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New cancer treatment may reawaken the immune system

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Immunotherapy is a promising strategy to treat cancer by stimulating the body’s own immune system to destroy tumor cells, but it only works for a handful of cancers. MIT researchers have now discovered a new way to jump-start the immune system to attack tumors, which they hope could allow immunotherapy to be used against more types of cancer.

Their novel approach involves removing tumor cells from the body, treating them with chemotherapy drugs, and then placing them back in the tumor. When delivered along with drugs that activate T cells, these injured cancer cells appear to act as a distress signal that spurs the T cells into action.

“When you create cells that have DNA damage but are not killed, under certain conditions those live, injured cells can send a signal that awakens the immune system,” says Michael Yaffe, who is a David H. Koch Professor of Science, the director of the MIT Center for Precision Cancer Medicine, and a member of MIT’s Koch Institute for Integrative Cancer Research.

In mouse studies, the researchers found that this treatment could completely eliminate tumors in nearly half of the mice.

Yaffe and Darrell Irvine, who is the Underwood-Prescott Professor with appointments in MIT’s departments of Biological Engineering and Materials Science and Engineering, and an associate director of the Koch Institute, are the senior authors of the study, which appears today in Science Signaling . MIT postdoc Ganapathy Sriram and Lauren Milling PhD ’21 are the lead authors of the paper.

T cell activation

One class of drugs currently used for cancer immunotherapy is checkpoint blockade inhibitors, which take the brakes off of T cells that have become “exhausted” and unable to attack tumors. These drugs have shown success in treating a few types of cancer but do not work against many others.

Yaffe and his colleagues set out to try to improve the performance of these drugs by combining them with cytotoxic chemotherapy drugs, in hopes that the chemotherapy could help stimulate the immune system to kill tumor cells. This approach is based on a phenomenon known as immunogenic cell death, in which dead or dying tumor cells send signals that attract the immune system’s attention.

Several clinical trials combining chemotherapy and immunotherapy drugs are underway, but little is known so far about the best way to combine these two types of treatment.

The MIT team began by treating cancer cells with several different chemotherapy drugs, at different doses. Twenty-four hours after the treatment, the researchers added dendritic cells to each dish, followed 24 hours later by T cells. Then, they measured how well the T cells were able to kill the cancer cells. To their surprise, they found that most of the chemotherapy drugs didn’t help very much. And those that did help appeared to work best at low doses that didn’t kill many cells.

The researchers later realized why this was so: It wasn’t dead tumor cells that were stimulating the immune system; instead, the critical factor was cells that were injured by chemotherapy but still alive.

“This describes a new concept of immunogenic cell injury rather than immunogenic cell death for cancer treatment,” Yaffe says. “We showed that if you treated tumor cells in a dish, when you injected them back directly into the tumor and gave checkpoint blockade inhibitors, the live, injured cells were the ones that reawaken the immune system.”

The drugs that appear to work best with this approach are drugs that cause DNA damage. The researchers found that when DNA damage occurs in tumor cells, it activates cellular pathways that respond to stress. These pathways send out distress signals that provoke T cells to leap into action and destroy not only those injured cells but any tumor cells nearby.

“Our findings fit perfectly with the concept that ‘danger signals’ within cells can talk to the immune system, a theory pioneered by Polly Matzinger at NIH in the 1990s, though still not universally accepted,” Yaffe says.  

Tumor elimination

In studies of mice with melanoma and breast tumors, the researchers showed that this treatment eliminated tumors completely in 40 percent of the mice. Furthermore, when the researchers injected cancer cells into these same mice several months later, their T cells recognized them and destroyed them before they could form new tumors.

The researchers also tried injecting DNA-damaging drugs directly into the tumors, instead of treating cells outside the body, but they found this was not effective because the chemotherapy drugs also harmed T cells and other immune cells near the tumor. Also, injecting the injured cells without checkpoint blockade inhibitors had little effect.

“You have to present something that can act as an immunostimulant, but then you also have to release the preexisting block on the immune cells,” Yaffe says.

Yaffe hopes to test this approach in patients whose tumors have not responded to immunotherapy, but more study is needed first to determine which drugs, and at which doses, would be most beneficial for different types of tumors. The researchers are also further investigating the details of exactly how the injured tumor cells stimulate such a strong T cell response.

The research was funded, in part, by the National Institutes of Health, the Mazumdar-Shaw International Oncology Fellowship, the MIT Center for Precision Cancer Medicine, and the Charles and Marjorie Holloway Foundation.

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Refractoriness to surgical resection and chemotherapy makes intrahepatic cholangiocarcinoma (ICC) a fatal cancer of the digestive system with high mortality and poor prognosis. Important function invests circR...

Unveiling the gastric microbiota: implications for gastric carcinogenesis, immune responses, and clinical prospects

High-throughput sequencing has ushered in a paradigm shift in gastric microbiota, breaking the stereotype that the stomach is hostile to microorganisms beyond H. pylori . Recent attention directed toward the compo...

The histone lysine acetyltransferase KAT2B inhibits cholangiocarcinoma growth: evidence for interaction with SP1 to regulate NF2-YAP signaling

Cholangiocarcinoma (CCA) is a highly malignant cancer of the biliary tract with poor prognosis. Further mechanistic insights into the molecular mechanisms of CCA are needed to develop more effective target the...

PRMT6-mediated transcriptional activation of ythdf2 promotes glioblastoma migration, invasion, and emt via the wnt–β-catenin pathway

Protein arginine methyltransferase 6 (PRMT6) plays a crucial role in various pathophysiological processes and diseases. Glioblastoma (GBM; WHO Grade 4 glioma) is the most common and lethal primary brain tumor ...

CCAAT enhancer binding protein delta activates vesicle associated membrane protein 3 transcription to enhance chemoresistance and extracellular PD-L1 expression in triple-negative breast cancer

Chemoresistance and immunosuppression are two major obstacles in the current anti-cancer treatments. This study investigates the involvements of a CCAAT enhancer binding protein delta (CEBPD)/vesicle associate...

Inhibition of autophagy-related protein 7 enhances anti-tumor immune response and improves efficacy of immune checkpoint blockade in microsatellite instability colorectal cancer

The efficacy of anti-PD-1 therapy is primarily hindered by the limited T-cell immune response rate and immune evasion capacity of tumor cells. Autophagy-related protein 7 (ATG7) plays an important role in auto...

Correction: Targeting of focal adhesion kinase enhances the immunogenic cell death of PEGylated liposome doxorubicin to optimize therapeutic responses of immune checkpoint blockade

The original article was published in Journal of Experimental & Clinical Cancer Research 2024 43 :51

Augmented ERO1α upon mTORC1 activation induces ferroptosis resistance and tumor progression via upregulation of SLC7A11

The dysregulated mechanistic target of rapamycin complex 1 (mTORC1) signaling plays a critical role in ferroptosis resistance and tumorigenesis. However, the precise underlying mechanisms still need to be full...

METTL3 recruiting M2-type immunosuppressed macrophages by targeting m6A-SNAIL-CXCL2 axis to promote colorectal cancer pulmonary metastasis

The regulatory role of N6-methyladenosine (m6A) modification in the onset and progression of cancer has garnered increasing attention in recent years. However, the specific role of m6A modification in pulmonar...

HERC5 downregulation in non-small cell lung cancer is associated with altered energy metabolism and metastasis

Metastasis is the leading cause of cancer-related death in non-small cell lung cancer (NSCLC) patients. We previously showed that low HERC5 expression predicts early tumor dissemination and a dismal prognosis ...

Targeting FTO induces colorectal cancer ferroptotic cell death by decreasing SLC7A11/GPX4 expression

Ferroptosis is a newly identified iron-dependent form of death that is becoming increasingly recognized as a promising avenue for cancer therapy. N6-methyladenosine (m 6 A) is the most abundant reversible methylati...

The Correction to this article has been published in Journal of Experimental & Clinical Cancer Research 2024 43 :131

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Cancer patients often do better with less intensive treatment, new research finds

Scaling back treatment for some cancers can make life easier for patients without hurting the outcomes.

Scaling back treatment for three kinds of cancer can make life easier for patients without compromising outcomes, doctors reported at the world’s largest cancer conference.

It’s part of a long-term trend toward studying whether doing less — less surgery, less chemotherapy, or less radiation — can help patients live longer and feel better. The latest studies involved ovarian and esophageal cancer and Hodgkin’s lymphoma.

Thirty years ago, cancer research was about doing more. In one sobering example, women with advanced breast cancer were pushed to the brink of death with massive doses of chemotherapy and bone marrow transplants. The approach didn’t work any better than regular chemotherapy, and patients suffered.

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Now, in a quest to optimize cancer care, researchers are asking: “Do we need all that treatment that we have used in the past?”

It’s a question, “that should be asked over and over again,” said Dr. Tatjana Kolevska, medical director for the Kaiser Permanente National Cancer Excellence Program, who was not involved in the new research.

Often, doing less works because of improved drugs.

“The good news is that cancer treatment is not only becoming more effective, it’s becoming easier to tolerate and associated with less short-term and long-term complications,” said Dr. William G. Nelson of Johns Hopkins School of Medicine, who was also not involved in the new research.

Studies demonstrating the trend were discussed over the weekend at an American Society of Clinical Oncology conference in Chicago. Three cancers were highlighted:

• Ovarian cancer. French researchers found that it’s safe to avoid removing lymph nodes that appear healthy during surgery for advanced ovarian cancer. The study compared the results for 379 patients: Half had their lymph nodes removed and half did not. After nine years, there was no difference in how long the patients lived, and those with less-extreme surgery had fewer complications, such as the need for blood transfusions. The research was funded by the National Institute of Cancer in France.
• Esophageal cancer. A German study looked at 438 people with a type of cancer of the esophagus that can be treated with surgery. Half received a common treatment plan that included chemotherapy and surgery on the esophagus, the tube that carries food from the throat to the stomach. Half got another approach that includes radiation. Both techniques are considered standard. Which one patients get can depend on where they get treatment. After three years, 57 percent of those who got chemo and surgery were alive, compared to 51 percent of those who got chemo, surgery, and radiation. The German Research Foundation funded the study.
• Hodgkin’s lymphoma. A comparison of two chemotherapy regimens for advanced Hodgkin’s found the less intensive treatment was more effective for the blood cancer and caused fewer side effects. After four years, the less harsh chemo kept the disease in check in 94 percent of people, compared to 91 percent of those who had the more intense treatment. The trial included 1,482 people in nine countries — Germany, Austria, Switzerland, the Netherlands, Denmark, Sweden, Norway, Australia, and New Zealand — and was funded by Takeda Oncology, the maker of one of the drugs used in the gentler chemo that was studied.

Leading Change in Cancer Clinical Research, Because Our Patients Can’t Wait

May 31, 2024 , by W. Kimryn Rathmell, M.D., Ph.D., and Shaalan Beg, M.D.

Greater use of technologies that can increase participation in cancer clinical trials is just one of the innovations that can help overcome some of the bottlenecks holding up progress in clinical research. 

Thanks to advances in technology, data science, and infrastructure, the pace of discovery and innovation in cancer research has accelerated, producing an impressive range of potential new treatments and other interventions that are being tested in clinical studies . The extent of the innovative ideas that might help people live longer, improve our ability to detect cancer early, or otherwise transform care is staggering. 

Our understanding of tumor biology is also evolving, and those gains in knowledge are being translated into the continued discovery of targets for potential interventions  and the development of novel types of treatments. Some of these therapies are producing unprecedented clinical responses  in studies, including in traditionally difficult-to-treat cancers. 

These advances have contributed to a record number of Food and Drug Administration (FDA) approvals in recent years with, arguably, the most notable approvals being those for drugs that can be used for any cancer, regardless of where it is in the body . 

In some instances, the activity of new agents has been so profound that clinical investigators are having to rethink their criteria for implementation in patient care and their definitions of treatment response. 

For example, although HER2 has been a known therapeutic target in breast cancer for many decades, the new antibody-drug conjugates  (ADCs) that target HER2 have proven to be vastly more effective than the original HER2-targeted therapies. This has forced researchers to rethink fundamental questions about how these ADCs are used in patient care: Can they be effective in people whose tumors have lower expression of HER2 than we previously thought was needed ? And, if so, do we need to redefine how we classify HER2-positive cancer? 

As more innovative therapies like ADCs hit the clinic at a far more rapid cadence than ever before, the research community is being inundated with such fundamentally important questions.

However, the remarkable progress we're experiencing with novel new therapies is tempered by a critical bottleneck: the clinical research infrastructure can’t be expected to keep pace in this new landscape. 

Currently, many studies struggle to enroll enough participants. At the same time, there are patients who don’t have ready access to studies from which they might benefit. Furthermore, ideas researchers have today for studies of innovative new interventions might not come to fruition for 2 or 3 years, or even longer—years that people with cancer don’t have. 

The key to overcoming this bottleneck is to invite innovation to help reshape our clinical trials infrastructure. And here’s how we plan to accomplish that.

Testing Innovation in Cancer Clinical Trials

A transformation in cancer clinical research is already underway. That transformation has been led in part by the success of novel precision oncology approaches, such as those tested in the NCI-MATCH trial .

This innovative study ushered in novel ways of recruiting participants and involving oncologists at centers big and small. And NCI-MATCH has spawned several successor studies that are incorporating and building on its innovations and achievements.

An innovation that emerged from the COVID pandemic was the increase of remote work, even in the clinical trials domain. Indeed, staffing shortages have caused participation in NCI-funded trials to decline. In response, NCI is piloting a Virtual Clinical Trials Office to offer remote support staff to participating study sites. This support staff includes research nurses, clinical research associates, and data specialists, all of whom will help NCI-Designated Cancer Centers and community practices engaged in clinical research activities.

Such technology-enabled services can allow us to reimagine how clinical trials are designed and run. This includes developing technologies and processes for remotely identifying clinical trial participants, shipping medications to participants at home, having imaging performed in the health care settings where our patients live, and empowering local physicians to participate in clinical trials.

We also need mechanisms to test and implement innovations in designing and conducting clinical studies. 

For example, NCI recently established the Clinical Trials Innovation Unit (CTIU) to pressure test a variety of innovations. One of the first trials to emerge from the CTIU’s initial efforts was the Pragmatica-Lung Cancer Treatment Trial , a phase 3 study designed to be easy to launch, enroll, and interpret its results. 

The CTIU, which includes leadership from FDA and NCI’s National Clinical Trials Network , is already working on future innovations, including those that will streamline data collection and apply innovative approaches for other cancers, all with the goal of making cancer clinical studies less burdensome to run and easier for patients to participate.

Data-Driven Solutions

The era of data-driven health care is here, providing still more opportunities to transform cancer clinical research. 

The emergence of artificial intelligence (AI) solutions, large language models, and informatics brings real potential for wholesale changes in how we match patients to clinical studies, assess side effects, and monitor events like disease progression. 

Recognizing this potential, NCI is offering funding opportunities and other resources that will fuel the development of AI tools for clinical research, allow us to carefully test their usefulness, and ultimately deploy them across the oncology community. 

Creating Partnerships and Expanding Health Equity

To be sure, none of this will be, or can be, done by NCI alone. All these innovations require partnerships. We will increase our engagement with partners in the public- and private-sectors, including other government agencies and nonprofits. 

That includes high-level engagement with the Office of the National Coordinator for Health Information Technology (ONC), with input from FDA, Centers for Medicare & Medicaid Services, and Centers for Disease Control and Prevention.

Dr. W. Kimryn Rathmell, M.D., Ph.D.

NCI Director

One example of such a partnership is the USCDI+ Cancer program . Conducted under the auspices of the ONC, this program will further the aims of the White House's reignited Cancer Moonshot SM by encouraging the adoption and utilization of interoperable cancer health IT standards, providing resources to support cancer-specific use cases, and promoting alignment between federal partners. 

And just as importantly, the new partnerships we create must include those with patients, advocates, and communities in ways we have never considered before.

A central feature of this community engagement must involve intentional efforts to expand health equity, to create study designs that are inclusive and culturally appropriate. Far too many marginalized communities and populations today are further harmed by studies that fail to provide findings that apply to their unique situations and needs.

Very importantly, the future will require educating our next generation of clinical investigators and empowering them with the tools that enable new ways of managing clinical studies. By supporting initiatives spearheaded by FDA and professional groups like the American Society of Clinical Oncology, NCI is making it easier for community oncologists to participate in clinical trials and helping clarify previously misunderstood regulatory requirements. 

These efforts must also ensure that we have a clinical research workforce that is representative of the people it is intended to serve. Far too many structural barriers have prevented this from taking place in the past, and it’s time for that to change. 

Expanding our capacity doesn’t mean doing more of the same, it means challenging ourselves to work differently. This will let us move forward to a new state, one in which clinical research is integrated in everyday practice. It is only with more strategic partnerships and increased inclusivity that we can open the doors to seeing clinical investigation in new ways, with new standards for success.

A Collaborative Effort

Shaalan Beg, M.D.

Senior Advisor for Clinical Research

To make the kind of progress we all desire, we have to recognize that our clinical studies system needs to evolve.

There was a time when taking years to design, launch, and complete a clinical trial was acceptable. It isn’t acceptable anymore. We are in an era where we have the tools and the research talent to make far more rapid progress than we have in the past. 

And we can do that by engaging with many different communities and stakeholders in unique and dynamic ways—making them partners in our effort to end cancer as we know it.

Together, our task is to capitalize on this work so we can move faster and enable cutting-edge research that benefits as many people as possible. 

We also know that there are more good ideas in this space, and part of this transformation includes grass roots efforts to drive systemic change. So, we encourage you to share your ideas on how we can transform clinical research. Because achieving this goal can’t be done by any one group alone. We are all in this together. 

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National Cancer Institute - Cancer.gov

Clinical trial researching combination immunotherapy for colorectal cancer

Image credit: Canva

Colorectal cancer that has returned or progressed after treatment and spread to other organs is known as metastatic colorectal cancer (mCRC). Most people with mCRC survive only about two years. A trial led by Jason M. Redman, M.D. , Assistant Research Physician in the Center for Immuno-Oncology , is studying combination immunotherapy, including a tumor-targeted vaccine, for the disease. The trial includes two mandatory biopsies.

The trial will take place at the NIH Clinical Center in Bethesda, Maryland, and there is no cost for participation.

For more information, please contact the NCI Medical Oncology Referral Office at (888) 624-1937 or  [email protected] .

Clinicaltrials.gov identifier:   NCT06149481

NCI Protocol ID:  IRB001563

Official Title:  Phase I/II Study of the Combination Immunotherapy Regimen: SX-682, TriAdeno Vaccine, Retifanlimab and IL-15 Agonist N-803 (STAR15) for Metastatic Colorectal Cancer (mCRC)

The Center for Cancer Research is NCI’s internal cancer center, a publicly funded organization working to improve the lives of cancer patients by solving important, challenging and neglected problems in cancer research and patient care. Highly trained physician-scientists develop and carry out clinical trials to create the medicines of tomorrow, treating patients at the world’s largest dedicated research hospital on the campus of the National Institutes of Health in Bethesda, Maryland. 

For more information on CCR clinical trials click  here , and  subscribe  to have the latest CCR clinical trials sent directly to your inbox.

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Clinical trial researching combination therapy for solid tumors

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Collection  10 March 2022

Top 100 in Cancer

This collection highlights our most downloaded* cancer papers published in 2021. Featuring authors from aroud the world, these papers showcase valuable research from an international community.

*Data obtained from SN Insights which is based on Digital Science's Dimensions.

Radiotherapy for brain metastasis and long-term survival

• Kawngwoo Park
• Gi Hwan Bae
• Jaehun Jung

The Angelina Jolie effect: Contralateral risk-reducing mastectomy trends in patients at increased risk of breast cancer

• Narendra Nath Basu
• James Hodson
• D. Gareth Evans

Deep learning classification of lung cancer histology using CT images

• Tafadzwa L. Chaunzwa
• Ahmed Hosny
• Hugo J. W. L. Aerts

Pancancer survival analysis of cancer hallmark genes

• Gyöngyi Munkácsy
• Balázs Győrffy

Anti-estrogenic and anti-aromatase activities of citrus peels major compounds in breast cancer

• Dina M. El-Kersh
• Shahira M. Ezzat
• Mohey M. Elmazar

Arsenic exposure in Indo Gangetic plains of Bihar causing increased cancer risk

• Mohammad Ali
• Ashok Kumar Ghosh

CIBERSORT analysis of TCGA and METABRIC identifies subgroups with better outcomes in triple negative breast cancer

• Kelly E. Craven
• Yesim Gökmen-Polar
• Sunil S. Badve

The incidence and clinical analysis of non-melanoma skin cancer

• Magdalena Ciążyńska
• Grażyna Kamińska-Winciorek
• Aleksandra Lesiak

Real-world outcomes versus clinical trial results of immunotherapy in stage IV non-small cell lung cancer (NSCLC) in the Netherlands

• Christine M. Cramer-van der Welle
• Marjon V. Verschueren
• The Santeon NSCLC Study Group

Anti-tumour activity of deer growing antlers and its potential applications in the treatment of malignant gliomas

• Louis Chonco
• Tomás Landete-Castillejos
• Tomás Segura

Risk of cancer development in patients with keloids

• Hung-Pin Tu
• Chih-Hung Lee

Neutrophil to lymphocyte ratio influences impact of steroids on efficacy of immune checkpoint inhibitors in lung cancer brain metastases

• Bicky Thapa
• Manmeet S. Ahluwalia

Prediction of survival in patients with advanced, refractory colorectal cancer in treatment with trifluridine/tipiracil: real-world vs clinical trial data

• Ana Fernández Montes
• Alberto Carmona-Bayonas
• Teresa Garcia García

Hyperbaric oxygen suppressed tumor progression through the improvement of tumor hypoxia and induction of tumor apoptosis in A549-cell-transferred lung cancer

• Shao-Yuan Chen
• Koichi Tsuneyama
• Shih-Ming Huang

Histopathological analysis of mucinous breast cancer subtypes and comparison with invasive carcinoma of no special type

• Michał Piotr Budzik
• Marta Magdalena Fudalej
• Anna Maria Badowska-Kozakiewicz

Copper-67 radioimmunotheranostics for simultaneous immunotherapy and immuno-SPECT

• Guiyang Hao
• Tara Mastren
• Xiankai Sun

Associations between the gut microbiome and fatigue in cancer patients

• Joud Hajjar
• Tito Mendoza

cGAS–STING cytosolic DNA sensing pathway is suppressed by JAK2-STAT3 in tumor cells

• Manuel Adrian Suter
• Nikki Y. Tan
• Y. L. Zhang

Iodine containing porous organosilica nanoparticles trigger tumor spheroids destruction upon monochromatic X-ray irradiation: DNA breaks and K-edge energy X-ray

• Yuya Higashi
• Kotaro Matsumoto
• Fuyuhiko Tamanoi

COVID-19 engages clinical markers for the management of cancer and cancer-relevant regulators of cell proliferation, death, migration, and immune response

• Serhiy Souchelnytskyi
• Andriy Nera
• Nazariy Souchelnytskyi

High-dose methotrexate-based regimens and post-remission consolidation for treatment of newly diagnosed primary CNS lymphoma: meta-analysis of clinical trials

• Haowen Xiao

Sensitivity, specificity, and accuracy of a liquid biopsy approach utilizing molecular amplification pools

• Jessica Garcia
• Nick Kamps-Hughes
• Cristian Ionescu-Zanetti

A survival analysis of surgically treated incidental low-grade glioma patients

• Lingcheng Zeng

Integrated multi-omics analysis of ovarian cancer using variational autoencoders

• Muta Tah Hira
• M. A. Razzaque
• Mosharraf Sarker

Cell-free DNA concentration and fragment size as a biomarker for prostate cancer

• Emmalyn Chen
• Clinton L. Cario
• John S. Witte

Real-world outcomes of first-line pembrolizumab plus pemetrexed-carboplatin for metastatic nonsquamous NSCLC at US oncology practices

• Vamsidhar Velcheti
• Thomas Burke

Graphene oxide loaded with tumor-targeted peptide and anti-cancer drugs for cancer target therapy

Comprehensive analysis of metastatic gastric cancer tumour cells using single-cell RNA-seq

• Yingyi Zhang
• Xianbao Zhan

Ex vivo culture of intact human patient derived pancreatic tumour tissue

• John Kokkinos
• George Sharbeen
• Phoebe A. Phillips

A phase 2a clinical study on the safety and efficacy of individualized dosed mebendazole in patients with advanced gastrointestinal cancer

• S. Mansoori

Palliative radiation therapy for symptomatic advance breast cancer

• Galia Jacobson
• Orit Kaidar-Person
• Merav Akiva Ben-David

Deep learning identifies morphological features in breast cancer predictive of cancer ERBB2 status and trastuzumab treatment efficacy

• Dmitrii Bychkov
• Nina Linder
• Johan Lundin

A prostate-specific membrane antigen (PSMA)-targeted prodrug with a favorable in vivo toxicity profile

• Srikanth Boinapally
• Hye-Hyun Ahn
• Martin G. Pomper

Comparison of microsatellite instability detection by immunohistochemistry and molecular techniques in colorectal and endometrial cancer

• Franceska Dedeurwaerdere
• Kathleen BM Claes
• Geert Martens

Valerian and valeric acid inhibit growth of breast cancer cells possibly by mediating epigenetic modifications

• Fengqin Shi

Efficacy and safety of new anti-CD20 monoclonal antibodies versus rituximab for induction therapy of CD20 + B-cell non-Hodgkin lymphomas: a systematic review and meta-analysis

• Chengxin Luo

Morphofunctional analysis of human pancreatic cancer cell lines in 2- and 3-dimensional cultures

• Fuuka Minami
• Norihiko Sasaki
• Toshiyuki Ishiwata

Potentiality of multiple modalities for single-cell analyses to evaluate the tumor microenvironment in clinical specimens

• Yukie Kashima
• Yosuke Togashi
• Toshihiko Doi

Polysaccharide hydrogel based 3D printed tumor models for chemotherapeutic drug screening

• Aragaw Gebeyehu
• Sunil Kumar Surapaneni
• Mandip Singh

PTEN loss promotes oncogenic function of STMN1 via PI3K/AKT pathway in lung cancer

• Guangsu Xun

Co-culture model of B-cell acute lymphoblastic leukemia recapitulates a transcription signature of chemotherapy-refractory minimal residual disease

• Stephanie L. Rellick
• Gangqing Hu
• Laura F. Gibson

Effect of SSRI exposure on the proliferation rate and glucose uptake in breast and ovary cancer cell lines

• Britta Stapel
• Catharina Melzer

Impact of tumor-parenchyma biomechanics on liver metastatic progression: a multi-model approach

• Erik Brodin
• Paul Macklin

Pembrolizumab in vaginal and vulvar squamous cell carcinoma: a case series from a phase II basket trial

• Jeffrey A. How
• Amir A. Jazaeri

Relationship of breast volume, obesity and central obesity with different prognostic factors of breast cancer

• Daniel María Lubián López
• Carmen Aisha Butrón Hinojo
• Ernesto González Mesa

Meta-analysis of host transcriptional responses to SARS-CoV-2 infection reveals their manifestation in human tumors

• Fengju Chen
• Yiqun Zhang
• Chad J. Creighton

Selection and characterisation of Affimers specific for CEA recognition

• Shazana Hilda Shamsuddin
• David G. Jayne
• Paul A. Millner

Epidemiology and prognosis in young lung cancer patients aged under 45 years old in northern China

Real-world data of fulvestrant as first-line treatment of postmenopausal women with estrogen receptor-positive metastatic breast cancer

• M. Ruiz-Borrego

Classification of paediatric brain tumours by diffusion weighted imaging and machine learning

• Niloufar Zarinabad
• Andrew Peet

Metagenomic analysis of formalin-fixed paraffin-embedded tumor and normal mucosa reveals differences in the microbiome of colorectal cancer patients

• Gabriela Debesa-Tur
• Vicente Pérez-Brocal
• Andrés Moya

A novel proteomics approach to epigenetic profiling of circulating nucleosomes

• Priscilla Van den Ackerveken
• Alison Lobbens
• Marielle Herzog

A review and comparison of breast tumor cell nuclei segmentation performances using deep convolutional neural networks

• Andrew Lagree
• Majidreza Mohebpour
• William T. Tran

Comparative analysis of machine learning approaches to classify tumor mutation burden in lung adenocarcinoma using histopathology images

• Apaar Sadhwani
• Huang-Wei Chang
• Peter Cimermancic

Alteration of DNA mismatch repair capacity underlying the co-occurrence of non-small-cell lung cancer and nonmedullary thyroid cancer

• Shiro Fujita
• Katsuhiro Masago

Anticancer potential of rhizome extract and a labdane diterpenoid from Curcuma mutabilis plant endemic to Western Ghats of India

• T. Lakshmipriya
• P. R. Manish Kumar

Serum-derived exosomal PD-L1 expression to predict anti-PD-1 response and in patients with non-small cell lung cancer

• Yoshihisa Shimada
• Jun Matsubayashi
• Norihiko Ikeda

Transcript levels of keratin 1/5/6/14/15/16/17 as potential prognostic indicators in melanoma patients

• Guo-Liang Shen

Enhancing the landscape of colorectal cancer using targeted deep sequencing

• Chul Seung Lee
• In Hye Song
• Sung Hak Lee

PGMD/curcumin nanoparticles for the treatment of breast cancer

• Mankamna Kumari
• Nikita Sharma
• Surendra Nimesh

GATA3 somatic mutations are associated with clinicopathological features and expression profile in TCGA breast cancer patients

• Fahimeh Afzaljavan
• Ayeh Sadat Sadr
• Alireza Pasdar

Explainable drug sensitivity prediction through cancer pathway enrichment

• Yi-Ching Tang
• Assaf Gottlieb

A novel biosensor for the ultrasensitive detection of the lncRNA biomarker MALAT1 in non-small cell lung cancer

• Dongming Wu

Neuroendocrine prostate cancer has distinctive, non-prostatic HOX code that is represented by the loss of HOXB13 expression

• Siyuan Cheng

New combination chemotherapy of cisplatin with an electron-donating compound for treatment of multiple cancers

• Qinrong Zhang
• Qing-Bin Lu

Lung adenocarcinoma and lung squamous cell carcinoma cancer classification, biomarker identification, and gene expression analysis using overlapping feature selection methods

• Joe W. Chen
• Joseph Dhahbi

Similarities between pandemics and cancer in growth and risk models

• Lode K. J. Vandamme
• Ignace H. J. T. de Hingh
• Paulo R. F. Rocha

Flavonoids increase melanin production and reduce proliferation, migration and invasion of melanoma cells by blocking endolysosomal/melanosomal TPC2

• Ponsawan Netcharoensirisuk
• Carla Abrahamian
• Christian Grimm

Convolutional autoencoder based model HistoCAE for segmentation of viable tumor regions in liver whole-slide images

• Mousumi Roy
• Vandana Mukherjee

Low temperature plasma irradiation products of sodium lactate solution that induce cell death on U251SP glioblastoma cells were identified

• Hiromasa Tanaka
• Masaru Hori

CAD systems for colorectal cancer from WSI are still not ready for clinical acceptance

• Sara P. Oliveira
• Pedro C. Neto
• Jaime S. Cardoso

Applicability of pan-TRK immunohistochemistry for identification of NTRK fusions in lung carcinoma

• Simon Strohmeier

Sulforaphane induces S-phase arrest and apoptosis via p53-dependent manner in gastric cancer cells

• Huazhang Wu

Repositioning metformin and propranolol for colorectal and triple negative breast cancers treatment

• L. E. Anselmino
• M. V. Baglioni
• M. Menacho Márquez

Evaluation of wavelength ranges and tissue depth probed by diffuse reflectance spectroscopy for colorectal cancer detection

• Marcelo Saito Nogueira
• Siddra Maryam
• Stefan Andersson-Engels

C. elegans -based chemosensation strategy for the early detection of cancer metabolites in urine samples

• Enrico Lanza
• Martina Di Rocco
• Viola Folli

Detection of colorectal cancer in urine using DNA methylation analysis

• R. D. M. Steenbergen

Learning deep features for dead and living breast cancer cell classification without staining

• Gisela Pattarone
• Laura Acion
• Emmanuel Iarussi

Epidemiological overview of multidimensional chromosomal and genome toxicity of cannabis exposure in congenital anomalies and cancer development

• Albert Stuart Reece
• Gary Kenneth Hulse

Adipose-derived mesenchymal stem cells differentiate into heterogeneous cancer-associated fibroblasts in a stroma-rich xenograft model

• Yoshihiro Miyazaki
• Tatsuya Oda
• Yasuyuki S. Kida

Loss of Parkinson’s susceptibility gene LRRK2 promotes carcinogen-induced lung tumorigenesis

• Chandra Lebovitz
• Nicole Wretham
• Sharon M. Gorski

Enhanced anti-cancer activity of andrographis with oligomeric proanthocyanidins through activation of metabolic and ferroptosis pathways in colorectal cancer

• Tadanobu Shimura
• Priyanka Sharma

Differential expression of PD-L1 between primary and metastatic epithelial ovarian cancer and its clinico-pathological correlation

• Sandeep Kumar Parvathareddy
• Abdul K. Siraj
• Khawla S. Al-Kuraya

Fibroblast activation protein targeted near infrared photoimmunotherapy (NIR PIT) overcomes therapeutic resistance in human esophageal cancer

• Ryoichi Katsube
• Kazuhiro Noma
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Activity of docetaxel, carboplatin, and doxorubicin in patient-derived triple-negative breast cancer xenografts

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CD73 facilitates EMT progression and promotes lung metastases in triple-negative breast cancer

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Cancer patients often do better with less intensive treatment, new research finds

FILE - In this May 25, 2017 file photo, chemotherapy drugs are administered to a patient at a hospital in Chapel Hill, N.C. Scaling back treatment in some cancers — ovarian, esophageal and Hodgkin lymphoma — can make life easier for patients without compromising outcomes, doctors reported at the American Society of Clinical Oncology annual meeting in early June 2024. (AP Photo/Gerry Broome, File)

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Scaling back treatment for three kinds of cancer can make life easier for patients without compromising outcomes, doctors reported at the world’s largest cancer conference.

It’s part of a long-term trend toward studying whether doing less — less surgery , less chemotherapy or less radiation — can help patients live longer and feel better. The latest studies involved ovarian and esophageal cancer and Hodgkin lymphoma.

Thirty years ago, cancer research was about doing more, not less. In one sobering example, women with advanced breast cancer were pushed to the brink of death with massive doses of chemotherapy and bone marrow transplants. The approach didn’t work any better than chemotherapy and patients suffered.

Now, in a quest to optimize cancer care, researchers are asking: “Do we need all that treatment that we have used in the past?”

It’s a question, “that should be asked over and over again,” said Dr. Tatjana Kolevska, medical director for the Kaiser Permanente National Cancer Excellence Program, who was not involved in the new research.

Often, doing less works because of improved drugs.

“The good news is that cancer treatment is not only becoming more effective, it’s becoming easier to tolerate and associated with less short-term and long-term complications,” said Dr. William G. Nelson of Johns Hopkins School of Medicine, who was also not involved in the new research.

Studies demonstrating the trend were discussed over the weekend at an American Society of Clinical Oncology conference in Chicago. Here are the highlights:

OVARIAN CANCER

French researchers found that it’s safe to avoid removing lymph nodes that appear healthy during surgery for advanced ovarian cancer. The study compared the results for 379 patients — half had their lymph nodes removed and half did not. After nine years, there was no difference in how long the patients lived and those with less-extreme surgery had fewer complications, such as the need for blood transfusions. The research was funded by the National Institute of Cancer in France.

ESOPHAGEAL CANCER

This German study looked at 438 people with a type of cancer of the esophagus that can be treated with surgery. Half received a common treatment plan that included chemotherapy and surgery on the esophagus, the tube that carries food from the throat to the stomach. Half got another approach that includes radiation too. Both techniques are considered standard. Which one patients get can depend on where they get treatment.

After three years, 57% of those who got chemo and surgery were alive, compared to 51% of those who got chemo, surgery and radiation. The German Research Foundation funded the study.

HODGKIN LYMPHOMA

A comparison of two chemotherapy regimens for advanced Hodgkin lymphoma found the less intensive treatment was more effective for the blood cancer and caused fewer side effects.

After four years, the less harsh chemo kept the disease in check in 94% of people, compared to 91% of those who had the more intense treatment. The trial included 1,482 people in nine countries — Germany, Austria, Switzerland, the Netherlands, Denmark, Sweden, Norway, Australia and New Zealand — and was funded by Takeda Oncology, the maker of one of the drugs used in the gentler chemo that was studied.

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Science and Educational Media Group. The AP is solely responsible for all content.

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New approaches and procedures for cancer treatment: Current perspectives

Dejene tolossa debela.

1 Center for Innovative Drug Development and Therapeutic Trials for Africa (CDT-Africa), College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia

Seke GY Muzazu

2 Enteric Diseases and Vaccines Research Unit, Centre for Infectious Disease Research in Zambia (CIDRZ), Lusaka, Zambia

Kidist Digamo Heraro

3 Wachemo University, Hossana, Ethiopia

Maureen Tayamika Ndalama

Betelhiem woldemedhin mesele.

4 Kotebe Metropolitan University, Addis Ababa, Ethiopia

Dagimawi Chilot Haile

5 University of Gondar, Gondar, Ethiopia

Sophia Khalayi Kitui

Tsegahun manyazewal.

Cancer is a global health problem responsible for one in six deaths worldwide. Treating cancer has been a highly complex process. Conventional treatment approaches, such as surgery, chemotherapy, and radiotherapy, have been in use, while significant advances are being made in recent times, including stem cell therapy, targeted therapy, ablation therapy, nanoparticles, natural antioxidants, radionics, chemodynamic therapy, sonodynamic therapy, and ferroptosis-based therapy. Current methods in oncology focus on the development of safe and efficient cancer nanomedicines. Stem cell therapy has brought promising efficacy in regenerating and repairing diseased or damaged tissues by targeting both primary and metastatic cancer foci, and nanoparticles brought new diagnostic and therapeutic options. Targeted therapy possessed breakthrough potential inhibiting the growth and spread of specific cancer cells, causing less damage to healthy cells. Ablation therapy has emerged as a minimally invasive procedure that burns or freezes cancers without the need for open surgery. Natural antioxidants demonstrated potential tracking down free radicals and neutralizing their harmful effects thereby treating or preventing cancer. Several new technologies are currently under research in clinical trials, and some of them have already been approved. This review presented an update on recent advances and breakthroughs in cancer therapies.

Introduction

Cancer is a global health problem responsible for one in six deaths worldwide. In 2020, there were an estimated 19.3 million new cancer cases and about 10 million cancer deaths globally. Cancer is a very complicated sequence of disease conditions progressing gradually with a generalized loss of growth control. 1 – 3 There were only a few options of cancer treatment for patients for many decades which include surgery, radiation therapy, and chemotherapy as single treatments or in combination. 4 , 5 But recently, many pathways involved in cancer therapy progression and how they can be targeted has improved dramatically, with combinatorial strategies, involving multiple targeted therapies or “traditional” chemotherapeutics, such as the taxanes and platinum compounds, being found to have a synergistic effect. 6 New approaches, such as drugs, biological molecules, and immune-mediated therapies, are being used for treatment even if the excepted therapy level has not reached that resists the mortality rate and decreases the prolonged survival time for metastatic cancer.

The creation of a new revolution in neoplastic cancer or targeting drugs depends on the pathways and characteristics of different tumor entities. 7 Chemotherapy is considered the most effective and widely used modality in treating cancers as used alone or in combination with radiotherapy. Genotoxicity is how chemotherapy drugs target the tumor cells mainly producing reactive oxygen species that largely destroy tumor cells. 8 Hormonal treatments are also widely used for cancer malignancies and considered as cytostatic because it restricts tumor development by limiting the hormonal growth factors acting through the direction of hypothalamic–pituitary–gonadal axis (HPGA), hormone receptor blockage, and limiting of adrenal steroid synthesis. 9

In this narrative review, a general overview of the most advanced and novel cancer therapies was provided. In addition, also new strategies currently under investigation at the research stage that should overwhelm the drawbacks of standard therapies; different strategies to cancer diagnosis and therapy; and their current status in the clinical context, underlining their impact as innovative anti-cancer approaches.

Cancer treatment modalities

We can see cancer treatment modalities by dividing them into conventional (traditional) and advanced or novel or modern categories. In this era worldwide, over half of all ongoing medical treatment trials are focusing on cancer treatments. 7 Entities, such as the type of cancer, its site, and severity, guide to select treatment options and its progress. The most widely used traditional treatment methods are surgery, chemotherapy, and radiotherapy, while modern modalities include hormone therapy, anti-angiogenic, stem cell therapies, immunotherapy, and dendritic cell-based immunotherapy. 10

Conventional cancer therapies

The most recommended conventional cancer treatment strategies include surgical resection of the tumors followed by radiotherapy with x-rays and/or chemotherapy. 11 Of these modalities, surgery is most effective at an early stage of disease progression. Radiation therapy can damage healthy cells, organs, and tissues. Although chemotherapy has reduced morbidity and mortality, virtually all chemotherapeutic agents damage healthy cells, especially rapidly dividing and growing cells. 12 Drug resistance, a major problem with chemotherapy, is a phenomenon wherein cancer cells that initially were suppressed by an anti-cancer drug develop resistance to the drug. This is caused primarily by reduced drug uptake and increased drug efflux. 13 Limitations of conventional chemotherapeutic modality, such as dosage selection difficulty, lack of specificity, rapid drug metabolism, and mainly harmful side effects. 14

Advanced and innovative cancer therapies

Among the obstacles of cancer, drug resistance and its delivery systems are the most problem in cancer cure and decreasing signs and symptoms; but currently, there are many approved treatment approaches and drugs. The efficiency of conventional cancer is reduced due to tumor pathology and architectural abnormality of tumor tissue blood vessels. 15 The following are the advanced and innovative cancer therapy types with their benefits and challenges.

Stem cells therapy

Stem cells are undifferentiated cells present in the bone marrow (BM) with an ability to differentiate into any type of body cell. Stem cell therapeutic strategy is also one of the treatment options for cancer which are considered to be safe and effective. Application of stem cell is yet in the experimental clinical trial; for example, their use in the regeneration of other damaged tissue is being explored. Mesenchymal stem cells (MSCs) are currently being used in trials that are delivered from the BM, fat tissues, and connective tissues. 16

Pluripotent stem cells

Embryonic stem cells (ESCs) isolated from the uniform inner mass cells of the embryo possess the flexibility to administer rise to any or all kinds of cells except those within the placenta. In 2006, the invention of Yamanaka factors to induce pluripotent stem cells (iPSCs) from physical cells in a culture marked a breakthrough in cell biology. 17 Avoiding ethical issues from embryo destruction, iPSCs and ESCs have the same characteristics. Hematopoietic embryonic stem cells (hESCs) and iPSCs are currently used for the induction of effector T cells and natural killer (NK) cells, 18 and anti-tumor vaccine preparation. 19

Adult stem cells

Adult stem cells (ASCs) groups often used in tumor therapy include hematopoietic stem cells (HSCs), MSCs, and neural stem cells (NSCs). HSCs, located in BM, can form all mature blood cells in the body. Currently, only approved by the Food and Drug Administration (FDA) is the infusion of HSCs derived from cord blood to treat multiple myeloma and leukemia. 20 MSCs are found in many tissues and organs, playing important roles in tissue repair and regeneration into cells, such as osteocytes, adipocytes, and chondrocytes. MSCs have special biological characteristics and are used as complimentary with other approaches in treating tumors. 21 NSCs can self-renew and generate new neurons and glial cells and are used for treating both primary and metastatic breast and other tumors. 22

Cancer stem cells

Cancer stem cells (CSCs) are generated in normal stem cells or precursor/progenitor cells by the epigenetic mutations process. Their role in tumor treatment includes cancer growth, metastasis, and recurrence, so that it could give promise in the treatment of solid tumors. 23 Stem cells have several action mechanisms in treating the tumor. The homing process is one mechanism which is a rapid migration of HSCs into defined stem cell niches in BM after that the transplants undergo the engraftment process before giving rise to specialized blood cells. This mechanism is dependent on the active interaction between stem cell CXCR4 receptors and requires their interaction with endothelial cells through LFA-1, VLA-4/5, CD44, and the secretion of matrix degradable enzyme MMP-2/9. 22 The second mechanism is the tumor-tropic effect in which the migration of MSCs toward tumor microenvironment (TM) after attraction by CXCL16, SDF-1, CCL-25, and IL-6 secreted by tumor cells and differentiation of MSCs within the tumor cells which contributes to tumor stromal development. 24 Stem cells also act by paracrine factor secretion, including extracellular vesicles (EVs) and soluble materials, 25 and their differentiation capacity, such as transplanted HSCs, can give rise to all blood cell types. 26

Generally, cancer treatment using stem cell therapy by various strategies, including transplantation of HSC, 27 MSC infusion, 28 therapeutic carriers, 29 generation of immune effector cells, 30 and vaccine production. 31 The stem cell cancer therapy approach confronted the following side effects: (1) tumorigenesis, (2) adverse events in allogeneic HSC transplantation, (3) drug toxicity and drug resistance, (4) increased immune responses and autoimmunity, and (5) viral infection. 22 Despite several successes, there are challenges, such as therapeutic dose control, low cell targeting, and retention in tumor sites, that should be investigated and overcome in the future. In addition, existing results from stem cell technologies are highly encouraging for tumor treatment but it still needs further efforts to improve the safety and efficacy before they could enter clinical trials. Table 1 summarized the licensed list of stem cell therapies.

Licensed stem cell therapies.

AML: acute myelogenous leukemia; FDA: The US Food and Drug Administration; iPSC: induced pluripotent stem cell; MSC-INβ: mesenchymal stem cells with interferon beta.

Targeted drug therapy

Targeted cancer therapies are drugs or other substances which are sometimes interchangeably used as “molecularly targeted drugs,” “molecularly targeted therapies,” and “precision medicines.” Those drugs’ mechanism of action is by interfering with growth molecules which leads to blocking the growth and spreading of cancer. 34 Tumor initiation and progression are determined by the TM of an atypical tumor which comprises endothelial cells, pericytes, smooth muscle cells, fibroblasts, various inflammatory cells, dendritic cells, and CSCs. There are various signaling mechanisms and pathways that TM-forming cells dynamically interact with the cancerous cells which are suitable for sustaining a reasonably high cellular proliferation. So, it is the area of research interest using TM conditions to mediate effective targeting measures for cancer therapy. 35

Selectively treating cancer cells with conventional chemotherapy is difficult since it is similar to normal cells. So those problems are intervened by cellular mechanisms, such as cell cycle arrest, apoptosis induction, proliferation prevention, and interfering with metabolic reprogramming by targeted drug therapy agents. 36 Modifying TM and targeting TM for drug delivery for effective treatment are two strategies that can be used for the treatment of cancer. 37 Targeted therapy drugs do work in different ways from standard chemotherapy drugs treatment like attacking cancer cells while doing less damage to normal cells which is a programming that sets them apart from normal, healthy cells. 38

Using targeted therapy markedly increased the survival rate for some diseases, for example, from 17% to 24% in patients with advanced pancreatic cancer, the addition of erlotinib to standard chemotherapy. Imatinib has had a dramatic effect on chronic myeloid leukemia, and rituximab, sunitinib, and trastuzumab have revolutionized the treatment of renal cell carcinoma and breast cancer, respectively. 39

We can classify the targeted cell agents based on the mechanism of their work or their target site. Some enzymes serve as signals for cancer cells to grow. Some targeted therapies inhibit enzymes that are signals for cancer cells to grow. These drugs are called enzyme inhibitors. Blocking these cell signals can inhibit cancer from getting bigger and spreading. 40

Some targeted therapies are called apoptosis-inducing drugs because they are aimed right at the parts of the cell that control whether cells live or die. The examples are serine/threonine kinase, protein kinase B (PKB/Akt), which promotes cell survival, and inhibitors of this protein are in the preclinical phase. 41

These agents stop the tumors from making new blood vessels which helps cut off the tumors’ blood supply so that tumors cannot grow. In addition, they arrest tumor growth that involves by curtailing blood supply to the tumor by inhibiting angiogenic factors, such as vascular endothelial growth factor (VEGF) or its receptors. The study showed the survival of patients with advanced colorectal carcinoma extended by months after the use of Avastin (bevacizumab) in combination with 5-fluorouracil-based chemotherapy. 42

Types of target agents

Monoclonal antibodies.

Antibody drugs are man-made versions of immune system proteins administered intravenously to attack certain targets on cancer cells. They contain a more proportion of human components than murine components. 43 Their attack mechanisms of action are recruiting host immune functions to attack the target cell, binding to ligands or receptors thereby interrupting essential cancer cell processes, and carrying a lethal payload, such as radioisotope or toxin, to the target cell. 44 Gemtuzumab is an example of a CD-33-specific monoclonal antibody currently used for AML treatment by conjugating with calicheamicin. 45 In addition, ibritumomab tiuxetan is an anti-CD20, a 90Y metal isotope-based is developed in clinical therapy. 46 Delivery of active therapeutics, prodrug activation enzymes, and chemotherapy toxins are also another use of target agents of monoclonal antibodies. 47

Small molecule inhibitors

These are smaller protein in size (⩽500 Da) than monoclonal antibodies, so that they can simply translocate through plasma membranes and can be taken orally. Their main function is interrupting cellular processes by interfering with the intracellular signaling of tyrosine kinases which leads to the inhibition of tyrosine kinase signaling and initiates a molecular cascade that can lead to the inhibition of cell growth, proliferation, migration, and angiogenesis in malignant tissues. 48 Examples of small molecule inhibitors are gefitinib and erlotinib which inhibit epidermal growth factor receptor (EGFR) kinase and EGFR in non-small cell lung cancer (NSCLC) patients, respectively. There are also lapatinib and sorafenib which act on the inhibition of EGFR/Erb-B2 Receptor Tyrosine Kinase 2 (ERBB2) for ERBB2-positive breast cancer and VEGFR kinase, in renal cancer. 49

Ablation cancer therapy

Ablation is a treatment technique that destroys tumors without removing them mostly indicated for small-size tumors of less than 3 cm and the surgical option is contraindicated. Ablation is also used with embolization for larger tumors. However, this technique might not be indicated for treating tumors near major blood vessels, the diaphragm, or major bile ducts due to destroying some of the normal tissue around the tumor. 50

Thermal ablation

This technique uses extreme hyperthermia or hypothermia to destruct tumor tissue concentrating on a focal zone in and around the tumor. Similar to surgery, thermal ablation removes the tumor and a 5–10 mm thick margin of seemingly normal tissue but the tissue is killed in situ and then absorbed by the body later. The procedure is similar to surgery using an open, laparoscopic, or endoscopic approach but is commonly applied using a percutaneous or non-invasive approach. The type of tumor, site, physician’s choice, and health status determine the approach. 51

Radiofrequency ablation (RFA), microwave ablation, high-intensity focused ultrasound, and cryoablation are currently being used in the clinical setting. Cryoablation uses a hypothermic modality to induce tissue damage by a freeze-thaw process against others. All these treatments operate on the principle of hyperthermia except cryoablation. Of all the ablation techniques, cryoablation demonstrated the highest potential to elicit a post-ablative immunogenic response. 52

Recent studies showed additional to tissue disruption RFA and cryoablation can modulate the immune system that they were applied as therapy on TM and in the systematic circulation. Evidence has shown that ablation procedures affect carcinogenesis due to its local inflammatory response leading to an immunogenic gene signature. 53

The advantage of this procedure over surgery is that it provides a minimal (e.g. percutaneously or laparoscopically) or non-invasive approach to cancer therapy and gets attention as an alternative to standard surgical therapies. 54

Cryoablation

Cryoablation is one of the ablation techniques which ablates the extensive tissue by freezing to lethal temperatures followed by liquid formation, causing extensive tissue. Benign and malignant primary tumors are mostly treated by this therapy. 55 James Arnott reported that the freezing temperatures can impair cancer cell viability after he attempted the usage of cold temperatures by salt and ice solutions for the generation of local numbness before surgical operations in the nineteenth century. He suggested cryoablation as an attractive therapeutic option and increased a patient’s survival. 56

Cryoablation techniques are based on the principle of the Joule–Thomson effect which was studied in the 1930s by many researchers and concluded using liquid CO 2 under high pressure, liquid air, and liquid oxygen to achieve the cooling effect and the subsequent formation of ice crystals so employed to treat lesions, warts, and keratosis. However, after 1950, Allington replaced liquid N 2 for the treatment of various skin lesion disorders. 47

RFA therapy

RFA is a minimally invasive procedure and an image-guided technique using hyperthermic (high-frequency electrical currents) conditions to destroy cancer cells. Imaging techniques, such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI), guide needle electrodes into a tumor cell. Generally, RFA is the most effective approach for treating small-size tumors of less than 3 cm in diameter. RFA can be used in combination with other conventional cancer treatment options. 57 After starting the use of deployable devices or multiple-electrode systems, RFA can treat medium tumors (up to 5 cm diameter). 58

Gene therapy

Gene therapy is the insertion of a normal copy of a defective gene in the genome to cure a specific disorder. The first application dates back to 1990 when a retroviral vector was exploited to deliver the adenosine deaminase (ADA) gene to T cells in patients with severe combined immunodeficiency (SCID). Approximately, about 2900 gene therapy clinical trials are currently ongoing, two-third of which are related to cancer. Strategies, such as expression of proapoptotic and chemosensitizing genes, expression of wild-type tumor suppressor genes, expression of genes able to solicit specific anti-tumor immune responses, and targeted silencing of oncogenes, are under evaluation for cancer gene therapy. 47

Thymidine kinase (TK) gene delivery is effective for the administration of prodrug ganciclovir to activate its expression and induce specific cytotoxicity. 59 The p53 tumor suppressor gene which is vectors carrying has been assessed for the clinical purpose very recently. ONYX-015 has been tested in NSCLC patients and gave a high response rate when given alone or combined with chemotherapy. 60 Gendicine, a recombinant adenovirus carrying wild-type p53-induced complete disease regression in head and neck squamous cell cancer had similar success when combined with radiotherapy. 61

Some challenges that have been faced with gene therapy are the selection of the right conditions and the choice of the best delivery mechanism. Identified drawbacks of this therapy are genome integration, limited efficacy in specific subsets of patients, and high chances of being neutralized by the immune system. Basic research and medical translation used RNA interference (RNAi) as an efficient technology that able to produce targeted gene silencing. 62 RNA-induced silencing complex (RISC) mediates the targeted gene silencing process by cleaving the messenger RNA (mRNA) and interference with protein synthesis. 63 A siRNAs can be designed to block desired targets, involving cell proliferation and metastatic invasion; hence, precise molecular mechanisms are a triggering factor for tumor formation. This method relies on siRNA-mediated gene silencing of anti-apoptotic proteins, transcription factors (i.e. c-myc gene), 64 , 65 or cancer mutated genes (i.e. K-RAS). 66

Advantages of siRNA-based drugs are safety, high efficacy, specificity, few side effects, and low costs of production. 67 However, occasionally, they can induce off-target effects or elicit innate immune responses, followed by specific inflammation. 68 Delivery methods currently under study are chemical modification (insertion of a phosphorothioate at 3’ end, introduction of a 2’ O-methyl group, and modification by 2,4-dinitrophenol) and lipid encapsulation, or conjugation with organic molecules (polymers, peptides, lipids, antibodies, small molecules) efficiently target to spontaneously cross cell membranes of naked siRNAs. 69 Interaction of cationic liposomes with negatively charged nucleic acids facilitates easy transfection by simple electrostatic interactions. 70 They can be constituted by 1,2-dioleoyl-3-trimethylammonium propane (DOTAP) and N-[1-(2,3-dioleoyloxy) propyl]-N, Ntrimethylammonium methyl sulfate (DOTMA). 71 Currently, a Phase I clinical trial is recruiting patients for evaluating the safety of Eph receptor A2 (EphA2) targeting 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) encapsulated siRNA (siRNA-EphA2- DOPC) in patients with advanced and recurrent cancer. 72 siRNAs can be concentrated in cationic polymers, such as chitosan, cyclodextrin, and polyethyleneimine (PEI). 73 CALAA-01 is one of the cyclodextrin polymers conjugated with human transferrin is being entered a Phase I clinical trial. PEI has been used as an anti-cancer by forming small cationic nanoparticles and loading with human epidermal growth factor receptor 2 (HER-2 receptor)-specific siRNA. 74 Phase II clinical trial has been started to evaluate Local Drug EluteR (siG12D LODER) directed to mutated Kirsten rat sarcoma (K-RAS) oncogene for the treatment of advanced pancreatic cancer. Conjugating to peptides, antibodies, and aptamers improves stability during circulation and enhances cellular uptake of siRNAs. 75 The introduction of nanocarriers has largely improved siRNAs stability, pharmacokinetics and biodistribution properties, and targeting specificity. Polyallylamine phosphate nanocarriers have been developed to release siRNAs in the cytoplasm after disassembly at low endosomal pH. 76

Dose correction and variabilities between individuals and different stages of disease are challenging issues on clinical translation of the siRNA-based approach. In the future, the needed research is on setting up the best-personalized therapy and toward controlled release to reach only specific targets on treating the tumor. Table 2 summarizes the gene therapy drugs based on their mechanism of action and induction.

Summary of gene therapy approaches.

Natural antioxidants

Day to day, the anatomy undergoes many exogenous insults, such as ultraviolet (UV) rays, pollution, and tobacco smoke, that end in the assembly of reactive species, particularly oxidants and free radicals, liable for the onset of many diseases, together with cancer. These molecules can even be made as a consequence of clinical administration of medication; however, they are additionally naturally created within our cells and tissues by mitochondria and peroxisomes, and from macrophages metabolism, throughout traditional physiological aerobic processes. 47

Oxidative stress and radical oxygen species can significantly change the regulation of transcription factors by damaging the DNA and other bio-macromolecule. 77

Vitamins, polyphenols, and plant-derived bioactive compounds are natural antioxidants used as preventive and therapeutic drugs against these molecules that damage the body due to their anti-inflammatory and antioxidant properties. 78 Studies added to cancer therapy after appreciating their anti-proliferative and proapoptotic properties. Compounds, such as vitamins, alkaloids, flavonoids, carotenoids, curcumin, berberine, quercetin, and others, are examples of natural antioxidants screened in vitro and in vivo. 79

Limited bioavailability and/ or toxicity is one of the challenges of natural drugs while their translation into clinical practice. 47 Curcumin has cytotoxic effects in different kinds of tumors, such as the brain, lung, leukemia, pancreatic, and hepatocellular carcinoma, 80 while sparing normal cells at effective therapeutic doses. The curcumin’s biological properties, treatment duration and efficient therapeutic doses are under study. 80 This day, about 27 clinical trials are done, while 40 are under study on curcumin.

Berberine is an alkaloid compound that has been studied to be effective against different cancers as a chemopreventive agent, modulating many signaling pathways. Different nanotechnological strategies have been developed to facilitate its delivery across cell membranes due to their poorly soluble in water. 81 Six clinical trials are under study and two have been completed.

Quercetin is another natural plant origin agent that is effective alone and also in combination with chemotherapeutic agents in treating many cancers, such as lung, prostate, liver, colon, and breast cancers. 82 Quercetin’s mechanism of action is by binding to cellular receptors and the interference of several signaling pathways. 83 Currently, six clinical trials are under study and seven studies have been completed.

Current clinical trials

In recent years, analysis of cancer medication has taken outstanding steps toward more practical, precise, and fewer invasive cancer treatments in the research of clinical trials ( Figure 1 ).

Current status of clinical trials of innovative and novel strategies of cancer therapy.

Currently, the most frequent entries focusing on cancer therapies in the database of clinical trials ( www.clinicalTrials.gov ) include the terminologies stem cell, targeted therapy, immunotherapy, and gene therapy because they are very promising and effective. Table 3 summarizes the potential advantages and disadvantages of the new treatment approaches.

Comparison of advantageous and disadvantageous of new cancer therapies.

MRI: magnetic resonance imaging.

Table 4 summarizes the approaches to advanced cancer therapies and their respective delivery systems with examples.

Advanced therapy approaches and delivery systems.

Current methods in oncology focus on the development of safe and efficient cancer nanomedicines. Targeted medical care helped rising the biodistribution of recent or already tested chemotherapeutical agents around the specific tissue to be treated; different methods, such as sequence medical care, siRNAs delivery, therapy, and inhibitor molecules, supply new potentialities to cancer patients. Gene therapy acts by direct in situ insertion of exogenous genes into benign tumors. Noticeably, stem cells can be used as regenerative medicine, therapeutic carriers, drug targeting, and generation of immune cells because of having unique biological actions on other cells. 22 On the opposite hand, thermal ablation and magnetic hyperthermia are promising alternatives to the growth surgical process. Finally, radionics and pathomics approaches facilitate the management of huge knowledge sets from cancer patients to enhance prognosis and outcomes. Much progress has been made, but many others are likely to come soon, producing more and more ad hoc personalized therapies. Further development and refinement of drug delivery systems are essential for improving therapeutic outcomes.

Acknowledgments

The authors thank the Center for Innovative Drug Development and Therapeutic Trials for Africa (CDT-Africa), Addis Ababa University, for the support rendered.

Author contributions: D.T.D. is a major contributor in writing the manuscript. All others reviewed and approved the manuscript.

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The author(s) received no financial support for the research, authorship, and/or publication of this article.

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Scaling back treatment for three kinds of cancer can make life easier for patients without compromising outcomes, doctors reported at the world’s largest cancer conference.

It’s part of a long-term trend toward studying whether doing less — less surgery, less chemotherapy or less radiation — can help patients live longer and feel better. The latest studies involved ovarian and esophageal cancer and Hodgkin lymphoma.

Thirty years ago, cancer research was about doing more, not less.

In one sobering example, women with advanced breast cancer were pushed to the brink of death with massive doses of chemotherapy and bone marrow transplants.

The approach didn’t work any better than chemotherapy and patients suffered.

Now, in a quest to optimize cancer care, researchers are asking: “Do we need all that treatment that we have used in the past?”

It’s a question, “that should be asked over and over again,” said Dr. Tatjana Kolevska, medical director for the Kaiser Permanente National Cancer Excellence Program, who was not involved in the new research.

Often, doing less works because of improved drugs.

“The good news is that cancer treatment is not only becoming more effective, it’s becoming easier to tolerate and associated with less short-term and long-term complications,” said Dr. William G. Nelson of Johns Hopkins School of Medicine, who was also not involved in the new research.

Studies demonstrating the trend were discussed over the weekend at an American Society of Clinical Oncology conference in Chicago. Here are the highlights:

OVARIAN CANCER

French researchers found that it’s safe to avoid removing lymph nodes that appear healthy during surgery for advanced ovarian cancer. The study compared the results for 379 patients — half had their lymph nodes removed and half did not.

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After nine years, there was no difference in how long the patients lived and those with less-extreme surgery had fewer complications, such as the need for blood transfusions.

The research was funded by the National Institute of Cancer in France.

ESOPHAGEAL CANCER

This German study looked at 438 people with a type of cancer of the esophagus that can be treated with surgery.

Half received a common treatment plan that included chemotherapy and surgery on the esophagus, the tube that carries food from the throat to the stomach.

Half got another approach that includes radiation too. Both techniques are considered standard. Which one patients get can depend on where they get treatment.

After three years, 57% of those who got chemo and surgery were alive, compared to 51% of those who got chemo, surgery and radiation. The German Research Foundation funded the study.

HODGKIN LYMPHOMA

A comparison of two chemotherapy regimens for advanced Hodgkin lymphoma found the less intensive treatment was more effective for the blood cancer and caused fewer side effects.

After four years, the less harsh chemo kept the disease in check in 94% of people, compared to 91% of those who had the more intense treatment.

The trial included 1,482 people in nine countries — Germany, Austria, Switzerland, the Netherlands, Denmark, Sweden, Norway, Australia and New Zealand — and was funded by Takeda Oncology, the maker of one of the drugs used in the gentler chemo that was studied.

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