved challenging. Here we describe the relatively few dietary factors that clearly influence risk of cancers along the digestive tract (from top to bottom) and of other common types of cancer, 7 8 as well as challenges for future research.

Cancers of the oral cavity and pharynx

Nasopharyngeal cancer is common in a few populations around the globe, such as the Cantonese population in southern China and some indigenous populations of South East Asia, the Arctic, north Africa, and the Middle East. 9 Consumption of foods preserved with salt has been linked with this cancer, and the mechanism might be through nitrosamine formation or reactivation of the Epstein-Barr virus. 10 Based on case-control studies, Chinese style salted fish has been classified as a carcinogen by the International Agency for Research on Cancer (IARC), part of the World Health Organization. 10

For oral and pharyngeal cancers overall, eating more fruits, vegetables, and related micronutrients such as vitamin C and folate is associated with lower cancer risk ( boxes 1 and 2 ). These associations, however, might be influenced by residual confounding by smoking (a major non-dietary risk factor 7 14 ) and alcohol consumption, so the evidence is only suggestive of a protective effect. 8 14

Are fruit and vegetables important determinants of cancer risk—and what about vegetarians?

Early case-control studies indicated that higher intakes of fruit and vegetables were associated with a lower risk of several types of cancer. 11 But subsequent prospective studies, which are not affected by recall or selection bias, produced much weaker findings. In the 2018 World Cancer Research Fund report neither fruits nor vegetables were considered to be convincingly or probably associated with the risk of any cancer. 8 There was suggestive evidence for protection of some cancers, and risk might increase at very low intakes. Specific components of certain fruits and vegetables might have a protective action.

Vegetarians eat no meat or fish and usually eat more fruit and vegetables than comparable non-vegetarians. The risk of all cancer sites combined might be slightly lower in vegetarians and vegans than in non-vegetarians, but findings for individual cancers are inconclusive. 12

Do vitamins and minerals reduce cancer risk?

By definition, deficiencies of vitamins and essential minerals cause ill health; this might include increased susceptibility to some types of cancer, but establishing the details of any such effects has proved difficult. High dose vitamin or mineral supplements have not reduced cancer risk in well nourished populations and might increase risk; for example, high dose β carotene might increase the risk of lung cancer. 13 Vitamin and mineral supplements should not be used for cancer prevention, although they can be important for other aspects of health, such as folic acid supplements for women before conception.

Oesophageal cancer

There are two types of oesophageal cancer: squamous cell carcinoma and adenocarcinoma. The squamous form predominates in most of the world, whereas adenocarcinoma is relatively common only in Western countries, where rates have recently increased. Obesity is an established risk factor for adenocarcinoma, probably partly owing to reflux of stomach contents into the oesophagus. 15 16 Alcohol increases the risk of squamous cell carcinoma but not of adenocarcinoma. 17 Smoking increases the risk of both types, with a larger effect for squamous cell carcinoma. 17

Oesophageal cancer incidence rates are very high in parts of eastern and southern Africa, Linzhou (China), and Golestan (Iran). 6 17 People in high risk populations have often consumed a restricted diet, low in fruit, vegetables, and animal products, so deficiencies of micronutrients have been postulated to explain the high risk ( boxes 1 and 2 ). Despite several observational studies and some randomised trials, however, the relative roles of various micronutrients are not yet clear. 17 18 19 20 In Western countries early case-control studies indicated a protective role for fruit and vegetables, 21 22 but more recently published prospective studies show weaker associations, which might be due to residual confounding from smoking and alcohol consumption. 16

Consumption of drinks such as tea and mate when scalding hot is associated with an increased risk of oesophageal cancer, 23 24 25 and drinking beverages above 65°C is classified by IARC as probably carcinogenic to humans. 26

Stomach cancer

Stomach cancer is the fifth most common cancer worldwide, with the highest rates in eastern Asia. 6 Eating large amounts of salted foods, such as salt preserved fish, is associated with an increased risk 27 ; this might be caused by the salt itself or by carcinogens derived from the nitrites in many preserved foods. Salted food might increase the risk of Helicobacter pylori infection (an established cause of stomach cancer) 28 and act synergistically to promote development of the disease. 29 Some evidence indicates that eating large amounts of pickled vegetables increases the risk of stomach cancer because of the production of N-nitroso compounds by mould or fungi, which are sometimes present in these foods. 30 31

The risk of stomach cancer might be decreased by diets high in fruit and vegetables and for people with high plasma concentrations of vitamin C ( boxes 1 and 2 ). 32 A trial in Linzhou, China, showed that supplementation with β carotene, selenium, and α tocopherol resulted in a significant reduction in stomach cancer mortality, 18 and other trials have indicated enhanced regression of precancerous lesions with the use of supplements of vitamin C, β carotene, or both. 33 34 Prospective studies in Japan have also shown an inverse association between stomach cancer risk and green tea consumption in women (the majority of whom are non-smokers), perhaps related to polyphenols. 35 These studies indicate a protective role of antioxidant micronutrients or other antioxidant compounds, but these associations need clarification.

Colorectal cancer

Colorectal cancer is the third most common cancer in the world. 6 Overweight and obesity increase risk, 8 36 37 as do alcohol and smoking. 7

Ecological analyses show striking positive correlations between eating meat and colorectal cancer rates. 3 38 In 2015 IARC classified processed meat as carcinogenic to humans and unprocessed red meat as probably carcinogenic, 39 40 partly based on a meta-analysis reporting an increase in risk of 17% for each daily 50 g increment in consumption of processed meat and 18% for each 100 g increment in consumption of red meat. 41 More recent systematic reviews have reported smaller increases in risk for unprocessed red meat. 8 42

The chemicals used to preserve processed meat, such as nitrates and nitrites, might increase exposure of the gut to mutagenic N-nitroso compounds. 40 Both processed and unprocessed red meat also contain haem iron, which might have a cytotoxic effect in the gut and increase formation of N-nitroso compounds. Cooking meat at high temperatures can generate mutagenic heterocyclic amines and polycyclic aromatic hydrocarbons. 40 Whether any of these putative mechanisms explain the association between eating red and processed meat and risk for colorectal cancer is unclear. 39 40

Higher consumptions of milk and calcium are associated with a moderate reduction in risk of colorectal cancer. 8 43 44 45 Calcium might be protective by forming complexes with secondary bile acids and haem in the intestinal lumen. Higher circulating concentrations of vitamin D are associated with a lower risk, 46 but this might be confounded by other factors such as physical activity. Mendelian randomisation studies of genetically determined vitamin D have not supported a causal relation. 47 48

In the 1970s Burkitt suggested that the low rates of colorectal cancer in parts of Africa were caused by the high consumption of dietary fibre. 49 Prospective studies have shown that consuming 10 g more total dietary fibre a day is associated with an average 10% reduction in risk of colorectal cancer; further analyses suggest that cereal fibre and wholegrain cereals are protective, but not fibre from fruit or vegetables. 50 51

High dietary folate intake has been associated with reduced risk of colorectal cancer, and adequate folate status maintains genomic stability, 8 but high folate status might promote the growth of colorectal tumours. 52 Whether folate or folic acid have any material impact on the risk of colorectal cancer is uncertain. Most randomised trials of folic acid supplementation have found no effect, 53 54 and although studies of the gene for methylenetetrahydrofolate reductase have indicated that lower circulating folate is associated with a slightly lower risk, the interpretation of these genetic data is not straightforward. 55

Liver cancer

Alcohol is the main diet related risk factor for liver cancer, probably through the development of cirrhosis and alcoholic hepatitis. 7 Overweight and obesity also increase risk. 8 Aflatoxin, a mutagenic compound produced by the fungus Aspergillus in foods such as grains, nuts, and dried fruit when stored in hot and humid conditions, is classified as a carcinogen by IARC and is an important risk factor in some low income countries (for people with active hepatitis virus infection). 56 The major non-dietary risk factor is chronic infection with hepatitis B or C viruses.

Some studies indicate an inverse association between coffee drinking and risk of liver cancer. 8 Coffee might have a true protective effect because it contains many bioactive compounds, 57 58 but the association might be influenced by residual confounding, as well as by reverse causation if subclinical liver disease reduces appetite for coffee.

Pancreatic cancer

Obesity increases risk of pancreatic cancer by about 20%. 8 Diabetes is also associated with increased risk, and a mendelian randomisation analysis indicates that this is due to raised insulin rather than diabetes itself. 59 Studies of dietary components and risk have been inconclusive. 8

Lung cancer

Lung cancer is the most common cancer in the world, and heavy smoking increases risk around 40-fold. 6 7 Prospective studies have indicated that diets higher in fruits and vegetables are associated with a slightly lower risk of lung cancer in smokers, but not in never smokers. 60 61 The weak inverse association of fruit and vegetables with lung cancer risk in smokers might perhaps indicate some true protective effect, but it might simply be due to residual confounding by smoking ( box 1 ). Trials that tested supplements of β carotene (and retinol in one trial) to prevent lung cancer showed an unexpected higher risk of lung cancer in participants in the intervention group. 13 62

Breast cancer

Breast cancer is the second most common cancer in the world. 6 Reproductive and hormonal factors are key determinants of risk. 63 Obesity increases breast cancer risk in postmenopausal women, probably by increasing circulating oestrogens, which are produced by aromatase in adipose tissue. 64 Most studies have shown that obesity in premenopausal women is associated with a reduction in risk, perhaps due to lower hormone levels related to an increased frequency of anovulation. 65 Alcohol increases risk by about 10% for each drink consumed daily 8 66 ; the mechanism might involve increased oestrogens.

Much controversy has surrounded the hypothesis that a high fat intake in adulthood increases breast cancer risk. Early case-control studies supported this hypothesis, but prospective observational studies have overall been null, 8 and two randomised controlled trials of a reduced fat diet were also null. 67 68

Studies of other dietary factors including meat, dairy products, and fruit are generally inconclusive. 8 Some recent studies have indicated an inverse association between vegetable intake and risk of oestrogen receptor negative breast cancer 8 69 70 and between dietary fibre and overall risk. 8 71 Isoflavones, largely from soya, have been associated with a lower risk of breast cancer in Asian populations. 72 These associations are potentially important and should be investigated for causality.

Prostate cancer

Prostate cancer is the fourth most common cancer in the world. 6 The only well established risk factors are age, family history, black ethnicity, and genetic factors. 73 Obesity probably increases the risk for more aggressive forms of prostate cancer. 8

Lycopene, primarily from tomatoes, has been associated with a reduced risk, but the data are not conclusive. 8 Some studies have indicated that risk might be reduced with higher levels of other micronutrients including β carotene, vitamin D, vitamin E, and selenium, but the findings from trials and mendelian randomisation analyses are overall null or inconclusive. 47 74 75 76

Isoflavones, largely from soya foods, have been associated with a reduced risk for prostate cancer in Asian men, 77 and plasma concentrations of the isoflavone equol might be inversely associated with prostate cancer risk in men in Japan. 78

Substantial evidence shows that prostate cancer risk is increased by high levels of the hormone insulin-like growth factor 1, which stimulates cell division, and further research is needed to determine whether dietary factors, such as animal protein, might influence prostate cancer risk by affecting production of this hormone. 79

Evaluations by expert groups

Given the huge variation in diets around the world and the large number of cancers that diets can influence, how do we know which foods or diets should be avoided and which should be recommended? The World Cancer Research Fund (WCRF) and IARC have reviewed the carcinogenic risk of foods and nutrients using systematic reviews of the evidence and evaluation by expert panels. As with much nutritional research the topic is complex, but the WCRF and IARC have identified nutritional factors with convincing evidence or probable evidence of cancer risk.

WCRF and IARC concluded that obesity and alcohol cause cancer at several sites ( fig 1 ). For overweight and obesity, increases in risk for every 5 kg/m 2 rise in body mass index (BMI) vary from 5% for colorectal cancer to 50% for cancer of the endometrium (IARC also considered the evidence to be sufficient for meningioma, thyroid cancer, and multiple myeloma). 80 For alcohol, risk increases for each 10 g rise in consumption a day vary from 4% for liver cancer to 25% for squamous cell carcinoma of the oesophagus.

Body mass index (BMI), alcohol, and cancer risk. Convincing associations according to the World Cancer Research Fund 8 or the International Agency for Research on Cancer (marked by asterisks), or both, 10 80 with relative risks from meta-analyses. 8 We also consider the association between BMI and risk of breast cancer in premenopausal women to be convincing. 65 RR, relative risk (plotted with squares proportional to amount of statistical information); CI, confidence interval

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Processed meat was judged to be a convincing cause of cancer by both WCRF and IARC; in the most recent WCRF report the relative risk for colorectal cancer was 1.16 (1.08 to 1.26) for each 50 g/day increment. 8 IARC judged Chinese-style salted fish to be a carcinogen (with a relative risk of nasopharyngeal cancer of 1.31 (1.16 to 1.47) for each additional serving per week), 8 10 as well as foods contaminated with aflatoxin. 56 Neither expert body judged any dietary factor to be convincingly protective against cancer.

Uncertainty remains

WCRF and IARC judged some associations between nutritional factors and cancer risk to be “probably” causal or protective ( table 1 ). Some researchers might think that the criteria for “probable” are not stringent enough. Further evidence might change the conclusions, and this should be kept in mind when using the reports to estimate the likely effects of diet or to make dietary recommendations. Notably, WCRF also categorised adult and young adulthood body fatness as probably protective for premenopausal breast cancer; with new evidence 65 we consider this convincing, so the association is shown in figure 1 rather than table 1 .

Still uncertain: dietary and nutritional factors that expert groups have classified as “probable” causal or protective factors for cancer

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Obesity probably increases the risk of cancers of the oral cavity and pharynx and of aggressive prostate cancer. Alcohol probably increases the risk of stomach cancer but is inversely associated with the risk of kidney cancer, which might indicate a true biological effect or reflect residual confounding or bias. 81 Very hot drinks probably increase the risk of cancer of the oesophagus, foods preserved by salting probably increase the risk of stomach cancer, and several dietary factors probably reduce the risk of colorectal cancer. The expert panels also concluded that the risk of endometrial cancer is probably increased by a diet with a high glycaemic load. Coffee was judged to probably be protective for liver and endometrial cancer, but some of the current authors think that this conclusion is too strong and that the data on coffee and endometrial cancer might be affected by selective publication of only part of the evidence. 82

Independently from overweight and obesity, greater adult height is associated with the risk of several cancers ( box 3 ).

Why do taller people have a higher risk of cancer?

The risk for most types of cancer increases with height. A WCRF systematic review showed that increases in risk for each 5 cm increment in height ranged from 4% for prostate cancer to 12% for malignant melanoma. 83 The mechanism is uncertain but might be related to taller people having more stem cells at risk of cancer or a factor such as insulin-like growth factor 1 having effects on both height and cancer risk. 84 Undernutrition causes restricted growth, and some aspects of adequate nutrition during childhood and adolescence, such as an ample intake of energy and protein, might lead to relatively greater height and a higher overall cancer risk. 83 It is not clear, however, whether better understanding of this pathway could lead to strategies for reducing cancer risk.

Acrylamide, a chemical produced during high temperature cooking and in the manufacture of many types of carbohydrate-rich foods (such as potato chips, cereal crispbreads, and coffee), is classified by IARC as probably carcinogenic to humans. 85 This conclusion was based largely on studies in experimental animals; epidemiological studies have been mostly null or inconclusive 86 but are limited by the difficulty of estimating long term exposure and by confounding owing to smoking. Recent research on possible mutational signatures of this chemical indicate that it might contribute to risk. 87

How important is diet as a preventable cause of cancer?

Figure 2 shows recent estimates of the proportions of cancer cases in the UK attributable to modifiable risk factors, including dietary factors classified by WCRF or IARC as convincing causes of cancer. 88 Overweight and obesity is the second largest attributable cause, responsible for 6.3% of cancers in the UK, and is the largest cause in non-smokers. Alcohol (3.3%), dietary fibre (3.3%), and processed meat (1.5%) are also among the top 10 causes (although dietary fibre is currently classed by WCRF as only “probable”). Analyses from some other countries have produced broadly similar estimates; recent estimates for Brazil were 4.9% for overweight and obesity, 3.8% for alcohol, 0.8% for dietary fibre, and 0.6% for processed meat. 89 In Japan, however, where the prevalence of obesity is lower, estimates were 1.1% for overweight and obesity and 6.3% for alcohol (and 1.6% for salt). 90

Percentages of cancer cases in the UK attributable to different exposures. 88

The way forward

Research into the effects of nutrition on health is difficult. 91 We have summarised here the relatively few well established clear links between nutrition and cancer, but future research might show further important risk factors—perhaps for specific food components or for broader dietary patterns, such as so called plant based diets. To move forward, the new generation of studies needs to improve estimates of long term exposure with, for example, repeated dietary records, which are now feasible using web based questionnaires. 92 Biomarkers of dietary intake and nutritional status can be used more extensively, and new biomarkers might be found through metabolomics, for example, but they will need to be validated and interpreted in the light of possible confounding and reverse causation. For some exposures, both for intake and nutritional status, mendelian randomisation will help to clarify causality, 93 and randomised trials will be needed to test specific hypotheses. It will also be important to attempt to coordinate systematic analyses of all the data available worldwide, to reduce the risk of publication bias. 94 For public health and policy, the top priority should be tackling the known major diet related risk factors for cancer, particularly obesity and alcohol.

Key messages

Obesity and alcohol increase the risk of several types of cancer; these are the most important nutritional factors contributing to the total burden of cancer worldwide

For colorectal cancer, processed meat increases risk and red meat probably increases risk; dietary fibre, dairy products, and calcium probably reduce risk

Foods containing mutagens can cause cancer; certain types of salted fish cause nasopharyngeal cancer, and foods contaminated with aflatoxin cause liver cancer

Fruits and vegetables are not clearly linked to cancer risk, although very low intakes might increase the risk for aerodigestive and some other cancers

Other nutritional factors might contribute to the risk of cancer, but the evidence is currently not strong enough to be sure

Contributors and sources: All authors contributed to the first draft of the manuscript and provided critical revisions. All authors gave intellectual input to improve the manuscript and have read and approved the final version. TJK is the guarantor. The authors all have experience in nutritional epidemiology, with particular expertise in cancers of the gastrointestinal tract (KEB, RS, ST), breast cancer (TJK), prostate cancer (TJK, APC), cancer in Asia (RS, ST), and mendelian randomisation (KKT). Sources of information for this article included published systematic reviews and primary research articles based on prospective observational studies and randomised controlled trials.

Competing interests: We have read and understood BMJ policy on declaration of interests and have no relevant interests to declare.

This research was partly supported by Cancer Research UK (C8221/A19170) and the Wellcome Trust Our Planet Our Health (Livestock, Environment and People, LEAP 205212/Z/16/Z). KEB is supported by the Girdlers’ New Zealand Health Research Council Fellowship. KKT is supported by WCRF (2014/1180).

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ .

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104 Cancer Essay Topic Ideas & Examples

Inside This Article

Cancer is a complex and devastating disease that affects millions of people worldwide. Writing an essay on this topic allows for a deeper understanding of the various aspects of cancer, including its causes, prevention, treatment, and impact on individuals and society. Here are 104 cancer essay topic ideas and examples to guide and inspire your writing:

• The history of cancer research and treatment: From ancient times to modern advancements.
• The role of genetics in cancer development: Exploring inherited and acquired genetic mutations.
• Environmental factors and their association with cancer risk: Analyzing the impact of pollution, radiation, and lifestyle choices.
• The most common types of cancer: In-depth exploration of breast, lung, prostate, colorectal, and other prevalent cancers.
• Childhood cancer: Understanding the unique challenges and treatment options for pediatric patients.
• The emotional and psychological impact of cancer on patients and their families.
• The economics of cancer: Assessing the financial burden on patients and healthcare systems.
• The impact of cancer on caregiver mental health: Examining the emotional toll on those who support cancer patients.
• The role of exercise and nutrition in cancer prevention and recovery.
• The development and effectiveness of cancer vaccines: Discussing breakthroughs and future prospects.
• The influence of lifestyle choices on cancer risk: Tobacco, alcohol, diet, and exercise.
• The stigma surrounding cancer: Addressing societal attitudes and misconceptions.
• Alternative therapies for cancer treatment: Exploring complementary medicine and its potential benefits.
• The ethics of experimental cancer treatments: Balancing patient rights and scientific progress.
• Cancer prevention strategies in low-income countries: Identifying challenges and potential solutions.
• The impact of cancer on workplace productivity: Analyzing the economic consequences for employees and employers.
• Cancer survivors' quality of life: Examining the long-term physical and emotional effects.
• The role of support groups and counseling in cancer care: Assessing their benefits and limitations.
• Cancer and gender: Investigating the disparities in cancer incidence, treatment, and outcomes.
• The psychological impact of cancer on children and adolescents.
• The role of technology in early cancer detection: Discussing advancements in screening methods.
• The impact of cancer on sexual health and intimacy: Addressing the challenges and available support.
• The correlation between cancer and mental health disorders: Analyzing the reciprocal relationship.
• The impact of cancer on fertility and reproductive choices: Exploring the options available to patients.
• The intersection of cancer and chronic diseases: Investigating the complexities of dual diagnoses.
• The role of palliative care in cancer treatment: Discussing end-of-life care and patient comfort.
• The influence of social media on cancer awareness and fundraising campaigns.
• The role of governmental policies in cancer prevention and control.
• Cancer and the elderly population: Addressing unique challenges and treatment approaches.
• The impact of race and ethnicity on cancer disparities: Investigating socioeconomic and cultural factors.
• The effects of cancer on children's education and academic development.
• The role of artificial intelligence in cancer diagnosis and treatment planning.
• Cancer prevention campaigns: Analyzing their effectiveness and potential limitations.
• The impact of cancer on sexual minorities: Investigating disparities in diagnosis, treatment, and support.
• The role of spirituality and faith in cancer patients' coping mechanisms.
• Cancer prevention in the workplace: Assessing occupational hazards and protective measures.
• The correlation between cancer and obesity: Exploring the link and potential interventions.
• The impact of cancer on siblings: Addressing the emotional and practical challenges.
• The role of precision medicine in personalized cancer treatment: Discussing targeted therapies.
• The influence of media portrayal on public perception of cancer and cancer patients.
• The impact of cancer on caregivers' professional lives: Analyzing the challenges and potential support systems.
• Cancer and the LGBTQ+ community: Investigating unique challenges and disparities in healthcare access.
• The role of music and art therapy in cancer care: Assessing their benefits and limitations.
• The correlation between cancer and socioeconomic status: Analyzing the disparities in diagnosis and outcomes.
• The impact of cancer on young adults: Discussing fertility preservation and long-term survivorship issues.
• Cancer and the rural population: Addressing barriers to access and treatment options.
• The role of emotional support animals in cancer care: Investigating their benefits and ethical considerations.
• The impact of cancer on intimate partner relationships: Addressing the challenges and available resources.
• The influence of mindfulness and meditation on cancer patients' well-being.
• The impact of cancer on military veterans: Analyzing the intersection of post-traumatic stress disorder and cancer.
• Cancer and the incarcerated population: Addressing the challenges and potential solutions.
• The role of patient advocacy in cancer care: Discussing the importance of empowering patients.
• Cancer prevention through public health initiatives: Assessing community-based interventions.
• The correlation between cancer and air pollution: Investigating the link and potential policy implications.
• The impact of cancer on body image and self-esteem: Addressing psychological and social consequences.
• Cancer and the transgender population: Exploring unique challenges and healthcare disparities.
• The role of social determinants of health in cancer outcomes: Analyzing the influence of socioeconomic factors.
• Cancer and the homeless population: Addressing the barriers to access and supportive care.
• The impact of cancer on the LGBTQ+ youth: Investigating mental health disparities and support systems.
• Cancer prevention in minority populations: Analyzing cultural factors and tailored interventions.
• The role of exercise in cancer rehabilitation: Discussing the benefits of physical activity during and after treatment.
• Cancer and the refugee population: Addressing the challenges and barriers to healthcare.
• The impact of cancer on veterans' mental health: Analyzing post-traumatic stress disorder and survivorship.
• The correlation between cancer and sleep disturbances: Investigating the link and potential interventions.
• Cancer and the disabled population: Addressing unique challenges and supportive care.
• The role of artificial intelligence in cancer prognosis: Discussing predictive models and decision support systems.
• Cancer prevention through HPV vaccination: Analyzing the impact on cervical and other related cancers.
• The impact of cancer on children's social development and peer relationships.
• Cancer and the prison population: Addressing the disparities in access and treatment.
• The role of telemedicine in cancer care: Discussing remote consultations and monitoring.
• Cancer prevention in the aging population: Analyzing challenges and tailored interventions.
• The correlation between cancer and smoking: Investigating the link and effective cessation strategies.
• Cancer and mental health: Exploring the reciprocal relationship and potential interventions.
• The impact of cancer on the LGBTQ+ elderly population: Addressing unique challenges and supportive care.
• Cancer prevention through lifestyle modifications: Analyzing the role of diet, exercise, and stress management.
• The role of genetic counseling in cancer risk assessment: Discussing the benefits and ethical considerations.
• Cancer and environmental justice: Analyzing disparities in exposure to carcinogens.
• The impact of cancer on adolescents' educational attainment and career prospects.
• Cancer and the indigenous population: Addressing cultural and access barriers to care.
• The role of social media influencers in cancer awareness campaigns: Assessing their impact and ethical considerations.
• Cancer prevention through workplace policies: Analyzing the importance of occupational safety measures.

These essay topic ideas offer a wide range of possibilities for exploring the complex and multifaceted nature of cancer. Depending on your interests and expertise, you can choose a topic that resonates with you and delve into it with extensive research, analysis, and critical thinking. Remember to approach the topic with sensitivity and empathy, as cancer affects millions of lives and demands a compassionate approach to understanding and addressing its challenges.

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Cell Phones and Cancer Risk

Why has there been concern that cell phones may cause cancer.

There are two main reasons why people are concerned that cell (or mobile) phones might have the potential to cause certain types of cancer or other health problems: Cell phones emit radiation (in the form of radiofrequency radiation , or radio waves ), and cell phone use is widespread. Even a small increase in cancer risk from cell phones would be of concern given how many people use them.

Brain and central nervous system cancers have been of particular concern because hand-held phones are used close to the head and because ionizing radiation—a higher energy form of radiation than what cell phones emit—has been found to cause some brain cancers. Many different kinds of studies have been carried out to try to investigate whether cell phone use is dangerous to human health.

However, the evidence to date suggests that cell phone use does not cause brain or other kinds of cancer in humans.

Is the radiation from cell phones harmful?

Cell phones emit radiation in the radiofrequency region of the electromagnetic spectrum . Second-, third-, and fourth-generation cell phones (2G, 3G, 4G) emit radiofrequency in the frequency range of 0.7–2.7 GHz. Fifth-generation (5G) cell phones are anticipated to use the frequency spectrum up to 80 GHz. 

These frequencies all fall in the nonionizing range of the spectrum, which is low frequency and low energy. The energy is too low to damage DNA. By contrast, ionizing radiation , which includes x-rays , radon , and cosmic rays, is high frequency and high energy. Energy from ionizing radiation can damage DNA. DNA damage can cause changes to genes that may increase the risk of cancer.

The NCI fact sheet Electromagnetic Fields and Cancer lists sources of radiofrequency radiation . More information about ionizing radiation can be found on the Radiation page.

The human body does absorb energy from devices that emit radiofrequency radiation. The only consistently recognized biological effect of radiofrequency radiation absorption in humans that the general public might encounter is heating to the area of the body where a cell phone is held (e.g., the ear and head). However, that heating is not sufficient to measurably increase core body temperature. There are no other clearly established dangerous health effects on the human body from radiofrequency radiation.

Has the incidence of brain and central nervous system cancers changed during the time cell phone use increased?

No. Investigators have studied whether the incidence of brain or other central nervous system cancers (that is, the number of new cases of these cancers diagnosed each year) has changed during the time that cell phone use increased dramatically. These studies found:

• stable incidence rates for adult gliomas in the United States ( 1 ), Nordic countries ( 2 ) and Australia ( 3 ) during the past several decades
• stable incidence rates for pediatric brain tumors in the United States during 1993–2013 ( 4 )
• stable incidence rates for acoustic neuroma ( 5 ), which are nonmalignant tumors , and meningioma ( 6 ), which are usually nonmalignant, among US adults since 2009 

In addition, studies using cancer incidence data have tested different scenarios (simulations) determining whether the incidence trends are in line with various levels of risk as reported in studies of cell phone use and brain tumors between 1979 and 2008 ( 7 , 8 ). These simulations showed that many risk changes reported in case–control studies  were not consistent with incidence data, implying that biases  and errors in the study may have distorted the findings.

Because these studies examine cancer incidence trends over time in populations rather than comparing risk in people who do and don’t use cell phones, their ability to observe potential small differences in risk among heavy users or susceptible populations is limited. Observational/epidemiologic studies—including case–control and cohort studies  (described below)—are designed to measure individual exposure to cell phone radiation and ascertain specific health outcomes.

How is radiofrequency radiation exposure measured in studies of groups of people?

Epidemiologic  studies use information from several sources, including questionnaires and data from cell phone service providers, to estimate radiofrequency radiation exposure in groups of people. Direct measurements are not yet possible outside of a laboratory setting. Estimates from studies reported to date take into account the following:

• How regularly study participants use cell phones (the number of calls per week or month)
• The age and the year when study participants first used a cell phone and the age and the year of last use (allows calculation of the duration of use and time since the start of use)
• The average number of cell phone calls per day, week, or month (frequency)
• The average length of a typical cell phone call
• The total hours of lifetime use, calculated from the length of typical call times, the frequency of use, and the duration of use

What has research shown about the link between cell phone use and cancer risk?

Researchers have carried out several types of population studies to investigate the possibility of a relationship between cell phone use and the risk of tumors, both malignant (cancerous) and nonmalignant (not cancer). Epidemiologic  studies (also called observational studies ) are research studies in which investigators observe groups of individuals (populations) and collect information about them but do not try to change anything about the groups. 

Two main types of epidemiologic studies— cohort studies  and case–control studies —have been used to examine associations between cell phone use and cancer risk. In a case–control study, cell phone use is compared between people who have tumors and people who don’t. In a cohort study, a large group of people who do not have cancer at the beginning of the study is followed over time and tumor development in people who did and didn’t use cell phones is compared. Cohort studies are limited by the fact that they may only be able to look at cell phone subscribers, who are not necessarily the cell phone users.

The tumors that have been investigated in epidemiologic studies include malignant brain tumors, such as gliomas , as well as nonmalignant tumors, such as acoustic neuroma (tumors in the cells of the nerve responsible for hearing that are also known as vestibular schwannomas), meningiomas (usually nonmalignant tumors in the membranes that cover and protect the brain and spinal cord ), parotid gland tumors (tumors in the salivary glands ), skin cancer, and thyroid gland tumors.

Four large epidemiologic studies have examined the possible association between cell phone use and cancer: Interphone, a case–control study, and three cohort studies, the Danish Study, the Million Women Study, and the Cohort Study on Mobile Phones and Health (COSMOS). The findings of these studies are mixed, but overall, they do not show an association between cell phone use and cancer ( 9 – 23 ).

Interphone Case–Control Study

How the study was done: This is the largest case–control study of cell phone use and the risk of head and neck tumors. It was conducted by a consortium of researchers from 13 countries. The data came from questionnaires that were completed by study participants in Europe, Israel, Canada, Australia, New Zealand, and Japan.

What the study showed: Most published analyses from this study have shown no increases overall in brain or other central nervous system cancers (glioma and meningioma) related to higher amounts of cell phone use. One analysis showed a statistically significant , although small, increase in the risk of glioma among study participants who spent the most total time on cell phone calls. However, for a variety of reasons the researchers considered this finding inconclusive ( 11 – 13 ).

An analysis of data from all 13 countries reported a statistically significant association between intracranial distribution of tumors within the brain and self-reported location of the phone ( 14 ). However, the authors of this study noted that it is not possible to draw firm conclusions about cause and effect based on their findings.

An analysis of data from five Northern European countries showed an increased risk of acoustic neuroma in those who had used a cell phone for 10 or more years ( 15 ). 

In subsequent analyses of Interphone data, investigators investigated whether tumors were more likely to form in areas of the brain with the highest exposure. One analysis showed no relationship between tumor location and level of radiation ( 16 ). However, another found evidence that glioma and, to a lesser extent, meningioma were more likely to develop where exposure was highest ( 17 ).

Danish Cohort Study

How the study was done: This cohort study linked billing information from more than 358,000 cell phone subscribers with brain tumor incidence data from the Danish Cancer Registry.

What the study showed: No association was observed between cell phone use and the incidence of glioma, meningioma, or acoustic neuroma, even among people who had been cell phone subscribers for 13 or more years ( 18 – 20 ).

Million Women Cohort Study

How the study was done: This prospective cohort study conducted in the United Kingdom used data obtained from questionnaires that were completed by study participants.

What the study showed: Self-reported cell phone use was not associated with an increased risk of glioma, meningioma, or non-central nervous system tumors. Although the original published findings reported an association with an increased risk of acoustic neuroma ( 21 ), it was not observed with additional years of follow-up of the cohort ( 22) .

Cohort Study of Mobile Phones and Health (COSMOS)

How the study was done: This large prospective cohort study conducted in Denmark, Finland, Sweden, the Netherlands, and the United Kingdom used data on health, lifestyle, and current and past cell phone use obtained from a questionnaire completed by participants when they joined the study. That information was supplemented with cancer occurrence data obtained from linkage to national cancer registries and cell phone records obtained from mobile network operators. 

What the study showed: Among 264,574 participants with a median follow-up of just over 7 years, the cumulative amount of mobile phone call-time was not associated with the risk of developing glioma, meningioma, or acoustic neuroma ( 23 ). No associations with cancer risk were seen in the heaviest mobile phone users or among among those with the longest history of mobile phone use (15 or more years).

Other Epidemiologic Studies

In addition to these four large studies, other, smaller epidemiologic studies have looked for associations between cell phone use and individual cancers in both adults and children. These include:

• Two NCI-sponsored case–control studies, each conducted in multiple US academic medical centers or hospitals between 1994 and 1998 that used data from questionnaires ( 24) or computer-assisted personal interviews ( 25 ). Neither study showed a relationship between cell phone use and the risk of glioma, meningioma, or acoustic neuroma in adults.
• The CERENAT study, another case–control study conducted in multiple areas in France from 2004 to 2006 using data collected in face-to-face interviews using standardized questionnaires ( 26 ). This study found no association for either gliomas or meningiomas when comparing adults who were regular cell phone users with non-users. However, the heaviest users had significantly increased risks of both gliomas and meningiomas.
• A pooled analysis of two case–control studies conducted in Sweden that reported statistically significant trends of increasing brain cancer risk for the total amount of cell phone use and the years of use among people who began using cell phones before age 20 ( 27 ).
• Another case–control study in Sweden, part of the Interphone pooled studies, did not find an increased risk of brain cancer among long-term cell phone users between the ages of 20 and 69 ( 28 ).
• The CEFALO study, an international case–control study of children diagnosed with brain cancer between ages 7 and 19, found no relationship between their cell phone use and risk for brain cancer ( 29 ).
• The MOBI-Kids study, a large international case–control study of young people ages 10 to 24 years diagnosed with brain tumors, found no evidence of an association between wireless phone use and the risk of brain tumors ( 30 ). 
• A population-based case–control study conducted in Connecticut found no association between cell phone use and the risk of thyroid cancer ( 31 ).

What are the findings from studies of the human body?

Researchers have carried out several kinds of studies to investigate possible effects of cell phone use on the human body. In 2011, two small studies were published that examined brain glucose metabolism in people after they had used cell phones. The results were inconsistent. One study showed increased glucose metabolism in the region of the brain close to the antenna compared with tissues on the opposite side of the brain ( 32 ); the other study ( 33 ) found reduced glucose metabolism on the side of the brain where the phone was used.

The authors of these studies noted that the results were preliminary and that possible health outcomes from changes in glucose metabolism in humans were unknown. Such inconsistent findings are not uncommon in experimental studies of the physiological effects of radiofrequency electromagnetic radiation in people ( 11 ). Some factors that can contribute to inconsistencies across such studies include assumptions used to estimate doses, failure to consider temperature effects, and investigators not being blinded to exposure status.

Another study investigated blood flow in the brain of people exposed to radiofrequency radiation from cell phones and found no evidence of an effect on blood flow in the brain ( 34 ).

What are the findings from experiments in laboratory animals?

Early studies involving laboratory animals showed no evidence that radiofrequency radiation increased cancer risk or enhanced the cancer-causing effects of known chemical carcinogens ( 35 – 38 ).

Because of inconsistent findings from epidemiologic studies in humans and the lack of clear data from previous experimental studies in animals, in 1999 the Food and Drug Administration (FDA) nominated radiofrequency radiation exposure associated with cell phone exposures for study in animal models by the US National Toxicology Program (NTP). NTP is an interagency program that coordinates toxicology research and testing across the US Department of Health and Human Services and is headquartered at the National Institute of Environmental Health Sciences, part of NIH.

The NTP studied radiofrequency radiation (2G and 3G frequencies) in rats and mice ( 39 , 40 ). This large project was conducted in highly specialized labs. The rodents experienced whole-body exposures of 3, 6, or 9 watts per kilogram of body weight for 5 or 7 days per week for 18 hours per day in cycles of 10 minutes on, 10 minutes off. A research overview of the rodent studies , with links to the peer-review summary, is available on the NTP website. The primary outcomes observed were a small number of cancers of Schwann cells  in the heart and non-cancerous changes ( hyperplasia ) in the same tissues for male rats, but not female rats, nor in mice overall.

These experimental findings raise new questions because cancers in the heart are extremely rare in humans. Schwann cells of the heart in rodents are similar to the kind of cells in humans that give rise to acoustic neuromas (also known as vestibular schwannomas), which some studies have suggested are increased in people who reported the heaviest use of cell phones. The NTP plans to continue to study radiofrequency exposure in animal models to provide insights into the biological changes that might explain the outcomes observed in their study.

Another animal study, in which rats were exposed 7 days per week for 19 hours per day to radiofrequency radiation at 0.001, 0.03, and 0.1 watts per kilogram of body weight was reported by investigators at the Italian Ramazzini Institute ( 41 ). Among the rats with the highest exposure levels, the researchers noted an increase in heart schwannomas in male rats and nonmalignant Schwann cell growth in the heart in male and female rats. However, key details necessary for interpretation of the results were missing: exposure methods, other standard operating procedures, and nutritional/feeding aspects. The gaps in the report from the study raise questions that have not been resolved.

ICNIRP (an independent nonprofit organization that provides scientific advice and guidance on the health and environmental effects of nonionizing radiation) critically evaluated both studies. It concluded that both followed good laboratory practice, including using more animals than earlier research and exposing the animals to radiofrequency radiation throughout their lifetimes. However, it also identified what it considered major weaknesses in how the studies were conducted and statistically analyzed and concluded that these limitations prevent drawing conclusions about the ability of radiofrequency exposures to cause cancer ( 42 ).

Why are the findings from different studies of cell phone use and cancer risk inconsistent?

A few studies have shown some evidence of statistical association of cell phone use and brain tumor risks in humans, but most studies have found no association. Reasons for these discrepancies include the following:

• Recall bias , which can occur when data about prior habits and exposures are collected from study participants using questionnaires administered after diagnosis of a disease in some of the participants. Study participants who have brain tumors, for example, may remember their cell phone use differently from individuals without brain tumors.
• Inaccurate reporting , which can happen when people say that something has happened more often or less often than it actually did. For example, people may not remember how much they used cell phones in a given time period.
• Morbidity and mortality among study participants who have brain cancer. Gliomas are particularly difficult to study because of their high death rate and the short survival of people who develop these tumors. Patients who survive initial treatment are often impaired, which may affect their responses to questions.
• Participation bias , which can happen when people who are diagnosed with brain tumors are more likely than healthy people (known as controls) to enroll in a research study.
• Changing technology. Older studies evaluated radiofrequency radiation exposure from analog cell phones. Today, cell phones use digital technology, which operates at a different frequency and a lower power level than analog phones, and cellular technology continues to change ( 43 ). 
• Exposure assessment limitations. Different studies measure exposure differently, which makes it difficult to compare the results of different studies ( 44 ). Investigations of sources and levels of exposure, particularly in children, are ongoing ( 45 ).
• Insufficient follow-up of highly exposed populations. It may take a very long time to develop symptoms after exposure to radiofrequency radiation, and current studies may not yet have followed participants long enough.
• Inadequate statistical power and methods to detect very small risks or risks that affect small subgroups of people specifically 
• Chance as an explanation of apparent effects may not have been considered.

What are other possible health effects from cell phone use?

The most consistent health risk associated with cell phone use is distracted driving and vehicle accidents ( 46 , 47 ). Several other potential health effects have been reported with cell phone use. Neurologic effects are of particular concern in young persons. However, studies of memory, learning, and cognitive function have generally produced inconsistent results ( 48 – 51 ).

What have expert organizations said about the cancer risk from cell phone use?

In 2011, the International Agency for Research on Cancer (IARC) , a component of the World Health Organization, appointed an expert working group to review all available evidence on the use of cell phones. The working group classified cell phone use as “possibly carcinogenic to humans,” based on limited evidence from human studies, limited evidence from studies of radiofrequency radiation and cancer in rodents, and inconsistent evidence from mechanistic studies ( 11 ).

The working group indicated that, although the human studies were susceptible to bias, the findings could not be dismissed as reflecting bias alone, and that a causal interpretation could not be excluded. The working group noted that any interpretation of the evidence should also consider that the observed associations could reflect chance, bias, or confounding variables rather than an underlying causal effect. In addition, the working group stated that the investigation of brain cancer risk associated with cell phone use poses complex research challenges.

The American Cancer Society’s cell phones page states “It is not clear at this time that RF (radiofrequency) waves from cell phones cause dangerous health effects in people, but studies now being done should give a clearer picture of the possible health effects in the future.” 

The National Institute of Environmental Health Sciences (NIEHS) states that the weight of the current scientific evidence has not conclusively linked cell phone use with any adverse health problems, but more research is needed.

The US Food and Drug Administration (FDA) notes that studies reporting biological changes associated with radiofrequency radiation have failed to be replicated and that the majority of human epidemiologic studies have failed to show a relationship between exposure to radiofrequency radiation from cell phones and health problems. FDA, which originally nominated this exposure for review by the NTP in 1999, issued a statement on the draft NTP reports released in February 2018, saying “based on this current information, we believe the current safety limits for cell phones are acceptable for protecting the public health.” FDA and the Federal Communications Commission (FCC) share responsibility for regulating cell phone technologies.

The US Centers for Disease Control and Prevention (CDC) states that no scientific evidence definitively answers whether cell phone use causes cancer.

The Federal Communications Commission (FCC) concludes that currently no scientific evidence establishes a definite link between wireless device use and cancer or other illnesses.

In 2015, the European Commission Scientific Committee on Emerging and Newly Identified Health Risks concluded that, overall, the epidemiologic studies on cell phone radiofrequency electromagnetic radiation exposure do not show an increased risk of brain tumors or of other cancers of the head and neck region ( 9 ). The committee also stated that epidemiologic studies do not indicate increased risk for other malignant diseases, including childhood cancer ( 9 ).

Has radiofrequency radiation from cell phone use been associated with cancer risk in children?

There are theoretical considerations as to why the potential health effects of cell phone use should be investigated separately in children. Their nervous systems are still developing and, therefore, more vulnerable to factors that may cause cancer. Their heads are smaller than those of adults and consequently have a greater proportional exposure to radiation emitted by cell phones. And, children have the potential of accumulating more years of cell phone exposure than adults.

Thus far, the data from studies of children with cancer do not suggest that children are at increased risk of developing cancer from cell phone use. The first published analysis came from a large case–control study called CEFALO, which was conducted in Europe. The study included 352 children who were diagnosed with brain tumors between 2004 and 2008 at the ages of 7 to 19 years. They were matched by age, sex, and geographical region with 646 young people randomly selected from population registries. Researchers did not find an association between cell phone use and brain tumor risk by amount of use or by the location of the tumor ( 29 ).

The largest case–control study among children, a 14-country study known as MOBI-Kids, included 899 young people ages 10 to 24 years who were diagnosed with brain tumors between 2010 and 2015. They were matched by sex, age, and region with 1,910 young people who were undergoing surgery for appendicitis. Researchers found no evidence of an association between wireless phone use and brain tumors in young people ( 30 ).

Which US federal agencies have a role in evaluating the effects of or regulating cell phones?

The National Institutes of Health (NIH), including the National Cancer Institute (NCI), conducts research on cell phone use and the risks of cancer and other diseases.

FDA and FCC share regulatory responsibilities for cell phones. FDA is responsible for testing and evaluating electronic product radiation and providing information for the public about the radiofrequency energy emitted by cell phones. FCC sets limits on the emissions of radiofrequency energy by cell phones and similar wireless products.

Where can I find more information about radiofrequency radiation from my cell phone?

The dose of the energy that people absorb from any source of radiation is estimated using a measure called the specific absorption rate (SAR), which is expressed in watts per kilogram of body weight ( 52 ). The SAR decreases very quickly as the distance to the exposure source increases. For cell phone users who hold their phones next to their head during voice calls, the highest exposure is to the brain, acoustic nerve, salivary gland, and thyroid.

The FCC provides information about the SAR of cell phones produced and marketed within the previous 1 to 2 years. Consumers can access this information using the phone’s FCC ID number, which is usually located on the case of the phone, and the FCC’s ID search form . SARs for older phones can be found by checking the phone settings or by contacting the manufacturer.

What can cell phone users do to reduce their exposure to radiofrequency radiation?

FDA has suggested some steps that concerned cell phone users can take to reduce their exposure to radiofrequency radiation :

• Reduce the amount of time spent using your cell phone.
• Use speaker mode, head phones, or ear buds to place more distance between your head and the cell phone.
• Avoid making calls when the signal is weak as this causes cell phones to boost RF transmission power.
• Consider texting rather than talking, but don’t text while you are driving. 

Use of wired or wireless headsets reduces the amount of radiofrequency radiation exposure to the head because the phone is not placed against the head ( 53 ). Exposures decline dramatically when cell phones are used hands-free. For example, wireless (Bluetooth) devices (such as headphones and earbuds) use short-range signals that typically transmit radiofrequency waves at power levels 10–400 times lower than cell phones ( 54 ).

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What to know about cancer

Cancer causes cells to divide uncontrollably. This can result in tumors, damage to the immune system, and other impairment that can be fatal.

Cancer can affect various parts of the body, such as the breasts, lungs, prostate, and skin.

In this article, we examine types of cancer, how the disease develops, and how doctors may treat it. We also explore different types of cancer and disease outlook. Finally, we answer some common questions about cancer.

Cancer resources

To discover more evidence-based information and resources for cancer, visit our dedicated hub .

What is cancer?

Cancer is a broad term. It describes the disease that results when cellular changes cause the uncontrolled growth and division of cells .

Some types of cancer cause rapid cell growth, while others cause cells to grow and divide at a slower rate.

Certain forms of cancer result in visible growths called tumors , while others, such as leukemia , do not.

Most of the body’s cells have specific functions and fixed lifespans. Cell death is part of a natural and beneficial phenomenon, which healthcare professionals call apoptosis.

A cell receives instructions to die so that the body can replace it with a newer cell that functions better. Cancerous cells lack the components that instruct them to stop dividing and to die.

As a result, they build up in the body, using oxygen and nutrients that would usually nourish other cells. Cancerous cells can form tumors, impair the immune system and cause other changes that prevent the body from functioning regularly.

Cancerous cells may appear in one area, then spread via the lymph nodes . These are clusters of immune cells located throughout the body.

There are many causes of cancer, and some are preventable.

Risk factors

Preventable risk factors for cancer include :

• heavy alcohol consumption
• excess body weight
• physical inactivity
• poor nutrition
• human papillomavirus infection

Other risk factors for cancer are not preventable. Currently, the most significant unpreventable risk factor is age. According to the American Cancer Society (ACS), doctors in the United States diagnose 88% of cancer cases in people ages 50 years or older.

Is cancer genetic?

Genetic factors can contribute to the development of cancer.

A person’s genetic code tells their cells when to divide and expire. Changes in the genes can lead to faulty instructions, and cancer can result.

Genes also influence the cells’ production of proteins, and proteins carry many of the instructions for cellular growth and division.

Some genes change proteins that would usually repair damaged cells. This can lead to a predisposition for cancer. If a parent has these genes, they may pass on the altered instructions to their offspring. A doctor may refer to this as an inherited gene mutation. These mutations may contribute to the development of up to 10% of cancer cases.

Some genetic mutations that increase the risk of developing cancer occur after birth. Healthcare professionals refer to these changes as “acquired gene mutations”. Possible causes include smoking and sun exposure. These genetic changes cause cancer more commonly than inherited gene mutations.

Other changes that can result in cancer take place in the chemical signals that determine how the cells turn specific genes on and off. Doctors may call these “epigenetic changes”.

Doctors usually prescribe treatments based on the type of cancer, its stage at diagnosis, and the person’s overall health.

Some examples of cancer treatment include :

• Chemotherapy aims to kill cancerous cells with medications that target rapidly dividing cells. The drugs can also help shrink tumors, but the side effects can be severe.
• Hormone therapy involves taking medications that change how certain hormones work or interfere with the body’s ability to produce them. When hormones play a significant role, as with prostate and breast cancers , this is a common approach.
• Immunotherapy uses medications and other treatments to boost the immune system and encourage it to fight cancerous cells.
• Radiation therapy uses high-dose radiation to kill cancerous cells. Also, a doctor may recommend using radiation to shrink a tumor before surgery or reduce tumor-related symptoms.
• Stem cell transplant can be especially beneficial for people with blood-related cancers, such as leukemia or lymphoma . It involves removing cells, such as red or white blood cells , that chemotherapy or radiation has destroyed. Lab technicians then strengthen the cells and put them back into the body.
• Surgery is often a part of a treatment plan when a person has a cancerous tumor. Also, a surgeon may remove lymph nodes to reduce or prevent the disease’s spread.
• Targeted therapies perform functions within cancerous cells to prevent them from multiplying. They can also boost the immune system. Two examples of these therapies are small-molecule drugs and monoclonal antibodies.

Doctors will often employ more than one type of treatment to maximize effectiveness.

The most common type of cancer in the U.S. is breast cancer, followed by lung and prostate cancers, according to the National Cancer Institute, which excluded nonmelanoma skin cancers from these findings.

Each year, more than 40,000 people in the country receive a diagnosis of one of the following types of cancer:

• colon and rectal
• endometrial
• non-Hodgkin’s lymphoma

Other forms are less common. According to the National Cancer Institute, there are over 100 types of cancer.

Cancer development and cell division

Doctors classify cancer by its location in the body and the tissues that it forms in.

For example, sarcomas develop in bones or soft tissues, while carcinomas form in cells that cover internal or external surfaces in the body. Basal cell carcinomas develop in the skin, while adenocarcinomas can form in the glands.

When cancerous cells spread to other parts of the body, the medical term for this is metastasis.

A person can also have more than one type of cancer at a time.

Improvements in cancer detection, increased awareness of the risks of smoking, and a drop in tobacco use have all contributed to a year-on-year decrease in the number of cancer diagnoses and deaths.

According to the ACS, the overall cancer death rate declined by 33% between 1991 and 2020.

When a person has cancer, their outlook will depend on whether the disease has spread and on its type, severity, and location.

Frequently asked questions

Below are some common questions and answers about cancer.

How do I recognize cancer before it starts to cause serious health problems?

Some cancers cause early symptoms, but others do not exhibit symptoms until they are more advanced. Many of these symptoms are often from causes unrelated to cancer.

The best way to identify cancer early is to report any unusual, persistent symptoms to a doctor so they can offer advice about any further testing that may be needed.

Can people with cancer live a long life?

Each individual’s outlook varies depending on the type of cancer they have and other factors, such as their overall health and whether the disease has spread.

However, the ACS indicates that the overall cancer death rate has declined by 33% between 1991 and 2020.

How long can someone live with cancer without knowing?

Some types of cancer do not cause symptoms in the early stages. Therefore, a person may not know they are living with the disease until it reaches more advanced stages.

For example, research indicates that carcinoid tumors may not present with any symptoms for years .

Cancer causes cells to divide uncontrollably. It also prevents them from dying at the natural point in their life cycle.

Genetic factors and lifestyle choices, such as smoking, can contribute to the development of the disease. Several elements affect the ways that DNA communicates with cells and directs their division and death.

After nonmelanoma skin cancer, breast cancer is the most common type in the U.S.

Treatments are constantly improving. Examples of current methods include chemotherapy, radiation therapy, and surgery. Some people benefit from newer options, such as stem cell transplantation and precision medicine.

The diagnosis and death rates of cancer are dropping yearly.

Last medically reviewed on January 24, 2024

• Cancer / Oncology

How we reviewed this article:

• About cancer. (n.d.). https://www.cancer.gov/about-cancer
• All about cancer. (n.d.). https://www.cancer.org/cancer.html
• Cancer facts & figures 2023. (2023). https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2023/2023-cancer-facts-and-figures.pdf
• Cingam SR, et al. (2022). Carcinoid tumors. https://www.ncbi.nlm.nih.gov/books/NBK448101/
• Common cancer types. (2018). https://www.cancer.gov/types/common-cancers
• Risk factors and cancer. (2023). https://www.cdc.gov/cancer/risk_factors.htm

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Can cancer be prevented?

Not all cancers can be prevented but there are things you can do to reduce your risk.

These include not smoking and keeping a healthy weight.

The world around us can make being healthy hard, and this can affect some people more than others. We need the government to help make it easier for us all. 

How can making healthy changes reduce my cancer risk?

A person’s risk of cancer depends on many different things. Research shows that things like stopping smoking and keeping a healthy weight can reduce the risk of cancer. By making healthy changes now, you can make a difference to your health in the future.

Use this page to explore six things that can reduce cancer risk.

And remember, you can also talk to your doctor if you’re worried about your cancer risk.

Can I make sure I don’t get cancer?

No, but making healthy changes does help reduce the risk.  There are some things we can’t change that increase the risk of cancer. These include things like getting older and a family history of cancer. 

The world around us also affects how healthy we are. There are some things we can do to help us form healthy habits. But we also need the government to help make it easier for everyone to be healthy.

4_in_10_infographic.jpg

Not smoking

Not smoking is the best thing you can do to reduce your risk of cancer.  Harmful chemicals in cigarette smoke affect the entire body, not just our lungs. If you smoke, the best thing you can do for your health is quit.

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Keep a healthy weight

Being a healthy weight has lots of health benefits, including reducing the risk of cancer. But the world around us can make this difficult, which is why the government needs to help too.

Have a healthy balanced diet

Having healthy food and drink can reduce your risk of cancer. Aim to have plenty of fruit and vegetables, wholegrain foods high in fibre and healthy proteins. Cut down on processed and red meat, alcohol and high calorie foods and drinks.

healthy-balanced-meal-plate-digital-social1_1_final_-_copy.png

Enjoy the sun safely

Being safe in the sun reduces the risk of skin cancer. Too much UV radiation from the sun or sunbeds damages our skin cells. When the sun is strong, take extra care to protect your skin- spend time in the shade, cover up with clothing, and use sunscreen.

sun_safety_screen1.png

Cut back on alcohol

The HPV Vaccine

The HPV vaccine is offered for free to children aged 11-13, and some other groups. It helps protect against HPV infection, reducing the risk of some types of cancer. The vaccine has been proven to be safe and effective.  

How does cancer start?

DNA is a set of instructions inside our cells that tells them how to behave. Cancer is caused by damage to our DNA that has built up over time.

Some things can increase the chances of this, such as UV rays from the sun and drinking alcohol.

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The Unique Hell of Getting Cancer as a Young Adult

W hen I got diagnosed with Stage 3b Hodgkin Lymphoma at age 32, it was almost impossible to process. Without a family history or lifestyle risk factors that put cancer on my radar, I stared at the emergency room doctor in utter disbelief when he said the CT scan of my swollen lymph node showed what appeared to be cancer—and lots of it. A few days away from a bucket list trip to Japan, I’d only gone to the emergency room because the antibiotics CityMD prescribed to me when I was sick weren’t working.I didn’t want to be sick in a foreign country. So when the doctor told me of my diagnosis, the  only question I could conjure was: “So Tokyo is a no-go?”

Around the world, cancer rates in people under 50 are surging, with a recent study in BMJ Oncology showing that new cases for young adults have risen 79% overall over the past three decades. In the U.S. alone, new cancer diagnoses in people under 50 hit 3.26 million, with the most common types being breast, windpipe, lung, bowel, and stomach. A new feature in the Wall Street Journal highlights the mad dash among doctors and researchers to determine what’s causing this troubling rise. Strangely, overall cancer rates in the U.S. have dropped over the past three decades, while young people—particularly with colorectal cancers—are increasingly diagnosed at late stages. “We need to make it easier for adolescents and young adults to participate in clinical trials to improve outcomes and study the factors contributing to earlier onset cancers so we can develop new cures,” says Julia Glade Bender, MD, co-lead of the Stuart Center for Adolescent and Young Adult (AYA) Cancers at Memorial Sloan Kettering in New York City (where I am currently a patient.)

Doctors suspect that lifestyle factors and environmental elements, from microplastics to ultra-processed foods, could be to blame. But many adults in their 20s and 30s, such as myself, were otherwise healthy before their diagnoses. It felt like all those years of forcing myself to run, eat high-fiber foods, and choke down kombucha were for nothing. 

Cancer is hell at any age, but the challenges facing young adults are especially steep, as the disease disrupts a formative period for building a career, family, and even healthy self-esteem, from body image to gender identity. It’s critical that our approach to treating and supporting these patients reflects the severity of this disruption. In recent years, a growing number of cancer hospitals have developed young adult-specific programming like support groups, information sessions on dating and sexual health, and even mobile apps to help counter social alienation. But there is still a long way to go.

Read more: Why I Stopped Being A “Good” Cancer Patient

Shockingly enough, canceling my trip to Japan was the least of my worries. Beyond the excruciating physical side effects of high-dose chemotherapy and a number of life-threatening complications, cancer pulverized my self-esteem into nothingness, as I watched peers get married and promoted from my bed. Thankfully, after switching to a new hospital, I found support groups that connected me with a community of peers who got it, as well as social workers who work exclusively with young adults and thus recognized many of my biggest challenges, like social isolation, financial strain, the dating nightmare, and hating my bald head.

Perhaps the biggest reason I resented cancer was for disrupting a milestone I’d worked for my whole life: a book launch. (My diagnosis came two months before my first book was published.) Young adulthood is meant to be littered with these kinds of professional and personal benchmarks, many of which are hard enough to accomplish without tumors; dating, for instance, is impossible for me even as a healthy person. Now I have to re-enter the pool older, weaker, and more traumatized? 

“Young adult patients may be trying to assert independence from parents, establish a career or intimate relationship, or even be parents themselves,” says Bender. “Most will be naïve to the medical system or a serious health condition.” And so they require flexible, creative clinicians who can help navigate them “to and through the best available therapy and back to their lives, inevitably ‘changed’ but intact.” Not only do these patients need specialized psychosocial support, but research initiatives should prioritize developing treatments that minimize long-term toxicities.

Given that many young patients haven’t yet built financial stability and are often in some form of debt, organizations like Young Adults Survivors United (YASU) have emerged to support young adult survivors and patients through the financial overwhelm. Stephanie Samolovitch, MSW and founder of YASU, says that there’s still an enormous need for resources supporting young adult cancer patients and survivors.

“Cancer causes a young adult to be dependent again, whether it’s moving back in with parents, getting rides to appointments, or asking for financial help,” says Samolovitch, who was diagnosed with leukemia in 2005, two weeks before her 20th birthday. “Young adults never expect to apply for Medicaid or Social Security Disability during our twenties or thirties, yet cancer doesn't give us a choice sometimes. That causes stress, shame, depression, and anxiety when trying to navigate the healthcare system.”

Read more: How to Create an Action Plan After a Cancer Diagnosis

When Ana Calderone, a 33-year-old magazine editor, was diagnosed with stage 2 breast cancer at 30, the most challenging part of getting diagnosed so young was “everything.”

“I felt like it set my whole life back, which sounds stupid because I was literally fighting for my life,” she says. “Who cares if I had to delay my wedding a year because I was still getting radiation treatment? But it was really hard at the time. Everything was delayed, and still is.”

During chemo, Calderone’s doctors gave her a shot that she still receives to try and preserve her ovaries, and she’s been able to try IVF twice. She says she had to proactively advocate for those things with her care team. While Calderone is currently cancer free, she still must take medication that has further delayed her plans to build a family. “I’m fairly confident I’d have a child by now if I didn’t get cancer. That’s been the most devastating part,” she says. “My oncologist would consider letting me get pregnant in two more years, which would be 4.5 years post-diagnosis, and even that is still a risk.”

For 32-year-old Megan Koehler, whose son was one and a half when she was diagnosed with Hodgkin Lymphoma, the hardest part “was knowing the world continued on while I spent days in bed,” she says. “My coworkers still worked on projects I was supposed to be part of, and the worst was knowing my son was growing up, learning to speak sentences, and just becoming a toddler without me – or so it felt that way.” 

She remembers crying for most of his second birthday because she was in bed post chemo, feeling devastated that she didn’t have the energy to spend the day with him. During a 50-plus day hospital stay caused by an adverse reaction to a chemotherapy drug, she would Facetime him and cry when he spoke in sentences, because he wasn’t doing that before she was admitted. While she’s grateful for the support she had from her husband and mother, she felt alienated. “I spoke to a few people my age via social media, but no one in person. My center mostly catered to the older generations, so it was somewhat isolating. I did have a great relationship with a few of the infusion nurses who were around my age.”

While oncologists may be rightly focused on saving patients’ lives, there must be more consideration for quality of life during and after treatment – both physical and mental. “More questions need to be asked about their relationships, fertility options, and any mental health concerns or symptoms,” says Samolovitch. From a research perspective, initiatives must expand to pinpoint not only the reason for the rise of cancer in young adults, but find ways to screen and diagnose earlier.

Towards the beginning of my treatment, before I switched hospitals, my oncologist seemed to treat my concerns about self-esteem and hair loss as trivial compared to the real work of saving my life. At my weakest, I had to advocate repeatedly to get accurate information on cold capping, a process of scalp cooling that can preserve most of your hair during chemotherapy, and I had to beg again and again for a social worker to reach out to me, which took weeks. 

It’s a beautiful thing that more young adults with cancer are surviving their illnesses. But that means they’ll have decades of life ahead of them. Providers must do a better job supporting young adult patients through all the collateral damage that comes with cancer and its treatment.  

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Cancer prevention: 7 tips to reduce your risk

Concerned about cancer prevention? Take charge by making changes such as eating a healthy diet and getting regular screenings.

How do people lower the chances of getting cancer? There's plenty of advice. But at times, advice from one study goes against the advice from another.

Cancer prevention information continues to develop. However, it's well accepted that lifestyle choices affect the chances of getting cancer.

Consider these lifestyle tips to help prevent cancer.

1. Don't use tobacco

Smoking has been linked to many types of cancer, including cancer of the lung, mouth, throat, voice box, pancreas, bladder, cervix and kidney. Even being around secondhand smoke might increase the risk of lung cancer.

But it's not only smoking that's harmful. Chewing tobacco has been linked to cancer of the mouth, throat and pancreas.

Staying away from tobacco — or deciding to stop using it — is an important way to help prevent cancer. For help quitting tobacco, ask a health care provider about stop-smoking products and other ways of quitting.

2. Eat a healthy diet

Although eating healthy foods can't ensure cancer prevention, it might reduce the risk. Consider the following:

• Eat plenty of fruits and vegetables. Base your diet on fruits, vegetables and other foods from plant sources — such as whole grains and beans. Eat lighter and leaner by choosing fewer high-calorie foods. Limit refined sugars and fat from animal sources.
• Drink alcohol only in moderation, if at all. Alcohol increases the risk of various types of cancer, including cancer of the breast, colon, lung, kidney and liver. Drinking more increases the risk.
• Limit processed meats. Eating processed meat often can slightly increase the risk of certain types of cancer. This news comes from a report from the International Agency for Research on Cancer, the cancer agency of the World Health Organization.

People who eat a Mediterranean diet that includes extra-virgin olive oil and mixed nuts might have a reduced risk of breast cancer. The Mediterranean diet focuses mostly on plant-based foods, such as fruits and vegetables, whole grains, legumes and nuts. People who follow the Mediterranean diet choose healthy fats, such as olive oil, over butter. They eat fish instead of red meat.

3. Maintain a healthy weight and be physically active

Being at a healthy weight might lower the risk of some types of cancer. These include cancer of the breast, prostate, lung, colon and kidney.

Physical activity counts too. Besides helping control weight, physical activity on its own might lower the risk of breast cancer and colon cancer.

Doing any amount of physical activity benefits health. But for the most benefit, strive for at least 150 minutes a week of moderate aerobic activity or 75 minutes a week of hard aerobic activity.

You can combine moderate and hard activity. As a general goal, include at least 30 minutes of physical activity in your daily routine. More is better.

4. Protect yourself from the sun

Skin cancer is one of the most common kinds of cancer and one of the most preventable. Try these tips:

• Avoid midday sun. Stay out of the sun between 10 a.m. and 4 p.m. when the sun's rays are strongest.
• Stay in the shade. When outdoors, stay in the shade as much as possible. Sunglasses and a broad-brimmed hat help too.
• Cover your skin. Wear clothing that covers as much skin as possible. Wear a head cover and sunglasses. Wear bright or dark colors. They reflect more of the sun's harmful rays than do pastels or bleached cotton.
• Don't skimp on sunscreen. Use a broad-spectrum sunscreen with an SPF of at least 30, even on cloudy days. Apply a lot of sunscreen. Apply again every two hours, or more often after swimming or sweating.
• Don't use tanning beds or sunlamps. These can do as much harm as sunlight.

5. Get vaccinated

Protecting against certain viral infections can help protect against cancer. Talk to a health care provider about getting vaccinated against:

Hepatitis B. Hepatitis B can increase the risk of developing liver cancer. Adults at high risk of getting hepatitis B are people who have sex with more than one partner, people who have one sexual partner who has sex with others, and people with sexually transmitted infections.

Others at high risk are people who inject illegal drugs, men who have sex with men, and health care or public safety workers who might have contact with infected blood or body fluids.

• Human papillomavirus (HPV). HPV is a sexually transmitted virus that can lead to cervical cancer and other genital cancers as well as squamous cell cancers of the head and neck. The HPV vaccine is recommended for girls and boys ages 11 and 12. The U.S. Food and Drug Administration recently approved the use of the vaccine Gardasil 9 for males and females ages 9 to 45.

6. Avoid risky behaviors

Another effective cancer prevention tactic is to avoid risky behaviors that can lead to infections that, in turn, might increase the risk of cancer. For example:

Practice safe sex. Limit the number of sexual partners and use a condom. The greater the number of sexual partners in a lifetime, the greater the chances of getting a sexually transmitted infection, such as HIV or HPV .

People who have HIV or AIDS have a higher risk of cancer of the anus, liver and lung. HPV is most often associated with cervical cancer, but it might also increase the risk of cancer of the anus, penis, throat, vulva and vagina.

• Don't share needles. Injecting drugs with shared needles can lead to HIV, as well as hepatitis B and hepatitis C — which can increase the risk of liver cancer. If you're concerned about drug misuse or addiction, seek professional help.

7. Get regular medical care

Doing regular self-exams and having screenings for cancers — such as cancer of the skin, colon, cervix and breast — can raise the chances of finding cancer early. That's when treatment is most likely to succeed. Ask a health care provider about the best cancer screening schedule for you.

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• Cancer prevention overview (PDQ) — Patient version. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/patient-prevention-overview-pdq. Accessed Oct. 24, 2022.
• Lewandowska AM, et al. Cancer prevention — Review paper. Annals of Agriculture and Environmental Medicine. 2021; doi:10.26444/aaem/116906.
• Colditz GA. Overview of cancer prevention. https://www.uptodate.com/contents/search. Accessed Oct. 24, 2022.
• Fletcher GS. Evidence-based approach to prevention. https://www.uptodate.com/contents/search. Accessed Oct. 24, 2022.
• Patel AV, et al. American College of Sports Medicine roundtable report on physical activity, sedentary behavior and cancer prevention and control. Medicine & Science in Sports & Exercise. 2019; doi:10.1249/MSS.0000000000002117.
• Health risks of smokeless tobacco. American Cancer Society. https://www.cancer.org/cancer/cancer-causes/tobacco-and-cancer/smokeless-tobacco.html. Accessed Oct. 24, 2022.
• Diet and physical activity: What's the cancer connection? American Cancer Society. https://www.cancer.org/cancer/cancer-causes/diet-physical-activity/diet-and-physical-activity.html. Accessed Oct. 24, 2022.
• Physical activity and cancer. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/physical-activity-fact-sheet. Accessed Oct. 24, 2022.
• HPV vaccines. American Cancer Society. https://www.cancer.org/cancer/cancer-causes/infectious-agents/hpv/hpv-vaccines.html. Accessed Oct. 24, 2022.
• How do I protect myself from ultraviolet (UV) rays? American Cancer Society. https://www.cancer.org/healthy/be-safe-in-sun/uv-protection.html. Accessed Oct. 24, 2022.
• Recommended vaccines for healthcare workers. Centers for Disease Control and Prevention. https://www.cdc.gov/vaccines/adults/rec-vac/hcw.html. Accessed Oct. 24, 2022.
• Cancers caused by HPV. Centers for Disease Control and Prevention. https://www.cdc.gov/hpv/parents/cancer.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fhpv%2Fcancer.html. Accessed Oct. 24, 2022.
• HIV infection and cancer risk. American Cancer Society. https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hiv-fact-sheet. Accessed Oct. 24, 2022.
• IARC Working Group on the Evaluation of Carcinogenic Risk to Humans. Vol. 114: Red meat and processed meat. In: IARC Monographs on the Evaluation of Carcinogenic Risk to Humans. Lyon, France: International Agency for Research on Cancer; 2018. https://monographs.iarc.fr/monographs-and-supplements-available-online/. Accessed Nov. 4, 2018.
• FDA approves expanded use of Gardasil 9 to include individuals 27 through 45 years old. U.S. Food and Drug Administration. https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm622715.htm. Accessed Oct. 24, 2022.

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Cellular (Cell) Phones

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How do cell phones work?

How are people exposed, cell phone specific absorption rate (sar), do cell phones cause tumors, how can i lower my exposure to rf waves from cell phones, are phones on 5g networks any different, what about cordless phones.

• What about Bluetooth® devices (including earbuds)?

Cellular (cell or mobile) phones first became widely available in the United States in the 1990s. Since then, along with the large and still growing number of cell phone users (both adults and children), the amount of time people spend on their phones has also risen sharply.

Cell phones give off a form of energy known as radiofrequency (RF) waves , so the safety of cell phone use has raised some concerns. The main concerns have focused on whether cell phones might increase the risk of brain tumors or other tumors in the head and neck area, as these areas are closest to where the phone is usually held while talking or listening on a call.

Cell phones send signals to (and receive them from) nearby cell towers (base stations) using RF waves. This is a form of energy in the electromagnetic spectrum that falls between FM radio waves and microwaves. Like FM radio waves, microwaves, visible light, and heat, RF waves are a form of non-ionizing radiation . They don’t have enough energy to cause cancer by directly damaging the DNA (genes) inside cells. RF waves are different from stronger ( ionizing ) types of radiation such as x-rays, gamma rays , and ultraviolet (UV) rays . Ionizing radiation can break the chemical bonds in DNA, which might lead to cancer.

The electromagnetic spectrum illustration shows the possible frequencies of electromagnetic energy, ranging from extremely low frequencies (such as those from power lines) to exposures from extremely high frequencies (x-rays and gamma rays), and includes both non-ionizing and ionizing radiation.

At very high levels, RF waves can heat up body tissues. But the levels of energy given off by cell phones are much lower, and are not enough to raise temperatures in the body.

The RF waves come from the cell phone's antenna, which is part of the body of a hand-held phone. The waves are strongest at the antenna and lose energy quickly as they travel away from the phone. The phone is often held against the head when a person is on a call. The closer the antenna is to a user's head, the greater their expected exposure to RF waves. The body tissues closest to the phone absorb more energy from RF waves than tissues farther away.

Many factors can affect the amount of energy from RF waves that a person is exposed to, including:

• The amount of time the person is on the phone.
• Whether the person is holding the phone close to the head, or is instead using the speaker mode or a hands-free device. The farther away from a person's body the phone is, the less they are exposed.
• The distance and path to the nearest cell phone tower. Cell phones adjust their power to use the minimum amount for a good signal. Being farther away from the tower requires more energy to get a good signal, as does being inside a building.
• The amount of cell phone traffic in the area at the time. Higher traffic (from many people using cell phones) may require more energy to get a good signal.
• The model of phone being used. Different phones give off different amounts of energy.

The specific absorption rate (SAR) is the amount of RF energy from the phone absorbed by the user’s body. Different cell phones have different SAR levels. Cell phone makers are required to report the maximum SAR level of their product to the US Federal Communications Commission (FCC). This information can often be found on the manufacturer’s website or in the user manual for the phone. The upper limit of SAR allowed in the United States according to FCC safety guidelines is 1.6 watts per kilogram (W/kg) of body weight.

But according to the FCC, comparing SAR values between phones can be misleading. The listed SAR value is based only on the phone operating at its highest power, not on what users would typically be exposed to with normal phone use. The actual SAR during use varies based on a number of factors, so it’s possible that a phone with a lower listed SAR value might sometimes expose a person to more energy from RF waves than one with a higher listed SAR value.

Because cell phones usually are held near the head when a person is on a call, the main concern has been whether the phones might cause or contribute to tumors in this area, including:

• Malignant (cancerous) brain tumors, such as gliomas
• Non-cancerous tumors of the brain, such as meningiomas
• Non-cancerous tumors of the nerve connecting the brain to the ear (vestibular schwannomas, also known as acoustic neuromas)
• Tumors of the salivary glands

A few studies have also looked at possible links to other types of cancer.

What do studies show?

Researchers use 2 main types of studies to try to determine if something might cause cancer:

• Studies done in the lab (using lab animals or cell cultures)
• Studies looking at groups of people

In most cases neither type of study provides enough evidence on its own to show if something causes cancer in people, so researchers usually look at both lab-based and human studies.

The following is a brief summary of some of the major studies that have looked at this issue to date. However, this is not a comprehensive review of all studies that have been done .

Lab studies of RF waves

As noted above, the RF waves given off by cell phones don’t have enough energy to damage DNA directly or to heat body tissues. Because of this, it’s not clear how cell phones might be able to cause cancer. Some studies have found possible increased rates of certain types of tumors in lab animals exposed to RF radiation, but overall, the results of these types of studies have not provided clear answers so far.

Large studies published in 2018 by the US National Toxicology Program (NTP) and by the Ramazzini Institute in Italy exposed groups of lab rats (as well as mice, in the case of the NTP study) to RF waves over their entire bodies for many hours a day, starting before birth and continuing for most or all of their natural lives. Both studies found an increased risk of uncommon heart tumors called malignant schwannomas in male rats, but not in female rats (nor in male or female mice, in the NTP study). The NTP study also reported possible increased risks of certain types of tumors in the brain and in the adrenal glands.

While both of these studies had strengths, they also had limitations that make it hard to know how they might apply to humans being exposed to RF waves from cell phones. A 2019 review of these two studies by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) determined that the limitations of the studies didn’t allow conclusions to be drawn regarding the ability of RF energy to cause cancer.

Still, the results of these studies do not rule out the possibility that RF waves from cell phones might somehow impact human health.

Studies in people

Several dozen studies have looked at possible links between cell phone use and tumors. Most of these studies have focused on brain tumors. Many of these have been case-control studies, in which patients with brain tumors (cases) were compared to people who didn't have brain tumors (controls), in terms of their past cell phone use.

These studies have had mixed results. Some studies have found a possible link between cell phone use and brain tumors, while others have not. For example, several studies published by the same research group in Sweden have reported an increased risk of brain tumors in people using cell phones. However, there was no apparent overall increase in brain tumors in Sweden during the years that correspond to these reports.

Three large studies deserve special mention:

The INTERPHONE study

The 13-country INTERPHONE study, the largest case-control study done to date, looked at cell phone use among more than 5,000 people who developed brain tumors (gliomas or meningiomas) and a similar group of people without tumors. Overall, the study found no link between brain tumor risk and the frequency of calls, longer call time, or cell phone use for 10 or more years. There was a suggestion of a possible increased risk of glioma, and a smaller suggestion of an increased risk of meningioma, in the 10% of people who used their cell phones the most. But this finding was hard to interpret because some people in the study reported implausibly high cell phone use. The researchers noted that the shortcomings of the study prevented them from drawing any firm conclusions, and that more research was needed.

Another part of the INTERPHONE study compared more than 1,000 people with acoustic neuromas to more than 2,000 people without tumors, who served as matched controls. As with gliomas and meningiomas, there was no overall link between cell phone use and acoustic neuromas. There was again a suggestion of a possible increased risk in the 10% of people who used their cell phones the most, but this finding was hard to interpret because some people reported implausibly high cell phone use.

The Danish cohort study

A large, long-term study has been comparing all of the people in Denmark who had a cell phone subscription between 1982 and 1995 (about 400,000 people) to those without a subscription to look for a possible increase in brain tumors. The most recent update of the study followed people through 2007. Cell phone use, even for more than 13 years, was not linked with an increased risk of brain tumors, salivary gland tumors, or cancer overall, nor was there a link with any brain tumor subtypes or with tumors in any location within the brain.

This type of study (following a large group of people going forward in time and not relying on people’s memories about cell phone use) is generally thought to provide stronger evidence than a case-control study.

But this study also has some drawbacks. First, it is based only on whether or not people had a cell phone subscription at the time. It didn’t measure how often these people used their phones (if at all), or if people who didn’t have a subscription used someone else’s phone. There are also limits as to how well this study might apply to people using cell phones today. For example, while the cell phones used at the time of the study tended to emit higher levels of RF waves than modern cell phones do, people also probably used their phones quite a bit less than people use their phones today.

The Million Women Study

A large prospective (forward-looking) study of nearly 800,000 women in the UK examined the risk of developing brain tumors over an average of about 14 years in relation to self-reported cell phone use. This study found no link between cell phone use and the risk of brain tumors overall or of several common brain tumor subtypes. But again, there are limits as to how well this study might apply to people using cell phones today. For example, when the women in this study were first asked about their cell phone use back in 2001, fewer than 1 in 5 users reported talking on a cell phone for 30 minutes or more each week.

All studies done so far have limitations

In summary, studies of people published so far have not established a clear link between cell phone use and the development of tumors. However, these studies have had some important limitations that make them unlikely to end the controversy about whether cell phone use affects cancer risk.

First, studies have not yet been able to follow people for very long periods of time. After a known cancer-causing exposure, it often takes decades for tumors to develop. Because cell phones have been widely used for only about 20 years in most countries, it is not possible to rule out possible future health effects.

Second, cell phone usage is constantly changing. People are using their cell phones much more than they were even 10 years ago, and the phones themselves are very different from what was used in the past. This makes it hard to know if the results of studies looking at cell phone use in years past still apply today.

Third, most of the studies published so far have focused on adults, rather than children. (One case-control study looking at children and teens did not find a significant link to brain tumors, but the small size of the study limited its power to detect modest risks.) Cell phone use is now widespread even among younger children. It is possible that if there are health effects, they might be more pronounced in children because their bodies might be more sensitive to RF energy. Another concern is that children’s lifetime exposure to RF waves from cell phones will be greater than adults’, who started using cell phones when they were older.

Finally, the measurement of cell phone use in most studies has been crude. Most have been case-control studies, which have relied on people’s memories about their past cell phone use. In these types of studies, it can be hard to interpret any possible link between cancer and an exposure. People with cancer are often thinking about possible reasons for it, so they may sometimes recall their phone usage differently from people without cancer.

With these limitations in mind, it is important to continue to study the possible risk of cell phone exposure, especially with regard to use by children and longer-term use.

What do expert agencies say?

The American Cancer Society (ACS) does not have any official position or statement on whether or not radiofrequency (RF) radiation from cell phones, cell phone towers, or other sources is a cause of cancer. ACS generally looks to other expert organizations to determine if something causes cancer (that is, if it is a carcinogen), including:

• The International Agency for Research on Cancer (IARC) , which is part of the World Health Organization (WHO)
• The US National Toxicology Program (NTP) , which is formed from parts of several different government agencies, including the National Institutes of Health (NIH), the Centers for Disease Control and Prevention (CDC), and the Food and Drug Administration (FDA)

Other major organizations also sometimes comment on the ability of certain exposures (such as cell phone use) to cause cancer.

Based on a review of studies published up until 2011, the International Agency for Research on Cancer (IARC) has classified RF radiation as “possibly carcinogenic to humans,” based on limited evidence of a possible increase in risk for brain tumors among cell phone users, and inadequate evidence for other types of cancer. (For more information on the IARC classification system, see Known and Probable Human Carcinogens .) 

More recently, the US Food and Drug Administration (FDA) issued a technical report based on studies published between 2008 and 2018, as well as national trends in cancer rates. The report concluded: “Based on the studies that are described in detail in this report, there is insufficient evidence to support a causal association between radiofrequency radiation (RFR) exposure and [tumor formation].”

So far, the National Toxicology Program (NTP) has not included RF radiation in its Report on Carcinogens , which lists exposures that are known to be or reasonably anticipated to be human carcinogens. (For more on this report, see Known and Probable Human Carcinogens .)

According to the US Federal Communications Commission (FCC) :

“[C]urrently no scientific evidence establishes a causal link between wireless device use and cancer or other illnesses. Those evaluating the potential risks of using wireless devices agree that more and longer-term studies should explore whether there is a better basis for RF safety standards than is currently used.”

According to the US Centers for Disease Control and Prevention (CDC) :

“At this time we do not have the science to link health problems to cell phone use. Scientific studies are underway to determine whether cell phone use may cause health effects.”

It is not clear at this time that RF waves from cell phones cause harmful health effects in people, but studies now being done should give a clearer picture of the possible health effects in the future. Until more is known, there are several things that people who are concerned about RF waves can do to limit their exposure.

Use the speaker mode or video chat feature on the phone, or a hands-free device such as a corded or cordless earpiece. This moves the antenna away from your head, which decreases the amount of RF waves that reach the head. Corded earpieces emit virtually no RF waves (although the phone itself still emits small amounts of RF waves that can reach parts of the body if close enough, such as on the waist or in a pocket). Bluetooth ® earpieces typically transmit RF waves at much lower power levels than cell phones themselves (see below).

Texting instead of talking on the phone may be another way to reduce your exposure. But it may not be a good option in some situations, especially if you are driving. For safety reasons, it is especially important to limit or avoid the use of cell phones (especially texting) while driving.

Limit your (and your children’s) cell phone use. This is one of the most obvious ways to limit your exposure to RF waves from cell phones. For example, you may want to limit the amount of time you spend talking on the phone (at least with your phone up to your ear). Parents who are concerned about their children’s exposure can limit how much time they spend talking on the phone.

Consider choosing a phone with a low SAR value. Different models of phones can give off different levels of RF waves. But as noted above, according to the FCC the SAR value is not always a good indicator of a person’s exposure to RF waves during normal cell phone use. One way to get information on the SAR level for a specific phone model is to visit the phone maker’s website. The FCC has links to some of these sites. If you know the FCC identification (ID) number for your phone model (which can often be found somewhere on the phone or in the user manual), you can also go to the following web address: www.fcc.gov/oet/ea/fccid. On this page, you will see instructions for entering the FCC ID number.

Fifth generation (5G) cellular networks are now being rolled out in many parts of the United States and in other countries. 5G networks are capable of transmitting much larger amounts of data over shorter periods of time than previous generations (4G, 3G, etc.).

5G networks (and the phones that use them) operate on some higher frequency (higher energy) RF wavelengths than older generation networks (although newer phones can typically still use the older networks as well). But the newer 5G signals still use RF waves, so they are still forms of non-ionizing radiation, which is not thought to have the ability to directly damage DNA.

The studies that have been done so far to look at possible links between cell phone use and cancer have focused on older generation (mainly 2G and 3G) signals. At this time, there has been very little research showing that the RF waves used in 5G networks are any more (or less) of a concern than the other RF wavelengths used in cellular communication. For more on 5G networks, see Cell Phone Towers .

Cordless phones, commonly used in homes, have base units that are plugged into telephone jacks and wired to a local telephone service. They are not considered cell phones. Cordless phones operate at about 1/600 the power of cell phones, so they are much less likely to be a concern in terms of health effects.

What about Bluetooth ® devices (including earbuds)?

Many wireless devices now communicate over shorter distances using Bluetooth technology. For example, many phones now have the option of using wireless (Bluetooth) earbuds. Phones can also connect to other devices (tablets, laptops, car dashboard computers, etc.) using Bluetooth.

Bluetooth devices use RF waves in a similar wavelength range as those used for cell phones. But because the signals only need to travel a short distance (such as from the phone to a person’s ears), they can operate at much lower power levels than those used by phones, which in theory might make them less of a health concern. But as with other devices that give off RF waves, possible health effects from these devices cannot be ruled out completely at this time.

• Additional resources

The American Cancer Society medical and editorial content team

Our team is made up of doctors and oncology certified nurses with deep knowledge of cancer care as well as editors and translators with extensive experience in medical writing.

Along with the American Cancer Society, other sources of information include:

Centers for Disease Control and Prevention (CDC) Frequently Asked Questions about Cell Phones and Your Health Website:  https://www.cdc.gov/nceh/radiation/cell_phones._FAQ.html

Federal Communications Commission (FCC) Wireless Devices and Health Concerns Website:  https://www.fcc.gov/consumers/guides/wireless-devices-and-health-concerns

Food and Drug Administration (FDA) Cell Phones Website:  https://www.fda.gov/radiation-emitting-products/home-business-and-entertainment-products/cell-phones

National Cancer Institute (NCI) Cell Phones and Cancer Risk Website:  https://www.cancer.gov/about-cancer/causes-prevention/risk/radiation/cell-phones-fact-sheet

National Institute of Environmental Health Sciences (NIEHS) Cell Phone Radio Frequency Radiation: https://www.niehs.nih.gov/health/topics/agents/cellphones/index.cfm Cell Phone Radio Frequency Radiation Studies: https://www.niehs.nih.gov/health/materials/cell_phone_radiofrequency_radiation_studies_508.pdf

* Inclusion on this list does not imply endorsement by the American Cancer Society.

Aydin D, Feychting M, Schuz J, et al. Mobile phone use and brain tumors in children and adolescents: A multicenter case-control study.  J Natl Cancer Inst . 2011;103:1264-1276.

Cardis E, Armstrong BK, Bowman JD, et al. Risk of brain tumours in relation to estimated RF dose from mobile phones: Results from five Interphone countries.  Occup Environ Med . 2011;68:631-640.

Christensen HC, Schuz J, Kosteljanetz M, et al. Cellular telephone use and risk of acoustic neuroma.  Am J Epidemiol . 2004;159:277-283.

Centers for Disease Control and Prevention. Frequently Asked Questions about Cell Phones and Your Health. 2014. Accessed at www.cdc.gov/nceh/radiation/cell_phones._FAQ.html on March 25, 2020.

Coureau G, Bouvier G, Lebailly P, et al. Mobile phone use and brain tumours in the CERENAT case-control study.  Occup Environ Med . 2014;7:514-522.

Falcioni L, Bua L, Tibaldi E, et al. Report of final results regarding brain and heart tumors in Sprague-Dawley rats exposed from prenatal life until natural death to mobile phone radiofrequency field representative of a 1.8 GHz GSM base station environmental emission. Environ Res . 2018;165:496-503.

Federal Communications Commission (FCC). Specific Absorption Rate (SAR) For Cell Phones: What It Means For You. 2019. Accessed at www.fcc.gov/guides/specific-absorption-rate-sar-cell-phones-what-it-means-you on March 25, 2020.

Federal Communications Commission (FCC). Wireless Devices and Health Concerns. 2019. Accessed at https://www.fcc.gov/consumers/guides/wireless-devices-and-health-concerns on March 25, 2020.

Federal Communications Commission, Office of Engineering and Technology. RF Safety FAQ. 2015. Accessed at https://www.fcc.gov/engineering-technology/electromagnetic-compatibility-division/radio-frequency-safety/faq/rf-safety on March 23, 2020.

Food and Drug Administration. Do Cell Phones Pose a Health Hazard? 2020. Accessed at https://www.fda.gov/radiation-emitting-products/cell-phones/do-cell-phones-pose-health-hazard on March 25, 2020.

Food and Drug Administration. Review of Published Literature between 2008 and 2018 of Relevance to Radiofrequency Radiation and Cancer. 2020. Accessed at https://www.fda.gov/media/135043/download on March 19, 2020.

Frei P, Poulsen AH, Johansen C, et al. Use of mobile phones and risk of brain tumours: Update of Danish cohort study.  BMJ . 2011 Oct 19;343:d6387.

Hardell L, Carlberg M. Mobile phone and cordless phone use and the risk for glioma - Analysis of pooled case-control studies in Sweden, 1997-2003 and 2007-2009. Pathophysiology . 2015;22(1):1-13.

Hardell L, Carlberg M, Mild K. Case-control study on cellular and cordless telephones and the risk for acoustic neuroma or meningioma in patients diagnosed 2000-2003.  Neuroepidemiology .   2005;25:120-128.

Hardell L, Nasman A, Pahlson A, et al. Use of cellular telephones and the risk for brain tumors: A case-control study.  Int J Oncol . 1999;15:113-116.

Hardell L, Hallquist A, Mild KH, et al. Cellular and cordless telephones and the risk of brain tumours.  Eur J Cancer Prev . 2002;159:277-283.

Inskip PD, Tarone RE, Hatch EE, et al. Cellular telephone use and brain tumors.  N Engl J Med . 2001;344:79-86.

International Agency for Research on Cancer.  IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 102. Non-Ionizing Radiation, Part 2: Radiofrequency Electromagnetic Fields . 2013. Accessed at: https://publications.iarc.fr/126 on March 23, 2020.

International Commission on Non-Ionizing Radiation Protection (ICNIRP). ICNIRP Note: Critical Evaluation of Two Radiofrequency Electromagnetic Field Animal Carcinogenicity Studies Published in 2018. Health Phys . 2019 Aug 27. [Epub ahead of print]

INTERPHONE Study Group. Acoustic neuroma risk in relation to mobile telephone use: Results of the INTERPHONE international case-control study.  Cancer Epidemiol . 2011;35:453-464.

INTERPHONE Study Group. Brain tumor risk in relation to mobile telephone use: Results of the INTERPHONE international case-control study.  Int J Epidemiol . 2010;39:675-694.

Lagorio S, Roosli M. Mobile phone use and risk of intracranial tumors: A consistency analysis.  Bioelectromagnetics . 2014;35:79-90.

Lai H, Singh NP. Acute low-intensity microwave exposure increases DNA single-strand breaks in rat brain cells.  Bioelectromagnetics . 1995;16:204-210.

Lonn S, Ahlbom A, Hall P, Swedish Interphone Study Group. Long-term mobile phone use and brain tumor risk.  Am J Epidemiol . 2005; 161:526-535.

Malyapa RS, Ahern EW, Straube WL, et al. DNA damage in rat brain cells after in vivo exposure to 2450 MHz electromagnetic radiation and various methods of euthanasia.  Radiat Res . 1998;149:637-645.

Muscat JE, Malkin MG, Thompson S, et al. Handheld cellular telephone use and risk of brain cancer.  JAMA .   2000;284:3001-3007.

Muscat JE, Malkin MG, Shore RE, et al. Handheld cellular telephone use and risk of acoustic neuroma.  Neurology . 2002;58:1304-1306.

National Cancer Institute. Cell Phones and Cancer Risk. 2019. Accessed at https://www.cancer.gov/about-cancer/causes-prevention/risk/radiation/cell-phones-fact-sheet on March 25, 2020.

National Institute of Environmental Health Sciences. Cell Phone Radio Frequency Radiation Studies. 2019. Accessed at https://www.niehs.nih.gov/health/materials/cell_phone_radiofrequency_radiation_studies_508.pdf on March 23, 2020.

Pettersson D, Mathiesen T, Prochazka M, et al. Long-term mobile phone use and acoustic neuroma risk.  Epidemiology . 2014;25:233-241.

Repacholi MH. Radiofrequency field exposure and cancer: What do the laboratory studies suggest?  Environ Health Perspect . 1997;105:1565-1568.

Schoemaker M J, Swerdlow AJ, Ahlbom A, et al. Mobile phone use and risk of acoustic neuroma: Results of the Interphone case-control study in five North European countries.  Br J Cancer . 2005;93:842-848.

Schuz J, Pirie K, Reeves GK, Floud S, Beral V; Million Women Study Collaborators. Cellular telephone use and the risk of brain tumors: Update of the UK Million Women Study. J Natl Cancer Inst . 2022 Mar 29:djac042. doi: 10.1093/jnci/djac042. Online ahead of print.

Schuz J, Steding-Jessen M, Hansen S, et al. Long-term mobile phone use and the risk of vestibular schwannoma: A Danish nationwide cohort study.  Am J Epidemiol . 2011;174:416-422.

Vijayalaxmi, Prihoda TJ. Genetic damage in human cells exposed to non-ionizing radiofrequency fields: A meta-analysis of the data from 88 publications (1990-2011).  Mutat Res . 2012;749:1-16.

Volkow ND, Tomasi D, Wang GJ, et al. Effects of cell phone radiofrequency signal exposure on brain glucose metabolism.  JAMA . 2011;305:808-813.

Last Revised: March 31, 2022

American Cancer Society medical information is copyrighted material. For reprint requests, please see our Content Usage Policy .

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Essay on Cancer

List of essays on cancer, essay on cancer – introduction, types and conclusion (essay 1 – 150 words), essay on cancer (essay 2 – 250 words), essay on cancer – for school students (essay 3 – 300 words), essay on cancer – for medical students (essay 4 – 400 words), essay on cancer – for science students (essay 5 – 500 words), essay on cancer (essay 6 – 600 words), essay on cancer – written in english (essay 7 – 750 words), essay on cancer – for ias, civil services, upsc, ips and other competitive exams (essay 8 – 1000 words).

Cancer is a disease which is related to the abnormal growth of cells in a particular part of the body. Since the last decade, cancer has become one of the most feared diseases of all times, particularly due to the difficult treatment one has to undergo and the limitations of the treatment in curing this disease during later stages of cancer.

Audience: The below given essays are exclusively written for school and college students. Furthermore, those students preparing for IAS, IPS, UPSC, Civil Services and other competitive exams can also increase their knowledge by studying these essays.

Introduction:

Cancer is a group of more than 100 diseases that can develop in almost anywhere in the body. Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body.

Types of Cancer:

There are various types of cancer. They include:

1] Breast cancer: This is type of cancer that forms in the cells of the breast.

2] Prostate cancer: This is type of cancer that occurs in a man’s prostate. This is a small walnut sized gland that has the duty of producing seminal fluid.

3] Lung cancer: This is a type of cancer that begins in the lungs and this occurs mostly in people who smoke.

4] Leukemia: A cancer of blood forming tissues, hindering the body’s ability to fight infection.

Conclusion:

We have seen various types of cancer but the types of cancer we have are hundreds but we had mentioned just a few. Each type of cancer comes with various symptoms and various ways of curbing it.

Cancer is a disease that has been around for centuries, but it has never had such an impact on public health as it has now. Cancer is the increase in the number of cells in human beings at an abnormal rate. Doctors have been discussing the reasons behind this increase for the past fifty years. One is tempted to think that there are no reasons behind this occurrence and that it is just a natural phenomenon, people die all the time. Right?

The thing is that the number of cancer cases has increased in the past decades and a lot of this increase is attributed to the influence of different types of radiation. Even though most of the really dangerous substances (or sources of radiation) are not allowed near people. What else can be causing such an increase in cancer cases?

Some doctors have made a discovery regarding cancer that can really help us get rid of this problem. Following down the line of the argumentation presented in the famous “China Study” more doctors are advising their patients to change their diet because it can help  in their fight against cancer. Not only that but a proper diet can also be the best prevention.

When you are a student your metabolism is young so you do not feel the bad effect of your habits as much as older people do but as we age the side effects of our bad choices will become obvious. We can teach ourselves to listen to our bodies and to prevent cancer but to do that we, first of all, have to defeat our habits.

Cancer is uncontrolled and unchecked development of abnormal cells in a part of the body. Cancerous cells develop just like another cell in the body. They, however, keep growing and can form a mass then subsequently becomes tumors. Since cells are present in every part of our body, cancer can also grow in all parts of our body.

Causes of Cancer:

One great scientific mystery in our world is the cause of cancer. Scientists from all over have tried and failed in isolating any particular action, substance or environmental factors that can lead to cancer.

However, scientists all over the world agree that cancer is caused by substances known as carcinogens. These substances are introduced to the body when we are exposed to or consume materials containing them. One of the confirmed sources of carcinogens is exposure to radiation from x-ray machines.

Cancer Treatment:

There are various ways to treat a person infected with cancer. These modes of treatment are chosen depending on the type of cancer, the stage of development and the health peculiarities of the cancer patient. In other cases, several modes of treatment are combined to treat a single patient.

Some of the modes of treating cancer are in fly highlighted below:

1. Surgery to remove Cancerous tumors from the body.

2. Radiation therapy to reduce the growth of cells.

3. Chemotherapy for destroying cancer cells.

4. Stem cell transplant.

Prevention of Cancer:

Just as there are no agreed actions, materials and exposure that causes cancer, there are no generally accepted means of preventing cancer. However, there are certain habits that can limit a person’s exposure.

Some of them are highlighted below:

1. Healthy environment and diet.

2. Reduction of exposure from the sun.

3. Keep your weight low.

4. Avoid the use of tobacco.

Early detection of cancer has been hailed as the most potent way of treating this menace. Though scientists are still in the business of searching for a cure, we as humans can prevent cancer by regular medical check-ups.

Cancer is one of the second largest fatal illnesses across the world. One of the horrific words a human being can listen to is being diagnosed with Cancer. The word Cancer brings alarm and anxiety to the listener. Cancer is the abnormal growth of cells in one part of the body which can even spread to other parts if not treated at an early stage. Neoplasms or tumour are the subset of these abnormally grown-up cells which often results in a mass or lump.

What causes Cancer?

Those agents which cause cancer are termed as Carcinogens . These can be classified into physical, chemical and biological. Physical Carcinogens include ultra violet and other ionizing radiations. Food adulterants such as aflatoxin, tobacco smoke, drinking water contaminant such as Arsenic, asbestos etc., are termed as Chemical Carcinogens. Viruses, Bacteria and other parasites which cause infections and eventually lead to Cancer are categorized under Biological Carcinogens. Ageing also causes cancer as the risk of the cellular repair mechanism weakens as we age.

Significant Symptoms of Cancer:

Some of the major symptoms of cancer include unexplained weight loss, extreme fatigue, persistent sores that do not heal, changes in the bladder and bowel movements, odd bleeding and discharges, change in voice due to cancer indication in larynx and lumps and bumps on the skin.

Preventive Measures:

Some of the risk factors which needs to be addressed to prevent cancer may include avoidance of tobacco, being overweight or obese, unhealthy eating with less vegetables and greens, physical in-activity, avoiding pollution etc. Apart from the mentioned, vaccination against HPV and Hepatitis B Virus, controlling hazards while at work, reducing exposure to ultra violet and ionizing radiation etc., can help prevent being infected by Cancer.

Assessing the type of cancer and the stage is very important because every cancer type has a different pattern of treatment from surgery, radiotherapy and chemotherapy . The treatment that is used to relieve the cancer patient from their pain and enhance the quality of life for the patients and their families is termed as Palliative care.

World Health Organization has partnered with UNO and other non-profit organizations to ensure every country is being made aware of the non-communicable diseases and the prevention of cancer and its control. Insights to develop Centers of Excellence to provide quality treatments and to conduct research on the carcinogenesis should be provided to governments and to help the people.

The abnormal cell growth in our body which spreads to other parts as well is what is termed as cancer. Around four lakh of people in India are known to be affected by this disease every year. More so, around half of them are not able to survive as they are usually detected in the last stages of cancer. Hence it is all the more important to educate the people about this disease and its symptoms so that it can be detected early and the lives of the people suffering from it can be saved.

Cancer can affect any body part. The part that is affected gives it the name, for instance, lung cancer which affects the lungs, skin cancer in which the skin is affected and so on. However, we can broadly divide cancer into four types. The first one is Sarcoma which is known to affect the blood vessels, bones, muscles cartilages and connective tissues. The second type of cancer is Carcinoma which affects the internal organs of the body or the skin. The third type is the Lymphoma. This cancer affects the lymph glands and the lymph nodes. The last type in which cancer can be categorised is Leukaemia which largely affects the parts forming blood such as the bone marrow.

Symptoms of Cancer:

Although no particular cause is known to trigger this disease, some activities have been associated as the cause of different types of cancer. The first and foremost is smoking. Excess smoking affects the entire respiratory system thereby leading to the onset of lung cancer. More so chewing tobacco is also attributed to giving rise to mouth and throat cancer. Similarly, alcohol is attributed to be the cause of stomach, liver and gallbladder cancer. Summarising it, all the ill habits of society and urbanisation have been attributed to this disease. Even radiations coming from X-ray machines can prove harmful and lead to cancer. That is why there are proper laws an protection in place when exposing people to these harmful radiations.

Treatments Available:

If detected in early stages, cancer can surely be curable. Surgery is one of the primary steps of curing this disease. If required, doctors remove the body part affected such as the uterus, gallbladder or the breast. Thereafter, through radiotherapy, the cancerous cells on the other affected parts of the body are killed so that they don’t spread to other parts. Chemotherapy is done using the strong chemical in order to kill the cancerous cells. Other methods such as tumour suppressing genes are used in different types of cancer as may be the need advised by the doctors. Whatever the method, it is extremely difficult to go through the pain and social stigma such as loss hair which comes alongside the treatment of cancer.

Living with this Disease:

It is indeed very difficult to live with this disease as not only this disease is not fully curable but the treatment is so tough that it scares even the toughest of individuals. We, as a society, must support the people suffering from cancer and help in their difficult times. We must not discriminate them and must understand that is already suffering a lot and must not do anything which further aggravates their sufferings.

Cancer is a severe disease in which there is abnormal growth of cell that spreads around the human body. Many people in the world are struggling with this disease. Consistently around 10 million cases are analyzed. These number of cases are expected to increase around 20 million by 2020. It turns into the most widely recognized reasons for death. Due to abnormal cell growth, it develops & affects the overall body weight. Prolonged cough and abnormal bleeding are some symptoms of this severe disease. The developed abnormal cells first make their impact on organs then slowly moved as poison. Cancer disease can be identified in the beginning periods. The medical professionals are still trying to catch this disease.

One of the main causes of cancer is smoking. Other causes include tobacco, consumption of alcohol, obesity, lack of physical activities, exposure to UV radiations, etc. Age factor and changes in genes are yet other factors that cause cancer.

Cancer has different types which can be divided into various forms:

i. Skin Cancer:

It is the most common type of cancer which can be seen in many people. Every year more than 1 million people are affected by skin cancer. Skin cancer happens due to the overexposure from the sun. The thicker ozone layers directly harms our skin, which increases the chances of skin cancer.

ii. Lung Cancer:

This type of cancer is related to the cells inside the lungs. The symptoms of this type of cancer are chest pain & sudden weight loss. It is also known as lung carcinoma. As a process of metastasis, the growth of abnormal cell growth spread inside the lungs. Smoking is a fundamental driver of Lung cases.

iii. Kidney Cancer:

Another name of kidney cancer is renal cancer. Renal Cell Carcinoma and Transitional Cell Carcinoma are the types of kidney cancer. This development of cancer happens after the age of 40 years. Smoking can twofold the danger of kidney malignant growth.

iv. Leukemia:

This cancer starts developing in the bone marrow, which leads to a high number of abnormal white cells. Acute myeloid leukemia or acute lymphocytic leukemia are the sorts of leukemia. Chemotherapy or radiation therapy can be used as the treatment for Leukemia.

Cancer Staging:

It is important to understand the staging factor of this severe disease. Diagnosis of cancer in early stages helps to tackle this disease by proper treatments. During the initial stages of cancer, proper surgeries or radiotherapy can help to overcome cancer. When the broken cancer cells move to other parts of the human body, then advance treatment is suggested by the professionals. But when a patient is in the final stages of cancer, he needs a treatment which covers his whole body. Chemotherapy is a therapy which is used to circulate the bloodstream. Professional doctors use various test techniques to identify the stages of cancer. Stages are used to describe the severity of cancer.

In the initial stage, cancer can be prevented through medication, proper surgeries and light treatment. In the advance stages of cancer, chemotherapy and radiation therapy is useful. Above all, the best way to keep cancer away is to stay away from smoking and tobacco, eat healthy food and a lot of green vegetables, and do some physical exercise daily.

It is very difficult for a cancer patient to fight with the final stages of cancer. To deal with this severe problem cancer symptoms should never be ignored. More than 70% of cases are seen only due to smoking. At every stage, it is essential that everyone must adopt a healthy diet plan & exercise daily to prevent this disease. A person who has a good and healthy lifestyle can fight with cancer more strongly.

Current trends in global health mention cancer. Cancer is currently one of the leading causes of death globally. It is an illness in which abnormal cell growth develops and affects parts of the human body as it advances, it has the potential to spread from one part of the body to the other. It is a chronic illness that imposes a great economic burden on a nation because its management is costly. Cancer occurs in different parts of the body and are classified according to where it has affected. In India, men are mostly acted by lung, oral, lip and neck cancers whereas women are affected by cervical, breast and ovarian cancer. The detection procedure varies with the type of cancer while the treatment varies with the stage of the cancer progression. Mostly early stages of cancer have better prognosis compared to late stages of cancer.

There are modifiable and non-modifiable factors that predispose an individual to cancer. Non modifiable factors include age and genetics. With an increase in age, the rate of cancer incidence increases. The genetic predisposition to cancer increases the incidences of suffering the disease. Modifiable factors include lifestyle habits like drinking and smoking tobacco which increase the incidences of lung, oral, esophageal among other cancers. Diet is also a predisposing factor especially one that is less in vitamin supplements.

Physical inactivity and obesity predispose to cancers of the colon, breast and others. Sexual activity in women with multiple sexual partners predisposes them to cervical cancer due to the transmission of HPV (Human Papilloma Virus). The environment also predisposes to cancer because of the chemicals, radicals and radiations that interact with human beings.

Detection of Cancer:

The detection varies with the type of cancer and so screening is done for each type differently. It is advisable that people get regular checkups of the whole body so that early detection facilitates effective and curative treatment. Screening of cancer is done using detailed examination of the physique, laboratory and histology tests, radiological and magnetic imaging techniques among other methods.

The campaigns against cancer advocate for early detection by teaching the public on the early signs of cancer. In breast cancer awareness for example, the public is made aware of physical examination of the breast and if they detect any abnormal growth or lump, they are to seek further investigation. Early detection is important because it results in successful treatment. In the detection, the cancer staging is done, which is usually four stages, stage one, two, three and four. Stage one has the best prognosis whereas stage four has the poorest prognosis.

Treatment of Cancer:

Once cancer is detected, a range of treatment options is provided. Treatment depends on the types of cancer and the staging. It can be treated by surgery whereby excision of the abnormal growth is done. Surgery is done for non-hematological cancers and those that have not metastasized to other parts of the body. An example of surgery is mastectomy to treat breast cancer.

Chemotherapy is another treatment option that involves the administration of anticancer medication that eliminate the abnormal cells in the body. Another treatment option is radiation therapy that uses ionizing radiations to destroy cancer cells. Radiation is also used to make tumors small. It is used to treat solid tumors and it depends on the sensitivity of the tumor to the radiations. It is targeted at the nucleic acid destruction in the tumor cells.

Consequences of Cancer:

Cancer is a chronic illness that could result in very serious consequences even with treatment. Cachexia is the extreme wasting of the body that causes death in cancer patients. Economic burden to both the individual and the nation is experienced in cancer treatment because the treatment modalities are costly. The economic burden results in decline of the nation’s economy and increased healthcare costs to the population.

Mental illnesses result from cancer because it is a terminal illness and most patients become mentally unstable upon diagnosis. The quality of health is affected in a country when there is high incidences of cancer and the performance is greatly affected, which cause poverty and economic crisis for individuals.

Cancer is a serious illness that impacts the lives of people and the nation negatively. It is evident that cancer has diverse treatment options but the problem is that people do not go for checkups. Checkups are important in early detection, which usually results in successful treatment and less burden of cancer in a nation and in individuals.

Cancer is basically an agglomeration of various diseases that involves the abnormal growth of cells with the ability to spread or invade other body parts. Cancers are quite different from benign tumours in that the latter does not spread or invade other body parts. Some of the many symptoms and signs of cancer include abnormal bleeding, a lump, weight loss that is unusual, prolonged cough and bowel movement change. Even though these listed symptoms and signs of cancer, they might be caused by other things so it is necessary to be diagnosed. Today, we have more than 100 various kinds of cancer that affect us humans.

History of Cancer:

It is believed that cancer has been in existence for a majority if not all of the history of man. Breast cancer was the first form of cancer that was recorded and this happened around 1600 BC in Egypt. Between 460 BC and 370 BC, Hippocrates spent time analysing various types of cancer and referred to them as crayfish or crab. The name was as a result of the crab-like look of the malignant tumour and the lateral extension of the distended veins and tumours.

Factors Causing Cancer:

It has been discovered that the major cause of deaths as a result of cancer is the use of tobacco and it accounts for about 22 percent of the total number of deaths due to cancer. Poor diet, obesity, excessive alcohol consumption and a lack of exercise and physical activities accounts for another 10 percent of deaths caused by cancer. Some other causes and factors that contribute to cancer include environmental pollutants, ionizing radiation exposure and certain infections.

In most developing countries, infections like hepatitis B, Helicobacter pylori, papillomavirus infection of humans, Hepatitis C, HIV and Epstein Barr contribute to fifteen percent of all cancers. All of the factors listed above change the cell genes. There are always a lot of genetic changes before the development of cancer. About 10% of all cancers are as a result of genetic defects that are inherited from a parent. Asides the symptoms and signs that are used to detect cancer, screening tests are also a good way of detecting cancer. Cancer is normally thoroughly investigated using medical imaging; it is then confirmed through biopsy.

Development of Cancer:

A tumour or neoplasm is a collection of cells which have gone through growth that is not regulated and most times form a lump or mass. Every tumour cell exhibits the six important characters that are necessary for the production of the malignant tumour.

The six characteristics are:

1. Cell division and growth without all the signals that are proper.

2. Continuous division and growth even though the signals given are contrary.

3. Cell death that is usually programmed is avoided.

4. The divisions of the cell are quite limitless in number.

5. The construction of blood vessel is promoted.

6. The tissues are invaded and metastases are formed.

Cancer Prevention:

The prevention of a lot of cancers can be ensured by trying to maintain a weight that is healthy, not smoking, consuming a lot of whole grains, fruits and vegetable, avoiding the consumption of a lot of alcohol, reduction in the amount of red and processed meat that is consumed, getting vaccinated against some infectious diseases and the avoidance of too much exposure to sunlight. It is sometimes useful that there is early detection in cases of colorectal and cervical cancer and this can be achieved through screening. The usefulness of breast cancer screening is highly controversial.

The treatment of cancer is usually done by combining surgery, radiation therapy, targeted therapy and chemotherapy. A very important element of care is the management of symptoms and pain. In cases of advanced disease, palliative care is of utmost importance. The extent of the disease at the commencement of treatment and also the form of cancer that is involved go a long way to determine the odds of survival. Using the adopted survival rate at five years, children that were under the age of 15 when they were diagnosed have an average rate of survival of 80% in most developed countries. In the US, the average rate of survival for the five year period is 66%.

90.5 million  people were living with different cancers in 2015. It has been reported that every year, close to 15 million reports of new cancer cases are filed. These do not include the cases of skin cancer. Cancer results in more than eight million deaths every year which is about 15.7% of the total number of deaths every year.

In males, prostate cancer, lung cancer, stomach cancer and colorectal cancer are the most widespread cancer types. In females, colorectal cancer, breast cancer, cervical cancer and lung cancer are the most widespread cancer types. Apart from melanoma, if we include skin cancer in the amount of new cases of cancer every year, it is going to be 40% of the total number of cases.

Brain tumours and lymphoblastic leukemia that is acute are the most widespread cancer types in children but in Africa, lymphoma that is no-Hodgkin is the most widespread. The total number of children that are under the age of 15 that ended up being diagnosed with one type of cancer or the other in 2012 is around 165,000.

With an increase in age, it has been seen that the risk of getting cancer also increases significantly and the number and occurrence of cases of cancer in developed countries in more than the number and occurrence of cancer cases in other countries. The change in lifestyle and increase in the number of people living to a very old age in countries that are developing contributes to the increase in the rate of the occurrence of cancer. Cancer is believed to have a financial cost of up to 1.16 trillion dollars every year.

Cancer can be extremely dangerous when it is not discovered early and when adequate and proper care and attention is not given to the treatment. Therefore it is very important to go for regularly screening to find out if there is need for caution or treatment.

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Epidemiology: Lung Cancer Risk Essay

Introduction, edward jenner, application of the epidemiological methods to current public health issues.

European countries recorded the 17th century as undoubtedly dangerous due to pestilential epidemics occurrence at the time. The Great Plague of London is one of the notable pandemics, which occurred from 1665 to 1666 (“John Graunt,” 2020). The plague affected many people as it happened in the spring and summer of 1665. It led to the deaths of about 100,000 people, most of who were London residents.

At the time, London was anticipated to be about 448 acres of land surrounded by a city wall. Maintaining proper hygiene was difficult due to congestion, as well as open sewage. The residents were also subject to poor sanitation and reckless disposal of rubbish (“John Graunt,” 2020). The below-average living conditions instigated shanties’ formation while rats started inhabiting the structures. In 1894, Alexandre Yersin identified the pandemic’s cause to be a bacterial agent Yersinia pestis , from the rat fleas (“John Graunt,” 2020). The continued exploration of the factors, as well as agents, leading to the spread of pandemics led to a quantitative and qualitative examination and the development of immunization to reduce infections.

John Graunt composed a book, namely Natural and Political Observations Made upon the Bills of Mortality , combining the Bills of Mortality data. His quantitative publication demonstrated birth and disease incident patterns, differences between males and females, and newborn death rates (“John Graunt,” 2020). He also reviewed the insufficiencies of the data, including geographical inconsistencies, from which the calculations were derived.

Some of the notable challenges included unbalanced intervals between recordings, lack of thoroughness, erroneous age approximations, and an indefinite disease categorization. These factors are used in evaluating important data in the present day. Other than statistical scrutiny, which led to public health development, John’s work was important in establishing principles for epidemiology and demography (“John Graunt,” 2020). He was among the pioneers for deriving patterns from a disease occurrence in a geographical area or based on sex.

John Snow (1813 – 1858), a renowned English physician, is remembered for his extensive study of Cholera. His work entailed probing into London’s Broad Street pump outbreak of malady, which happened in 1854 (Frerichs, 2020). His work was dubbed the “Grand experiment” to compare two regions in a city reported with waterborne cholera cases. One of the regions was getting fairly safe water, while the other was supplied with sewage-contaminated water.

In the 1854 outbreak at the Broad Street pump in London, Snow demonstrated that the ongoing cholera outbreak was a result of contaminated water from the pump. At the time, the epidemic had claimed several lives in the SoHo neighborhood (Frerichs, 2020). In the same year, in his “Grand Experiment” study, Snow compared London communities that received water supply from two companies.

One company used water upstream of the River Thames, which was relatively safe from urban pollution. In contrast, the second firm largely used water from other London inlets (“Location of Water, “n.d.). Using this information, he developed the harmful effect of contaminated water and proposed interventions. The “Grand Experiment” was not exactly a true experiment, as Snow had not allocated two study groups for the process (“Location of Water, “n.d.). He instead took advantage of the natural settings, which had provided room for two distinct study scenarios. He used the classical epidemiological design of exposure and disease presence to analyze his data and draw relevant conclusions.

During this period, a notion had been spread that the intake of contaminated air transmitted Cholera. On the contrary, Snow stated that a microbe-like agent was causing Cholera, a concept that was later substantiated in the 1880s when the causative agent, Vibrio cholera , was characterized. His works were published in his book On the Mode of Communication of Cholera in 1855 and later republished as an epidemiological piece, which would later bolster his recognition in the field of epidemiology (Frerichs, 2020). His book explains in detail the results of his quantitative epidemiological study, and the inferences therein that have been used to shape modern practice.

Out of every ten inhabitants, three who were infected by smallpox passed away. One of the methods used to control smallpox was a procedure called variolation. Material from smallpox sores was provided for people who had never had the illness (“History of Smallpox,” 2016). They would then be scratched on the arm or made to inhale. Some of the people subjected to the variolation conditions had fever or rashes, but only a few died. The number of deaths as a result of the curative mechanism was significantly lower than the one caused by the illness.

Immunization is based on the findings of Dr. Edward Jenner, who established that variolation had positive outcomes, especially if administered to milkmaids who had at one time contracted cowpox. He experimented with a substance from an open patch on the maid’s hand and introduced it into a boy’s arm (“History of Smallpox,” 2016). Edward then exposed the boy several times to the variola virus, but he was never infected. After several tests, in 1801 he published his work “On the Origin of the Vaccine Inoculation.” He showed optimism concerning the eradication of smallpox. Consequently, immunization was acknowledged and replaced the art of variolation (“History of Smallpox,” 2016). Almost two centuries afterward, the World Health Assembly affirmed smallpox eradication, a feat measured to be one of the biggest international public health achievements.

Dr. Jenner’s effort is largely regarded as the foundation of immunology, which started with a hypothesis formulated by an epidemiologic observation; he and others who used the same method by counting and comparing smallpox cases in cowpox vaccinated and unvaccinated individuals discovered a lower percentage of smallpox disease in cowpox vaccinated individuals, demonstrating the usefulness of the vaccine (“History of Smallpox,” 2016). Although the field of epidemiology had not been discovered, Jenner and those who adopted his findings were practicing it by collecting and scrutinizing data to ascertain the efficiency of the procedure for vaccination.

One of the current public health issues that the world is facing is Lung Cancer. Literature research is being used to provide a basis for identifying and shortening key reports on people’s behaviors concerning lung cancer risk, including smoking cigarettes and other tobacco products (Dubey, Gupta, & Jain, 2016). For the arithmetic study, prevalence and death, as well as endurance rates, are being used to better identify the grave condition of lung cancer (Dubey et al., 2016). These study patterns and approaches are founded on earlier inferences for collecting and interpreting large data sets, as well as producing reports.

Dubey, A., Gupta, U., & Jain, S. (2016). Epidemiology of lung cancer and approaches for its prediction: A systematic review and analysis. Chinese Journal of Cancer , 35 (1). Web.

Frerichs, R. (2020). John Snow | British physician . Web.

History of smallpox . (2016) Web.

John Graunt (2020). Web.

Location of water companies . (n.d.) Web.

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Example Of Essay On Cancer- Risk Factors

Type of paper: Essay

Topic: Obesity , Life , Risk , Smoking , Body , Cancer , Animals , Fat

Published: 03/11/2020

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According to the WebMD assessment feedback, the two cancers I am at risk of are blood cancer and prostate cancer. The risk of getting these two types of cancer is not high as I watch my health and keep off unhealthy habits. According to the WebMD feedback, factors that decrease cancer include living a healthy life, quitting smoking and eating a balanced diet.

Controllable and uncontrollable factors

Controllable risk factors Achieving and maintaining a body weight that is healthy; Consuming less animal fat; Consuming soy food; Consuming fruits and vegetables; Moderating alcohol consumption; Consuming fiber on a daily basis.

Uncontrollable factors

Old age- Age comes with a high chance of contracting cancer Pregnancy- Increases the probability of getting cancer Inheritance (family history) - Genes play a big role in determining the risk one has to get cancer BRCA- This genetic mutation significantly increases the risk Foods that lower cancer risks Vegetables such as carrots, cabbage and cucumber- They contain vitamin c, beta and lycopene. These chemicals protect body cells from compounds that are harmful to the body. Beans and legumes such as dried peas, navy beans and soy sauce- These help fight prostate cancer. They have a powerful anti-oxidant which reduces the risk of getting cancer.

Lifestyle changes that would positively influence modifiable risk factors

Stop smoking- Smoking increases the risk of getting throat cancer. Drinking tea instead of coffee- Green and black tea is far much protective when compared to coffee. Consuming or quitting animal fat: This applies to women. Taking less animal fat reduces the risk of getting breast cancer.

Implementing these changes

A total or partial lifestyle change is necessary for preventing cancer. The best way of implementing these changes is through adopting the alternative ways of life. For instance, one can watch the food they take. This will protect them from getting cancer.

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Can aspirin work its wonders to prevent cancer?

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Doctors have appreciated the healing potential of aspirin for centuries. Its longevity and versatility as a pain reliever and anti-inflammatory have led some to herald it as a “miracle drug."

Aspirin is used to relieve headaches and arthritis. It helps reduce fevers and soothe toothaches. Because aspirin thins the blood, doctors may recommend it to some patients to help prevent blood clots and reduce the risk of a stroke or heart attack.

Now, evidence is mounting that an aspirin regimen may also help reduce the risk of certain cancers, especially colorectal cancer .

“Epidemiological studies have shown aspirin to reduce the incidence of formation of polyps and thus reduce the probability of developing colon cancer,” says Pankaj Vashi , MD, a Gastroenterologist and Vice Chief of Staff at City of Hope® Cancer Center Chicago . “Recent studies have shown that aspirin also has an immunologic effect, which explains why low metastatic colon cancers   may be seen in patients who were on aspirin.”

Despite the studies touting aspirin’s ability to reduce cancer risk   and improve heart health, not everyone is convinced.

In this article, we’ll explore:

What is aspirin?

• How does aspirin target inflammation?

What does the research say?

What does the u.s. preventive services task force say, what are the potential side effects of aspirin use.

If you’ve been diagnosed with cancer and are interested in a second opinion on your diagnosis and treatment plan, call us or chat online with a member of our team.

Aspirin, acetylsalicylic acid (ASA), is a nonsteroidal anti-inflammatory drug, a class of medications used to reduce pain and inflammation. The drug was invented in 1897 by Dr. Felix Hoffman, but its base ingredient salicylic acid has been used for centuries to reduce fever and pain. Salicylic acid is found in willow trees, and ancient healers used willow bark and willow leaf tea to treat fevers. Salicin, an active ingredient in salicylic acid, also is found in the meadowsweet flower.

According to The Pharmaceutical Journal , the first clinical trial of salicin in 1876 found that the substance reduced fever and joint pain. Two years after Hoffman’s acetylsalicylic acid compound was developed, the Friedrich Bayer and Co. coined the name aspirin. According to the journal, “The letter ‘A’ stands for acetyl, ‘spir’ is derived from the plant known as Spiraea ulmaria (meadowsweet), which yields salicin, and ‘in’ was a common suffix used for drugs at the time of the first stable synthesis of acetylsalicylic acid.”

Aspirin is among the most commonly used drugs in the world. It’s also among the most-frequently researched drugs. That research has produced evidence that aspirin may not only reduce fever, pain and inflammation; it may also improve cardiovascular health and reduce cancer risk.

Targeting inflammation

Aspirin works by targeting enzymes known as cyclooxygenases (COX). Two types of this enzyme—COX1 and COX2—help produce substances in the body that contribute to inflammation, a common response to injury or illness.

When inflammation becomes chronic, it may cause DNA damage in cells in the inflamed area, which in turn may lead to serious diseases, such as colitis or cancer.

Long-term aspirin use may reduce the inflammation that sometimes leads to cancer. Research also shows aspirin may help limit the production of a gene called c-Myc, a " master regulator " protein that helps control cell growth and division. The c-Myc protein is considered an oncogene , which has the potential to mutate a healthy cell into a cancer cell.

Research abounds in aspirin’s potential to reduce cancer risk. The latest research, published in April by scientists in Italy, suggest that “regular aspirin use may have an active role in enhancing immunosurveillance” against colorectal cancer.

“The Italian study speculates that due to an immunological effect, patients with colon cancer may have less metastatic cancer  in the lymph nodes if they have been on long-term, low-dose aspirin,” Dr. Vashi says. “This still needs to be studied more before we claim ASA as a therapeutic option for colon cancer.”

In a 2016 report published in the Journal of the American Medical Association , researchers who studied aspirin use in 135,000 patients concluded "long-term aspirin use was associated with a modest but significantly reduced risk for overall cancer, especially gastrointestinal tract tumors. Regular aspirin use may prevent a substantial proportion of colorectal cancers."

Two studies in 2011 also concluded that aspirin may help reduce cancer risk. One of those studies , of patients with Lynch syndrome , an inherited condition that increases the risk of colorectal cancer , concluded that an aspirin regimen "substantially reduced cancer incidence … in carriers of hereditary colorectal cancer."

The other, a review of several studies involving more than 660,000 men and women, found "clear evidence that aspirin in doses as low as 325 mg per day reduces [colorectal cancer] risk."

While touted as a wonder drug by many, the U.S. Preventive Services Task Force (USPSTF) has a more measured approach to the drug’s benefits.

The USPSTF is an independent panel of experts convened by the government to help develop guidelines on health care issues, such as cancer screening and aspirin use. In an extensive 2022 article in the Journal of the American Medical Association (JAMA), the USPSTF altered its recommendation on using aspirin to prevent cardiovascular disease (CVD). The agency no longer recommends a daily, low-dose aspirin regimen to prevent CVD in people 60 years or older.

“The USPSTF concludes with moderate certainty that aspirin use for the primary prevention of CVD events in adults aged 40 to 59 years who have a 10 percent or greater 10-year CVD risk has a small net benefit,” the report says. “The USPSTF concludes with moderate certainty that initiating aspirin use for the primary prevention of CVD events in adults 60 years or older has no net benefit.”

The agency also backtracked on a previous recommendation on aspirin use to reduce the risk of colorectal cancer (CRC) and now has “concluded that the evidence is inadequate that low-dose aspirin use reduces CRC incidence or mortality.” But the agency says more research is needed to better evaluate aspirin’s potential to reduce CVD and CRC.

In a response to the USPSTF’s recommendations, the American Cancer Society says it “recognizes the evidence that long-term regular aspirin use has both harms and benefits, including reduced risk of colorectal cancer, but has not formally reviewed this evidence and does not currently have recommendations for or against aspirin use.”

Still, the American Heart Association and the American College of Cardiology (ACC) recommend that those at high risk of a heart attack talk to their doctor about taking low-dose aspirin to help reduce the risk of blood clots that may lead to a heart attack or stroke.

"It is very important to recognize that the USPSTF recommendation on the initiation of aspirin does not apply to patients with a prior history of heart attack, stroke, bypass surgery or recent stent procedure," says Eugene Yang, MD, chair of the ACC's Prevention of Cardiovascular Disease Section. "All patients should consult with their physicians about whether they can safely discontinue aspirin. This decision should be made after a careful review of the risks and benefits."

Before taking aspirin daily, consult your doctor. Aspirin is a powerful acid, and patients taking daily doses may develop side effects, including gastrointestinal issues and bleeding.

“ASA should not be used in patients who are high risk for gastrointestinal bleeding,” Dr. Vashi says. “Caution should be taken in patients who have stomach ulcers or who are on anticoagulants. Cancer patients who are at risk of bleeding due to low platelet counts from chemotherapy  should not take ASA.”

Experts also urge parents not to give aspirin to children, and they warn nursing mothers that the drug may be passed onto babies through breast milk.

Despite the documented side effects, millions of Americans still take aspirin regularly. A University of Michigan poll found that one-quarter of Americans 50 to 80 years old take aspirin at least three times a week.

“Aspirin is no longer a one-size-fits-all preventive tool for older adults, which for decades it was touted as,” says Michigan Medicine Hematologist Jordan Schaefer, MD.

“This poll shows we have a long way to go to make sure aspirin use is consistent with current knowledge.”

Related Articles

Does ejaculating often reduce your risk of prostate cancer?

Senior Lecturer in Biochemistry, Sheffield Hallam University

Disclosure statement

Daniel Kelly does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Sheffield Hallam University provides funding as a member of The Conversation UK.

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In terms of men’s health issues, prostate cancer features high on the agenda. It’s the second most diagnosed cancer in men globally – closely followed by lung cancer. And it’s the most common cancer in men in the UK.

As the prostate is a reproductive organ with its main job being to help make semen – the fluid that carries sperm in ejaculate – researchers have long questioned the effect of sexual factors on a man’s prostate cancer risk. Specifically, does ejaculation protect against prostate cancer risk?

Interestingly, there is some evidence that supports this idea. A recent review looking at all the relevant medical investigations taking place over the last 33 years showed that seven out of the 11 studies reported some beneficial effect of ejaculation frequency on prostate cancer risk.

Although the mechanisms are not completely understood, these studies fit with the idea that ejaculation can reduce prostate cancer by decreasing the concentration of toxins and crystal-like structures that can accumulate in the prostate and potentially cause tumours.

Similarly, ejaculation may alter the immune response within the prostate reducing inflammation – a known risk factor for cancer development – or by increasing immune defence against tumour cells.

Alternatively, by reducing psychological tension ejaculation may lower the activity of the nervous system which then prevents certain prostate cells from dividing too rapidly and increasing the chance of them becoming cancerous.

Despite these suggested mechanisms, in the research implying ejaculation is protective, it appears that specifics are important.

Age plays its part. Sometimes frequency of ejaculation was only protective at ages 20-29 , or 30-39 , and sometimes only in later life (50s and older) and actually increased the risk in younger life (20s).

Other times, ejaculation in adolescence (when the prostate is still developing and maturing) had the greatest impact on the risk of prostate cancer decades later.

But how frequent is frequent? Well, very frequent in some cases.

A study from Harvard University found that men who ejaculated 21 or more times a month enjoyed a 31% lower risk of prostate cancer compared with men who reported four to seven ejaculations per month across their lifetimes.

Similar findings have come from Australia where prostate cancer is 36% less likely to be diagnosed before the age of 70 in men who averaged about five to seven ejaculations a week compared with men who ejaculated less than two to three times a week.

Other research has a much more modest view with greater than four per month being the ejaculation frequency to give protective effects in some age groups and patients.

No firm conclusion

Drawing overall conclusions from this research is difficult, especially when the studies differ so much in the way they were conducted.

Factors like the varied populations of men investigated, the numbers of men included in the analyses, and differences in the way ejaculation frequency is measured (whether this includes intercourse, masturbation and unprompted release usually at night) can all cloud the picture.

In fact, measurement of ejaculation frequency relies on self-reporting and often from many years and decades ago. So this is an estimate at best and can be biased by attitudes, both personal and societal, towards sexual activity and masturbation potentially leading to both over- and under-reporting.

There may also be a bias in the detection of prostate tumours with highly sexually active men delaying or not going to the hospital for the fear that cancer treatment may stop their sexual activity. These men with high ejaculation frequency may therefore actually have prostate cancer that goes unreported in these studies.

It is also possible that ejaculation may not guard against prostate cancer and the links may be due to other factors. For example, men who ejaculate more often might have healthier lifestyles that lower their chances of being diagnosed with cancer.

Reduced ejaculation frequency is related to increased body mass index (BMI), reduced physical activity and divorce – all factors related to poorer general health that in turn may contribute to cancer development.

Testosterone may be important

Testosterone, the main male sex hormone, is also a crucial part of the picture.

It is well known to increase sex drive, so a man with low levels of testosterone may not have the same desire for sexual activity leading to ejaculation as a man with higher levels.

Contrary to early opinions that high testosterone levels in men raise prostate cancer risk, the current view suggests that not only does it not elevate this risk, it is actually low testosterone concentrations that increase risk . This is particularly true for men with existing prostate cancer who have a worse disease outcome when their testosterone is low.

So it may be testosterone reducing a man’s risk of prostate cancer and additionally driving their motivation for sexual activity.

Despite this, most studies do not measure testosterone levels and, at best, only recognise it as a possible influencing factor. One study that did measure the male sex hormone found that men who ejaculated frequently had higher testosterone levels. And it was these men who also had a reduced risk of prostate cancer.

There are benefits of sexual activity and ejaculation beyond the prostate including positive effects on the heart, brain, immune system, sleep and mood. So while the link between ejaculation frequency and prostate cancer is not fully understood and there is a real need for more research, frequent ejaculation (within reason) will certainly do no harm, probably does good and should therefore form part of a man’s healthy lifestyle.

• Prostate cancer
• Male health
• ejaculation

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Improving Fall Risk Screening in Oncology Patients: Implementing an Oncology-Specific Fall Risk Screening Tool in an Outpatient Adult Blood Cancer Center

Add to collection, downloadable content.

• Affiliation: School of Nursing
• ABSTRACT Carmen Everhart Raborn: Improving Fall Risk Screening in Oncology Patients: Implementing an Oncology-Specific Fall Risk Screening Tool in an Outpatient Adult Blood Cancer Center (Under the direction of Ashley Kellish) BACKGROUND: Patients with cancer are at higher risk for falls than those without cancer, yet there is lack of risk assessment tools that are validated in the oncology population. This evidence-based, quality improvement (QI) project aimed to improve screening adherence and identification of patients with cancer who are at an increased risk for falls in the outpatient setting by implementation of a validated, oncology-specific falls risk screening tool. METHODS: The IOWA Model of Research-Based Practice to Promote Quality Care model and the Plan Do Study Act (PDSA) method of quality improvement were used to guide this project. A literature review was conducted to identify oncology specific fall risk screening tools. Interventions: The intervention was implementation of a validated oncology-specific fall risk screening tool over a 10-week period. The validated fall risk tool was the Cleveland ClinicCapone Albert (CC-CA) screening tool. The intervention was focused on patients receiving treatment in the adult blood cancer center (BCC). RESULTS: Of the 496 patients that were treated by nurse champions in the BCC, 492 met criteria to be screened using the CC-CA tool. Of the 492 patients who met criteria, 431 patients were screened by a nurse champion. 61 patients were missed, and 4 patients were excluded for not meeting eligibility criteria. Total fall screen adherence was 87.6% during the pilot period. There were zero reported patient falls during the screening timeframe. CONCLUSION: This project surpassed the benchmarks to increase fall risk screening adherence. However, results are limited as there were no documented falls during the timeframe of the pilot study.
• Screening Tool
• https://doi.org/10.17615/032x-1208
• Dissertation
• In Copyright - Educational Use Permitted
• Kellish, Ashley
• Vernon-Platt, Tracy
• Thigpen, April
• Doctor of Nursing Practice
• University of North Carolina at Chapel Hill Graduate School

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Breast Cancer—Epidemiology, Risk Factors, Classification, Prognostic Markers, and Current Treatment Strategies—An Updated Review

Sergiusz Łukasiewicz.

1 Department of Surgical Oncology, Center of Oncology of the Lublin Region St. Jana z Dukli, 20-091 Lublin, Poland; lp.lzoc@zciweisakulS (S.Ł.); [email protected] (A.S.)

Marcin Czeczelewski

2 Department of Forensic Medicine, Medical University of Lublin, 20-090 Lublin, Poland; [email protected] (M.C.); lp.teno@amrofa (A.F.)

Alicja Forma

3 Department of Human Anatomy, Medical University of Lublin, 20-090 Lublin, Poland; [email protected]

Robert Sitarz

Andrzej stanisławek.

4 Department of Oncology, Chair of Oncology and Environmental Health, Medical University of Lublin, 20-081 Lublin, Poland

Simple Summary

Breast cancer is the most common cancer among women. It is estimated that 2.3 million new cases of BC are diagnosed globally each year. Based on mRNA gene expression levels, BC can be divided into molecular subtypes that provide insights into new treatment strategies and patient stratifications that impact the management of BC patients. This review addresses the overview on the BC epidemiology, risk factors, classification with an emphasis on molecular types, prognostic biomarkers, as well as possible treatment modalities.

Breast cancer (BC) is the most frequently diagnosed cancer in women worldwide with more than 2 million new cases in 2020. Its incidence and death rates have increased over the last three decades due to the change in risk factor profiles, better cancer registration, and cancer detection. The number of risk factors of BC is significant and includes both the modifiable factors and non-modifiable factors. Currently, about 80% of patients with BC are individuals aged >50. Survival depends on both stage and molecular subtype. Invasive BCs comprise wide spectrum tumors that show a variation concerning their clinical presentation, behavior, and morphology. Based on mRNA gene expression levels, BC can be divided into molecular subtypes (Luminal A, Luminal B, HER2-enriched, and basal-like). The molecular subtypes provide insights into new treatment strategies and patient stratifications that impact the management of BC patients. The eighth edition of TNM classification outlines a new staging system for BC that, in addition to anatomical features, acknowledges biological factors. Treatment of breast cancer is complex and involves a combination of different modalities including surgery, radiotherapy, chemotherapy, hormonal therapy, or biological therapies delivered in diverse sequences.

1. Introduction

Being characterized by six major hallmarks, carcinogenesis might occur in every cell, tissue, and organ, leading to the pathological alternations that result in a vast number of cancers. The major mechanisms that enable its progression include evasion of apoptosis, limitless capacity to divide, enhanced angiogenesis, resistance to anti-growth signals and induction of own growth signals, as well as the capacity to metastasize [ 1 ]. Carcinogenesis is a multifactorial process that is primarily stimulated by both—genetic predispositions and environmental causes. The number of cancer-related deaths is disturbingly increasing every year ranking them as one of the major causes of death worldwide. Even though a significant number of cancers do not always need to result in death, they significantly lower the quality of life and require larger costs in general.

Breast cancer is currently one of the most prevalently diagnosed cancers and the 5th cause of cancer-related deaths with an estimated number of 2.3 million new cases worldwide according to the GLOBOCAN 2020 data [ 2 ]. Deaths due to breast cancer are more prevalently reported (an incidence rate approximately 88% higher) in transitioning countries (Melanesia, Western Africa, Micronesia/Polynesia, and the Caribbean) compared to the transitioned ones (Australia/New Zealand, Western Europe, Northern America, and Northern Europe). Several procedures such as preventive behaviors in general as well as screening programs are crucial regarding a possible minimization of breast cancer incidence rate and the implementation of early treatment. Currently, it is the Breast Health Global Initiative (BHGI) that is responsible for the preparation of proper guidelines and the approaches to provide the most sufficient breast cancer control worldwide [ 3 ]. In this review article, we have focused on the female breast cancer specifically since as abovementioned, it currently constitutes the most prevalent cancer amongst females.

2. Breast Cancer Epidemiology

According to the WHO, malignant neoplasms are the greatest worldwide burden for women, estimated at 107.8 million Disability-Adjusted Life Years (DALYs), of which 19.6 million DALYs are due to breast cancer. [ 4 ]. Breast cancer is the most frequently diagnosed cancer in women worldwide with 2.26 million [95% UI, 2.24–2.79 million] new cases in 2020 [ 5 ]. In the United States, breast cancer alone is expected to account for 29% of all new cancers in women [ 6 ]. The 2018 GLOBOCAN data shows that age-standardized incidence rates (ASIR) of breast cancer are strongly and positively associated with the Human Development Index (HDI) [ 7 ]. According to 2020 data, the ASIR was the highest in very high HDI countries (75.6 per 100,000) while it was more than 200% lower in medium and low HDI countries (27.8 per 100,000 and 36.1 per 100,000 respectively) [ 5 ].

Besides being the most common, breast cancer is also the leading cause of cancer death in women worldwide. Globally, breast cancer was responsible for 684,996 deaths [95% UI, 675,493–694,633] at an age-adjusted rate of 13.6/100,000 [ 5 ]. Although incidence rates were the highest in developed regions, the countries in Asia and Africa shared 63% of total deaths in 2020 [ 5 ]. Most women who develop breast cancer in a high-income country will survive; the opposite is true for women in most low-income and many middle-income countries [ 8 ].

In 2020 breast cancer mortality-to-incidence ratio (MIR) as a representative indicator of 5-year survival rates [ 9 ] was 0.30 globally [ 5 ]. Taking into consideration the clinical extent of breast cancer, in locations with developed health care (Hong-Kong, Singapore, Turkey) the 5-year survival was 89.6% for localized and 75.4% for regional cancer. In less developed countries (Costa Rica, India, Philippines, Saudi Arabia, Thailand) the survival rates were 76.3% and 47.4% for localized and regional breast cancer respectively [ 10 ].

Breast cancer incidence and death rates have increased over the last three decades. Between 1990 and 2016 breast cancer incidence has more than doubled in 60/102 countries (e.g., Afghanistan, Philippines, Brazil, Argentina), whereas deaths have doubled in 43/102 countries (e.g., Yemen, Paraguay, Libya, Saudi Arabia) [ 11 ]. Current projections indicate that by 2030 the worldwide number of new cases diagnosed reach 2.7 million annually, while the number of deaths 0.87 million [ 12 ]. In low- and medium-income countries, the breast cancer incidence is expected to increase further due to the westernization of lifestyles (e.g., delayed pregnancies, reduced breastfeeding, low age at menarche, lack of physical activity, and poor diet), better cancer registration, and cancer detection [ 13 ].

3. Risk Factors of Breast Cancer

The number of risk factors of breast cancer is significant and includes both modifiable factors and non-modifiable factors ( Table 1 ).

Modifiable and non-modifiable risk factors of breast cancer.

3.1. Non-Modifiable Factors

3.1.1. female sex.

Female sex constitutes one of the major factors associated with an increased risk of breast cancer primarily because of the enhanced hormonal stimulation. Unlike men who present insignificant estrogen levels, women have breast cells which are very vulnerable to hormones (estrogen and progesterone in particular) as well as any disruptions in their balance. Circulating estrogens and androgens are positively associated with an increased risk of breast cancer [ 14 ]. The alternations within the physiological levels of the endogenous levels of sex hormones result in a higher risk of breast cancer in the case of premenopausal and postmenopausal women; these observations were also supported by the Endogenous Hormones and Breast Cancer Collaborative Group [ 15 , 16 , 17 ].

Less than 1% of all breast cancers occur in men. However, breast cancer in men is a rare disease that’s at the time of diagnosis tends to be more advanced than in women. The average age of men at the diagnosis is about 67. The important factors increase a man’s risk of breast cancer are: older age, BRCA2/BRCA1 mutations, increased estrogen levels, Klinefelter syndrome, family history of breast cancer, and radiation exposure [ 18 ].

3.1.2. Older Age

Currently, about 80% of patients with breast cancer are individuals aged >50 while at the same time more than 40% are those more than 65 years old [ 19 , 20 , 21 ]. The risk of developing breast cancer increases as follows—the 1.5% risk at age 40, 3% at age 50, and more than 4% at age 70 [ 22 ]. Interestingly, a relationship between a particular molecular subtype of cancer and a patient’s age was observed –aggressive resistant triple-negative breast cancer subtype is most commonly diagnosed in groups under 40 age, while in patients >70, it is luminal A subtype [ 21 ]. Generally, the occurrence of cancer in older age is not only limited to breast cancer; the accumulation of a vast number of cellular alternations and exposition to potential carcinogens results in an increase of carcinogenesis with time.

3.1.3. Family History

A family history of breast cancer constitutes a major factor significantly associated with an increased risk of breast cancer. Approximately 13–19% of patients diagnosed with breast cancer report a first-degree relative affected by the same condition [ 23 ]. Besides, the risk of breast cancer significantly increases with an increasing number of first-degree relatives affected; the risk might be even higher when the affected relatives are under 50 years old [ 24 , 25 , 26 ]. The incidence rate of breast cancer is significantly higher in all of the patients with a family history despite the age. This association is driven by epigenetic changes as well as environmental factors acting as potential triggers [ 27 ]. A family history of ovarian cancer—especially those characterized by BRCA1 and BRCA2 mutations—might also induce a greater risk of breast cancer [ 28 ].

3.1.4. Genetic Mutations

Several genetic mutations were reported to be highly associated with an increased risk of breast cancer. Two major genes characterized by a high penetrance are BRCA1 (located on chromosome 17) and BRCA2 (located on chromosome 13). They are primarily linked to the increased risk of breast carcinogenesis [ 29 ]. The mutations within the above-mentioned genes are mainly inherited in an autosomal dominant manner, however, sporadic mutations are also commonly reported. Other highly penetrant breast cancer genes include TP53 , CDH1 , PTEN , and STK11 [ 30 , 31 , 32 , 33 , 34 ]. Except for the increased risk of breast cancer, carriers of such mutations are more susceptible to ovarian cancer as well. A significant number of DNA repair genes that can interact with BRCA genes including ATM , PALB2 , BRIP1 , or CHEK2 , were reported to be involved in the induction of breast carcinogenesis; those are however characterized by a lower penetrance (moderate degree) compared to BRCA1 or BRCA2 ( Table 2 ) [ 29 , 35 , 36 , 37 , 38 ]. According to quite recent Polish research, mutations within the XRCC2 gene could also be potentially associated with an increased risk of breast cancer [ 39 ].

Major genes associated with an increased risk of breast cancer occurrence.

3.1.5. Race/Ethnicity

Disparities regarding race and ethnicity remain widely observed among individuals affected by breast cancer; the mechanisms associated with this phenomenon are not yet understood. Generally, the breast cancer incidence rate remains the highest among white non-Hispanic women [ 51 , 52 ]. Contrarily, the mortality rate due to this malignancy is significantly higher among black women; this group is also characterized by the lowest survival rates [ 53 ].

3.1.6. Reproductive History

Numerous studies confirmed a strict relationship between exposure to endogenous hormones—estrogen and progesterone in particular—and excessive risk of breast cancer in females. Therefore, the occurrence of specific events such as pregnancy, breastfeeding, first menstruation, and menopause along with their duration and the concomitant hormonal imbalance, are crucial in terms of a potential induction of the carcinogenic events in the breast microenvironment. The first full-term pregnancy at an early age (especially in the early twenties) along with a subsequently increasing number of births are associated with a reduced risk of breast cancer [ 54 , 55 ]. Besides, the pregnancy itself provides protective effects against potential cancer. However, protection was observed at approximately the 34th pregnancy week and was not confirmed for the pregnancies lasting for 33 weeks or less [ 56 ]. Women with a history of preeclampsia during pregnancy or children born to a preeclamptic pregnancy are at lower risk of developing breast cancer [ 57 ]. No association between the increased breast cancer risk and abortion was stated so far [ 58 ].

The dysregulated hormone levels during preeclampsia including increased progesterone and reduced estrogen levels along with insulin, cortisol, insulin-like growth factor-1, androgens, human chorionic gonadotropin, corticotropin-releasing factor, and IGF-1 binding protein deviating from the physiological ranges, show a protective effect preventing from breast carcinogenesis. The longer duration of the breastfeeding period also reduces the risk of both the ER/PR-positive and -negative cancers [ 59 ]. Early age at menarche is another risk factor of breast cancer; it is possibly also associated with a tumor grade and lymph node involvement [ 60 ]. Besides, the earlier age of the first menstruation could result in an overall poorer prognosis. Contrarily, early menopause despite whether natural or surgical, lowers the breast cancer risk [ 61 ].

3.1.7. Density of Breast Tissue

The density of breast tissue remains inconsistent throughout the lifetime; however, several categories including low-density, high-density, and fatty breasts have been established in clinical practice. Greater density of breasts is observed in females of younger age and lower BMI, who are pregnant or during the breastfeeding period, as well as during the intake of hormonal replacement therapy [ 62 ]. Generally, the greater breast tissue density correlates with the greater breast cancer risk; this trend is observed both in premenopausal and postmenopausal females [ 63 ]. It was proposed that screening of breast tissue density could be a promising, non-invasive, and quick method enabling rational surveillance of females at increased risk of cancer [ 64 ].

3.1.8. History of Breast Cancer and Benign Breast Diseases

Personal history of breast cancer is associated with a greater risk of a renewed cancerous lesions within the breasts [ 65 ]. Besides, a history of any other non-cancerous alternations in breasts such as atypical hyperplasia, carcinoma in situ, or many other proliferative or non-proliferative lesions, also increases the risk significantly [ 66 , 67 , 68 ]. The histologic classification of benign lesions and a family history of breast cancer are two factors that are strongly associated with breast cancer risk [ 66 ].

3.1.9. Previous Radiation Therapy

The risk of secondary malignancies after radiotherapy treatment remains an individual matter that depends on the patient’s characteristics, even though it is a quite frequent phenomenon that arises much clinical concern. Cancer induced by radiation therapy is strictly associated with an individual’s age; patients who receive radiation therapy before the age of 30, are at a greater risk of breast cancer [ 69 ]. The selection of proper radiotherapy technique is crucial in terms of secondary cancer risk—for instance, tangential field IMRT (2F-IMRT) is associated with a significantly lower risk compared to multiple-field IMRT (6F-IMRT) or double partial arcs (VMAT) [ 70 ]. Besides, the family history of breast cancer in patients who receive radiotherapy additionally enhances the risk of cancer occurrence [ 71 ]. However, Bartelink et al. showed that additional radiation (16 Gy) to the tumor bed combined with standard radiotherapy might decrease the risk of local recurrence [ 72 ].

3.2. Modifiable Factors

3.2.1. chosen drugs.

Data from some research indicates that the intake of diethylstilbestrol during pregnancy might be associated with a greater risk of breast cancer in children; this, however, remains inconsistent between studies and requires further evaluation [ 73 , 74 ]. The intake of diethylstilbestrol during pregnancy is associated with an increased risk of breast cancer not only in mothers but also in the offspring [ 75 ]. This relationship is observed despite the expression of neither estrogen nor progesterone receptors and might be associated with every breast cancer histological type. The risk increases with age; women at age of ≥40 years are nearly 1.9 times more susceptible compared to women under 40. Moreover, breast cancer risk increases with greater diethylstilbestrol doses [ 76 ]. Numerous researches indicate that females who use hormonal replacement therapy (HRT) especially longer than 5 or 7 years are also at increased risk of breast cancer [ 77 , 78 ]. Several studies indicated that the intake of chosen antidepressants, mainly paroxetine, tricyclic antidepressants, and selective serotonin reuptake inhibitors might be associated with a greater risk of breast cancer [ 79 , 80 ]. Lawlor et al. showed that similar risk might be achieved due to the prolonged intake of antibiotics; Friedman et al. observed that breast risk is mostly elevated while using tetracyclines [ 81 , 82 ]. Attempts were made to investigate a potential relationship between hypertensive medications, non-steroidal anti-inflammatory drugs, as well as statins, and an elevated risk of breast cancer, however, this data remains highly inconsistent [ 83 , 84 , 85 ].

3.2.2. Physical Activity

Even though the mechanism remains yet undeciphered, regular physical activity is considered to be a protective factor of breast cancer incidence [ 86 , 87 ]. Chen et al. observed that amongst females with a family history of breast cancer, physical activity was associated with a reduced risk of cancer but limited only to the postmenopausal period [ 88 ]. However, physical activity is beneficial not only in females with a family history of breast cancer but also in those without such a history. Contrarily to the above-mentioned study, Thune et al. pointed out more pronounced effects in premenopausal females [ 89 ]. There are several hypotheses aiming to explain the protective role of physical activity in terms of breast cancer incidence; physical activity might prevent cancer by reducing the exposure to the endogenous sex hormones, altering immune system responses or insulin-like growth factor-1 levels [ 88 , 90 , 91 ].

3.2.3. Body Mass Index

According to epidemiological evidence, obesity is associated with a greater probability of breast cancer. This association is mostly intensified in obese post-menopausal females who tend to develop estrogen-receptor-positive breast cancer. Yet, independently to menopausal status, obese women achieve poorer clinical outcomes [ 92 ]. Wang et al. showed that females above 50 years old with greater Body Mass Index (BMI) are at a greater risk of cancer compared to those with low BMI [ 93 ]. Besides, the researchers observed that greater BMI is associated with more aggressive biological features of tumor including a higher percentage of lymph node metastasis and greater size. Obesity might be a reason for greater mortality rates and a higher probability of cancer relapse, especially in premenopausal women [ 94 ]. Increased body fat might enhance the inflammatory state and affects the levels of circulating hormones facilitating pro-carcinogenic events [ 95 ]. Thus, poorer clinical outcomes are primarily observed in females with BMI ≥ 25 kg/m 2 [ 96 ]. Interestingly, postmenopausal women tend to present poorer clinical outcomes despite proper BMI values but namely due to excessive fat volume [ 97 ]. Greater breast cancer risk with regards to BMI also correlates with the concomitant family history of breast cancer [ 98 ].

3.2.4. Alcohol Intake

Numerous evidences confirm that excessive alcohol consumption is a factor that might enhance the risk of malignancies within the gastrointestinal tract; however, it was proved that it is also linked to the risk of breast cancer. Namely, it is not alcohol type but rather the content of alcoholic beverages that mostly affect the risk of cancer. The explanation for this association is the increased levels of estrogens induced by the alcohol intake and thus hormonal imbalance affecting the risk of carcinogenesis within the female organs [ 99 , 100 ]. Besides, alcohol intake often results in excessive fat gain with higher BMI levels, which additionally increases the risk. Other hypotheses include direct and indirect carcinogenic effects of alcohol metabolites and alcohol-related impaired nutrient intake [ 101 ]. Alcohol consumption was observed to increase the risk of estrogen-positive breast cancers in particular [ 102 ]. Consumed before the first pregnancy, it significantly contributes to the induction of morphological alterations of breast tissue, predisposing it to further carcinogenic events [ 103 ].

3.2.5. Smoking

Carcinogens found in tobacco are transported to the breast tissue increasing the plausibility of mutations within oncogenes and suppressor genes ( p53 in particular). Thus, not only active but also passive smoking significantly contributes to the induction of pro-carcinogenic events [ 104 ]. Besides, longer smoking history, as well as smoking before the first full-term pregnancy, are additional risk factors that are additionally pronounced in females with a family history of breast cancer [ 105 , 106 , 107 , 108 ].

3.2.6. Insufficient Vitamin Supplementation

Vitamins exert anticancer properties, which might potentially benefit in the prevention of several malignancies including breast cancer, however, the mechanism is not yet fully understood. Attempts are continually made to analyze the effects of vitamin intake (vitamin C, vitamin E, B-group vitamins, folic acid, multivitamin) on the risk of breast cancer, nevertheless, the data remains inconsistent and not sufficient to compare the results and draw credible data [ 108 ]. In terms of breast cancer, most studies are currently focused on vitamin D supplementation confirming its potentially protective effects [ 109 , 110 , 111 ]. High serum 25-hydroxyvitamin D levels are associated with a lower incidence rate of breast cancer in premenopausal and postmenopausal women [ 110 , 112 ]. Intensified expression of vitamin D receptors was shown to be associated with lower mortality rates due to breast cancer [ 113 ]. Even so, further evaluation is required since data remains inconsistent in this matter [ 108 , 114 ].

3.2.7. Exposure to Artificial Light

Artificial light at night (ALAN) has been recently linked to increased breast cancer risk. The probable causation might be a disrupted melatonin rhythm and subsequent epigenetic alterations [ 115 ]. According to the studies conducted so far, increased exposure to ALAN is associated with a significantly greater risk of breast cancer compared to individuals with lowered ALAN exposure [ 116 ]. Nonetheless, data regarding the excessive usage of LED electronic devices and increased risk of breast cancer is insufficient and requires further evaluation as some results are contradictory [ 116 ].

3.2.8. Intake of Processed Food/Diet

According to the World Health Organization (WHO), highly processed meat was classified as a Group 1 carcinogen that might increase the risk of not only gastrointestinal malignancies but also breast cancer. Similar observations were made in terms of an excessive intake of saturated fats [ 117 ]. Ultra-processed food is rich in sodium, fat, and sugar which subsequently predisposes to obesity recognized as another factor of breast cancer risk [ 118 ]. It was observed that a 10% increase of ultra-processed food in the diet is associated with an 11% greater risk of breast cancer [ 118 ]. Contrarily, a diet high in vegetables, fruits, legumes, whole grains, and lean protein is associated with a lowered risk of breast cancer [ 119 ]. Generally, a diet that includes food containing high amounts of n-3 PUFA, vitamin D, fiber, folate, and phytoestrogen might be beneficial as a prevention of breast cancer [ 120 ]. Besides, lower intake of n-6 PUFA and saturated fat is recommended. Several in vitro and in vivo studies also suggest that specific compounds found in green tea might present anti-cancer effects which has also been studied regarding breast cancer [ 121 ]. Similar properties were observed in case of turmeric-derived curcuminoids as well as sulforaphane (SFN) [ 122 , 123 ].

3.2.9. Exposure to Chemical

Chronic exposure to chemicals can promote breast carcinogenesis by affecting the tumor microenvironment subsequently inducing epigenetic alterations along with the induction of pro-carcinogenic events [ 124 ]. Females chronically exposed to chemicals present significantly greater plausibility of breast cancer which is further positively associated with the duration of the exposure [ 125 ]. The number of chemicals proposed to induce breast carcinogenesis is significant; so far, dichlorodiphenyltrichloroethane (DDT) and polychlorinated biphenyl (PCB) are mostly investigated in terms of breast cancer since early exposure to those chemicals disrupts the development of mammary glands [ 126 , 127 ]. A potential relationship was also observed in the case of increased exposure to polycyclic aromatic hydrocarbons (PAH), synthetic fibers, organic solvents, oil mist, and insecticides [ 128 ].

3.2.10. Other Drugs

Other drugs that might constitute potential risk factors for breast cancer include antibiotics, antidepressants, statins, antihypertensive medications (e.g., calcium channel blockers, angiotensin II-converting enzyme inhibitors), as well as NSAIDs (including aspirin, ibuprofen) [ 129 , 130 , 131 , 132 , 133 ].

4. Breast Cancer Classification

4.1. histological classification.

Invasive breast cancers (IBC) comprise wide spectrum tumors that show a variation concerning their clinical presentation, behavior, and morphology. The World Health Organization (WHO) distinguish at least 18 different histological breast cancer types [ 134 ].

Invasive breast cancer of no special type (NST), formerly known as invasive ductal carcinoma is the most frequent subgroup (40–80%) [ 135 ]. This type is diagnosed by default as a tumor that fails to be classified into one of the histological special types [ 134 ]. About 25% of invasive breast cancers present distinctive growth patterns and cytological features, hence, they are recognized as specific subtypes (e.g., invasive lobular carcinoma, tubular, mucinous A, mucinous B, neuroendocrine) [ 136 ].

Molecular classification independently from histological subtypes, invasive breast cancer can be divided into molecular subtypes based on mRNA gene expression levels. In 2000, Perou et al. on a sample of 38 breast cancers identified 4 molecular subtypes from microarray gene expression data: Luminal, HER2-enriched, Basal-like, and Normal Breast-like [ 137 ]. Further studies allowed to divide the Luminal group into two subgroups (Luminal A and B) [ 138 , 139 ]. The normal breast-like subtype has subsequently been omitted, as it is thought to represent sample contamination by normal mammary glands. In the Cancer Genome Atlas Project (TCGA) over 300 primary tumors were thoroughly profiled (at DNA, RNA, and protein levels) and combined in biological homogenous groups of tumors. The consensus clustering confirmed the distinction of four main breast cancer intrinsic subtypes based on mRNA gene expression levels only (Luminal A, Luminal B, HER2-enriched, and basal-like) [ 140 ]. Additionally, the 5th intrinsic subtype—claudin-low breast cancer was discovered in 2007 in an integrated analysis of human and murine mammary tumors [ 141 ].

In 2009, Parker et al. developed a 50-gene signature for subtype assignment, known as PAM50, that could reliably classify particular breast cancer into the main intrinsic subtypes with 93% accuracy [ 142 ]. PAM50 is now clinically implemented worldwide using the NanoString nCounter ® , which is the basis for the Prosigna ® test. The Prosigna ® combines the PAM50 assay as well as clinical information to assess the risk of distant relapse estimation in postmenopausal women with hormone receptor-positive, node-negative, or node-positive early-stage breast cancer patients, and is a daily-used tool assessing the indication of adjuvant chemotherapy [ 143 , 144 , 145 ].

4.2. Luminal Breast Cancer

Luminal breast cancers are ER-positive tumors that comprise almost 70% of all cases of breast cancers in Western populations [ 146 ]. Most commonly Luminal-like cancers present as IBC of no special subtype, but they may infrequently differentiate into invasive lobular, tubular, invasive cribriform, mucinous, and invasive micropapillary carcinomas [ 147 , 148 ]. Two main biological processes: proliferation-related pathways and luminal-regulated pathways distinguish Luminal-like tumors into Luminal A and B subtypes with different clinical outcomes.

Luminal A tumors are characterized by presence of estrogen-receptor (ER) and/or progesterone-receptor (PR) and absence of HER2. In this subtype the ER transcription factors activate genes, the expression of which is characteristic for luminal epithelium lining the mammary ducts [ 149 , 150 ]. It also presents a low expression of genes related to cell proliferation [ 151 ]. Clinically they are low-grade, slow-growing, and tend to have the best prognosis.

In contrast to subtype A, Luminal B tumors are higher grade and has worse prognosis. They are ER positive and may be PR negative and/or HER2 positive. Additionally, it has high expression of proliferation-related genes (e.g., MKI67 and AURKA) [ 152 , 153 , 154 ]. This subtype has lower expression of genes or proteins typical for luminal epithelium such as the PR [ 150 , 155 ] and FOXA1 [ 146 , 156 ], but not the ER [ 157 ]. ER is similarly expressed in both A and B subtypes and is used to distinguish luminal from non-luminal disease.

4.3. HER2-Enriched Breast Cancer

The HER2-enriched group makes up 10–15% of breast cancers. It is characterized by the high expression of the HER2 with the absence of ER and PR. This subtype mainly expresses proliferation—related genes and proteins (e.g., ERBB2/HER2 and GRB7), rather than luminal and basal gene and protein clusters [ 154 , 156 , 157 ]. Additionally, in the HER2-enriched subtype there is evidence of mutagenesis mediated by APOBEC3B. APOBEC3B is a subclass of APOBEC cytidine deaminases, which induce cytosine mutation biases and is a source of mutation clusters [ 158 , 159 , 160 ].

HER2-enriched cancers grow faster than luminal cancers and used to have the worst prognosis of subtypes before the introduction of HER2-targeted therapies. Importantly, the HER2-enriched subtype is not synonymous with clinically HER2-positive breast cancer because many ER-positive/HER2-positive tumors qualify for the luminal B group. Moreover, about 30% of HER2-enriched tumors are classified as clinically HER2-negative based on immunohistochemistry (IHC) and/or fluorescence in situ hybridization (FISH) methods [ 161 ].

4.4. Basal-Like/Triple-Negative Breast Cancer

The Triple-Negative Breast Cancer (TNBC) is a heterogeneous collection of breast cancers characterized as ER-negative, PR-negative, and HER2-negative. They constitute about 20% of all breast cancers. TNBC is more common among women younger than 40 years of age and African-American women [ 161 ]. The majority (approximately 80%) of breast cancers arising in BRCA1 germline mutation are TNBC, while 11–16% of all TNBC harbor BRCA1 or BRCA2 germline mutations. TNBC tends to be biologically aggressive and is often associated with a worse prognosis [ 162 ]. The most common histology seen in TNBC is infiltrating ductal carcinoma, but it may also present as medullary-like cancers with a prominent lymphocytic infiltrate; metaplastic cancers, which may show squamous or spindle cell differentiation; and rare special type cancers like adenoid cystic carcinoma (AdCC) [ 163 , 164 , 165 ].

The terms basal-like and TNBC have been used interchangeably; however, not all TNBC are of the basal type. On gene expression profiling, TNBCs can be subdivided into six subtypes: basal-like (BL1 and BL2), mesenchymal (M), mesenchymal stem-like (MSL), immunomodulatory (IM), and luminal androgen receptor (LAR), as well as an unspecified group (UNS) [ 166 , 167 ]. However, the clinical relevance of the subtyping still unclear, and more research is needed to clarify its impact on TNBC treatment decisions [ 168 ].

4.5. Claudin-Low Breast Cancer

Claudin-low (CL) breast cancers are poor prognosis tumors being mostly ER-negative, PR-negative, and HER2-negative. CL tumors account for 7–14% of all invasive breast cancers [ 147 ]. No differences in survival rates were observed between claudin-low tumors and other poor-prognosis subtypes (Luminal B, HER2-enriched, and Basal-like). CL subtype is characterized by the low expression of genes involved in cell-cell adhesion, including claudins 3, 4, and 7, occludin, and E-cadherin. Besides, these tumors show high expression of epithelial-mesenchymal transition (EMT) genes and stem cell-like gene expression patterns [ 169 , 170 ]. Moreover, CL tumors have marked immune and stromal cell infiltration [ 171 ]. Due to their less differentiated state and a preventive effect of the EMT-related transcription factor, ZEB1 CL tumors are often genomically stable [ 172 , 173 ].

4.6. Surrogate Markers Classification

In clinical practice, the key question is the discrimination between patients who will or will not benefit from particular therapies. By using molecular assays, more patients can be spared adjuvant chemotherapy, but these tests are associated with significant costs. Therefore, surrogate subgroups based on pathological morphology and widely available immunohistochemical (IHC) markers are used as a tool for risk stratification and guidance of adjuvant therapy [ 174 ]. A combination of the routine pathological markers ER, PR, and HER2 is used to classify tumors into intrinsic subtypes [ 175 ]. Semiquantitative evaluation of Ki-67 and PR is helpful for further typing of the Luminal subtype [ 176 , 177 ]. Moreover, evaluation of cytokeratin 5/6 and epidermal growth factor receptor is utilized to identify the Basal-like breast cancer among the TNBC [ 178 ].

In St. Gallen’s 2013 guidelines the IHC-based surrogate subtype classification was recommended for clinical decision making [ 179 ]. However, these IHC-based markers are only a surrogate and cannot establish the intrinsic subtype of any given cancer, with discordance rates between IHC-based markers and gene-based assays as high as 30% [ 180 ].

4.7. American Joint Committee on Cancer Classification

The baseline tool to estimate the likely prognosis of patients with breast cancer is the AJCC staging system that includes grading, immunohistochemistry biomarkers, and anatomical advancement of the disease. Since its inception in 1977, the American Joint Committee on Cancer (AJCC) has published an internationally accepted staging system based on anatomic findings: tumor size (T), nodal status (N), and metastases (M). However, gene expression profiling has identified several molecular subtypes of breast cancer [ 181 ]. The eighth edition of the AJCC staging manual (2018), outlines a new prognostic staging system for breast cancer that, in addition to anatomical features, acknowledges biological factors [ 182 ]. These factors—ER, PR, HER2, grade, and multigene assays—are recommended in practice to define prognosis [ 183 , 184 ].

The most widely used histologic grading system of breast cancer is the Elston-Ellis modification [ 185 ] of Scarff-Bloom-Richardson grading system [ 186 ], also known as the Nottingham grading system. The grade of a tumor is determined by assessing morphologic features: (a) formation of tubules, (b) mitotic count, (c) variability, and the size and shape of cellular nuclei. A score between 1 (most favorable) and 3 (least favorable) is assigned for each feature. Grade 1 corresponds to combined scores between 3 and 5, grade 2 corresponds to a combined score of 6 or 7, and grade 3 corresponds to a combined score of 8 or 9.

In addition to grading and biomarkers, the commercially available multigene assays provide additional prognostic information suitable for incorporation in the AJCC 8th edition. The 21-gene assay Oncotype DX ® assessed by reverse transcription-polymerase chain reaction (RT-PCR) was the only assay sufficiently evaluated and included in the staging system. This assay is valuable in the staging of patients with hormone receptor-positive, HER2-negative, node-negative tumors that are <5 cm. Patients with results of the assay (Recurrence Score) less than 11 had excellent disease-free survival at 6.9 years of 98.6% with endocrine therapy alone [ 187 ]. Hence, adjuvant systemic chemotherapy can be safely omitted in patients with a low-risk multigene assay [ 188 ].

The AJCC staging manual includes a pathological and a clinical-stage group. The clinical prognostic stage group should be utilized in all patients on initial evaluation before any systemic therapy. Clinical staging uses the TNM anatomical information, grading, and expression of these three biomarkers. When patients undergo surgical resection of their primary tumor, the post-resection anatomic information coupled with the pretreatment biomarker findings results in the final Pathologic Prognostic Stage Group.

The recent update of breast cancer staging by the biologic markers improved the outcome prediction in comparison to prior staging based only on anatomical features of the disease. The validation studies involving the reassessment of the Surveillance, Epidemiology, and End Results (SEER) database ( n = 209,304, 2010–2014) and the University of Texas MD Anderson Cancer Center database ( n = 3327, years of treatment 2007–2013) according to 8th edition AJCC manual proved the more accurate prognostic information [ 189 , 190 ].

5. Prognostic Biomarkers

5.1. estrogen receptor.

Estrogen receptor (ER) is an important diagnostic determinant since approximately 70–75% of invasive breast carcinomas are characterized by significantly enhanced ER expression [ 191 , 192 ]. Current practice requires the measurement of ER expression on both—primary invasive tumors and recurrent lesions. This procedure is mandatory to provide the selection of those patients who will most benefit from the implementation of the endocrine therapy mainly selective estrogen receptor modulators, pure estrogen receptor downregulators, or third-generation aromatase inhibitors [ 193 ]. Even though the diagnosis of altered expression of ER is particularly relevant in terms of the proper therapy selection, ER expression might also constitute a predictive factor—patients with high ER expression usually present significantly better clinical outcomes [ 194 ]. A relationship was observed between ER expression and the family history of breast cancer which further facilitates the utility of ER expression as a diagnostic biomarker of breast cancer especially in cases of familial risk [ 195 ]. Besides, Konan et al. reported that ERα-36 expression could constitute one of the potential targets of PR-positive cancers and a prognostic marker at the same time [ 196 ].

5.2. Progesterone Receptor

PR is highly expressed (>50%) in patients with ER-positive while quite rarely in those with ER-negative breast cancer [ 197 ]. PR expression is regulated by ER therefore, physiological values of PR inform about the functional ER pathway [ 197 ]. However, both ER and PR are abundantly expressed in breast cancer cells and both are considered as diagnostic and prognostic biomarkers of breast cancer (especially ER-positive ones) [ 198 ]. Greater PR expression is positively associated with the overall survival, time to recurrence, and time to either treatment failure or progression while lowered PR levels are usually related to a more aggressive course of the disease as well as poorer recurrence and prognosis [ 199 ]. Thus, favorable management of breast cancer patients highly depends on the assessment of PR expression. Nevertheless, the predictive value of PR expression still remains controversial [ 200 ].

5.3. Human Epidermal Growth Factor Receptor 2

The expression of human epidermal growth factor receptor 2 (HER2) accounts for approximately 15–25% of breast cancers and its status is primarily relevant in the choice of proper management with breast cancer patients; HER2 overexpression is one of the earliest events during breast carcinogenesis [ 201 ]. Besides, HER2 increases the detection rate of metastatic or recurrent breast cancers from 50% to even more than 80% [ 202 ]. Serum HER2 levels are considered to be a promising real-time marker of tumor presence or recurrence [ 203 ]. HER2 amplification leads to further overactivation of the pro-oncogenic signaling pathways leading to uncontrolled growth of cancer cells which corresponds with poorer clinical outcomes in the case of HER2-positive cancers [ 204 ]. Overexpression of HER2 also correlates with a significantly shorter disease-free period [ 205 ] as well as histologic type, pathologic state of cancer, and a number of axillary nodes with metastatic cancerous cells [ 205 ].

5.4. Antigen Ki-67

The Ki-67 protein is a cellular marker of proliferation and the Ki-67 proliferation index is an excellent marker to provide information about the proliferation of cancerous cells particularly in the case of breast cancer. The proliferative activities determined by Ki-67 reflect the aggressiveness of cancer along with the response to treatment and recurrence time [ 206 ]. Thus, Ki-67 is crucial in terms of the choice of the proper treatment therapy and the potential follow-ups due to recurrence. Though, due to several limitations of the analytical validity of Ki-67 immunohistochemistry, Ki-67 expression levels should be considered benevolently in terms of definite treatment decisions. Ki-67 might be considered as a potential prognostic factor as well; according to a meta-analysis of 68 studies involving 12,155 patients, the overexpression of Ki-67 is associated with poorer clinical outcomes of patients [ 207 ]. High expression of Ki-67 also reflects poorer survival rates of breast cancer patients [ 208 ]. There are speculations whether Ki-67 could be considered as a potential predictive marker, however, such data is still limited and contradictory.

Mib1 (antibody against Ki-67) proliferation index remains a reliable diagnostic biomarker of breast cancer, similarly to Ki-67. A decrease in both Mib1 and Ki-67 expression levels is associated with a good response of breast cancer patients to preoperative treatment [ 209 ]. Mib1 levels are significantly greater in patients with concomitant p53 mutations [ 210 ]. Mib1 assessment might be especially useful in cases of biopsy specimens small in size, inappropriate for neither mitotic index nor S-phase fraction evaluation [ 211 ].

5.6. E-Cadherin

E-cadherin is a critical protein in the epithelial-mesenchymal transition (EMT); loss of its expression leads to the gradual transformation into mesenchymal phenotype which is further associated with increased risk of metastasis. The utility of E-cadherin as a breast biomarker is yet questionable, however, some research indicated that its expression is potentially associated with several breast cancer characteristics such as tumor size, TNM stage, or lymph node status [ 212 ]. Low or even total loss of E-cadherin expression might be potentially useful in the determination of histologic subtype of breast cancer [ 213 , 214 ]. E-cadherin levels do not seem to be promising in terms of patients’ survival rates assessment, however, there are some reports indicating that higher levels of E-cadherin were associated with shorter survival rates in patients with invasive breast carcinoma [ 213 , 215 ]. Lowered E-cadherin expression is positively associated with lymph node metastasis [ 216 ].

5.7. Circulating Circular RNA

Circulating circular RNAs (circRNAs) belong to the group of non-coding RNA and were quite recently shown to be crucial in terms of several hallmarks of breast carcinogenesis including apoptosis, enhanced proliferation, or increased metastatic potential [ 217 ]. One of the most comprehensively described circRNAs, mostly specific to breast cancer include circFBXW7—which was proposed as a potential diagnostic biomarker as well as therapeutic tool for patients with triple-negative breast cancer (TNBC), as well as hsa_circ_0072309 which is abundantly expressed in breast cancer patients and usually associated with poorer survival rates [ 218 ]. Has_circ_0001785 is considered to be promising as a diagnostic biomarker of breast cancer [ 219 ]. The number of circRNAs dysregulated during breast carcinogenesis is significant; their expression might be either upregulated (e.g., has_circ_103110, circDENND4C) or downregulated (e.g., has_circ_006054, circ-Foxo3) [ 220 ]. Besides, specific circRNAs have been reported in different types of breast cancer such as TNBC, HER2-positive, and ER-positive [ 221 ]. Recently it was showed that an interaction between circRNAs and micro-RNA—namely in the form of Cx43/has_circ_0077755/miR-182 post-transcriptional axis, might predict breast cancer initiation as well as further prognosis. Cx43 is transmembrane protein responsible for epithelial homeostasis that mediates junction intercellular communication and its loss dysregulates post-transcriptional axes in breast cancer initiation [ 222 ].

Loss-of-function mutations in the TP53 (P53) gene have been found in numerous cancer types including osteosarcomas, leukemia, brain tumors, adrenocortical carcinomas, and breast cancers [ 223 , 224 ]. P53 protein is essential for normal cellular homeostasis and genome maintenance by mediating cellular stress responses including cell cycle arrest, apoptosis, DNA repair, and cellular senescence [ 225 ]. The silencing mutation of the P53 gene is evident at an early stage of cancer progression. In breast cancer, the prevalence of TP53 mutations is present in approximately 80% of patients with the TNBC and 10% of patients with Luminal A disease [ 226 ].

There have been many studies showing the prognostic role of p53 loss-of-function mutation in breast cancer [ 227 , 228 ]. However, the missense mutations may alters p53 properties causing not only a loss of wild-type function, but also acquisition novel activities-gain of function [ 229 ]. The IHC status of p53 has been proposed as a specific prognostic factor in TNBC, and a feature that divides TNBC into 2 distinct subgroups: a p53-negative normal breast-like TN subgroup, and a p53-positive basal-like subgroup with worse overall survival [ 230 , 231 , 232 ]. However, there is not enough evidence to utilize p53 gene mutational status or immunohistochemically measured protein for determining standardized prognosis in patients with breast cancer [ 233 ].

5.9. MicroRNA

MicroRNAs (miRNA) are a major class of endogenous non-coding RNA molecules (19–25 nucleotides) that have regulatory roles in multiple pathways [ 234 ]. Some miRNAs are related to the development, progression, and response of the tumor to therapy [ 235 ]. Several studies have investigated abnormally expressed miRNAs as biomarkers in breast cancer tissue samples. According to meta-analysis by Adhami et al. two miRNAs (miRNA-21 and miRNA-210) were upregulated consistently and six miRNAs (miRNA-145, miRNA-139-5p, miRNA-195, miRNA-99a, miRNA-497, and miRNA-205) were downregulated consistently in at least three studies [ 236 ].

The miRNA-21 overexpression was observed in TNBC tissues and was associated with enhanced invasion and proliferation of TNBC cells as well as downregulation of the PTEN expression [ 237 ]. Similarly, the high expression of miRNA-210 is related to tumor proliferation, invasion, and poor survival rates in breast cancer patients [ 238 , 239 ].

The miRNA-145 is an anti-cancer agent having the property of inhibiting migration and proliferation of breast cancer cells via regulating the TGF-β1 expression [ 240 ]. However, the miRNA-145 is downregulated in both plasma and tumors of breast cancer patients [ 241 ]. Similarly, miRNA-139-5p and miRNA-195 have tumor suppressor activity in various cancers [ 242 , 243 ].

Nevertheless, further clinical researches focusing on these miRNAs are needed to utilize them as reproducible, disease-specific markers that have a high level of specificity and sensitivity.

5.10. Tumor-Associated Macrophages

Macrophages are known for their immunomodulatory effects and they can be divided according to their phenotypes into M1- or M2-like states [ 244 , 245 ]. M1 macrophages secrete IL-12 and tumor necrosis factor with antimicrobial and antitumor effects. M2 macrophages produce cytokines, including IL-10, IL-1 receptor antagonist type II, and IL-1 decoy receptor. Therefore, macrophages with M1-like phenotype have been linked to good disease course while M2-like phenotype has been associated with adverse outcome, potentially through immunosuppression and the promotion of angiogenesis and tumor cell proliferation and invasion [ 246 , 247 ]. In literature, tumor-associated macrophages (TAMs) are associated with M2 macrophages which promote tumor growth and metastasis.

For breast cancer, studies have shown that the density of TAMs is related to hormone receptor status, stage, histologic grade, lymph node metastasis, and vascular invasion [ 248 , 249 , 250 , 251 ]. According to meta-analysis conducted by Zhao et al. high density of TAMs was related to overall survival disease-free survival [ 252 ].

Conversely, M1 polarized macrophages are linked to favorable prognoses in various cancers [ 253 , 254 , 255 ]. In breast cancer, the high density of M1-like macrophages predicted improved survival in patients with HER2+ phenotype and may be a potential prognostic marker [ 256 ].

However, further studies are needed to clarify the influence of macrophages on breast cancer biology as well as investigate the role of their intratumoral distribution and surface marker selection.

5.11. Inflammation-Based Models

The host inflammatory and immune responses in the tumor and its microenvironment are critical components in cancer development and progression [ 257 ]. The tumor-induced systemic inflammatory response leads to alterations of peripheral blood white blood cells [ 258 ]. Therefore, the relationship between peripheral blood inflammatory cells may serve as an accessible and early method of predicting patient prognosis. Recent studies have reported the predictive role of the inflammatory cell ratios: neutrophil-to-lymphocyte ratio, the lymphocyte-to-monocyte ratio, and the platelet-to-lymphocyte ratio for prognosis in different cancers [ 258 , 259 , 260 , 261 ].

5.11.1. The Neutrophil-to-Lymphocyte Ratio (NLR)

In an extensive study on 27,031 cancer patients, Proctor et al. analyzed the prognostic value of NLR and found a significant relationship between NLR and survival in various cancers including breast cancer [ 262 ]. There are pieces of evidence of the role of lymphocytes in breast cancer immunosurveillance [ 263 , 264 ]. Opposingly neutrophils suppress the cytolytic activity of lymphocytes, leading to enhanced angiogenesis and tumor growth and progression [ 265 ].

Azab et al. first reported that NLR before chemotherapy was an independent factor for long-term mortality and related it to age and tumor size in breast cancer [ 266 ]. In a recent meta-analysis by Guo et al., performed on 17,079 individuals, the high NLR level was associated with both poor overall survival as well as disease-free survival for breast cancer patients. Moreover, it was reported that association between NLR and overall survival was stronger in TNBC patients than in HER2-positive ones [ 267 ].

5.11.2. Lymphocyte-to-Monocyte Ratio

The association of the lymphocyte-to-monocyte ratio (LMR) with patients’ prognosis has been reported for several cancers [ 268 , 269 ]. As lymphocytes have an antitumor activity by inducing cytotoxic cell death and inhibiting tumor proliferation [ 270 ], the monocytes are involved in tumorigenesis, including differentiation into TAMs [ 246 , 247 , 271 ]. In the tumor microenvironment, cytokines, and free radicals that are secreted by monocytes and macrophages are associated with angiogenesis, tumor cell invasion, and metastasis [ 271 ].

A meta-analysis investigating the prognostic effect of LMR showed that low LMR levels are associated with shorter overall survival outcomes in Asian populations, TNBC patients, and patients with non-metastatic and mixed stages [ 272 ]. Moreover, high LMR levels are associated with favorable disease-free survival of breast cancer patients under neoadjuvant chemotherapy [ 273 ].

5.11.3. Platelet-to-Lymphocyte Ratio (PLR)

A high platelet count has been associated with poor prognosis in several types of cancers [ 274 , 275 , 276 ]. Platelets contain both pro-inflammatory molecules and cytokines (P-selectin, CD40L, and interleukin (IL)-1, IL-3, and IL-6) and many anti-inflammatory cytokines. Tumor angiogenesis and growth may be stimulated by the secretion of platelet-derived growth factor, vascular endothelial growth factor, transforming growth factor-beta, and platelet factor 4 [ 277 , 278 , 279 ].

A meta-analysis study investigated the prognostic importance of PLR by analyzing 5542 breast cancer patients. High PLR level was associated with poor prognosis (overall survival and disease-free survival), yet, its prognostic value was not determined for molecular subtypes of breast cancer. Nevertheless, an association was found between PLR and clinicopathological features of the tumor, including stage, lymph node metastasis, and distant metastasis [ 280 ]. In the aforementioned meta-analysis, there was a difference in the incidence of high levels of PLR between HER2 statuses [ 280 ], while other studies found a difference between hormone ER or PR statuses [ 281 , 282 ].

6. Treatment Strategies

6.1. surgery.

There are two major types of surgical procedures enabling the removal of breast cancerous tissues and those include (1) breast-conserving surgery (BCS) and (2) mastectomy. BCS—also called partial/segmental mastectomy, lumpectomy, wide local excision, or quadrantectomy—enables the removal of the cancerous tissue with simultaneous preservation of intact breast tissue often combined with plastic surgery technics called oncoplasty. Mastectomy is a complete removal of the breast and is often associated with immediately breast reconstruction. The removal of affected lymph nodes involves sentinel lymph node biopsy (SLNB) and axillary lymph node dissection (ALND). Even though BCS seems to be highly more beneficial for patients, those who were treated with this technique often show a tendency for a further need for a complete mastectomy [ 283 ]. However, usage of BCS is mostly related to significantly better cosmetic outcomes, lowered psychological burden of a patient, as well as reduced number of postoperative complications [ 284 ]. Guidelines of the European Society for Medical Oncology (ESMO) for patients with early breast cancer make the choice of therapy dependent to tumor size, feasibility of surgery, clinical phenotype, and patient’s willingness to preserve the breast [ 285 ].

6.2. Chemotherapy

Chemotherapy is a systemic treatment of BC and might be either neoadjuvant or adjuvant. Choosing the most appropriate one is individualized according to the characteristics of the breast tumor; chemotherapy might also be used in the secondary breast cancer. Neoadjuvant chemotherapy is used for locally advanced BC, inflammatory breast cancers, for downstaging large tumors to allow BCS or in small tumors with worse prognostics molecular subtypes (HER2 or TNBC) which can help to identify prognostics and predictive factors of response and can be provided intravenously or orally. Currently, treatment includes a simultaneous application of schemes 2–3 of the following drugs—carboplatin, cyclophosphamide, 5-fluorouracil/capecitabine, taxanes (paclitaxel, docetaxel), and anthracyclines (doxorubicin, epirubicin). The choice of the proper drug is of major importance since different molecular breast cancer subtypes respond differently to preoperative chemotherapy [ 286 ]. Preoperative chemotherapy is comparably effective to postoperative chemotherapy [ 287 ].

Even though chemotherapy is considered to be effective, its usage very often leads to several side effects including hair loss, nausea/vomiting, diarrhea, mouth sores, fatigue, increased susceptibility to infections, bone marrow supression, combined with leucopenia, anaemia, easier bruising or bleeding; other less frequent side effects include cardiomyopathy, neuropathy, hand-foot syndrome, impaired mental functions. In younger women, disruptions of the menstrual cycle and fertility issues might also appear. Special form of chemotherapy is electrochemotherapy which can be used in patients with breast cancer that has spread to the skin, however, it is still quite uncommon and not available in most clinics.

6.3. Radiation Therapy

Radiotherapy is local treatment of BC, typically provided after surgery and/or chemotherapy. It is performed to ensure that all of the cancerous cells remain destroyed, minimizing the possibility of breast cancer recurrence. Further, radiation therapy is favorable in the case of metastatic or unresectable breast cancer [ 288 ]. Choice of the type of radiation therapy depends on previous type of surgery or specific clinical situation; most common techniques include breast radiotherapy (always applied after BC), chest-wall radiotherapy (usually after mastectomy), and ‘breast boost’ (a boost of high-dose radiotherapy to the place of tumor bed as a complement of breast radiotherapy after BCS). Regarding breast radiotherapy specifically, several types are distinguished including

• (1) intraoperative radiation therapy (IORT)
• (2) 3D-conformal radiotherapy (3D-CRT)
• (3) intensity-modulated radiotherapy (IMRT)
• (4) brachytherapy—which refers to internal radiation in contrast to other above-mentioned techniques.

Irritation and darkening of the skin exposed to radiation, fatigue, and lymphoedema are one of the most common side effects of radiation therapy applied in breast cancer patients. Nonetheless, radiation therapy is significantly associated with the improvement of the overall survival rates of patients and lowered risk of recurrence [ 289 ].

6.4. Endocrinal (Hormonal) Therapy

Endocrinal therapy might be used either as a neoadjuvant or adjuvant therapy in patients with Luminal–molecular subtype of BC; it is effective in cases of breast cancer recurrence or metastasis. Since the expression of ERs, a very frequent phenomenon in breast cancer patients, its blockage via hormonal therapy is commonly used as one of the potential treatment modalities. Endocrinal therapy aims to lower the estrogen levels or prevents breast cancer cells to be stimulated by estrogen. Drugs that block ERs include selective estrogen receptor modulators (SERMs) (tamoxifen, toremifene) and selective estrogen receptor degraders (SERDs) (fulvestrant) while treatments that aim to lower the estrogen levels include aromatase inhibitors (AIs) (letrozole, anastrazole, exemestane) [ 290 , 291 ]. In the case of pre-menopausal women, ovarian suppression induced by oophorectomy, luteinizing hormone-releasing hormone analogs, or several chemotherapy drugs, are also effective in lowering estrogen levels [ 292 ]. However, approximately 50% of hormonoreceptor-positive breast cancer become progressively resistant to hormonal therapy during such treatment [ 293 ]. Endocrinal therapy combined with chemotherapy is associated with the reduction of mortality rates amongst breast cancer patients [ 294 ].

6.5. Biological Therapy

Biological therapy (targeted therapy) can be provided at every stage of breast therapy– before surgery as neoadjuvant therapy or after surgery as adjuvant therapy. Biological therapy is quite common in HER2-positive breast cancer patients; major drugs include trastuzumab, pertuzumab, trastuzumab deruxtecan, lapatinib, and neratinib [ 295 , 296 , 297 , 298 , 299 ]. Further, the efficacy of angiogenesis inhibitors such as a recombinant humanized monoclonal anti-VEGF antibody (rhuMAb VEGF) or bevacizumab are continuously investigated [ 300 ].

In the case of Luminal, HER2-negative breast cancer, pre-menopausal women more often receive everolimus -TOR inhibitor with exemestane while postmenopausal women often receive CDK 4–6 inhibitor palbociclib or ribociclib simultaneously, combined with hormonal therapy [ 301 , 302 , 303 ]. Two penultimate drugs along with abemaciclib and everolimus can also be used in HER2-negative and estrogen-positive breast cancer [ 304 , 305 ]. Atezolizumab is approved in triple-negative breast cancer, while denosumab is approved in case of metastasis to the bones [ 306 , 307 , 308 ].

7. Conclusions

In this review, we aimed to summarize and update the current knowledge about breast cancer with an emphasis on its current epidemiology, risk factors, classification, prognostic biomarkers, and available treatment strategies. Since both the morbidity and mortality rates of breast cancer have significantly increased over the past decades, it is an urgent need to provide the most effective prevention taking into account that modifiable risk factors might be crucial in providing the reduction of breast cancer incidents. So far, mammography and sonography is the most common screening test enabling quite an early detection of breast cancer. The continuous search for prognostic biomarkers and targets for the potential biological therapies has significantly contributed to the improvement of management and clinical outcomes of breast cancer patients.

Author Contributions

Conceptualization, A.F., R.S. and A.S.; critical review of literature, S.Ł., M.C., A.F., J.B., R.S., A.S.; writing—original draft preparation, M.C., A.F.; writing—review and editing, S.Ł., M.C., A.F., J.B., R.S., A.S.; supervision, R.S. All authors have read and agreed to the published version of the manuscript.

This research received no external funding.

Conflicts of Interest

The authors declare no conflict of interest.

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Vegetarian and vegan diets linked to lower risk of heart disease, cancer and death, large review finds

A plant-based diet is associated with a reduced risk of heart disease, cancer and death, according to a large-scale review published Wednesday. 

The research , which appears in the journal PLOS ONE, analyzed the results of nearly 50 studies published from 2000 to 2023.

The studies examined the health effects of either vegetarian diets or vegan regimens, which restrict any food derived from animals, including dairy.

A clear consensus emerged: Both eating patterns were associated with a lower risk of cancer and ischemic heart disease (heart problems caused by narrowed arteries). In particular, the diets seemed to reduce the risk of prostate cancer and gastrointestinal cancers like colon cancer. Vegetarian diets were also linked to a lower risk of dying from cardiovascular disease.

In addition, plant-based diets were associated with a reduction in risk factors for heart disease and cancer, including high body weight, inflammation and LDL or “bad” cholesterol. 

“This research shows, in general, that a plant-based diet can be beneficial, and taking small steps in that direction can make a difference,” said Matthew Landry, one of the review’s authors and an assistant professor of population health and disease prevention at the University of California, Irvine.

“You don’t have to go completely vegan to see some of these benefits,” he added. “Even reducing a day or two per week of animal-based consumption can have benefits over time.”

However, Dr. Walter Willett, a professor of epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, pointed out that not everyone who follows a plant-based diet eats the same foods, so levels of healthiness still vary.

“A vegetarian diet could be based primarily on refined starches and sugar, which we see to be the worst dietary pattern,” Willett, who was not involved in the new research, said in an email. 

A healthy plant-based diet, he said, should consist mostly of whole grains, fruits, vegetables, nuts, soy, beans and non-hydrogenated plant oils. 

Why are plant-based diets so healthy?

Researchers are still investigating the mechanisms through which plant-based diets lower the risk of disease. 

Some of it may have to do with preventing obesity, which is linked to heart disease and certain cancers . But the benefits likely extend beyond that, Landry said. 

“Some of it is independent of weight. Even when weight is maintained or doesn’t change, we still see reductions in some of these other clinical health outcomes, especially when it relates to cardiovascular disease,” he said.

One possible reason is that many fruits and vegetables are high in anti-inflammatory nutrients and antioxidants, which can reduce plaque buildup in the arteries.

Plant-based diets also tend to be high in fiber, which helps lower bad cholesterol, said Brie Turner-McGrievy, a professor of health promotion, education and behavior at the University of South Carolina. She published a study in 2014 which found that plant-based diets can reduce risk factors for heart disease, stroke and Type 2 diabetes. The research was included in the new review.

“Soluble fiber that’s found in things like beans and oats is really a powerful tool to help lower LDL cholesterol levels,” she said.

Turner-McGrievy noted, though, that much of that benefit can only be achieved through eating whole foods: “It’s not like you can take a fiber supplement and hope to have these same outcomes.”

Another benefit of a plant-based diet may come simply from the absence of meat, she said. People who are vegan tend to consume less saturated fat than meat eaters. 

“It’s just really hard to lower your saturated fat intake if you’re consuming animal-based foods,” Turner-McGrievy said. “Cheese, for example, is the No. 1 source of saturated fat in the diet.”

Processed meat products such as bacon or salami are also known to raise the risk of cancer , according to the World Health Organization. The agency considers red meat in general to be a “probable human carcinogen.”

Is a vegan or vegetarian diet right for everyone?

According to the Academy of Nutrition and Dietetics, vegetarian and vegan diets are adequate and healthy at all stages of life , including pregnancy, childhood and older adulthood. 

But the new review stopped short of recommending plant-based diets for everyone. 

“During pregnancy, it’s not recommended based on the data that we have to use a strict vegetarian diet,” said Dr. Federica Guaraldi, one of the review’s authors and an endocrinologist at the IRCCS Institute of Neurological Sciences of Bologna in Italy. 

Guaraldi and her co-authors found that the plant-based regimens studied didn’t lower the risk of gestational diabetes or hypertension in pregnant women. One study included in the review suggested that pregnant women who followed a vegetarian diet had lower levels of zinc — which is important for children's growth, development and immune function — than those who ate meat. Another study in the review found that vegetarian mothers had an increased risk of delivering babies with low birthweights. 

The review's authors also cautioned that plant-based diets might lead to vitamin B12 deficiencies in the general population. Landry said that can be addressed by taking a B12 supplement.  

“From my perspective as a dietitian, a healthy plant-based diet — either vegetarian or vegan — can really meet just about all your vitamin and mineral needs,” he said. 

Aria Bendix is the breaking health reporter for NBC News Digital.

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• Health Topics A-Z

Liver Cancer Basics

• You can lower your risk of getting liver cancer in several ways.
• Keep a healthy weight and get enough physical activity.
• Get vaccinated against hepatitis B and tested for hepatitis C.
• Avoid drinking too much alcohol.
• Don't smoke cigarettes.

Liver cancer is a disease in which cells in the liver grow out of control. The liver is in the upper abdomen near the stomach, intestines, gallbladder, and pancreas. Intrahepatic bile ducts are a network of small tubes that carry bile inside the liver.

The liver does many jobs, including:

• Storing nutrients.
• Removing waste products and worn-out cells from the blood.
• Filtering and processing chemicals in food, alcohol, and medications.
• Producing bile, a solution that helps digest fats and eliminate waste products.

© 2010 Terese Winslow LLC. US government has certain rights. Used with permission. Contact artist at www.teresewinslow.com for licensing.

In its early stages, liver cancer may not have symptoms that can be seen or felt. However, as the cancer grows larger, people may notice one or more of these common symptoms. It's important to remember that these symptoms could also be caused by other health conditions. If you have any of these symptoms, talk to your doctor.

Liver cancer symptoms may include:

• Discomfort in the upper abdomen on the right side.
• A swollen abdomen.
• A hard lump on the right side just below the rib cage.
• Pain near the right shoulder blade or in the back.
• Jaundice (yellowing of the skin and whites of the eyes).
• Easy bruising or bleeding.
• Unusual tiredness.
• Nausea and vomiting.
• Loss of appetite.
• Weight loss for no known reason.

Risk factors

Behaviors and conditions that increase risk for getting liver cancer are:

• Being overweight or having obesity.
• Having a long-term hepatitis B virus or hepatitis C virus infection.
• Smoking cigarettes.
• Drinking alcohol.
• Having cirrhosis (scarring of the liver, which can also be caused by hepatitis and alcohol use).
• Having nonalcoholic fatty liver disease (extra fat in the liver that is not caused by alcohol).
• Having diabetes.
• Having hemochromatosis, a condition in which the body takes up and stores more iron than it needs.
• Eating foods that have aflatoxin (a fungus that can grow on foods, such as grains and nuts that have not been stored properly).

I Have Liver Cancer, But You Don't Have To‎

Reducing risk.

You can lower your risk of getting liver cancer in the following ways:

• Get vaccinated against hepatitis B.
• Get tested for hepatitis C, and get medical care if you have it.
• Don't smoke, or quit if you do.

Preventing Liver Cancer Among Opioid Users ‎

The Data Visualizations tool makes it easy for anyone to explore and use the latest official federal government cancer data from United States Cancer Statistics. It includes the latest cancer data covering the US population.

• Cancer Statistics At a Glance : See rates or numbers of new liver and intrahepatic bile duct cancers, or cancer deaths, for the entire United States and individual states. Also, see the top 10 cancers for men and women.
• Cancers by Age, Sex, Race, and Ethnicity : See rates or numbers of new liver and intrahepatic bile duct cancers, or cancer deaths, by race and ethnicity, sex, and age group.
• Trends : See how the rates of new liver and intrahepatic bile duct cancers or cancer deaths changed over time for the entire United States and individual states.
• Liver and Bile Duct Cancer (National Cancer Institute)
• Video: Hepatitis and Liver Cancer Statistics (National Cancer Institute)
• Alcohol and Cancer (CDC)
• Viral Hepatitis and Liver Cancer Prevention Profiles

Liver Cancer

To lower your risk, get vaccinated against hepatitis B, get tested for hepatitis C, and avoid drinking too much alcohol.