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

In this episode of the Dementia together podcast, we learn about the UK's first dementia-friendly railway line.

The Bentham Line runs from the hubbub of Leeds to the seaside resort of Morecambe, past miles of incredible scenery. Yet it's no quaint heritage ride, but a fully functioning rail link.

We meet the people who've been making the experience of travelling by rail better for people affected by dementia, and the wonderful opportunities this has created.

You can visit alzheimers.org.uk/publications for our range of publications designed to support and inform anyone affected by dementia.

For personalised information and advice, call our Dementia Support Line on 0333 150 3456, or for Welsh speakers call 03300 947 400.

'It shows what can be achieved' – Dementia together podcast June 2025

Dr. Stefanie Morgan joins Dr. Robert Dudley from AgelessRx to discuss a #research paper she co-authored that was #published in Volume 17, Issue 4 of Aging, entitled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.”

DOI - https://doi.org/10.18632/aging.206235

Corresponding author - Stefanie L. Morgan - stefanie@agelessrx.com

Author interview - https://www.youtube.com/watch?v=2qlIiVh2OJs

Video short - https://www.youtube.com/watch?v=z5j2nyK2HZ8

Abstract

Design: This 48-week decentralized, double-blinded, randomized, placebo-controlled trial (NCT04488601) evaluated the long-term safety of intermittent low-dose rapamycin in a healthy, normative-aging human cohort. Participants received placebo, 5 mg or 10 mg compounded rapamycin weekly. The primary outcome measure was visceral adiposity (by DXA scan), secondary outcomes were blood biomarkers, and lean tissue and bone mineral content (by DXA scan). Established surveys were utilized to evaluate health and well-being. Safety was assessed through adverse events and blood biomarker monitoring.

Results: Adverse and serious adverse events were similar across all groups. Visceral adiposity did not change significantly (ηp2 = 0.001, p = 0.942), and changes in blood biomarkers remained within normal ranges. Lean tissue mass (ηp2 = 0.202, p = 0.013) and self-reported pain (ηp2 = 0.168, p = 0.015) improved significantly for women using 10 mg rapamycin. Self-reported emotional well-being (ηp2 = 0.108, p = 0.023) and general health (ηp2 = 0.166, p = 0.004) also improved for those using 5 mg rapamycin. No other significant effects were observed.

Conclusions: Low-dose, intermittent rapamycin administration over 48 weeks is relatively safe in healthy, normative-aging adults, and was associated with significant improvements in lean tissue mass and pain in women. Future work will evaluate benefits of a broader range of rapamycin doses on healthspan metrics for longevity, and will aim to more comprehensively establish efficacy.

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Keywords - aging, rapamycin, geroscience, longevity, healthspan

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Behind the Study: Rapamycin’s 1-Year Impact on Healthspan—PEARL Trial Results

BUFFALO, NY – June 9, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 20, 2025, titled “Cigarette smoke and decreased DNA repair by Xeroderma Pigmentosum Group C use a double hit mechanism for epithelial cell lung carcinogenesis.”

In this study, led by first author Nawar Al Nasralla and corresponding author Catherine R. Sears, from the Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Indianapolis and the Richard L. Roudebush Veterans Affairs Medical Center, researchers investigated how cigarette smoke and reduced DNA repair capacity contribute together to the development of lung cancer. They found that when a critical DNA repair protein called XPC is decreased and lung cells are exposed to cigarette smoke, the combination causes extensive damage and significantly increases cancer risk.

Non-small cell lung cancer (NSCLC) develops through both genetic and environmental factors. This study focused on how cigarette smoke affects the body’s natural ability to repair DNA. The researchers studied the role of XPC, a protein essential for recognizing and repairing harmful DNA changes caused by tobacco smoke. They found that low levels of XPC — commonly seen in lung cancer patients — made lung cells less capable of repairing DNA. This made the cells unstable and more likely to become cancerous. These changes were most pronounced in normal lung cells, suggesting that the earliest stages of disease occur before cancer is even detected.

The findings support a “double hit” model, where both cigarette smoke and reduced DNA repair work together to drive cancer development. In laboratory experiments, normal lung cells with low XPC levels showed more damage and cell death after cigarette smoke exposure. By contrast, lung cancer cells were more resistant to smoke damage, even when XPC was low, indicating that critical changes had likely occurred earlier in the disease process.

“Our study suggests that cigarette smoke exposure leads to decreased XPC mRNA expression, exacerbates total and oxidative DNA damage, hinders NER, and may contribute to lung cancer development.”

The study also showed that DNA repair ability declined significantly in healthy cells after smoke exposure, but this effect was not seen in cancer cells. In addition, the researchers confirmed that XPC gene activity was lower in actual lung tumor tissue compared to nearby healthy lung tissue. This pattern was consistent across both adenocarcinoma and squamous cell carcinoma, the two main types of NSCLC.

These results add to our understanding of how lung cancer begins at the molecular level. By showing how cigarette smoke and reduced DNA repair combine to create genetic instability, the research points toward new strategies for prevention. A better understanding of XPC’s role could help identify high-risk individuals and inform future efforts to stop lung cancer before it begins.

DOI - https://doi.org/10.18632/oncotarget.28724

Correspondence to - Catherine R. Sears - crufatto@iu.edu

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Keywords - cancer, DNA repair, DNA damage, lung adenocarcinoma, squamous cell carcinoma, Xeroderma Pigmentosum Group C (XPC)

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Oncotarget

Cigarette Smoke and DNA Repair Deficiency Drive Lung Cancer Development

BUFFALO, NY — June 10, 2025 — A new #research perspective was #published in Aging (Aging-US) Volume 17, Issue 5, on May 5, 2025, titled “Methylation clocks for evaluation of anti-aging interventions.”

In this perspective article, Dr. Josh Mitteldorf explores how current epigenetic clocks—used to estimate biological age—might mislead scientists trying to evaluate anti-aging therapies. The paper challenges a widespread assumption: that all changes in DNA methylation with age are equally valid for measuring biological decline. Dr. Mitteldorf proposes that failing to distinguish between different types of epigenetic changes could lead to inaccurate conclusions, potentially even favoring treatments that reduce repair processes rather than extend healthy lifespan.

Methylation clocks have become a popular tool in aging research. These clocks use patterns of DNA methylation, a form of gene regulation that changes over time, to predict a person’s biological age. Because human aging trials are long and expensive, these clocks offer a faster way to evaluate whether a therapy slows or reverses aging. However, this article warns that not all methylation changes are equal in meaning or effect.

The perspective identifies two main categories of methylation changes that occur with age. One type, called 'Type 1,' seems to support the idea that aging may be programmed, with gene activity changing in ways that could cause damage, such as more inflammation or increased cell loss. The second type, “Type 2,” involves increased gene activity aimed at repairing age-related damage. If a therapy reduces the activity of Type 2 genes, it may appear to slow aging while actually interfering with the body’s repair response.

“Paradoxically, an intervention that “sets back” the body’s methylation clock to a younger state is shutting off vital repair mechanisms, so it is likely inimical to health and longevity.” 

This distinction is important because most methylation clocks, including popular models like GrimAge, do not separate these two types. As a result, they may incorrectly suggest that a treatment is reversing aging when it is only suppressing beneficial repair mechanisms. According to Dr. Mitteldorf, this could lead researchers to draw the wrong conclusions and unintentionally slow down progress in anti-aging research.

The author also addresses a growing trend in the scientific community that aims to explain age-related methylation as random drift rather than directed change. In a pilot analysis using publicly available data, Dr. Mitteldorf attempted to construct a clock based purely on stochastic, or random, changes. The results showed a weak correlation with age, suggesting that random drift is an unreliable basis for assessing biological aging.

Dr. Mitteldorf argues that most age-related methylation changes are likely intentional and regulated, rather than random. If so, epigenetic clocks must be refined to reflect the biological purpose behind methylation shifts. Without distinguishing between changes that indicate damage and those that indicate repair, current clocks may not only mismeasure age but also misguide intervention strategies.

This article highlights the urgent need to improve how methylation data are interpreted before such clocks can reliably assess anti-aging therapies. A clearer understanding of these molecular patterns could help reshape the future of aging research and therapy evaluation.

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

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

To learn more about the journal, please visit our website at https://www.Aging-US.com.

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Why Epigenetic Clocks May Fail to Measure Anti-Aging Effects

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 Aging, Oncotarget, 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 Aging, Oncotarget 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 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

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Aging Sponsors Open Access Team in 2025 Ride for Roswell

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 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

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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

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

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