BUFFALO, NY - March 18, 2025 – A new precision oncology paper was #published in Oncotarget, Volume 16, on March 12, 2025, titled “Worldwide Innovative Network (WIN) Consortium in Personalized Cancer Medicine: Bringing next-generation precision oncology to patients."

Led by Oncotarget Editor-in-Chief Dr. Wafik S. El-Deiry and a global team of researchers, this special publication highlights the groundbreaking work of the Worldwide Innovative Network (WIN) Consortium, a global collaboration dedicated to transforming cancer care through personalized medicine. By leveraging artificial intelligence (AI), molecular profiling, and innovative clinical trials, WIN is helping clinicians tailor treatments to each patient’s unique cancer profile—moving beyond the traditional one-size-fits-all approach.

The WIN Consortium is a fast-moving, non-profit organization bringing together nearly 40 academic, industry, and research institutions, along with patient advocacy groups, across 18 countries and five continents. Founded in 2010 in France by Dr. John Mendelsohn (MD Anderson Cancer Center) and Dr. Thomas Tursz (Gustave Roussy), WIN has been led by different renowned experts. Currently under Dr. El-Deiry’s leadership, WIN continues to break barriers in cancer research, ensuring cutting-edge treatments reach patients worldwide.

“The WIN global consortium is ready to take up the challenge by bringing the best possible Precision Oncology trial to patients.”

One of WIN’s most significant contributions is the development of N-of-1 clinical trials, a revolutionary approach that personalizes cancer treatment based on a patient’s specific tumor characteristics. Unlike traditional trials that test drugs on large groups, N-of-1 trials focus on finding the best therapy for an individual patient using AI-driven algorithms, genomic analysis, and real-world data. WIN’s WINTHER trial was one of the first to use both DNA and RNA analysis to match patients with the most effective therapies, while the WINGPO trial builds on this approach by integrating AI and liquid biopsies to refine treatment selection. These innovations are helping clinicians make more precise treatment decisions and improving outcomes for cancer patients.

While advancing research, the WIN Consortium is also addressing major challenges in precision oncology, including drug accessibility, regulatory barriers, and disparities in global healthcare. By working closely with governments, pharmaceutical companies, and advocacy organizations, WIN is aiming to ensure that life-saving treatments are accessible to all patients, regardless of location or financial status.

WIN’s mission is clear: to accelerate the future of precision oncology by delivering the latest scientific advancements into real-world cancer care. As the field continues to evolve, WIN remains at the forefront, developing next-generation trials and leveraging AI-driven insights to improve patient outcomes. Through global collaboration and groundbreaking research, the WIN Consortium is shaping a future where every cancer patient receives the most effective, personalized treatment possible.

DOI - https://doi.org/10.18632/oncotarget.28703

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

Video short - https://www.youtube.com/watch?v=XAdYfFoMvUM

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

To learn more about Oncotarget, please visit https://www.oncotarget.com.

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Oncotarget

WIN Consortium Leading the Future of Precision Cancer Medicine

Because there are no symptoms in the early stages of pancreatic cancer “about 75 to 80 percent of patients are diagnosed in the later stages of the disease,” said Somashekar Krishna, MD, a James physician scientist who specializes in the early detection and screening of pancreatic cancer. 
Krishna and the team of pancreatic cancer experts at the James are using enhanced screening and artificial intelligence (AI) to better identify pre-cancerous cysts and cancerous tumors in the pancreas; and are the first in the world to use high-tech ablation techniques to attack and kill pancreatic cysts and tumors in a new clinical trial. Most pancreatic cancer tumors begin as pre-cancerous cysts and are most commonly found in people 60 and older. “For people in their 50s there is about a 10-percent prevalence, this doubles in people 60 to 70 to 20 percent and is 25 to 30 percent in people 70 to 80,” Krishna said, adding, “most are small and never grow and become cancerous.” 
Endoscopy procedures are used to better “see” these cysts and cancerous tumors, and the use of artificial intelligence is another tool to identify and determine the risk factor of pre-cancerous cysts. “The tip of the endoscopy probe can see even the tiniest structures in a very detailed manner, and we can pass a needle through the scope and do a biopsy and establish the risk,” Krishna said. Surgery is one option, but the procedure is quite invasive and not easily tolerated by older patient with other medical issues. “A new option is ablation, using heat, in a very precise and careful manner,” Krishna said. “We are the only ones doing this in the United States and have done this with nearly 30 patients in a clinical trial.” Krishna is determined to improve screening and treatment for pancreatic cancer and reduce the mortality rate. “Early in my career, 80 percent of patients diagnosed with pancreatic cancer did not make it more than a year,” he said. “We want to change these outcomes to intervene early and with better and better treatment options.”

Episode 186: Advances in Detecting & Treating Pancreatic Cancer, with Dr Krishna

Clinical Professor of Law Anika Singh Lemar talks about the struggle to build more affordable housing in Connecticut and the three clinics she leads at the Law School that work on housing issues. She also discusses her ideas about making it easier to build housing.

https://law.yale.edu/yls-today/news/podcast-anika-singh-lemar-confronts-connecticuts-housing-crisis

Anika Singh Lemar Confronts Connecticut’s Housing Crisis

Paula Cilleros-Holgado from Pablo de Olavide University discusses a #research paper she co-authored that was #published in Volume 17, Issue 2 of Aging (Aging-US), entitled “Mitochondrial dysfunction, iron accumulation, lipid peroxidation, and inflammasome activation in cellular models derived from patients with multiple sclerosis.”

DOI - https://doi.org/10.18632/aging.206198

Corresponding author - José Antonio Sánchez-Alcázar - jasanalc@upo.es

Video interview - https://www.youtube.com/watch?v=wIV0lAHPA_M

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Despite advancements in managing relapsing active illness, effective treatments for the irreversible progressive decline in MS remain limited.

Research employing skin fibroblasts obtained from patients with neurological disorders revealed modifications in cellular stress pathways and bioenergetics. However, research using MS patient-derived cellular models is scarce.

In this study, we collected fibroblasts from two MS patients to investigate cellular pathological alterations. We observed that MS fibroblasts showed a senescent morphology associated with iron/lipofuscin accumulation and altered expression of iron metabolism proteins. In addition, we found increased lipid peroxidation and downregulation of antioxidant enzymes expression levels in MS fibroblasts. When challenged against erastin, a ferroptosis inducer, MS fibroblasts showed decreased viability, suggesting increased sensitivity to ferroptosis. Furthermore, MS fibroblasts presented alterations in the expression levels of autophagy-related proteins. Interestingly, these alterations were associated with mitochondrial dysfunction and inflammasome activation. These findings were validated in 7 additional patient-derived cell lines.

Our findings suggest that the underlying stress phenotype of MS fibroblasts may be disease-specific and recapitulate the main cellular pathological alterations found in the disease such as mitochondrial dysfunction, iron accumulation, lipid peroxidation, inflammasome activation, and pro-inflammatory cytokine production.

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Keywords - aging, multiple sclerosis, iron accumulation, lipid peroxidation, inflammasome, mitochondrial dysfunction

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Aging (Aging-US)

Behind the Study: How Mitochondrial Dysfunction and Iron Buildup Drive Multiple Sclerosis

BUFFALO, NY - April 11, 2025 – A new research perspective was published in Oncotarget, Volume 16, on April 4, 2025, titled “GSK3β activation is a key driver of resistance to Raf inhibition in BRAF mutant melanoma cells."

In this work, first author Diana Crisan and corresponding author Abhijit Basu from the University Hospital Ulm led a team that presents experimental evidence pointing to the protein GSK3β as a key contributor to drug resistance in melanoma. Their findings suggest that GSK3β becomes increasingly active in cancer cells during treatment, helping them survive and adapt despite ongoing therapy with BRAF inhibitors.

Melanoma is a type of skin cancer in which nearly half of patients have mutations in the BRAF gene that accelerate tumor growth. While treatments targeting BRAF, known as BRAF inhibitors, initially work well, tumors often find ways to fight back. This research perspective explores how GSK3β, a protein involved in metabolism and cell survival, becomes more active in melanoma cells that develop resistance to BRAF inhibitors.

Researchers treated melanoma cells with a common BRAF mutation using Dabrafenib, a widely used BRAF inhibitor. Over time, the cancer cells developed resistance and showed a marked increase in GSK3β levels. This pattern was confirmed across multiple melanoma cell models, suggesting that the finding is consistent and reliable.

Importantly, the researchers observed that treating resistant cancer cells with a GSK3β inhibitor significantly reduced their growth. This result suggests that blocking this protein could restore sensitivity to treatment, highlighting GSK3β as a promising therapeutic target and supporting the idea of combining GSK3β inhibitors with existing melanoma therapies.

“Remarkably, treatment of BRAFi-resistant melanoma cells with the GSK3 inhibitor LY2090314 for three weeks could overcome resistance and significantly decreased melanoma cell growth, confirming the causal role of GSK3 activation for BRAFi resistance development.”

The research perspective adds to ongoing efforts to understand and overcome melanoma drug resistance. It shows that resistance is not driven only by genetic mutations but may also involve adaptive changes in the cell’s internal signaling and survival mechanisms. By identifying GSK3β as a potential contributor, the authors offer a new direction for improving the durability of targeted treatments in melanoma.

As research continues, GSK3β may be a critical factor in the long-term success of melanoma therapy, particularly for patients who have stopped responding to standard BRAF-targeted drugs.

Continue reading: DOI: https://doi.org/10.18632/oncotarget.28711

Correspondence to: Abhijit Basu — abhijit.basu@alumni.uni-ulm.de

Video short - https://www.youtube.com/watch?v=G2Tq4_r6xLw

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About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Protein GSK3β Offers New Angle on Overcoming Melanoma Drug Resistance

BUFFALO, NY — April 14, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 4, 2025, titled “Deciphering age-related transcriptomic changes in the mouse retinal pigment epithelium.”

The study, led by first authors Sushil K. Dubey and Rashmi Dubey with corresponding author Mark E. Kleinman from East Tennessee State University, reveals that aging causes inflammation, oxidative stress, and gene disruption in the retinal pigment epithelium (RPE), a vital layer of cells in the eye. These changes may explain why older adults are more vulnerable to age-related eye diseases. The researchers also developed a human cell model to study retinal aging and test future therapies.

The RPE plays a key role in maintaining retinal health. It recycles light-sensitive molecules, supports the visual cycle, and protects the retina from damage. When this layer becomes damaged, vision problems such as age-related macular degeneration can develop.

In this study, researchers compared gene activity in RPE cells from young and aged mice. They found that aging increased the activity of genes involved in immune system responses, inflammation, and oxidative stress, three known triggers of tissue damage. At the same time, genes related to vision and light detection became less active, weakening the RPE’s ability to support healthy vision.

To reinforce these findings, the research team also aged human RPE cells in the lab. Over time, these cells showed the same patterns: inflammation increased, while genes tied to visual function decreased. This human cell model offers a practical way to explore how RPE degeneration happens over time and how it might be slowed down or reversed.

The research also identified “hub genes,” which are central players of the gene networks involved in RPE aging. These are connected to immune signaling, oxidative damage, and changes in the eye’s structural support. Many of these genes are already known to be involved in age-related retinal degeneration, so they may become important targets for future treatments aimed at protecting vision in older adults.

“GO annotation of downregulated genes included processes related to visual perception, sensory perception of light stimulus, detection of light stimulus, detection of visible light, detection of external stimulus, detection of abiotic stimulus, phototransduction, cellular response to interferon-beta, response to interferon-beta, and response to light stimulus.”

By mapping how the RPE changes with age at the molecular level, this study provides a clearer understanding of why aging leads to eye disease. It also introduces a reliable laboratory model that researchers can use to test new therapies. Altogether, the work is a key step toward developing treatments to slow or prevent vision loss tied to retinal aging.

Read the full paper: DOI: https://doi.org/10.18632/aging.206219

Corresponding author: Mark E. Kleinman- kleinman@etsu.edu 

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Keywords: aging, transcriptome, retinal pigment epithelium, oxidative stress, inflammation, chronological aging

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Aging Triggers Inflammation and Stress in Retinal Cells, Raising Risk of Vision Loss

This week’s episode of the YJBM Science News podcast is all about papers that identify or help narrow down potential new targets and tools for cancer therapeutics. From protein modifications to autoantibodies to epigenetic markers and more, join co-hosts Majo and Roxanna as they break down recent Yale-affiliated biological and biomedical research.

Papers featured in this episode:
“Turnover atlas of proteome and phosphoproteome across mouse tissues and brain regions” - https://doi.org/10.1016/j.cell.2025.02.021
https://medicine.yale.edu/news-article/protein-turnover-mapping-may-offer-clues-for-alzheimers-cancer-treatment/
“A lupus-derived autoantibody that binds to intracellular RNA activates cGAS-mediated tumor immunity and can deliver RNA into cells” - https://doi.org/10.1126/scisignal.adk3320
https://medicine.yale.edu/news-article/lupus-related-antibody-shows-promise-in-enhancing-cancer-treatment-efficacy/
“BRCA2 prevents PARPi-mediated PARP1 retention to protect RAD51 filaments” - https://doi.org/10.1038/s41586-025-08749-x
https://news.yale.edu/2025/03/26/how-inherited-cancer-risks-can-be-used-effective-personalized-therapy
“An in vivo screen identifies NAT10 as a master regulator of brain metastasis” - https://doi.org/10.1126/sciadv.ads6021
https://medicine.yale.edu/news-article/a-genetic-screen-identifies-a-new-master-regulator-of-brain-metastasis/

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YJBM Science News 31: Clues to Cancer Care

The Rev'd John Burruss (The Leader's Way ’23 Fellow) and the Rev'd Mary Bea Sullivan join hosts Hannah Black and Brandon Nappi to tell the story of the Threshold Center, a vibrant space designed to address loneliness and foster connection in Birmingham, Alabama. Born from a tragic event in the life of St. Stephen's Episcopal Church, the Threshold Center nurtures well-being and connection by engaging practices of the heart, body, and imagination through innovative programs like trauma-informed yoga, listening as an act of love, and peace through poetry. This episode offers rich insights into the power of collaboration, creativity, and radical hospitality.

50: Innovative Parish Ministry with the Threshold Center

BUFFALO, NY - April 15, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on April 4, 2025, titled “Association between two single nucleotide polymorphisms of the Prostaglandin-Endoperoxide Synthase 1 and 2 genes and cell proliferative prostatic diseases in Lebanon."

The team of researchers led by first author Brock J. Sheehan and corresponding author Ruhul H. Kuddus, from Utah Valley University, discovered that a specific genetic variation in the PTGS2 gene is associated with a higher risk of benign prostate hyperplasia (BPH), a common condition in aging men. The study, which focused on Lebanese men, suggests that the C allele of the -765 G>C polymorphism in the PTGS2 gene may increase risk to this non-cancerous but problematic prostate condition. This finding could help identify men at greater risk earlier and lead to better treatment choices.

Benign prostate hyperplasia and prostate cancer are two common conditions that involve abnormal cell growth in the prostate gland. While prostate cancer is malignant and potentially life-threatening, BPH is a non-cancerous enlargement that can still significantly affect quality of life. Both conditions are widespread in older men, with BPH affecting over 70% of men above 60. Researchers have long suspected that inflammation-related genes may play a role in their development. In this study, the focus was to study PTGS1 and PTGS2, genes that help produce enzymes involved in inflammation.

Using DNA samples from 168 Lebanese men, including 61 with prostate cancer, 51 with BPH, and 56 healthy controls, the researchers analyzed two common gene variants. They found no link between the PTGS1 variant and either condition. However, the PTGS2 variant showed a strong association with BPH. Men carrying the C version of this gene were more than twice as likely to have BPH compared to those without it. While a similar trend was observed in men with prostate cancer, the results were less conclusive.

"The C allele of SNP-765G>C of the PTGS2 gene was significantly associated with an increased risk of BPH (OR = 2.30, p-value = 0.01)."

This is the first study to report a genetic link between the C allele of the -765 G>C polymorphism in the PTGS2 gene and BPH in Lebanese men. It builds on earlier findings that associated this gene variant with various cancers, including prostate, colon, and stomach cancers. Although based on a relatively small and specific population, the study offers new insight that could help improve genetic screening and guide prevention strategies.

The research also points to the potential benefits of COX-2 inhibitors—drugs already used to treat prostate conditions—which may be more effective for men with certain PTGS2 gene types. Further studies in larger and more diverse groups are needed to confirm these results and explore how this gene variant influences prostate disease. In the future, simple genetic tests could help identify men at higher risk before symptoms appear, allowing for earlier and more personalized care.

Continue reading: DOI: https://doi.org/10.18632/oncotarget.28710

Correspondence to: Ruhul H. Kuddus — ruhul.kuddus@uvu.edu

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Gene Variant Linked to Benign Prostate Hyperplasia Risk in Lebanese Men

BUFFALO, NY — April 16, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 12, 2025, titled “DNA methylation entropy is a biomarker for aging.”

Researchers Jonathan Chan, Liudmilla Rubbi, and Matteo Pellegrini from the University of California, Los Angeles, led a study that discovered a new way to measure changes in DNA that can help predict a person’s age. This method focuses on how random certain chemical tags on DNA become over time. The team compared this new measurement, called methylation entropy, to existing methods and found it performed just as well—or even better. These findings support the idea that changes in our epigenetic information are closely linked to aging and could offer new tools for studying age-related diseases.

The study focused on DNA methylation, a process where chemical marks are added to DNA and help control which genes are turned on or off. Scientists have traditionally measured average methylation levels to estimate biological age using “epigenetic clocks.” This study, however, takes a different approach. The researchers used buccal swabs (cells from inside the cheek) from 100 individuals between ages 7 and 84 and applied targeted bisulfite sequencing techniques to measure methylation entropy across 3,000 regions of the genome.

Entropy in this context reflects how disordered or varied the methylation patterns are at certain sites on the DNA. The researchers discovered that as people age, the entropy of methylation at many locations changes in a reproducible way. Sometimes it increases, reflecting more random patterns, and sometimes it decreases, showing more uniformity. These shifts are not always tied to how much methylation is happening, which suggests entropy provides new information beyond what traditional methods can offer.

To test how well this new metric could predict age, the team used both statistical and machine learning models. They found that methylation entropy predicted age as accurately as traditional methods, and the best results came from combining entropy with other measurements like average methylation and a method called CHALM. These combined models were able to estimate age with an average error of just five years.

"[...] methylation entropy is measuring different properties of a locus compared to mean methylation and CHALM, and that loci can become both more or less disordered with age, independently of whether the methylation is increasing or decreasing with age."

This research supports the growing theory that aging is partly caused by a gradual loss of epigenetic information—the biological “instructions” that help keep our cells working properly. This insight also connects with recent studies suggesting that restoring this lost information might reverse some signs of aging. While more research is needed to study methylation entropy in other tissues, this work points to a more precise and powerful way to measure biological aging, which could influence the future of aging-related treatments and therapies.

Read the full paper: DOI: https://doi.org/10.18632/aging.206220

Corresponding author: Matteo Pellegrini - matteope@gmail.com

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Keywords: entropy, DNA methylation, aging, epigenetics, epigenetic clocks

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DNA Methylation Entropy: A New Way to Track and Predict Aging

Breast cancer survivors are living longer than ever, thanks to research and medical advances, but new studies suggest that some treatments may come with a hidden cost: accelerated aging. A recent study, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors,” published in Aging (Aging-US), reveals that breast cancer and its treatments may speed up biological aging, with effects lasting up to a decade post-diagnosis.

Breast Cancer and Aging

Breast cancer is one of the most common cancers among women worldwide. Medical advancements have dramatically improved survival rates, making it one of the most treatable forms of cancer. Yet, many survivors report lasting symptoms like fatigue, memory issues, and reduced vitality that resemble accelerated aging. This pattern has led scientists to investigate whether treatments for breast cancer might be contributing to biological age acceleration.

Full blog - https://aging-us.org/2025/04/breast-cancer-treatments-hidden-impact-accelerated-aging-among-survivors/

Paper DOI - https://doi.org/10.18632/aging.206218

Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org

Video short - https://www.youtube.com/watch?v=cfuyzVyDeHY

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Keywords - aging, accelerated aging, PhenoAge, breast cancer, survivors

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Breast Cancer Treatment’s Hidden Impact: Accelerated Aging Among Survivors

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

WIN Consortium Leading the Future of Precision Cancer Medicine

Oncotarget Podcast

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