In this #episode of the Longevity & Aging Series, Dr. Shubhankar Suman from the Department of Oncology at Georgetown University Medical Center joins host Dr. Evgeniy Galimov to discuss a #research paper he co-authored in Volume 17, Issue 1 of Aging (Aging-US), titled: “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.”

DOI - https://doi.org/10.18632/aging.206183

Corresponding author - Shubhankar Suman - ss2286@georgetown.edu

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Keywords - aging, senescence-associated secretory phenotype, senolytic agent, carcinogenesis, inflammation, β-catenin

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Aging (Aging-US)

Longevity & Aging Series (S3, E4): Dr. Shubhankar Suman

BUFFALO, NY — June 10, 2025 — The Ride for Roswell, one of the USA’s largest cycling events supporting cancer research, returns to Buffalo on Saturday, June 28, 2025. Hosted annually by Roswell Park Comprehensive Cancer Center, this community-wide event brings together riders, volunteers, and supporters to raise funds for cancer research, celebrate survivors, and honor those lost to the disease. 

Among the returning participants is the Open Access Team, led by team captain Sergei Kurenov. This year, the team is once again proudly sponsored by Impact Journals, the publisher of open access journals Oncotarget, Aging, Genes & Cancer, and Oncoscience.

“For the last 10 years, I have continuously participated in the Ride for Roswell in honor of those who have bravely fought cancer,” said Kurenov. “This journey is deeply personal for me. My father battled cancer, and some of my closest friends have fought through prostate and lung cancer with incredible strength.”

This year, the Open Access Team rides in honor of Dr. Mikhail (Misha) Blagosklonny, a visionary scientist who dedicated his career to advancing cancer and aging research. As the founding Editor-in-Chief of Oncotarget, Aging, and Oncoscience, Dr. Blagosklonny was a pioneer of open-access publishing. His groundbreaking work on mTOR signaling and rapamycin transformed our understanding of cancer biology and healthy lifespan extension.

The 2025 Ride for Roswell features nine route options, ranging from 4 to 100 miles, all beginning at the University at Buffalo North Campus. Riders from across the USA and beyond are invited to participate and make a meaningful impact in the fight against cancer.

This ride is more than just a journey on two wheels—it’s a commitment to building a future where no one has to fear a cancer diagnosis. There is still time to support the Open Open Access Team in the 2025 Ride for Roswell. Whether by donating, joining the team, or sharing their story, every action brings us closer to better treatments, deeper understanding, and, ultimately, a cure.

Visit the Open Access Team page - https://give.roswellpark.org/site/TR/SpecialEvents/General?team_id=23320&pg=team&fr_id=2020

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

Oncotarget Sponsors Open Access Team in 2025 Ride for Roswell

BUFFALO, NY - June 11, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 29, 2025, 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.”

A team led by first author Jinah Kim, from the University of Vermont Medical Center, and corresponding author Young Kwang Chae, from the Feinberg School of Medicine, reports a clinical case in which a patient with advanced non-small cell lung cancer (NSCLC) carrying rare EGFR mutations responded remarkably to amivantamab after other treatments had failed. The patient experienced a complete resolution of brain and spinal fluid metastases, suggesting that amivantamab may be a viable option for patients with uncommon genetic profiles and limited therapy options.

Lung cancer remains one of the leading causes of cancer-related deaths worldwide. Patients with NSCLC who have rare mutations in the EGFR gene often face limited treatment options and poor outcomes, especially when the disease spreads to the brain or spinal fluid. This case involved a 67-year-old man diagnosed with NSCLC who had two rare EGFR mutations—G719A and A289V. After disease progression on osimertinib and other therapies, the patient began amivantamab monotherapy.

Within six weeks, his lung tumor shrank by over 30 percent. By six months, imaging confirmed the disappearance of brain metastases and leptomeningeal disease, a serious condition affecting the membranes of the brain and spinal cord. Blood tests showed no detectable cancer-related mutations, and the patient, previously wheelchair-bound, regained the ability to walk and perform daily activities. This response has been sustained for more than 19 months.

 “Treatment produced a durable response over 19 months, including a 32.2% reduction in tumor size at six weeks, and complete resolution of brain metastases and LMD by six months.”

Amivantamab is a bispecific antibody that targets EGFR and MET, two key drivers of tumor growth. While it is approved in combination regimens for common EGFR mutations, its effectiveness as a single agent in rare mutations or in treating brain metastases remains largely unproven. This case challenges the assumption that large antibody drugs cannot cross the blood-brain barrier and suggests that amivantamab may have potential in managing central nervous system involvement. Further research is needed to clarify how the drug achieves these effects and to explore its broader use in patients with rare EGFR mutations and limited treatment options.

This case highlights three key findings: amivantamab may be effective against rare EGFR mutations, can be used as monotherapy, and may overcome the challenges of the blood-brain barrier. Although based on a single patient, the results provide encouraging evidence to support further investigation of amivantamab in treating difficult-to-manage forms of NSCLC.

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=RJX3rmtH7h8

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

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Rare Non-Small Cell Lung Cancer with Brain Metastases Responds to Amivantamab Monotherapy

As we age, our brains become more sensitive to stress and disease. A recent study sheds light on a lesser-known risk: reduced oxygen levels. The study, titled “Defining the hypoxic thresholds that trigger blood-brain barrier disruption: the effect of age” and recently published as the cover for Volume 17, Issue 5 of Aging (Aging-US), found that low oxygen—also called hypoxia—can harm the aging brain by disrupting the blood-brain barrier (BBB). This damage may contribute to cognitive decline, memory problems, and an increased risk of dementia.

Understanding Hypoxia in the Brain

The brain relies on a steady supply of oxygen to stay healthy. When oxygen levels fall—a condition known as hypoxia—the brain undergoes changes to adapt. These changes include the remodeling of blood vessels and, importantly, a weakening of the blood-brain barrier. The BBB acts as a filter, protecting brain tissue from harmful substances. When it breaks down, it can lead to inflammation, brain cell damage, and cognitive issues.

Hypoxia is common in older adults, especially those with conditions like sleep apnea, chronic obstructive pulmonary disease (COPD), heart failure, and asthma. That is why understanding the connection between low oxygen and the aging brain is crucial for preventing long-term neurological damage.

Full blog - https://aging-us.org/2025/06/oxygen-deprivation-and-the-aging-brain-a-hidden-trigger-for-cognitive-decline/

Paper DOI - https://doi.org/10.18632/aging.206241

Corresponding author - Richard Milner - rmilner@sdbri.org

Video short - https://www.youtube.com/watch?v=Nr6rTm7aJRo

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Keywords - aging, blood-brain barrier integrity, endothelial, proliferation, microglia, chronic mild hypoxia, hypoxic threshold

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Oxygen Deprivation and the Aging Brain: A Hidden Trigger for Cognitive Decline

BUFFALO, NY — June 12, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 3, 2025, titled “APOE genotype and biological age impact inter-omic associations related to bioenergetics.”

In this study, led by first author Dylan Ellis and corresponding author Noa Rappaport from the Institute for Systems Biology, researchers discovered that different versions of the APOE gene—particularly ε2 and ε4—are linked to metabolic patterns associated with aging and Alzheimer’s disease risk. Both variants were linked to increased levels of diacylglycerols, a type of fat molecule connected to insulin resistance and inflammation, suggesting shared disruptions in how the body regulates energy.

The research team analyzed data from over 2,200 adults without an Alzheimer’s diagnosis, exploring how APOE genotypes influence biological age, a measure of health that reflects how quickly or slowly someone is aging at a cellular level. They found that the same metabolic disturbances seen in ε2 carriers were also present in people considered biologically older, revealing unexpected overlap between genetic risk and aging-related metabolic changes.

To examine these connections in more detail, the researchers used a multi-omics approach, combining blood-based metabolism and protein data, gut bacteria analysis from stool samples, and clinical chemistry data. This method allowed them to map how genetic differences and biological aging affect the body’s energy systems. They observed altered connections between glucose metabolism, inflammatory markers, and key molecules that play roles in energy production, indicating early disruptions that could contribute to age-related diseases.

One of the study’s surprising findings was that the ε2 variant, usually associated with longer life and reduced Alzheimer’s risk, showed metabolic traits similar to those found in insulin-resistant individuals. This suggests that ε2 may carry metabolic disadvantages earlier in life, with its protective effects becoming more pronounced later. Conversely, ε4—linked to greater Alzheimer’s risk—may exert its influence based on interactions with lifestyle factors like diet, sex, and overall health status.

“‘Omics association patterns of ε2-carriers and increased biological age were also counter-intuitively similar, displaying significantly increased associations between insulin resistance markers and energy-generating pathway metabolites.”

By identifying these shared biological signatures, this study offers a new framework for understanding how genes and metabolism work together to influence aging. These findings could support more personalized health strategies aimed at delaying biological aging and reducing the risk of chronic diseases. As aging populations grow worldwide, understanding these pathways is essential to improving healthspan.

DOI - https://doi.org/10.18632/aging.206243

Corresponding author - Noa Rappaport - noa.rappaport@isbscience.org

Video short - https://www.youtube.com/watch?v=75hZQoO5U0U

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Keywords - aging, apolipoprotein E (APOE), biological age, metabolism, Alzheimer’s disease (AD), insulin resistance

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APOE Gene Variants Linked to Metabolic Signatures of Aging and Alzheimer's Risk

BUFFALO, NY - June 13, 2025 – A new #review was #published in Volume 16 of Oncotarget on June 4, 2025, titled “Applying the unattainable triangle in cardio-oncology care: Balancing cost, quality, and time.”

In this review, first author John Hoverson, corresponding author Stella Pak, and colleagues from the University of Texas Health Science Center at San Antonio explore how the “unattainable triangle”—a business concept describing the trade-offs between cost, quality, and time—can help improve healthcare delivery in cardio-oncology. As cancer treatments become more complex and often affect the heart, this model highlights the challenge of providing care that is fast, effective, and affordable.

Cardio-oncology is an emerging field focused on preventing and managing heart problems caused by cancer therapies. The review explains that high-quality cancer care often requires advanced diagnostics and close collaboration between oncologists and cardiologists, which can drive up costs and time demands. Understanding how to balance these pressures is essential for delivering better outcomes for patients.

Many cancer survivors face long-term cardiovascular complications due to their treatment. Early monitoring and intervention can reduce these risks. However, these improvements often come with financial burdens, especially when key tests are not covered by insurance. Meanwhile, both patients and clinicians must manage the burden of tight appointment schedules, long clinic visits, and increasing demands on their time.

To improve care quality, the authors emphasize the need for interdisciplinary teamwork and ongoing education. Surveys show that many clinicians are still unfamiliar with cardio-oncology guidelines, which can compromise care. The review also highlights the potential for artificial intelligence and digital tools to streamline care delivery, reduce wait times, and support both patients and providers.

Importantly, the authors point out that improving one area—such as quality—can come at the expense of others, like cost or time. They encourage healthcare systems to take a balanced approach, setting clear goals and using integrated care models that consider all three elements of the triangle together.

“While a perfect model for managing the unattainable triangle may be simply that, ‘unattainable’, investments in research, patient-centered care, data-driven decision-making, and financial alignment with payers will be crucial to the long-term success of both patient outcomes and the organization’s profitability.”

While achieving perfect balance may be difficult, the review suggests that using the unattainable triangle as a guiding framework can help hospitals and clinicians make smarter, more sustainable decisions. As cardio-oncology continues to expand in response to the growing number of cancer survivors with cardiovascular needs, this approach could help improve patient outcomes and strengthen healthcare systems.

DOI - https://doi.org/10.18632/oncotarget.28738

Correspondence to - Stella Pak - stellacpak@outlook.com

Video short - https://www.youtube.com/watch?v=65-5eUuVyyk

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Keywords - cancer, cardio-oncology, quality improvement, cardiology, oncology

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Balancing Time, Cost, and Quality in Cardio-Oncology Care

BUFFALO, NY — June 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 1, 2025, titled “Oxytocin modulates insulin and GLP-1 secretion in pancreatic islets.”

In this study, scientists from Fukushima Medical University School of Medicine investigated how the hormone oxytocin (Oxt) influences insulin levels by acting on specific cells in the pancreas. The team led by first author Kasumi Hattori and corresponding authors Kenju Shimomura and Yuko Maejima discovered that oxytocin may indirectly increase insulin secretion by triggering another hormone, GLP-1, from within the pancreas. This finding could lead to new strategies for improving blood sugar control in people with diabetes.

Oxytocin is commonly known for its roles in childbirth and social bonding, but scientists have also been exploring its effects on metabolism. While previous studies offered mixed results about whether oxytocin raises or lowers blood sugar, this research brings new clarity. The study focused on oxytocin’s impact on insulin and a hormone called GLP-1, which helps regulate insulin production. Researchers tested this by using mice with and without oxytocin receptors and found that oxytocin’s ability to raise insulin levels depended on the presence of these receptors and high blood sugar conditions.

Researchers found that oxytocin stimulates the release of “intra-islet GLP-1,” a form of GLP-1 produced inside the pancreas rather than the intestine. In the pancreas, insulin is produced by beta cells, while alpha cells produce glucagon, a hormone that raises blood sugar. But recent research, including this study, has shown that alpha cells can also release GLP-1, which in turn helps beta cells secrete insulin. Oxytocin appears to increase this internal GLP-1 release, especially when blood sugar levels are high, thereby leading to insulin release in a natural and targeted way.

In this study researchers were also able to detect the difference between oxytocin’s effect on blood sugar and its effect on insulin. They observed that right after oxytocin was given, blood sugar levels rose in all mice—even in those that lacked oxytocin receptors. However, only the mice with working oxytocin receptors showed a later increase in insulin. This suggests that oxytocin may trigger insulin production through a separate, receptor-dependent pathway involving the hormone GLP-1.

"WT mice showed a significant increase in insulin levels at 15-min, while OxtR KO mice did not."

This indirect action—oxytocin triggering alpha cells to release GLP-1, which then acts on beta cells—may represent a novel mechanism for controlling insulin release. It also explains why oxytocin does not increase insulin in low-glucose conditions, making it a potentially safer option for regulating blood sugar.

As treatments for type 2 diabetes increasingly focus on GLP-1–based drugs, this study opens the door to using oxytocin or similar compounds to naturally enhance the body’s own insulin-producing system. With further research, this mechanism could help develop new therapies that better mimic the body’s natural glucose control, particularly beneficial for older adults with diabetes.

DOI - https://doi.org/10.18632/aging.206244

Corresponding authors - Kenju Shimomura - shimomur@fmu.ac.jp, and Yuko Maejima - maejimay@fmu.ac.jp

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New Hormonal Pathway Links Oxytocin to Insulin Secretion in the Pancreas

Bladder cancer remains a significant clinical concern, with more than 85,000 new diagnoses and nearly 19,000 deaths reported annually in the United States. While current treatments like surgery, chemotherapy, and radiation can be effective for early-stage disease, many patients with advanced or recurrent cancer face limited options.

A recent review, published in Oncotarget by researchers from the University of California, Irvine, analyzes the growing body of evidence supporting the combination of radiation therapy and immunotherapy for bladder cancer. Led by Nazmul Hasan, the work synthesizes clinical data and biological mechanisms that suggest this strategy could enhance anti-tumor responses in specific patient groups.

Full blog - https://www.oncotarget.org/2025/06/16/exploring-a-combined-approach-radiation-and-immunotherapy-in-bladder-cancer/

Paper DOI - https://doi.org/10.18632/oncotarget.28723

Correspondence to - Nazmul Hasan - nhasan1@hs.uci.edu

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Exploring a Combined Approach: Radiation and Immunotherapy in Bladder Cancer

BUFFALO, NY - June 17, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 10, 2025, titled “Exceptional responders to immunotherapy in pancreatic cancer: A multi-institutional case series of a rare occurrence.”

The study, led by first author Kavin Sugumar and corresponding author Jordan M. Winter, from University Hospitals Seidman Cancer Center, reports on a rare group of pancreatic cancer (PC) patients who responded remarkably well to immunotherapy, a treatment typically considered ineffective for this cancer type. The analysis, which includes data from 14 patients across multiple U.S. institutions, identifies outcomes that could help refine treatment strategies for one of the most aggressive and deadly forms of cancer.

“Between 2020–21, 471 oncologists from 91 major cancer centers in the United States were contacted.”

Pancreatic cancer has among the lowest survival rates and few effective therapies. While immunotherapy has transformed the treatment landscape for several other cancers, it generally offers little benefit for pancreatic cancer. However, this study highlights a small but important group of patients who experienced significant and sustained responses to immune-based treatment without chemotherapy. Most had advanced or metastatic disease and had already progressed after standard treatments.

Among the 14 patients, 82% had partial tumor shrinkage, and nearly one-third had a notable decrease in tumor markers. The median progression-free survival was 12 months, and most patients were still alive at follow-up, with survival rates of 80% at one year and 70% at two years. These outcomes contrast sharply with standard therapies, which often provide only a few months of benefit for similar patients.

Interestingly, while some patients had high microsatellite instability (MSI-high)—a known marker for immunotherapy success—more than half did not, suggesting other biological mechanisms may be involved. This result highlights the need for new biomarkers to be discovered to predict treatment response in future studies.

This case series is the largest focused exclusively on exceptional immunotherapy responders in pancreatic cancer. By excluding patients who received chemotherapy, the study isolates the effects of immune-based drugs, including PD-1 inhibitors such as pembrolizumab and nivolumab, CTLA-4 inhibitors like ipilimumab, and agents targeting macrophages.

While the sample size is small, the findings challenge the assumption that immunotherapy is ineffective for nearly all pancreatic cancer patients. The study suggests that, under certain biological conditions, this treatment can be remarkably successful. Further research is needed to understand the underlying mechanisms.

This work supports the need to reconsider how clinical trials are designed for pancreatic cancer and who is eligible for immunotherapy. Broader criteria and more personalized molecular profiling could help uncover hidden opportunities for treatment in this highly lethal cancer.

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

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

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Rare Pancreatic Cancer Patients Show Strong Response to Immunotherapy

BUFFALO, NY — June 18, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 12, 2025, titled “Frailty transitions in electronic health records: who first? what first?”

The study, led by Fabienne Hershkowitz Sikron from Meuhedet HMO, analyzed how frailty develops over time in older adults using electronic health record data from nearly 120,000 individuals aged 65 and above. Researchers found that frailty worsened in over 13% of participants within a year, particularly among women, adults aged 85 or older, and people with chronic illnesses, while nearly 3% showed signs of improvement. The findings highlight early indicators of decline that could help guide preventive care and improve outcomes for aging populations.

Frailty is a condition marked by increased vulnerability to health complications and tends to change gradually. The study used the Meuhedet Electronic Frailty Index (MEFI) to track yearly transitions in frailty among older adults in Israel. While many people remained in the same frailty category, a significant proportion experienced deterioration in just one year, and a smaller group improved.

“Worsening frailty is defined as a higher frailty level one year later in 2024 compared to 2023. A new frailty deficit is defined as a deficit appearing in 2024 that was not present in 2023.”

Those most at risk of worsening included adults over 85, women, individuals from lower socio-economic backgrounds, and members of the Arab sector. Additional predictors of decline included recent hospitalizations, multiple chronic diseases, and signs of cognitive or mobility issues. Importantly, the first signs of worsening were often not new chronic conditions but more manageable health deficits such as sleep disturbances, muscle weakness, hearing loss, and memory decline. Those who improved were more likely to be younger, male, from higher socio-economic backgrounds, and have fewer chronic conditions and hospitalizations.

The study also found that common chronic illnesses like diabetes and hypertension were often already present and did not usually signal the beginning of frailty progression. Instead, declines in overall function and quality of life were more frequently the first new issues to appear. This suggests that early intervention on modifiable health deficits could delay or prevent further decline.

This work is one of the first large-scale, real-world studies to identify both who is most likely to worsen first and what health problems typically appear first. The authors emphasize the importance of using routinely collected electronic medical data to monitor frailty and tailor care. By doing so, health providers can implement timely strategies to reduce disease burden and support aging individuals in maintaining independence.

These findings support the creation of proactive health programs focused on maintaining physical strength, cognitive function, and sensory abilities. Preventing frailty progression can reduce hospitalizations, ease disease burden, and help older adults maintain independence and a higher quality of life.

DOI - https://doi.org/10.18632/aging.206247

Corresponding author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.il

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Early Signs of Frailty Detected Through Health Records in Aging Adults

Dr. Josh Mitteldorf summarizes his #research perspective #published in Volume 17, Issue 5 of Aging (Aging-US), titled “Methylation clocks for evaluation of anti-aging interventions.”

DOI - https://doi.org/10.18632/aging.206245

Corresponding author - Josh Mitteldorf - aging.advice@gmail.com

Author interview - https://www.youtube.com/watch?v=efgNvr5ezTk

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

Abstract

Methylation clocks have found their way into the community of aging research as a way to test anti-aging interventions without having to wait for mortality statistics. But methylation is a primary means of epigenetic control, and presumably has evolved under strong selection. Hence, if methylation patterns change consistently at late ages it must mean one of two things. Either (1) the body is evolved to destroy itself (with inflammation, autoimmunity, etc.), and the observed methylation changes are a means to this end; or (2) the body detects accumulated damage, and is ramping up repair mechanisms in a campaign to rescue itself. My thesis herein is that both Type 1 and Type 2 changes are occurring, but that only Type 1 changes are useful in constructing methylation clocks to evaluate anti-aging interventions. This is because a therapy that sets back Type 1 changes to an earlier age state has stopped the body from destroying itself; but a therapy that sets back Type 2 changes has stopped the body from repairing itself. Thus, a major challenge before the community of epigenetic clock developers is to distinguish Type 2 from Type 1. The existence of Type 1 epigenetic changes is in conflict with conventional Darwinian thinking, and this has prompted some researchers to explore the possibility that Type 1 changes might be a form of stochastic epigenetic drift. I argue herein that what seems like directed epigenetic change really is directed epigenetic change. Of five recent articles on “stochastic methylation clocks,” only one (from the Conboy lab) is based on truly stochastic changes. Using the Conboy methodology and a methylation database, I construct a measure of true methylation drift, and show that its correlation with age is too low to be useful.

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Keywords - aging, methylation, stochastic, entropy, programmed aging, aging clock, epigenetic clock

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Behind the Study: Using Methylation Clocks to Evaluate Anti-Aging Interventions

Cancer and aging are two sides of age-related tumorigenesis.

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.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

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