Cancer News and Discussions

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Research identifies key enzyme target to fight deadly brain cancers

by Ohio State University Medical Center
https://medicalxpress.com/news/2025-04- ... ncers.html
Researchers have found that targeting an enzyme called PGM3 can help stop the growth of glioblastoma, the most dangerous type of brain tumor. Study findings are published online in the journal Science Advances.

This enzyme plays a vital role in the hexosamine synthesis pathway, which is involved in the processes of protein and lipid glycosylation that allow tumors to rapidly grow. Lipid glycosylation is a process where sugar molecules attach to fats (lipids) in the body.

Researchers with The Ohio State University Comprehensive Cancer Center—Arthur G. James and Richard J. Solove Research Institute believe that targeting PGM3 can reduce tumor growth and eliminate glioblastoma cells.
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New blood test detects tumor-derived cell-free RNA with high sensitivity
https://medicalxpress.com/news/2025-04- ... -free.html
by Justin Jackson , Medical Xpress
Somewhere in the body of a patient, a small clump of cells, growing undetected, has begun to form a tumor. It has yet to cause pain or visible symptoms of illness. Several months from now, or perhaps years, those first signs will prompt a doctor's inquiry, a referral to a specialist, and an eventual diagnosis. Treatment will depend on how long the cancer has gone unnoticed and how far it has spread.

There were early signs, though not ones the patient or doctor could have noticed. Small fragments of RNA, cast off from dying cells or spit out of the tumor's twisted transcriptions, floating about in the bloodstream—early signals of a tissue in distress.

A new method developed by Stanford researchers aims to bring the moment of detection much closer to the beginning. They have developed a blood-based method called RARE-seq that detects tumor-derived cell-free RNA with around 50 times the sensitivity of standard sequencing techniques.
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Himalayan fungus compound tweaked for 40x anti-cancer boost
By Nick Lavars
April 26, 2025
By using a compound derived from a Himalayan fungus and used for centuries in Chinese medicine as a jumping off point, scientists have developed a new chemotherapy drug with powerful anti-cancer effects. Doing so involved chemically altering the compound to better infiltrate cancerous cells, which proved to boost its potency by up to 40 times.

Editor's note: Readers often ask us for follow-ups on memorable stories. What has happened to this story over the years? This article was originally published in 2021 but has been re-edited and updated with new information current as of April 25, 2025. Enjoy!

The 2021 research was carried out by University of Oxford scientists in collaboration with biopharmaceutical company Nucana, and began with a compound called Cordycepin. This naturally-occurring nucleoside analogue has been used to treat inflammatory disease and cancer for hundreds of years, but runs into several barriers that severely limit its effectiveness when deployed to tackle tumors.
https://newatlas.com/cancer/cordycepin- ... e-2-trial/
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Anticancer Mechanisms of Indigenous Food Plants in Nigeria
January 26, 2025, featured in an article published in Eurekalert on April 28, 2025.

Abstract:
(XHP Publishing) Cancer continues to pose a substantial public health problem in Nigeria, characterized by rising rates of occurrence and mortality. While there is increasing interest in using natural products for cancer treatment, comprehensive data on the specific bioactive compounds in these plants and how they modulate different types of cancer are still lacking. Additionally, although traditional knowledge about these food plants is rich and valuable, it has not been fully integrated with modern scientific research to create standardized treatment protocols. Scientific databases like PubMed, ScienceDirect, Google Scholar, and ResearchGate were explored to retrieve empirical data. The key plants discussed are Spondias mombin, Xanthosoma sagittifolium, Elaeis guineensis, Irvingia gabonensis, Allium cepa, Blighia sapida, Dioscorea dumetorum, Psidium guajava, and Talinum triangulare. These plants demonstrate a wide range of anticancer properties, including the ability to induce apoptosis (cell death), halt the cell cycle, inhibit angiogenesis, and regulate inflammatory responses. They contain a variety of phytochemicals, such as flavonoids, tannins, terpenoids, alkaloids, and organosulfur compounds, which contribute to their anticancer effects. For example, Spondias mombin contains flavonoids that inhibit the formation of tumors, whereas Xanthosoma sagittifolium exhibits cytotoxic effects against leukemia cells. Additionally, Elaeis guineensis exhibits antioxidant properties that counteract oxidative stress, a crucial factor in cancer progression. This review highlights the significance of these plants in developing complementary cancer therapies that can be used alongside conventional treatments. By combining traditional knowledge with contemporary scientific methods, these medicinal plants have the potential to provide innovative approaches to cancer prevention and treatment, addressing the pressing demand for safer and more efficient therapeutic alternatives.
Conclusions:
Thus, encouraging the use and further research of these native plants could be a vital element in developing effective dietary approaches for cancer prevention, halting the carcinogenesis process, or producing reasonably priced and easily accessible cancer treatments in areas where medical resources are limited.
Read more here: https://www.xiahepublishing.com/2835-6 ... 4-00042
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caltrek
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News Release – Not subject to length limitations that might otherwise be due to copyright considerations

Why Some Cells are More Susceptible to Cancer
April 30, 2025

Introduction:
(Eurekalert) The ability of mutations to cause cancer depends on how fast they force cells to divide, Sinai Health researchers have found.
The study, led by Dr. Rod Bremner, a Senior Investigator at the Lunenfeld-Tanenbaum Research Institute, part of Sinai Health in Toronto, has identified cell cycle length – the time it takes one cell to divide into two daughter cells – as a critical factor in determining whether a mutation actually drives cancer or is completely harmless.

The research findings, published today in Nature, have implications for developing new treatments that enhance the body's natural defences against cancer.

Cancer starts when cells acquire genetic mutations that prompt them to proliferate out of control, forming tumours. Not all cells that carry such mutations will turn into cancer, however. This is because the body has evolved ways to prevent cancer from forming by neutralizing or destroying the suspect cancerous cells. The protective mechanisms include apoptosis, or programmed cell death and clearance by the immune system, among others.

“An average adult has millions and millions of cells which have mutations in them, yet thankfully, we don’t develop cancer all the time,” said Dr. Bremner, who is also a Professor in the Departments of Ophthalmology and Laboratory Medicine & Pathobiology at the
University of Toronto.

Now, Dr. Bremner and team have identified the speed at which mutated cells divide as another mechanism of cancer resistance.

Spearheaded by Dr. Danian Chen, Scientific Associate, their study shows that mutated cells that divide rapidly and have shorter cell cycles are more prone to turning cancerous. In comparison, those with longer cycles exhibit resistance. The finding was consistent across various tissues and types of cancer, including retinoblastoma, pituitary cancer, and lung cancer.
Read more here: https://www.eurekalert.org/news-releases/1081801
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Gene-editing therapy shows early success in fighting advanced gastrointestinal cancers
https://medicalxpress.com/news/2025-05- ... anced.html
by Alex Smith, University of Minnesota Medical School

Researchers at the University of Minnesota have completed a first-in-human clinical trial testing a CRISPR/Cas9 gene-editing technique to help the immune system fight advanced gastrointestinal (GI) cancers. The results, recently published in The Lancet Oncology, show encouraging signs of the safety and potential effectiveness of the treatment.

"Despite many advances in understanding the genomic drivers and other factors causing cancer, with few exceptions, stage IV colorectal cancer remains a largely incurable disease," said Emil Lou, MD, Ph.D., a gastrointestinal oncologist with the University of Minnesota Medical School, Masonic Cancer Center and M Health Fairview, and clinical principal investigator for the trial. "This trial brings a new approach from our research labs into the clinic and shows potential for improving outcomes in patients with late-stage disease."
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Diabetes drug shows potential to slow prostate cancer cell growth
https://medicalxpress.com/news/2025-05- ... ancer.html
by Medical University of Vienna

An international team of scientists led by the Medical University of Vienna has identified similarities in the mechanisms of diabetes and cancer: as the researchers show, the protein PPARγ, which is central to the regulation of metabolic processes, can also influence the growth of prostate cancer cells. PPARγ is already known to be a target of certain drugs used to treat type 2 diabetes.

The results of the study, published in Molecular Cancer, indicate that such drugs could also represent a promising approach for the treatment of prostate cancer.

PPARγ has been known in diabetes research for quite some time, as it has an influence on insulin sensitivity. For more than 20 years, the protein has been the target of certain medications, including so-called thiazolidinediones such as pioglitazone, which are used to treat type 2 diabetes.
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Novel cancer immunotherapy offers new hope for late-stage cancer patients
https://medicalxpress.com/news/2025-05- ... ients.html
by Agency for Science, Technology and Research (A*STAR), Singapore
Researchers from A*STAR Institute of Molecular and Cell Biology (A*STAR IMCB) and local biotechnology company Intra-ImmuSG have announced promising outcomes from a Phase II clinical trial of a novel cancer immunotherapy, PRL3-zumab.

Published in Cell Reports Medicine, the study shows PRL3-zumab safely slows disease progression in patients with advanced solid cancers unresponsive to existing treatments.

PRL3-zumab is a novel humanized antibody therapy uniquely designed to target PRL3, an intracellular protein highly expressed in about 80% of solid tumors but absent in healthy tissues.

Unlike conventional antibodies that only engage surface proteins, PRL3-zumab identifies cancer cells by targeting PRL3 when it transiently appears on the cell surface, flagging them for the immune system to attack and destroy through processes known as antibody-dependent cellular cytotoxicity and phagocytosis.
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Engineered T-cells that express both CARs and TCRs can better distinguish between cancerous and healthy tissues
https://phys.org/news/2025-05-cells-car ... erous.html
by NDORMS, University of Oxford
Researchers have developed an innovative dual-receptor T-cell therapy that promises safer and more effective cancer treatments. This study, published in Cell, demonstrates that engineering T-cells to express both a Chimeric Antigen Receptor (CAR) and a T-cell Receptor (TCR) can improve their ability to distinguish between cancerous and healthy tissues—addressing a major challenge in current immunotherapy.

Treatments involving the use of the body's immune system to fight cancer have led to significant improvements in patient survival in recent years, particularly using a method called CAR T-cell therapy. This treatment involves extracting a patient's own T-cells and modifying them in a lab to express a special receptor called a Chimeric antigen receptor (CAR) that recognizes a tumor protein. These are then reinfused back into the patient, where they can find and destroy cancer cells.

However, while CAR T-cells have shown great promise for the treatment of blood cancers, they have struggled to effectively target solid tumors. CARs are unable to easily distinguish tumor cells from healthy cells that have the same target protein, which is a major issue when treating solid tumors, as the healthy tissue surrounding a solid cancer is often critical for survival but expresses similar proteins to the tumors themselves.

In contrast, natural T-cells with T-cell receptors (TCRs) are better able to discriminate between tumor cells and healthy cells. However, TCR-based therapies often suffer from limited effectiveness against tumors.
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DiffInvex Reveals How Cancers Rewire Driver Genes to Beat Chemotherapy
May 13, 2025

Introduction:
Barcelona, 13 May 2025 – Just as species adapt over generations, our body’s cells accumulate DNA changes throughout life. Most are harmless, yet a few “driver” mutations give a cell a competitive edge and can spark cancer. Chemotherapy then adds a new evolutionary pressure, encouraging further genetic changes that let tumours bounce back.

Researchers at IRB Barcelona have developed DiffInvex, a computational framework that tracks how evolutionary pressures on genes change as healthy cells become tumours and as tumours face chemotherapy. Applied to more than 11,000 human cancer and healthy tissue genomes spanning ~30 tissue types, DiffInvex pinpoints the mutational “escape routes” cancers take to resist treatment and reveals which genes may ignite resistance. The findings of this research are published today in Nature Communications.
Additional extract:
“By disentangling treatment effects from background noise, DiffInvex could one day help clinicians predict the resistance pathways a patient’s tumour is likely to take – and cut them off in advance,” concludes Dr. Ahmed Khalil, first author of the study,…
Read more of the Eurekalert article here: https://www.eurekalert.org/news-releases/1083521

For a presentation of study results as published in Nature Communications:
https://www.nature.com/articles/s41467-025-59397-8
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First at-home test kit for cervical cancer approved by the FDA, company says

https://apnews.com/article/hpv-test-hom ... f589506c53
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New nanoparticle could make cancer treatment safer, more effective
Scientists have created a new nanoparticle that could make ultrasound-based cancer treatments more effective and safer, while also helping prevent tumors from coming back. To make the therapy even more powerful, the scientists also attached a potent chemotherapy drug to the peptide on the nanoparticle's surface. The ultrasound physically destroys the tumor, and the drug helps eliminate any leftover cancer cells that might cause the tumor to return.
https://www.sciencedaily.com/releases/2 ... 164330.htm
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Trump Administration Delays Funding To Cancer Research

Yesterday, the Trump Administration imposed a wide range of restrictions on the National Institutes of Health (NIH): a pause on all external communications, a hiring freeze, a travel ban and, perhaps most crucially, the cancellation of grant review panels, until at least February 1. These panels, where a team of NIH experts review research proposals, are required before the $47.4 billion agency will disburse money to support research by hospitals, universities and biotech companies.
https://www.forbes.com/sites/alexknapp/ ... -research/

Trump administration again blocked from cutting billions in federal health money
U.S. District Judge Mary McElroy in Rhode Island granted the preliminary injunction request in the lawsuit brought last month by a coalition of Democrat-led states, allowing the money to keep flowing.
“If we don’t have our health, we don’t have anything, and that’s why today’s preliminary injunction is such a critical win,” Rhode Island Attorney General Peter Neronha said in a statement, adding later: “A hacksaw approach to government reduction will never yield positive results for the American people, and we will continue to fight, and win, in court to minimize the harm the Trump Administration is causing the people of this country.”
https://www.msn.com/en-us/news/us/trump ... r-AA1EUOXs
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Cancer Research in the US is World Class Because of its Broad Base of Funding − With the Government Pulling Out, Its Future is Uncertain
by Jeffrey MacKeigan, Ph.D.
April 28, 2025

Extract:
(The Conversation) While private foundations are vital partners for cancer research, they cannot replace the scale and consistency of federal funding. Total U.S. philanthropic funding for cancer research is estimated at a few billion dollars per year, spread across hundreds of organizations. In comparison, the federal government has typically contributed roughly five to eight times more than philanthropy to cancer research each year.
Industry innovation − and its priorities

Private-sector innovation is essential for translating discoveries into treatments. In 2021, nearly 80% of the roughly $57 billion the U.S. spent on cancer drugs came from pharmaceutical and biotech companies. Many of the treatments used in oncology today, including immunotherapies and targeted therapies, emerged from collaborations between academic labs and industry partners.

But commercial priorities don’t always align with public health needs. Companies naturally focus on areas with strong financial returns: common cancers, projects that qualify for fast-track regulatory approval, and high-priced drugs. Rare cancers, pediatric cancers and basic science often receive less attention.

Industry is also saddled with uncertainty. Rising R&D costs, tough regulatory requirements and investor wariness have created a challenging environment to bring new drugs to market. Several biotech startups have folded or downsized in the past year, leaving promising new drugs stranded in limbo in the lab before they can reach clinical trials.

Without federal or philanthropic entities to pick up the slack, these discoveries may never reach the patients who need them.
Read more here: https://theconversation.com/cancer-re ... in-254536
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Biosynthetic advance could halve the cost of widely used cancer drug
https://phys.org/news/2025-05-biosynthe ... ancer.html
by University of Copenhagen

edited by Lisa Lock, reviewed by Robert Egan
The demand for the widely used cancer drug Taxol is increasing, but it's difficult and expensive to produce because it hasn't been possible to do it biosynthetically. Until now, that is. Researchers from the University of Copenhagen have cracked the last part of a code that science has struggled with for 30 years. The breakthrough could halve the price of the drug and make production far more sustainable.

Taxol is one of the most commonly prescribed chemotherapy drugs for breast, ovarian, cervical, and lung cancer. Yet producing the drug is complex, costly, and environmentally burdensome, as it currently relies on a complicated chemical semi-synthesis. For 30 years, scientists around the world have tried to understand how taxol, a natural compound derived from the Pacific yew tree, forms in nature. Decoding this process would allow for biotech-based production. But the final steps remained unknown—until now.

A research team from the University of Copenhagen has succeeded in finding the two missing pieces: They have identified the enzymes responsible for the two critical final steps in the biosynthetic pathway that makes Taxol active as a drug.
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Joe Biden was recently diagnosed with prostate cancer with a Gleason score of 9. Some, most especially Donald Trump, have confused this with "stage 9."

To clarify this in my own mind, I posed this question to Bing co-pilot:

caltrek: How long does it normally take for prostate cancer to reach "stage 9." Please provide sources.

Bing Co-pilot: Prostate cancer is typically staged using the TNM system, which classifies the cancer from Stage I to Stage IV based on how far it has spread(2). The Gleason score, which ranges from 6 to 10, is used to grade the aggressiveness of the cancer. A Gleason score of 9 indicates a high-grade cancer that is more likely to grow and spread quickly.

The progression of prostate cancer varies significantly depending on factors such as genetics, overall health, and treatment. High-grade prostate cancer (Gleason 9 or 10) can progress rapidly, often spreading beyond the prostate to bones and other organs. However, the exact timeline for progression depends on individual circumstances and medical intervention.

If you're looking for more details on prostate cancer staging and progression, you can check out WebMD, the American Cancer Society, or Healthline. If you have concerns about prostate cancer, consulting a healthcare professional is always the best approach.

1) https://www.cancer.org/cancer/types/pr ... aging.html

2) https://www.healthline.com/health/pros ... ges.html

3) https://www.webmd.com/prostate-cancer/ ... er-stages

4) https://www.msn.com/en-us/health/other ... -AA1F171q
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caltrek
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Biden’s prostate cancer diagnosis has heightened interest in this subject. Below is another article on prostate cancer. I have cited an interesting section regarding “a cancer’s genetic profile.”

Genetics: Uncovering Cancer’s DNA Blueprint
by Jason P. Joseph
May 21, 2025

Extract:
(The Conversation) In addition to grade and stage, doctors are increasingly using a cancer’s genomic profile – its specific genetic makeup – both for deeper insights into its aggressiveness and potential treatment pathways.

DNA acts like a detailed instruction manual for cells, dictating how they should grow and function as well as when they should stop dividing or die. In cancer, mutations act like typos in this genetic instruction manual, causing cells to ignore these normal controls, grow and spread.

Genomic testing can identify these specific genetic alterations. This can be performed on the tumor tissue itself to identify changes called somatic mutations that occurred after you were born. Or it can be carried out through blood or saliva samples to detect changes you inherited called germline mutations.

For men with early-stage prostate cancer, certain genomic tests on the tumor can help clarify the risk of the cancer progressing. This information is valuable in deciding whether active surveillance – closely monitoring the cancer without immediate treatment – is a safe approach, or whether more immediate treatment is warranted.

In advanced or metastatic prostate cancer, identifying specific mutations is particularly critical. For instance, mutations in genes such as BRCA1 or BRCA2 – more commonly associated with breast and ovarian cancer risk – can also occur in prostate cancer. These mutations can make the cancer more aggressive but also potentially susceptible to a specific type of drug called a PARP inhibitor, especially if the cancer becomes resistant to hormone therapy.
Read more here: https://theconversation.com/what-does- ... -257100
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