BUFFALO, NY – August 19, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 19, 2025, titled “The SCD1 inhibitor aramchol interacts with regorafenib to kill GI tumor cells in vitro and in vivo.”

In this study, led by first authors Laurence Booth and Michael R. Booth, along with corresponding author Paul Dent from Virginia Commonwealth University, researchers investigated how aramchol, a drug originally developed for liver disease, works with the cancer drug regorafenib in gastrointestinal (GI) tumor cells. They found that the combination is effective, especially in tumor cells with a specific genetic variant. The combined approach offers a potential new strategy for treating liver and colon cancers.

Gastrointestinal cancers, such as liver and colon cancer, are serious global health challenges. Regorafenib, already approved for cancer treatment, can have limited impact and frequently causes side effects. Aramchol, a drug developed to treat fatty liver disease, affects how cancer cells process fats and energy. In this study, researchers tested whether combining these two drugs could improve GI cancer treatment, both in cells and mouse models.

The results showed that the drug combination killed liver and colorectal cancer cells more effectively than either drug alone. In animal models, mice with human liver tumors had slower tumor growth, without showing signs of weight loss or other toxicity. 

The researchers also found that aramchol and regorafenib work together to block important survival pathways inside cancer cells. This combination was especially effective in cells with a genetic variant called ATG16L1 T300, which is more common in people of African ancestry. The treatment triggered stress responses in the cancer cells and disrupted key proteins required for survival. It also activated autophagy, a natural recycling process that clears out damaged parts, eventually leading to cancer cell death.

“Aramchol interacted with the multi-kinase inhibitors sorafenib, regorafenib or lenvatinib, to kill GI tumor cells, with regorafenib exhibiting the greatest effect.”

Aramchol is currently in clinical trials for fatty liver disease and has a well-established safety profile, while regorafenib is already FDA-approved for cancer treatment. Together, their combination could advance fast into clinical testing for patients with GI cancers. However, researchers note that additional studies are needed to support the launch of early-phase clinical trials.

Altogether, this study may offer a more effective and less toxic alternative to current treatments for GI cancers. It also highlights the role of genetic variants in shaping treatment response, suggesting that future therapies could be more precisely tailored to each patient’s unique genetic profile.

DOI - https://doi.org/10.18632/oncotarget.28762

Correspondence to - Paul Dent - paul.dent@vcuhealth.org

Video short - https://www.youtube.com/watch?v=5saAqsqxi-Q

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Keywords - cancer, macroautophagy, flux; ER stress, aramchol, regorafenib

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Oncotarget

Aramchol Boosts Regorafenib Effectiveness in Gastrointestinal Tumors

BUFFALO, NY — August 21, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 17, 2025, titled “The influence of cancer on a forensic age estimation tool.”

In this study by Charlotte Sutter, Daniel Helbling, Cordula Haas and Jacqueline Neubauer from the Zurich Institute of Forensic Medicine, University of Zurich and Onkozentrum Zurich, the researchers investigated how cancer might affect the accuracy of forensic tools used to estimate a person’s age from blood samples.

DNA methylation is a natural chemical modification of DNA that changes with age. Forensic scientists can use these changes to predict someone’s age from biological traces, such as blood found at a crime scene. However, medical conditions like cancer can alter these patterns and potentially reduce the accuracy of such predictions. This study investigated whether various cancer types influence the DNA markers used in age estimation.

“Our study is among the first to show whether it might be necessary to account for the influence of cancer on forensic age estimation tools in order to enhance estimation accuracy as much as possible.”

The researchers applied the VISAGE enhanced age estimation tool, a widely used DNA methylation-based method, to blood samples from 100 cancer patients and 102 healthy individuals. Age predictions in the control group were generally accurate, with small average errors. Patients with solid tumors, including breast and lung cancers, showed only slightly less accurate results. In contrast, individuals with blood cancers, particularly chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML), sometimes had large errors, with ages overestimated by as much as 50 years. 

Despite these few extreme cases, the study found that cancer does not typically have a strong impact on the accuracy of this forensic tool. Most cancer patients, even those undergoing treatment, had DNA methylation patterns similar to those of healthy individuals. The researchers found no consistent differences based on cancer type, stage, or treatment, except in isolated cases involving aggressive forms of cancer.

The findings support the continued use of current forensic age estimation methods. While aggressive cancers may occasionally affect prediction accuracy, such cases are rare. The researchers suggest noting these conditions as a possible factor in unusually large errors, without requiring changes to standard practice.

This study provides valuable information about how health conditions, such as cancer, may influence DNA-based age estimation. It strengthens confidence in the reliability of forensic age prediction tools, even when applied to individuals with a medical history of cancer.

DOI - https://doi.org/10.18632/aging.206281

Corresponding author - Cordula Haas - cordula.haas@irm.uzh.ch

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Keywords - aging, forensic age, estimation age prediction, cancer, DNA methylation, age acceleration

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Aging (Aging-US)

Impact of Cancer on Forensic DNA Methylation Age Estimation

BUFFALO, NY — August 26, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 21, 2025, titled “Association of DNA methylation age acceleration with digital clock drawing test performance: the Framingham Heart Study.”

In this study, led by first author Zexu Li from the Department of Anatomy and Neurobiology at Boston University Chobanian and Avedisian School of Medicine, and corresponding author Chunyu Liu from Boston University Chobanian and Avedisian School of Medicine and Boston University School of Public Health, researchers found that individuals with signs of faster biological aging had lower scores on a digital cognitive test taken seven years later. The findings suggest that the rate at which a person ages at the molecular level may be associated with how well their brain functions as they grow older.

Using data from the Framingham Heart Study, the researchers examined the relationship between biological aging and cognitive health. They used DNA methylation (DNAm) patterns—chemical changes that occur in the DNA with aging, known as epigenetic aging—to estimate biological age acceleration, and used the digital Clock Drawing Test (dCDT) to assess cognitive performance. The dCDT is a computerized version of a traditional pen-and-paper test that evaluates memory, thinking speed, and motor control. It provides an overall score and measures performance in specific areas such as spatial reasoning and movement.

Among 1,789 participants, higher levels of epigenetic age acceleration were associated with significantly lower cognitive scores, particularly those over age 65. Of all the epigenetic aging markers examined, the DunedinPACE measure showed the strongest association with reduced brain function in both younger and older adults. Other measures, such as Horvath and PhenoAge, were associated with lower scores only in older adults. Key areas affected included motor skills and spatial reasoning.

The researchers also studied blood-based protein markers used in an aging measure called GrimAge. Two proteins, PAI1 and ADM, were closely associated with lower cognitive scores, especially in older individuals. These results suggest that declines in brain and motor functions may reflect broader aging-related changes throughout the body.

“Digital cognitive measures displayed stronger associations with most DNAm aging metrics among older compared to younger participants, likely to reflect the cumulative and nonlinear age influences on both brain health and DNAm.”

This study supports the idea that epigenetic age may be a more accurate predictor of cognitive decline than chronological age. The dCDT, which is easy to use, automated, and more precise than traditional tools, may help detect early signs of brain aging. When combined with DNAm measures, it could become a valuable part of regular health screenings.

Overall, the findings provide strong evidence that faster biological aging is associated with cognitive decline. This research may lead to better ways of identifying and monitoring brain health in aging populations.

DOI - https://doi.org/10.18632/aging.206285

Corresponding author - Chunyu Liu - liuc@bu.edu

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Faster Biological Aging Linked to Cognitive Decline in Older Adults

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

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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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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.

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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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

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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

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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

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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.

Full blog - https://aging-us.org/2025/09/how-exosomes-spread-aging-signals-and-could-support-anti-aging-research/

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

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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