BUFFALO, NY — February 19, 2025 — A new #research paper was #published by Aging (Aging-US) on January 6, 2025, in Volume 17, Issue 1, titled “The profile of oxidative stress markers (arachidonic and linoleic acid derivatives) in patients with benign prostatic hyperplasia in relation to metabolic syndrome.”

A team of researchers, led by first author Weronika Ratajczak and corresponding author Olimpia Sipak from Pomeranian Medical University, examined how inflammation and metabolic health contribute to benign prostatic hyperplasia (BPH), a common condition that causes prostate enlargement in aging men, leading to urinary problems. Their findings suggest that inflammatory-related molecules in the blood may play a key role in BPH development, especially in men with metabolic syndrome—a group of conditions including obesity, high blood sugar, and high cholesterol.

BPH affects millions of men as they age, making urination more difficult and sometimes painful. While age and hormonal changes are known factors, the precise causes of prostate enlargement remain unclear. This study provides new evidence that inflammation, especially lipid-derived inflammatory markers, may be a driving factor behind BPH, particularly in those with poor metabolic health.

The research team analyzed blood samples from 219 men, including 144 with BPH and 75 without, measuring markers related to inflammation and oxidative stress. The results showed that men with BPH had significantly higher levels of pro-inflammatory molecules such as 12S-HETE and 5-HETE while having lower levels of anti-inflammatory substances like lipoxin A4. The imbalance was even more pronounced in men with both BPH and metabolic syndrome, indicating a possible link between poor metabolic health and worsening prostate conditions​.

“Furthermore, there is mounting evidence that links the onset of inflammation with the development of prostate diseases, including benign prostatic hyperplasia and prostate cancer.”

Metabolic dysfunction and chronic inflammation may not only contribute to BPH development but also exacerbate its severity. Monitoring metabolic health could play a role in reducing the risk of prostate enlargement.

Future research is needed and may focus on whether anti-inflammatory treatments or lifestyle changes—such as improved diet, weight management, and exercise—could help slow the progression of BPH or reduce its symptoms​.

DOI - https://doi.org/10.18632/aging.206187

Corresponding author - Olimpia Sipak - olimpiasipak-szmigiel@wp.pl

Video short - https://www.youtube.com/watch?v=O0VMvqaVsUs

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Keywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipid markers, inflammation, fatty acids derivatives

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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Aging (Aging-US)

Inflammation and Metabolic Syndrome Linked to Benign Prostatic Hyperplasia

Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality. While the development of targeted therapies has improved outcomes for many patients with EGFR-mutated NSCLC, those with rare EGFR variants often face limited treatment options, especially when the disease involves the central nervous system (CNS).

A recent research paper, titled “Durable complete response in leptomeningeal disease of EGFR mutated non-small cell lung cancer to amivantamab, an EGFR-MET receptor bispecific antibody, after progressing on osimertinib” published in Volume 16 of Oncotarget, describes a patient with NSCLC harboring two uncommon EGFR mutations—G719A and A289V—who experienced a prolonged and clinically significant response to amivantamab monotherapy, after prior treatments had failed.

Full blog - https://www.oncotarget.org/2025/08/26/amivantamab-monotherapy-in-rare-egfr-mutated-advanced-nsclc/

Paper DOI - https://doi.org/10.18632/oncotarget.28730

Correspondence to - Young Kwang Chae - young.chae@northwestern.edu

Video short - https://www.youtube.com/watch?v=UEiCz834a8c

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Keywords - cancer, amivantamab, monotherapy, rare EGFR mutation, NSCLC, leptomeningeal disease

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.

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Oncotarget

Amivantamab Monotherapy in Rare EGFR-Mutated Advanced NSCLC

Aiden Deacon from the University of Minnesota-Twin Cities, Minneapolis, discusses a research paper he co-authored that was published in Volume 16 of Oncotarget, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.”

DOI - https://doi.org/10.18632/oncotarget.28758

Correspondence to - Justin Hwang - jhwang@umn.edu

Video interview - https://www.youtube.com/watch?v=OXKhWWU1gnY

Abstract

This study investigates the R-spondin family of genes (RSPO1/2/3/4), a group of secreted proteins that act as Wnt regulators, and their subsequent role in advanced prostate cancer (PC). When evaluating transcriptomic data from primary and metastatic PC patients, we found that alterations in RSPO2 were more prevalent than in other RSPO family members or Wnt-regulating genes APC and CTNNB1. Further, we found that RSPO2 alterations in PCs were significantly associated with worse disease-free survival. Through our in silico modeling, RSPO2 exhibited strong positive associations with genes regulating epithelial-mesenchymal transition (EMT) and double-negative prostate cancer (DNPC), but had negative correlations with androgen receptor (AR) and AR-associated genes. Furthermore, 3D modeling of RSPO2 revealed structural differences between itself and other RSPOs. In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1. Conversely, this was not observed when CTNNB1 was overexpressed in the same models. These findings highlight that, in PC, RSPO2 functions as a unique member of the R-spondin family by promoting genes and signaling pathways associated with aggressive PC, and RSPO2 amplifications are associated with poor outcomes in PC patients.

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Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics

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.

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Oncotarget author interview: Aiden Deacon

Behind the Study: R-spondin Family Roles in Metastatic Prostate Cancer

BUFFALO, NY — August 27, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 24, 2025, titled “RNA-binding protein AUF1 suppresses cellular senescence and glycolysis by targeting PDP2 and PGAM1 mRNAs.”

In this study, Hyejin Mun, Chang Hoon Shin, Mercy Kim, Jeong Ho Chang, and Je-Hyun Yoon from the University of Oklahoma and Kyungpook National University investigated how changes in cellular metabolism contribute to aging. Their findings offer potential targets for therapies aimed at slowing or reducing the effects of aging.

As cells age, they often lose their ability to divide and begin releasing harmful signals that damage nearby tissues. This process, called cellular senescence, is linked to many age-related diseases. A key feature of senescent cells is their altered metabolism, where they use more glucose and oxygen, even when oxygen levels are low. This leads to the production of inflammatory substances and fatty acids, which can accelerate tissue damage. The study examined how these metabolic changes are controlled at the molecular level.

Researchers found that AUF1, a protein that binds to RNA, normally helps prevent aging by breaking down two enzymes involved in glucose metabolism: PGAM1 and PDP2. When AUF1 is missing or inactive, these enzymes build up. This causes the cell to produce more energy and inflammatory molecules, which are common features of senescent cells.

“Our high throughput profiling of mRNAs and proteins from Human Diploid Fibroblasts (HDFs) revealed that the expression of pyruvate metabolic enzymes is inhibited by the anti-senescent RNA-binding protein (RBP) AUF1 (AU-binding Factor 1).”

The team also identified another protein, MST1, which becomes active during cellular stress and aging. MST1 modifies AUF1 in a way that stops it from doing its protective job. As a result, PGAM1 and PDP2 accumulate, leading to faster aging of the cell. Experiments using human fibroblast cells and mouse models confirmed that higher levels of these enzymes are linked to stronger signs of cellular aging.

These findings improve our understanding of how metabolism affects the aging process. They highlight the MST1-AUF1-PDP2/PGAM1 pathway as a key factor in the metabolic shift seen in aging cells. Since these enzymes and proteins are already known to be involved in other diseases, existing or future therapies might be used to block this pathway and reduce the effects of aging.

This study offers a new direction for senotherapy—a field focused on treating or removing aging cells. By adjusting glucose metabolism through AUF1 and its targets, scientists believe it may be possible to slow aging or limit its effects on tissue function. More research is needed, but these insights could lead to new strategies for managing age-related diseases and promoting healthier aging.

DOI - https://doi.org/10.18632/aging.206286

Corresponding authors - Jeong Ho Chang - jhcbio@knu.ac.kr, and Je-Hyun Yoon - jehyun-yoon@ouhsc.edu

Video short - https://www.youtube.com/watch?v=Gbu6USUSkgg

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Keywords - aging, AUF1, MST1, senescence, glycolysis

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AUF1 Protein Plays Anti-Aging Role by Regulating Cellular Metabolism

BUFFALO, NY – August 29, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 29, 2025, titled “In vivo manipulation of the protein homeostasis network in rhabdomyosarcoma.”

In this study led by first author Kristen Kwong and corresponding author Amit J. Sabnis from the Department of Pediatrics, Division of Oncology, University of California San Francisco, researchers discovered that disrupting the protein quality control system in cancer cells slows tumor growth in rhabdomyosarcoma (RMS), the most common pediatric soft tissue cancer. This finding points to a new strategy for treating high-risk childhood cancers that often resist current therapies.

Rhabdomyosarcoma is a rare and aggressive cancer that primarily affects children and adolescents. Standard treatments like chemotherapy and radiation often have limited long-term success in high-risk cases. This study explored a different approach: targeting the cellular machinery that maintains protein quality, known as the proteostasis network. Cancer cells rely heavily on this system to survive stress caused by rapid growth and genetic instability.

“To examine whether MAL3-101 or more drug-like proteostasis inhibitors represent a new therapeutic strategy for RMS, we screened proteostasis components that might recapitulate the effects of MAL3-101 in vivo.”

The researchers first used a compound called MAL3-101 to disrupt protein control in RMS cells. They then identified which parts of the protein quality system were affected. Based on those findings, they searched for more drug-like compounds that could target the same pathways. 

They focused on a protein called p97, which plays a critical role in removing damaged or misfolded proteins. When they blocked p97 using a drug called CB-5083, the cancer cells could no longer manage internal stress and began to self-destruct. In both laboratory models and mice implanted with human RMS tumors, the treatment significantly slowed or stopped tumor growth. The drug triggered a stress response in the cells known as the unfolded protein response, which can lead to either recovery or programmed cell death.

However, not all tumors responded the same way. Some resisted the treatment by activating a backup system called autophagy, which allows cells to recycle parts of themselves under stress. By comparing tumors that responded well to those that did not, the researchers found that higher autophagy activity could serve as a warning sign for resistance. This insight may help identify which patients are more likely to benefit from therapies that target protein quality control.

While the results are promising, the drug’s effectiveness depended on the tumor’s genetic profile and how it handled stress. Combining p97 inhibition with other treatments or blocking alternative survival pathways like autophagy may improve outcomes. The researchers also noted the importance of developing safer and more targeted drugs to reduce side effects.

This study opens new possibilities for personalized cancer treatment, particularly for children with aggressive or relapsed RMS. By weakening the systems that cancer cells depend on to survive, rather than only using toxic treatments to kill them, scientists aim to develop more effective and less harmful therapies for young patients.

DOI - https://doi.org/10.18632/oncotarget.28764

Correspondence to - Amit J. Sabnis - amit.sabnis@ucsf.edu

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

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Blocking Protein Control Pathway Slows Rhabdomyosarcoma Growth in Mice

BUFFALO, NY — September 2, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 8 of Aging (Aging-US) was #published on July 30, 2025, titled “Exosomes released from senescent cells and circulatory exosomes isolated from human plasma reveal aging-associated proteomic and lipid signatures.”

In this study, led by first authors Sandip Kumar Patel and Joanna Bons, along with corresponding author Birgit Schilling from The Buck Institute for Research on Aging, researchers found that exosomes—tiny particles released by cells—carry molecular signatures that indicate both biological aging and cellular senescence. These signatures include proteins, lipids, and microRNAs associated with inflammation, oxidative stress, and tissue remodeling. The findings could enhance our understanding of biological aging and help in developing future anti-aging therapies.

Senescence is a state in which cells stop dividing but remain metabolically active. These cells often release harmful substances, known collectively as the senescence-associated secretory phenotype (SASP), that can affect nearby tissues. This study shows that exosomes are an important component of this secretory profile.

The researchers analyzed exosomes from senescent human lung cells and from the blood plasma of both young and older adults. They identified over 1,300 proteins and 247 lipids within these particles. Many of these molecules were significantly altered with age.

“In parallel, a small human plasma cohort from young (20–26 years) and old (65–74 years) individuals revealed 1,350 exosome proteins and 171 plasma exosome proteins were altered in old individuals.”

Exosomes from older individuals contained more inflammation-related proteins and fewer antioxidants, while those from senescent cells showed lipid changes associated with membrane integrity and cellular stress. These changes suggest that exosomes may play a role in spreading senescence to nearby cells, a process known as secondary senescence.

The study also identified distinct patterns in microRNAs—small molecules that regulate gene expression—found in the blood of older adults. Some of these, including miR-27a and miR-874, have previously been associated with cognitive decline and chronic illnesses, highlighting their potential as biomarkers for biological aging.

Although the study involved a limited number of samples, it provides strong early evidence that exosomes reflect the molecular changes associated with aging. By showing how these particles carry and possibly spread aging-related signals throughout the body, the research opens new possibilities for diagnosing and treating age-related diseases.

DOI - https://doi.org/10.18632/aging.206292

Corresponding author - Birgit Schilling – bschilling@buckinstitute.org

Video short - https://www.youtube.com/watch?v=tcyAZahw-g8

Keywords - aging, proteomics, senescence, exosomes, data-independent acquisitions

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New Study Links Exosomes to Biological Aging

BUFFALO, NY — September 4, 2025 — A new #research perspective was #published  in Volume 17, Issue 8 of Aging (Aging-US) on August 16, 2025, titled “Age-related diseases as a testbed for anti-aging therapeutics: the case of idiopathic pulmonary fibrosis.”

In this research perspective, Alex Zhavoronkov, Dominika Wilczok, Feng Ren, and Fedor Galkin, from Insilico Medicine, Buck Institute for Research on Aging, and Duke University, propose a new method to evaluate age-related diseases based on how closely they align with the biological processes of aging. Their analysis shows that idiopathic pulmonary fibrosis (IPF), a progressive lung condition, is one of the diseases most strongly associated with aging. This makes IPF a promising model for testing new anti-aging therapies with the potential to treat multiple age-related conditions.

“This perspective explores how aging-related diseases (ARDs) can serve as experimental platforms for discovering new geroprotective interventions.”

While many age-related diseases are used as models for aging research, not all accurately reflect the biology of aging. To address this, the authors developed a scoring system that measures how closely a disease is connected to the key hallmarks of aging, such as inflammation, genetic instability, and impaired cellular repair. Using this system, they evaluated 13 common age-related diseases and found that IPF had a particularly high overlap with aging biology.

IPF is a chronic disease that causes scarring in the lungs and a rapid decline in lung function. In contrast to the gradual loss of function seen in normal aging, IPF progresses more than five times faster. The authors highlight that IPF shares nearly all of the biological features associated with aging. These similarities make IPF a strong candidate for studying aging and testing therapies that target its underlying causes.

The authors also discuss different therapies currently being developed for IPF that are also designed to address aging itself. These include drugs that clear senescent cells, activate telomerase to maintain chromosome health, or repair damaged signaling between cells. Some of these treatments, such as senolytic combinations and AI-discovered compounds like rentosertib, are already showing early promise in preclinical or clinical trials.

In addition, the authors point out that IPF’s fast progression and clearly measurable outcomes offer an advantage for clinical testing. If a therapy proves effective in IPF, it may also be useful for other conditions that share similar aging-related mechanisms, including diabetes, arthritis, and heart disease. This approach could accelerate drug development and reduce costs by focusing on therapies that target shared biological pathways.

Overall, this perspective supports a shift in pharmaceutical research toward treating aging as an underlying cause of many chronic diseases. By positioning IPF as a model for aging-related drug development, the authors propose a strategic pathway for testing and expanding anti-aging therapies across a wide range of health conditions.

DOI - https://doi.org/10.18632/aging.206301

Corresponding author - Alex Zhavoronkov – alex@insilico.com

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Idiopathic Pulmonary Fibrosis Identified as a Model for Anti-Aging Drug Development

As the global population grows older, understanding what drives the aging process is becoming increasingly important. Diseases like Alzheimer’s, cardiovascular conditions, and cancer are more common with age, yet many current treatments only manage symptoms rather than addressing the underlying biological causes.

One contributor to aging is the buildup of “senescent” cells—cells that have stopped dividing but do not die. These cells can harm nearby tissues by releasing molecular signals, a process known as secondary senescence.

Scientists have found that senescent cells release tiny particles called exosomes. A research team from The Buck Institute for Research on Aging recently discovered that these exosomes carry aging-related messages through the bloodstream. Their study, titled “Exosomes released from senescent cells and circulatory exosomes isolated from human plasma reveal aging-associated proteomic and lipid signatures,” was featured as the cover article in Aging (Aging-US), Volume 17, Issue 8.

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Paper DOI - https://doi.org/10.18632/aging.206292

Corresponding author - Birgit Schilling - bschilling@buckinstitute.org

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Keywords - aging, proteomics, senescence, exosomes, data-independent acquisitions

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How Exosomes Spread Aging Signals and Could Support Anti-Aging Research

BUFFALO, NY — September 9, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 1, 2025, titled “Causal relationships between gut microbiome and hundreds of age-related traits: evidence of a replicable effect on ApoM protein levels.”

In this study, Federica Grosso, Daniela Zanetti, and Serena Sanna from the Institute for Genetic and Biomedical Research (IRGB) of the National Research Council (CNR), Italy, uncovered new associations between gut microbiome and the aging process. The researchers found that certain microbial characteristics may causally influence proteins in the blood linked to inflammation and heart health. These findings could help explain how age-related diseases like cardiovascular conditions and macular degeneration are influenced by changes in the gut ecosystem.

The gut microbiome, the collection of microorganisms living in the digestive system, plays a major role in immune function and metabolic health. As people age, this microbial community shifts, often leading to imbalances associated with inflammation and chronic disease. To explore how these changes might affect the body, the researchers used Mendelian Randomization—a method that leverages genetic data—to test over 55,000 possible causal connections between gut microbial characteristics and age-related health indicators.

The study identified 91 significant causal relationships. Among them, the researchers found that higher levels of certain gut bacteria were associated with increased risk of age-related macular degeneration. Another finding was the association between a metabolic pathway in the gut, called “purine nucleotides degradation II,” and lower levels of apolipoprotein M (ApoM), a protein that helps protect against heart disease. This result was validated using data from an independent study, strengthening the evidence.

“Unlike previous studies, we performed replication analyses for the significant results using independent GWAS datasets, a fundamental step that has often been overlooked.”

The study also revealed how some bacteria may affect protein levels differently depending on a person’s blood type. Specifically, in individuals with blood type A, certain gut microbes that can break down a sugar called GalNAc may influence proteins related to inflammation and cardiovascular health. This suggests that personalized approaches to managing age-related diseases could consider both gut microbiota and genetic factors like blood type.

The research team followed strict guidelines to reduce false findings and confirmed its key results in independent datasets. By carefully testing for reverse causality and other biases, the authors provided strong evidence that the gut microbiome can influence critical aspects of aging biology.

Although more research is needed to fully understand the biological pathways involved, these findings suggest that targeting the gut microbiota might help delay or reduce age-related inflammation and disease. The study lays a foundation for future therapeutic strategies that could include diet, probiotics, or other microbiome-based interventions.

DOI - https://doi.org/10.18632/aging.206293

Corresponding author - Serena Sanna - serena.sanna@cnr.it

Abstract video - https://www.youtube.com/watch?v=CWky6jlHKUs

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Aging-US

Gut Microbiome Influences Proteins That Drive Aging and Disease

BUFFALO, NY — September 11, 2025 — A new #research paper was #published  in Volume 17, Issue 8 of Aging-US on August 8, 2025, titled “AI-driven toolset for IPF and aging research associates lung fibrosis with accelerated aging.”

In this study, researchers Fedor Galkin, Shan Chen, Alex Aliper, Alex Zhavoronkov, and Feng Ren from Insilico Medicine used artificial intelligence (AI) to investigate the similarities between idiopathic pulmonary fibrosis (IPF), a severe lung disease, and the aging process. Their findings show that IPF is not simply accelerated aging, but a distinct biological condition shaped by age-related dysfunction. This insight may lead to a new approach in how scientists and clinicians treat this complex disease.

IPF mainly affects individuals over the age of 60. It causes scarring of lung tissue, making it harder to breathe and often leading to respiratory failure. Current treatments can slow the disease but rarely stop or reverse its progression. The researchers used AI to identify shared biological features between aging and fibrosis, finding new potential targets for therapy.

The team developed a “proteomic aging clock” based on protein data from more than 55,000 participants in the UK Biobank. This AI-driven tool accurately measured biological age and found that patients with severe COVID-19, who are at increased risk for lung fibrosis, also showed signs of accelerated aging. This suggests that fibrosis leaves a detectable biological trace, supporting the use of aging clocks in studying age-related diseases.

“For aging clock training, we used the UK Biobank collection of 55319 proteomic Olink NPX profiles annotated with age and gender.”

They also developed a custom AI model, ipf-P3GPT, to compare gene activity in aging lungs versus those with IPF. Although some genes were active in both, many showed opposite behavior. In fact, more than half of the shared genes had inverse effects. This means IPF does not just speed up aging but also disrupts the body’s normal aging pathways.

The study identified unique molecular signatures that distinguish IPF from normal aging. While both involve inflammation and tissue remodeling, IPF drives more damaging changes to lung structure and repair systems. This difference could guide the development of drugs that specifically target fibrosis without affecting normal aging.

By combining AI with large-scale biological data, the study also introduces a powerful toolset for examining other age-related conditions such as liver and kidney fibrosis. These models may support personalized treatments and expand understanding of the relationships between aging and disease, opening new directions for therapy development.

DOI - https://doi.org/10.18632/aging.206295

Corresponding author - Alex Zhavoronkov - alex@insilico.com

Abstract video - https://www.youtube.com/watch?v=24lX2lHbt7o

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Keywords - aging, IPF, generative AI, transformer, proteomics

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AI Tools Uncover New Link Between Idiopathic Pulmonary Fibrosis and Aging

Immunotherapy is not usually effective against pancreatic cancer (PC), but a new study published in Oncotarget (Volume 16, 2025) highlights rare cases where it did help. These examples, though uncommon, may offer valuable insights for future treatment.

Pancreatic Cancer and Immunotherapy

Pancreatic cancer is often diagnosed at an advanced stage, which limits treatment options and contributes to its poor prognosis. While chemotherapy remains the standard treatment, it usually offers only modest benefits in terms of survival. Immunotherapy—an approach that activates the immune system to fight cancer—has been effective in other cancers but has shown limited success in PC.

This is largely due to the tumor’s ability to suppress immune responses and create an environment that protects it from attack. Currently, these drugs are only approved for a small subset of patients whose tumors have a specific genetic feature called high microsatellite instability (MSI-high), found in just 1 to 2 percent of cases.

The Study: Pancreatic Cancer Immunotherapy Responders

The study, titled “Exceptional responders to immunotherapy in pancreatic cancer: A multi-institutional case series of a rare occurrence,” was led by first author Kavin Sugumar and corresponding author Jordan M. Winter, from University Hospitals Seidman Cancer Center. 

The researchers examined medical records from 14 patients with pancreatic ductal adenocarcinoma (PDAC) who had responded unexpectedly well to immune checkpoint inhibitors—drugs that help reactivate immune cells to attack cancer. The drugs included PD-1 inhibitors such as pembrolizumab and nivolumab, CTLA-4 inhibitors like ipilimumab, and agents targeting tumor-associated macrophages. To find these rare cases, the research team contacted 471 oncologists from 91 major U.S. cancer centers between 2020 and 2021.

Full blog - https://www.oncotarget.org/2025/09/11/immunotherapy-response-in-pancreatic-cancer-what-a-new-study-reveals/

Paper DOI - https://doi.org/10.18632/oncotarget.28739

Correspondence to - Jordan M. Winter - jordan.winter@UHHospitals.org

Abstract video - https://www.youtube.com/watch?v=VeWTcuVmqgM

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Keywords - cancer, pancreatic adenocarcinoma, immunotherapy, exceptional responders, microsatellite instability, survival

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Immunotherapy Response in Pancreatic Cancer: What a New Study Reveals

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.

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Inflammation and Metabolic Syndrome Linked to Benign Prostatic Hyperplasia

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