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BUFFALO, NY — August 12, 2026 — A new #research paper was #published in Volume 18 of Aging on July 27, 2026, titled “Transcriptomic aging clock analysis identifies key genes in opioid dependence.” The study was led by first author Hai Duc Nguyen from the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University. The corresponding author is Woong-Ki Kim, who is affiliated with the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University, and the Department of Microbiology and Immunology at Tulane University School of Medicine. Opioid dependence is a chronic and relapsing condition associated with substantial health and societal burdens. Chronic opioid exposure can affect neuronal signaling, immune function, metabolism, and other biological processes, yet the molecular mechanisms underlying dependence remain incompletely understood. Increasing evidence also suggests that substance use disorders may be associated with molecular changes related to aging, raising questions about how chronic opioid exposure interacts with age-dependent processes in the brain. To investigate these relationships, the researchers conducted an in silico study integrating three complementary approaches: RNA sequencing-based transcriptomic profiling, transcriptomic aging-clock modeling, and analysis of previously published genome-wide association studies (GWAS). The transcriptomic analysis used a publicly available brain RNA-seq dataset containing 42 samples—21 healthy controls and 21 individuals with opioid dependence—while the genetic analysis incorporated findings from six independent GWAS. Full press release - https://www.aging-us.com/news-room/transcriptomic-aging-clock-reveals-age-related-molecular-patterns-in-opioid-dependence DOI - https://doi.org/10.18632/aging.206405 Corresponding author - Woong-Ki Kim - wkim6@tulane.edu Abstract video - https://www.youtube.com/watch?v=7VwU0mFGkbg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206405 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, opioids, GWAS, transcriptomic clock To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
A #Research paper recently #Published in Volume 18 of Aging, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b,” examines whether the senolytic PROTAC 753b can slow age-related intervertebral disc degeneration (IDD) in mice. Long-term systemic treatment with 753b reduced key features of disc degeneration in 22-month-old male mice, including matrix breakdown, loss of disc aggrecan, age-related structural changes, and inflammatory markers such as IL-6 and TNFα. These benefits, however, were not observed in female mice, highlighting potential sex-based differences in the role of cellular senescence in IDD and the response to senolytic therapies. DOI - https://doi.org/10.18632/aging.206394 Corresponding author - Nam Viet Vo - nvv1@pitt.edu Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Colorectal cancer does not develop in isolation. Cancer cells exist within a complex tumor microenvironment made up of fibroblasts, immune cells, blood vessels, and extracellular matrix. Increasing evidence suggests that these surrounding cells and structures can influence whether tumors grow, regress, or evade the immune system. A research paper published in Volume 17 of Oncotarget, titled “Microenvironmental CTHRC1 has a pro-tumorigenic role in colorectal cancer,” investigated the role of collagen triple helix repeat containing 1 (CTHRC1), a secreted protein found in cancer-associated stroma. Full blog post - https://www.oncotarget.org/2026/08/10/cthrc1-in-the-tumor-microenvironment-drives-colorectal-cancer-growth-in-mouse-study/ DOI - https://doi.org/10.18632/oncotarget.28878 Correspondence to: Sergey Ryzhov - Sergey.Ryzhov@mainehealth.org; Volkhard Lindner- Volkhard.Lindner@mainehealth.org; Michaela R. Reagan - Michaela.Reagan@mainehealth.org Abstract video - https://www.youtube.com/watch?v=gTbYy6vGd7E Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28878 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Cthrc1, CRC, colorectal cancer, subcutaneous tumor model, immune analysis To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – August 10, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on August 7, 2026, titled “Delayed growth of SK-ES-1 Ewing sarcoma tumor xenografts is associated with reduced Trk and IGF1R pathway markers.” The study was led by first author Bruna Almeida dos Santos and corresponding author Caroline Brunetto de Farias, primarily affiliated with the Federal University of Rio Grande do Sul and the National Science and Technology Institute for Children's Cancer Biology and Pediatric Oncology (INCT BioOncoPed), with de Farias also affiliated with the Children's Cancer Institute (ICI) in Brazil. The research team investigated whether targeting tropomyosin receptor kinase (Trk) and related signaling pathways could interfere with Ewing sarcoma growth. Ewing sarcoma is an aggressive cancer that primarily affects children and adolescents and can arise in bone or soft tissue. Although modern multimodal treatments have substantially improved outcomes for patients with localized disease, the prognosis remains considerably poorer for metastatic or relapsed Ewing sarcoma. This has driven efforts to identify molecular pathways that could provide additional therapeutic targets. One potential target involves the Trk family of receptor tyrosine kinases. TrkA, TrkB, and TrkC are encoded by the NTRK1, NTRK2, and NTRK3 genes, respectively, and regulate intracellular signaling pathways involved in cell survival, differentiation, and growth. Previous work from the research group showed that TrkA and TrkB are expressed in Ewing sarcoma and that blocking these receptors can reduce tumor-cell proliferation. Full press release - https://www.oncotarget.com/news/pr/trk-and-igf1r-related-signaling-linked-to-delayed-ewing-sarcoma-growth/ DOI - https://doi.org/10.18632/oncotarget.28911 Correspondence to - Caroline Brunetto de Farias - cbfarias@zielbiosciences.com Abstract video - https://www.youtube.com/watch?v=ZG-vhYfHjuw Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28911 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Ewing sarcoma, K252a, Trk, NTRK, insulin-like growth factor 1 receptor To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 10, 2026 — A new #essay was #published in Volume 18 of Aging on August 6, 2026, titled “Misha Blagosklonny: a life of ideas.” The article was written by Aging Editorial Board member David Gems from the Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, United Kingdom, along with Aging Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, the Netherlands. Rather than presenting new experimental findings, the essay examines the life, scientific contributions, and lasting influence of Mikhail (“Misha”) Blagosklonny, whose ideas had a major influence on modern thinking about the biological mechanisms of aging. Dr. Blagosklonny was trained as a physician and experimental scientist before building an influential career in oncology and aging research after moving to the United States. His work combined cancer biology with theoretical biogerontology, leading to the proposal that aging is driven not primarily by the passive accumulation of molecular damage, but by developmental and growth-related programs that continue beyond their beneficial period. Through what he described as conceptual research, Misha synthesized evidence from diverse experimental studies to generate new hypotheses about aging and reinterpret existing biological observations. A central theme of the essay is Dr. Blagosklonny's development of the hyperfunction theory of aging. Building on observations that persistent activation of the mechanistic target of rapamycin (mTOR) pathway can drive cellular senescence, he proposed that many features of aging arise from the continued activity of biological programs that promote growth and reproduction earlier in life. Rather than viewing aging as an adaptive genetic program, Misha argued that it represents a quasi-program—a genetically determined continuation of normal developmental processes that become harmful later in life. This framework provided a mechanistic explanation linking evolutionary concepts such as antagonistic pleiotropy with molecular pathways that regulate growth, metabolism, and cellular senescence. Full press release - https://www.aging-us.com/news-room/misha-blagosklonnys-scientific-legacy-continues-to-shape-modern-aging-research DOI - https://doi.org/10.18632/aging.206412 Corresponding author - David Gems - david.gems@ucl.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206412 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail Blagosklonny To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
In this episode of the Longevity & Aging Series (S4, E5), Dr. Kan Cao of the Department of Cell Biology and Molecular Genetics at the University of Maryland joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.” Interview video - https://www.youtube.com/watch?v=2Por-Wh3AWo DOI - https://doi.org/10.18632/aging.206376 Corresponding author - Kan Cao - kcao@umd.edu Longevity & Aging Series - https://www.aging-us.com/longevity About Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206376 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, methylene blue, minoxidil, HFSCs, Wnt/β-catenin, GLP-1 RA To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 6, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 24, 2026, titled “A brief history of the hyperfunction theory of aging and future directions.” The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting new experimental findings, the perspective examines the historical development of the hyperfunction theory of aging, reviews evidence supporting programmatic mechanisms of aging, and discusses future directions for understanding why organisms age and how aging might eventually be modified. For decades, most aging research has been dominated by the idea that aging results primarily from the gradual accumulation of molecular damage, including DNA damage, oxidative stress, mitochondrial dysfunction, and protein deterioration. In contrast, the hyperfunction theory proposes that aging is driven largely by developmental and growth programs that continue operating beyond their beneficial period. Rather than being intentionally programmed, aging is viewed as a consequence of biological pathways that promote growth and reproduction early in life but become harmful when they continue later in adulthood. The perspective traces the historical roots of these ideas from early theories proposed in the nineteenth century through Clive McCay's pioneering caloric restriction experiments and George Williams' concept of antagonistic pleiotropy. Particular attention is given to the contributions of the late Mikhail Blagosklonny, whose hyperfunction theory proposed that aging results from “quasi-programs”—developmental processes that fail to switch off after their normal biological role has ended. The author argues that this framework provides a mechanistic explanation linking evolutionary theory with many biological features of aging. Full press release - https://www.aging-us.com/news-room/hyperfunction-theory-offers-a-new-perspective-on-why-we-age Paper DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.info Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 5, 2026 — A new #research paper was #published in Volume 18 of Aging on July 23, 2026, titled “Adipo-neuroinflammation, cognitive impairment and surrogate markers of cardiovascular risk in patients with Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).” The study was led by co-first authors Gaetano Pacinella from the University of Palermo, and the Internal Medicine and Stroke Care Ward, Policlinico “P. Giaccone”, Palermo, and Alessandro Del Cuore from the same institutions. Gaetano Pacinella also served as the corresponding author. Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease, is increasingly recognized as a systemic condition that extends beyond the liver. People with MASLD have an elevated risk of cardiovascular disease, cognitive decline, and other metabolic complications, yet the biological mechanisms connecting these conditions remain incompletely understood. In this study, researchers investigated whether lipocalin-2 (LCN2), a protein involved in inflammatory and metabolic signaling, is associated with early vascular dysfunction, cognitive impairment, and cardiovascular risk in patients with MASLD. Full press release - https://www.aging-us.com/news-room/fatty-liver-disease-linked-to-early-cardiovascular-and-cognitive-changes DOI - https://doi.org/10.18632/aging.206397 Corresponding author - Gaetano Pacinella - gaetano.pacinella@unipa.it Abstract video - https://www.youtube.com/watch?v=CrqTayKl8KI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206397 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, metabolic dysfunction, cardiovascular risk, lipocalin-2, cognitive impairment, endothelial dysfunction To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — August 3, 2026 — A new #research paper was #published in Volume 18 of Aging on July 17, 2026, titled “Selective targeting of cancer and senescence via shared metabolic shifts extends lifespan of old mice.” The study was led by first author Zachery R. Robinson, and corresponding author and Aging editorial board member Irina M. Conboy, both from the Department of Bioengineering and QB3 Institute, University of California, Berkeley. The researchers developed a new combination therapy that selectively targets both cancer cells and senescent cells by exploiting metabolic vulnerabilities shared by these two cell types. In laboratory studies and aged mice, the treatment selectively eliminated senescent cells and reduced cancer cell viability while improving physical performance and extending lifespan without significant toxicity to healthy tissues. Cancer and aging are closely linked. As people age, senescent cells accumulate throughout the body. Although these cells no longer divide, they remain metabolically active and release inflammatory molecules known as the senescence-associated secretory phenotype (SASP), which contributes to chronic inflammation, tissue dysfunction, and tumor progression. Existing therapies such as the BCL-2/BCL-xL inhibitor navitoclax (ABT-263) can eliminate both cancer cells and senescent cells but require doses that frequently cause thrombocytopenia, a potentially serious reduction in platelet counts that has limited their clinical use. Full press release - https://www.aging-us.com/news-room/new-drug-combination-targets-cancer-and-senescent-cells-while-extending-lifespan-in-old-mice DOI - https://doi.org/10.18632/aging.206399 Corresponding author - Irina M. Conboy - irina@generationlab.co Abstract video - https://www.youtube.com/watch?v=7p5JMvy9Twg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206399 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, cancer, metabolic shift, ATP To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Heart failure remains one of the leading causes of hospitalization among older adults worldwide. During episodes of acute decompensated heart failure (ADHF), excess fluid builds up in the lungs and body, making breathing difficult and increasing the risk of serious complications. Although intravenous loop diuretics such as furosemide are the standard treatment for relieving congestion, many patients continue to experience persistent inflammation, ongoing cardiac remodeling, and worsening heart function despite therapy. A research paper published in Volume 18 of Aging titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF),” investigated whether combining intravenous furosemide with small volumes of hypertonic saline solution (HSS) could improve biological markers associated with heart failure compared with furosemide alone. Full blog post - https://aging-us.org/2026/08/hypertonic-saline-plus-furosemide-improves-heart-failure-biomarkers-in-randomized-trial/ DOI - https://doi.org/10.18632/aging.206364 Corresponding author - Antonino Tuttolomondo - bruno.tuttolomondo@unipa.it Abstract video - https://www.youtube.com/watch?v=EG65XlcDJ3U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206364 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solution To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 30, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 16, 2026, titled “Towards integration of healthspan strategies into the Italian National Health Service.” The article was led by co-first authors Nicola Marino, affiliated with the AEON Foundation and the Women's Brain Foundation, and Matteo Fiore from the University of Bologna, with both serving as corresponding authors. Rather than presenting new clinical trial results, the authors propose a prevention-focused framework for the staged, evidence-based evaluation and integration of healthspan strategies into Italy's National Health Service (Servizio Sanitario Nazionale, SSN) to help address the challenges of an aging population. Italy has one of the oldest populations in the world. Although life expectancy has continued to increase, many older adults spend a substantial portion of those additional years living with chronic disease, disability, or reduced physical and cognitive function. The authors describe this mismatch as the lifespan–healthspan divide and argue that healthcare systems should increasingly focus not only on helping people live longer, but also on extending the years they remain healthy and functionally independent. To address this challenge, the authors outline the concept of longevity medicine, describing it as a prevention-oriented, life-course framework rather than a new medical specialty. The approach integrates principles from geroscience, preventive medicine, and personalized healthcare with the goal of identifying age-related risks earlier and promoting healthy aging before chronic diseases and functional limitations accumulate. At the same time, the paper emphasizes that many emerging tools—including biological-age biomarkers, multi-omic profiling, wearable sensor data, and artificial intelligence-based risk stratification—remain exploratory and should not be adopted routinely until they demonstrate clear clinical utility, cost-effectiveness, and meaningful benefits for patients. Full press release - https://www.aging-us.com/news-room/italy-proposes-a-healthspan-focused-framework-for-healthy-aging DOI - https://doi.org/10.18632/aging.206402 Corresponding authors - Nicola Marino - marino@aeonfoundation.eu, and Matteo Fiore - matteo.fiore@auslromagna.it Abstract video - https://www.youtube.com/watch?v=uc1tGVfiHMw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206402 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, preventive, longevity, national health system, health span, biomarkers To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Nutrition plays a critical role in cancer care, yet it is often overlooked. Many patients experience weight loss, muscle wasting, treatment-related side effects, and changes in appetite that can affect their ability to tolerate therapy and maintain quality of life. Although nutrition specialists can help manage these challenges, access to specialized nutritional care remains limited in many healthcare settings. An editorial published in Volume 17 of Oncotarget, titled “Artificial intelligence in nutritional oncology: From isolated screening tools to agentic intervention systems,” explores how advances in artificial intelligence (AI) could help address this gap. The editorial was written by Arnab Sarkar and corresponding author Yashbir Singh-Wolkenhauer, who is affiliated with the Department of Radiology, Mayo Clinic, Rochester, Minnesota. Rather than presenting new clinical trial data, the authors outline a future vision in which AI systems move beyond isolated tasks to continuously support nutritional care throughout a patient's cancer journey. Full blog post - https://www.oncotarget.org/2026/07/28/artificial-intelligence-could-transform-nutrition-care-for-cancer-patients/ DOI - https://doi.org/10.18632/oncotarget.28874 Correspondence to - Yashbir Singh-Wolkenhauer - singh.yashbir@mayo.edu Abstract video - https://www.youtube.com/watch?v=sVKhRSr5xaY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28874 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, artificial intelligence To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 27, 2026 — A new #research paper was #published in Volume 18 of Aging on July 13, 2026, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b.” The study was led by first author Peter G. Alexander from the Ferguson Laboratory for Spine Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, and corresponding author Nam Viet Vo from the same institution. Intervertebral disc degeneration is a leading cause of chronic low back pain and disability. As discs age, they lose important structural components, become less able to absorb mechanical stress, and accumulate senescent cells—dysfunctional cells that stop dividing but continue releasing inflammatory molecules that contribute to tissue degeneration. Senolytic therapies, which selectively eliminate these cells, have emerged as a promising strategy to slow age-related diseases. In this study, researchers evaluated PROTAC 753b, a next-generation senolytic designed to target the anti-apoptotic proteins BCL-2 and BCL-xL while reducing the platelet toxicity associated with earlier drugs in this class. The researchers treated 16-month-old male and female mice with PROTAC 753b for six months and evaluated their intervertebral discs at 22 months of age using histology, molecular analyses, and measurements of inflammatory markers. The treatment significantly improved several measures of intervertebral disc health in aged male mice, preserving the extracellular matrix protein aggrecan and reducing matrix metalloproteinase (MMP)-mediated aggrecan breakdown, a hallmark of disc degeneration. In contrast, female mice showed little overall improvement, revealing a sex-specific response to treatment. Full press release - https://www.aging-us.com/news-room/senolytic-protac-slows-age-related-intervertebral-disc-degeneration-in-male-mice DOI - https://doi.org/10.18632/aging.206394 Corresponding author - Nam Viet Vo - nvv1@pitt.edu Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 23, 2026 — A new #research paper was #published in Volume 18 of Aging on July 8, 2026, titled “TM4SF1 is a surface marker of senescent pancreatic β-cells.” The study was led by first author Ana Beathriz Leite Lorente from Joslin Diabetes Center and Harvard Medical School, and São Paulo State University (UNESP), Brazil, and corresponding author Cristina Aguayo-Mazzucato from Joslin Diabetes Center and Harvard Medical School. Type 2 diabetes is characterized by insulin resistance and the progressive loss of pancreatic β-cell function. With aging and metabolic stress, senescent β-cells accumulate within the pancreas, producing less insulin while releasing inflammatory signals that contribute to disease progression. Although eliminating these dysfunctional cells has emerged as a promising therapeutic strategy, a major challenge has been identifying markers that distinguish senescent β-cells from healthy cells with sufficient precision. This study identifies transmembrane 4 L six family member 1 (TM4SF1) as a highly selective surface marker of senescent β-cells, providing a promising candidate for the future development of more selective therapies for type 2 diabetes. In this study, the researchers searched for cell-surface proteins that specifically identify senescent β-cells. Using RNA sequencing, flow cytometry, immunofluorescence, and analyses of both mouse and human pancreatic tissue, they compared TM4SF1 with the previously established senescence marker urokinase-type plasminogen activator receptor (uPAR/PLAUR). Their findings showed that TM4SF1 is expressed predominantly in senescent β-cells while exhibiting much lower expression in non-senescent β-cells and other tissues, making it a more β-cell-specific surface marker than uPAR. Full press release - https://www.aging-us.com/news-room/new-surface-marker-could-advance-precision-therapies-for-type-2-diabetes DOI - https://doi.org/10.18632/aging.206398 Corresponding author - Cristina Aguayo-Mazzucato - Cristina.aguayo-mazzucato@joslin.harvard.edu Abstract video - https://www.youtube.com/watch?v=tNbFKdleTJo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206398 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescent β-cell, type 2 diabetes, transmembrane 4 l six family member 1, urokinase-type plasminogen activator receptor To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – July 22, 2026 – A new #PrecisionOncology paper was #Published in Volume 17 of Oncotarget on July 21, 2026, titled “WIN-MTB-2024017 – WIN International Molecular Tumor Board: A 48-year-old female with multiple primary cancers.” The study was led by Oncotarget Editor-in-Chief, Dr. Wafik S. El-Deiry, from the Worldwide Innovative Network (WIN) Association – WIN Consortium and Legorreta Cancer Center at Brown University. Patients who develop multiple primary cancers face unique diagnostic and treatment challenges because each tumor may have distinct biological characteristics requiring different therapeutic approaches. Advances in genomic profiling and precision oncology now enable clinicians to better distinguish between independent tumors and recurrent disease while identifying molecular alterations that may guide individualized treatment strategies. This case report demonstrates how an international molecular tumor board integrated comprehensive genomic data with multidisciplinary expertise to develop personalized recommendations for a patient with an exceptionally complex cancer history. The case describes the clinical journey of a 48-year-old woman carrying a germline BRCA1 mutation who developed multiple primary cancers over nearly two decades, including breast cancer, basal cell carcinoma of the skin, high-grade serous ovarian carcinoma, colon cancer, and small bowel adenocarcinoma. During this time, she underwent multiple surgeries, chemotherapy regimens, targeted therapy with the PARP inhibitor niraparib, and extensive molecular testing to characterize each malignancy. Full press release - https://www.oncotarget.com/news/pr/international-molecular-tumor-board-explores-personalized-treatment-strategies-for-a-patient-with-multiple-primary-cancers/ DOI - https://doi.org/10.18632/oncotarget.28899 Correspondence to - Wafik S. El-Deiry - wafik_el-deiry@brown.edu Abstract video - https://www.youtube.com/watch?v=4KIDbmq6ui8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28899 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, precision oncology, molecular tumor board To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 21, 2026 — A new #research paper was #published in Volume 18 of Aging on July 6, 2026, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.” The study was authored by Yash Flora, Dhriti Shastri, Kathryn R. DeLeo, and K. Adam Bohnert from the Department of Biological Sciences, Louisiana State University. Aging is accompanied by the gradual decline of many cellular structures that help maintain healthy tissues and organs. Among these are peroxisomes, which play essential roles in breaking down toxic molecules and metabolizing lipids, and mitochondria, which generate most of the cell's energy. Although these organelles work closely together, little has been known about how changes in one influence the aging of the other. This new study reveals that preserving peroxisomes helps maintain healthier mitochondria and extends lifespan in the nematode Caenorhabditis elegans, providing new insight into how communication between cellular organelles influences aging. In this study, the researchers investigated the function of PRX-11, a peroxisomal protein involved in peroxisome division. Previous work from the group showed that reducing PRX-11 activity prevents the age-related degradation of peroxisomes through a process known as pexophagy and increases lifespan. The new study explored why preserving peroxisomes produces these beneficial effects and found that maintaining peroxisomes also preserves mitochondrial health during aging. The researchers found that animals with reduced PRX-11 activity retained long, interconnected mitochondrial networks that resembled those seen in young adults, whereas normal aging was associated with progressive mitochondrial fragmentation. These preserved mitochondria also accumulated less calcium, generated lower levels of oxidative stress, maintained higher ATP-to-ADP ratios, and were associated with improved locomotor function in older animals. Together, these findings indicate that preventing age-related peroxisome loss supports multiple aspects of mitochondrial function during aging. Full press release - https://www.aging-us.com/news-room/preserving-peroxisomes-helps-maintain-mitochondrial-health-and-extend-lifespan-in-c-elegans DOI - https://doi.org/10.18632/aging.206395 Corresponding author - K. Adam Bohnert - bohnerta@lsu.edu Abstract video - https://www.youtube.com/watch?v=fbcqBsP90CY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206395 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular aging, lifespan, pexophagy, mitochondrial tubulation, inter-organelle crosstalk To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Coordinating both hands is something most people take for granted. Everyday activities such as buttoning a shirt, preparing a meal, driving, or using a knife and fork all depend on the brain's ability to precisely control movements on both sides of the body. As people age, however, these tasks often become more difficult, especially when they require both hands to perform different movements at the same time. A research paper published in Volume 18 of Aging titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance,” investigated how aging affects the brain's ability to adapt to increasingly complex hand-coordination tasks. The study was led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven. Full blog - https://aging-us.org/2026/07/brain-flexibility-is-linked-to-hand-coordination-during-aging/ DOI - https://doi.org/10.18632/aging.206363 Corresponding author - Koen Cuypers - koen.cuypers@uhasselt.be Abstract video - https://www.youtube.com/watch?v=3TbcGFCZV9s Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206363 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, bimanual coordination, Bimanual Tracking Task, BOLD variability, task modulation To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging chosen as the “Editors' Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases. Cellular senescence is a hallmark of aging and age-related disease, yet the diverse mechanisms that trigger this cellular state remain incompletely understood. The review recently published in Volume 18 of Aging, titled “The multifaceted inducers of cellular senescence,” examines the many intrinsic and extrinsic stimuli that induce senescence, including DNA damage, oxidative and mitochondrial stress, telomere attrition, oncogene activation, cell–cell fusion, and developmental signals. The authors, Hilah Gal and Valery Krizhanovsky, explain how these distinct pathways converge on a stable cell-cycle arrest. By highlighting the complexity and heterogeneity of senescent cells, the authors provide valuable insights that may guide the development of future therapies targeting senescence to promote healthy aging and combat age-related diseases. DOI - https://doi.org/10.18632/aging.206391 Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206391 Keywords - aging, cell senescence To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 16, 2026 — A new #research paper was #published in Volume 18 of Aging on July 1, 2026, titled “Senescent cells accumulate lipid droplets.” The study was led by first author Noa Rachmian-Cooper and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. Cellular senescence is a natural biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. Although senescence helps suppress tumor formation and supports normal processes such as tissue repair and development, senescent cells accumulate with age and contribute to chronic inflammation and numerous age-related diseases, including cancer, cardiovascular disease, and Alzheimer's disease. While many of the biological effects of senescent cells have been linked to inflammatory signaling, much less has been understood about the metabolic changes that accompany senescence. In this study, the researchers investigated how cellular metabolism changes during senescence, with a particular focus on lipid metabolism. Using comprehensive metabolic profiling of human fibroblasts, they discovered that senescent cells accumulate high levels of triacylglycerols—the major precursors of lipid droplets—alongside increased glycolytic activity. Additional laboratory experiments confirmed that senescent cells contain significantly more lipid droplets than actively dividing cells. Full press release - https://www.aging-us.com/news-room/senescent-cells-found-to-accumulate-lipid-droplets-across-aging-and-alzheimers-disease DOI - https://doi.org/10.18632/aging.206390 Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Abstract video - https://www.youtube.com/watch?v=GZbhY3wtGGI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206390 Keywords - aging, senescence, lipid droplets, metabolism, Alzheimer's disease To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the digestive tract. Although many GISTs can be effectively treated with targeted therapies, their response to treatment depends largely on the specific genetic alterations driving tumor growth. Advances in molecular testing have transformed the management of these tumors, allowing clinicians to tailor treatment based on each patient's genetic profile. A case report published in Volume 17 of Oncotarget, titled “Small bowel GIST harboring concurrent KIT exon 9 duplication and SDHC mutation: A case report,” describes an exceptionally rare case involving a patient whose tumor carried two genetic alterations that are traditionally considered mutually exclusive. Full blog post - https://www.oncotarget.org/2026/07/13/rare-genetic-combination-in-gastrointestinal-tumor-offers-new-insights-into-precision-cancer-care/ DOI - https://doi.org/10.18632/oncotarget.28863 Correspondence to - Joseph G. Crompton - jcrompton@mednet.ucla.edu Abstract video - https://www.youtube.com/watch?v=eB_QG2vBNCE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28863 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, GIST, KIT duplication, SDHC mutation, genetic testing, case report To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 13, 2026 — A new #review was #published in Volume 18 of Aging on June 26, 2026, titled “Hormonal dimorphism in sarcopenia disease.” The review was led by first author Romain Menard and corresponding author Romain Madelaine from the MDI Biological Laboratory, Kathryn W. Davis Center for Regenerative Biology and Aging, Bar Harbor, Maine, USA. Sarcopenia—the progressive loss of skeletal muscle mass, strength, and physical function with aging—is one of the leading causes of frailty and disability in older adults. Although the condition affects millions of people worldwide and has been recognized as a disease by the World Health Organization since 2016, treatment options remain largely limited to exercise and nutritional interventions, with no approved medications specifically targeting the disease. Growing evidence now suggests that one reason for this limited success is that sarcopenia develops through distinct biological mechanisms in women and men. In this comprehensive review, the authors examine how biological sex influences the hormonal mechanisms underlying muscle aging. They focus on three peptide hormones—apelin, insulin, and oxytocin—and describe how age-related changes in these interconnected signaling networks contribute to muscle decline through distinct biological pathways in women and men. According to the review, women often experience an abrupt decline in muscle health during menopause as estrogen levels fall rapidly. This hormonal transition disrupts apelin signaling, accelerates insulin resistance, reduces oxytocin-mediated muscle regeneration, and impairs the function of satellite cells, the muscle stem cells responsible for repair and regeneration. In contrast, men generally undergo a slower, more gradual decline in muscle function that parallels progressive reductions in testosterone, resulting in different patterns of hormonal dysregulation and disease progression. The review also highlights the central roles of apelin, insulin, and oxytocin in maintaining healthy skeletal muscle. Together, these hormones regulate muscle metabolism, glucose utilization, mitochondrial function, protein homeostasis, inflammation, and satellite-cell activity through overlapping signaling pathways. Disruption of this hormonal network during aging is proposed to contribute to impaired muscle repair, reduced metabolic function, chronic inflammation, and progressive muscle loss. Full press release - https://aging-us.net/2026/07/13/sex-specific-hormones-could-hold-the-key-to-better-sarcopenia-treatments/ DOI - https://doi.org/10.18632/aging.206392 Corresponding author - Romain Madelaine - rmadelaine@mdibl.org Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206392 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, sarcopenia, hormonal dimorphism, muscle aging, sex-stratified medicine, sexual dimorphism To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
In this episode of the Longevity & Aging Series (S4, E4), Dr. Maria Blasco of the Spanish National Cancer Centre (CNIO) joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Cross species activity of TERT human telomerase component.” Interview video - https://www.youtube.com/watch?v=DHeysGp9oPg DOI - https://doi.org/10.18632/aging.206372 Corresponding author - Maria A. Blasco - mblasco@cnio.es Longevity & Aging Series: https://www.aging-us.com/longevity About Dr. Yuan Zhao: https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206372 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, telomeres, telomerase To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 7, 2026 — A new #review was #published in Volume 18 of Aging on June 22, 2026, titled “The multifaceted inducers of cellular senescence.” The review was led by first author Hilah Gal and corresponding author Valery Krizhanovsky from the Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. Cellular senescence is a fundamental biological process in which damaged or stressed cells permanently stop dividing while remaining metabolically active. This response plays an essential role in suppressing tumor formation, supporting embryonic development, facilitating wound healing, and maintaining tissue integrity. However, as people age, senescent cells accumulate because they are no longer efficiently cleared by the immune system. Their persistence contributes to chronic inflammation, tissue dysfunction, cancer, and many age-related diseases. In this comprehensive review, the authors examine the diverse biological stimuli that trigger cellular senescence and describe how seemingly different stimuli ultimately converge on common molecular pathways that establish stable growth arrest. Rather than viewing senescence as a single process, the review emphasizes its remarkable biological diversity and the importance of understanding how different initiating events shape distinct senescent cell phenotypes. The review discusses several major biological inducers of cellular senescence. One of the best-established mechanisms is telomere attrition, in which repeated cell division gradually shortens chromosome ends until they trigger a persistent DNA damage response. Other important stimuli include direct DNA damage caused by ionizing radiation, ultraviolet light, chemotherapy, and oxidative injury, all of which activate cellular pathways that permanently halt proliferation. Full press release - https://aging-us.net/2026/07/07/multiple-biological-triggers-shape-cellular-senescence-in-aging-and-disease/ DOI - https://doi.org/10.18632/aging.206391 Corresponding author - Valery Krizhanovsky - valery.krizhanovsky@weizmann.ac.il Abstract video - https://www.youtube.com/watch?v=5Y7R_8GQ1gk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206391 Keywords - aging, cell senescence To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – July 6, 2026 – A new #casereport was #published in Volume 17 of Oncotarget on July 2, 2026, titled “Renal oncocytoma: Α case report and literature review.” The study was led by first and corresponding author Areti Kalfoutzou from the Second Propaedeutic Department of Internal Medicine, Attikon General Hospital, National and Kapodistrian University of Athens, Greece. Renal oncocytoma is a rare benign tumor of the kidney that accounts for approximately 5–9% of renal epithelial tumors. Although it is considered benign, it often resembles kidney cancer on imaging studies, making accurate diagnosis challenging. Because treatment strategies differ substantially between benign oncocytoma and malignant renal tumors, establishing the correct diagnosis is essential to avoid unnecessary surgery while ensuring appropriate patient care. In this report, the researchers describe the case of an 82-year-old woman who presented with two months of gross hematuria. Contrast-enhanced computed tomography (CT) identified a 55 × 34 mm exophytic lesion arising from the upper pole of the left kidney. Based on its imaging characteristics, the mass was initially classified as a Bosniak category IV renal lesion, raising strong suspicion for renal malignancy. Full press release - https://www.oncotarget.net/2026/07/06/rare-benign-kidney-tumor-case-highlights-value-of-biopsy-and-minimally-invasive-treatment/ DOI - https://doi.org/10.18632/oncotarget.28893 Correspondence to - Areti Kalfoutzou - areti.kalfoutzou@haf.gr Abstract video - https://www.youtube.com/watch?v=C7TBLT3tbfA Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28893 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, cryoablation, image-guided biopsy, kidney neoplasms, minimally invasive surgery, renal oncocytoma To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
As people live longer, maintaining good health is becoming just as important as extending lifespan. While chronological age simply reflects the number of years a person has lived, biological age measures how well the body is functioning and may better predict future health. Researchers have increasingly focused on lifestyle factors that may slow biological aging, and diet has emerged as one of the most promising. A research paper published in Volume 18 of Aging titled “Plant-based dietary patterns are associated with slower epigenetic aging,” investigated whether diets emphasizing plant foods are associated with slower biological aging as measured by DNA methylation-based epigenetic clocks. Full blog post - https://aging-us.org/2026/07/plant-based-dietary-patterns-are-associated-with-slower-biological-aging/ DOI - https://doi.org/10.18632/aging.206362 Corresponding author - Hyunju Kim - hyunjuk1@uw.edu Abstract video - https://www.youtube.com/watch?v=FcJ7oEZ-KFk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206362 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, plant-based diets, DNA methylation, epigenetic aging, all-cause mortality, middle-aged adults To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — July 6, 2026 — A new systematic #review was #published in Volume 18 of Aging on June 18, 2026, titled “Life expectancy and causes of death in classical laminopathic progeroid syndromes: systematic review with individual-patient data synthesis.” The study was led by co-first authors Carlos López-Vila, Manuel García-Cordeiro, and Luís Estévez-Martínez from the University of Santiago de Compostela, and corresponding author David Araújo-Vilar from the University of Santiago de Compostela and the University Clinical Hospital of Santiago de Compostela, Spain. Classical laminopathic progeroid syndromes are among the rarest inherited disorders known. Caused by mutations affecting the LMNA gene or the ZMPSTE24 enzyme, these conditions lead to premature aging, severe multisystem disease, and markedly shortened life expectancy. Although Hutchinson-Gilford progeria syndrome (HGPS), mandibuloacral dysplasia (MAD), and restrictive dermopathy (RD) all belong to this group, reliable information about survival and causes of death for each disorder has remained limited because most published reports describe only individual patients or small case series. In this study, researchers performed a comprehensive systematic review and individual-patient data analysis to date of classical laminopathic progeroid syndromes. Following PRISMA guidelines, they analyzed data from 169 published studies together with two additional genetically confirmed institutional cases, creating a cohort of 158 genetically confirmed patients for the primary survival analysis. By examining individual patient records rather than pooled summaries, the investigators were able to compare survival patterns and causes of death across each disease subtype with greater precision. Full press release - https://aging-us.net/2026/07/06/comprehensive-individual-patient-analysis-clarifies-life-expectancy-across-rare-progeria-disorders/ DOI - https://doi.org/10.18632/aging.206389 Corresponding author - David Araújo-Vilar - david.araujo@usc.es Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206389 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, progeria, Lamin A/C (LMNA), ZMPSTE24, survival, cause of death To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Multiple myeloma is the second most common blood cancer in the United States and has long been considered a difficult disease to treat. For decades, treatment options were limited, and survival remained poor. However, the therapeutic landscape has changed dramatically over the past several decades with the introduction of stem cell transplantation, targeted drugs, immunotherapies, and more recently, CAR T-cell therapy and bispecific antibodies. A research paper titled “Targeted therapeutics and U.S. population-level mortality trends in multiple myeloma: A SEER-based analysis from 1975 to 2023” was published in Volume 17 of Oncotarget. In this study, the researchers examined how these major treatment advances have coincided with changes in multiple myeloma mortality across the United States over nearly five decades. The study was led by first and corresponding author Navkirat Kahlon from the Mass General Cancer Center at Wentworth-Douglass Hospital in Dover, New Hampshire. Full blog - https://www.oncotarget.org/2026/06/29/targeted-therapies-have-coincided-with-a-dramatic-decline-in-multiple-myeloma-mortality-in-the-united-states/ Paper DOI - https://doi.org/10.18632/oncotarget.28877 Correspondence to - Navkirat Kahlon - nkahlon@mgb.org; (ORCID: https://orcid.org/0000-0003-1115-2029) Abstract video - https://www.youtube.com/watch?v=-TNWkG9FyUo Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28877 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, multiple myeloma, epidemiologic trends, mortality reduction, therapeutic advancements, SEER database To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 29, 2026 — A new #review was #published in Volume 18 of Aging on May 30, 2026, titled “The love and hate relationship between cellular senescence and stemness.” The review was led by first author Angelos Papaspyropoulos and corresponding author Vassilis G. Gorgoulis from the National and Kapodistrian University of Athens and the Biomedical Research Foundation of the Academy of Athens, Greece. Cellular senescence and stemness have traditionally been viewed as biological opposites. Senescent cells permanently stop dividing in response to cellular stress, helping prevent the spread of damaged cells, while stem cells maintain tissue repair by continuously renewing themselves and generating specialized cells. However, growing evidence suggests that the relationship between these two biological processes is far more complex and depends on the tissue type, physiological conditions, and disease context. In this review, the authors summarize recent research examining how senescence and stemness interact across normal tissues, aging, regeneration, and cancer. Rather than always opposing one another, the two processes can either suppress or reinforce each other depending on the biological setting. Under normal physiological conditions, senescence often limits stem cell activity. The review highlights studies showing that excessive senescence can impair the regenerative capacity of mesenchymal stem cells, muscle satellite cells, dental pulp stem cells, and pancreatic β-cell progenitors. In several experimental models, reducing senescence restored stem cell function and improved tissue regeneration. At the molecular level, multiple signaling pathways contribute to this balance, including the p53/p21 and p16INK4A/RB pathways, mTOR signaling, Wnt/β-catenin signaling, and the senescence-associated secretory phenotype (SASP). These pathways help determine whether cells maintain regenerative potential or enter a stable senescent state. The review also emphasizes that the relationship changes dramatically in cancer. In many tumors, senescent cells can promote the emergence of cancer stem cells through inflammatory signals released as part of the SASP or through cells escaping from the senescent state. This interaction has been reported in several malignancies, including B-cell lymphoma, liver cancer, colon cancer, lung cancer, and breast cancer, where stem cell-like properties may contribute to tumor progression, metastasis, and resistance to therapy. Full press release - https://www.aging-us.com/news-room/cellular-senescence-and-stem-cells-share-a-more-complex-relationship-than-previously-recognized DOI - https://doi.org/10.18632/aging.206387 Corresponding author - Vassilis G. Gorgoulis - vgorg@med.uoa.gr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206387 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, stemness To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 25, 2026 — A new #research paper was #published in Volume 18 of Aging on May 29, 2026, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial.” The study, selected as our Editors' Choice, was led by first author Tatsuki Nishimura and corresponding author Yukihiro Hishida from the R&D Division of Morinaga Milk Industry Co., Ltd., Japan. As researchers continue searching for practical ways to promote healthy aging, increasing attention has focused on interventions that target multiple biological pathways simultaneously. While exercise and healthy eating are widely recognized as important components of healthy aging, scientists are also investigating whether specific dietary components and gut microbes may influence biological aging processes measurable at the molecular level. In this study, researchers evaluated whether a 12-week lifestyle program could affect DNA methylation–based biomarkers of aging in overweight men aged 50 years and older. The intervention combined individualized exercise guidance, dietary counseling, and daily consumption of yogurt containing Bifidobacterium longum BB536, a probiotic strain that has previously been linked to beneficial effects on inflammation and gut health. The randomized controlled trial enrolled 48 participants, who were assigned either to the intervention group or to a control group that maintained their usual lifestyle habits. Participants in the intervention group received dietary counseling focused on reducing overeating, exercise guidance encouraging regular walking or stepper-based activity, and a daily serving of yogurt containing Bifidobacterium longum BB536. To assess biological aging, the investigators measured several DNA methylation–based aging biomarkers before and after the 12-week intervention. Particular attention was given to DunedinPACE, an epigenetic measure designed to estimate the current pace of biological aging rather than biological age itself. Full press release - https://aging-us.net/2026/06/25/lifestyle-intervention-linked-to-slower-biological-aging-markers-in-older-men/ DOI - https://doi.org/10.18632/aging.206386 Corresponding author - Yukihiro Hishida - yukihiro-hishida639@morinagamilk.co.jp Abstract video - https://www.youtube.com/watch?v=7W5sDpGgZtE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206386 Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536 To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – June 24, 2026 – A new research paper was published in Volume 17 of Oncotarget on June 9, 2026, titled “TRAIL-R2 in the shadows: Epigenetic silencing and clinical implications in breast cancer.” The study was led by first author Nuzhat Khursheed from the University of Kashmir and corresponding authors Asia Asiaf from the Central University of Kashmir and Showkat Ahmad Ganie from the University of Kashmir. Breast cancer remains one of the most common cancers affecting women worldwide. While advances in diagnosis and treatment have improved outcomes for many patients, researchers continue to investigate the molecular changes that enable tumor cells to survive, grow, and spread. One process receiving increasing attention is epigenetic regulation, in which genes are switched on or off without altering the underlying DNA sequence. In this study, researchers examined TRAIL-R2, also known as death receptor 5 (DR5), a protein that plays an important role in triggering apoptosis, the programmed cell death process that helps eliminate damaged or abnormal cells. Loss of apoptotic signaling is a hallmark of cancer, but the clinical significance and epigenetic regulation of TRAIL-R2 in breast cancer have remained incompletely understood. The investigators analyzed matched tumor and adjacent normal breast tissue samples from 67 patients. Using methylation-specific PCR, quantitative real-time PCR, and western blotting, they evaluated TRAIL-R2 promoter methylation as well as its gene and protein expression levels. The analysis revealed that TRAIL-R2 was frequently silenced in breast tumors. More than half of tumor samples showed promoter hypermethylation, a chemical modification that can suppress gene activity. At the same time, both TRAIL-R2 mRNA and protein expression levels were significantly lower in tumor tissues than in adjacent normal breast tissue. Further analysis demonstrated that TRAIL-R2 hypermethylation was more common in invasive ductal carcinoma, the most common subtype of breast cancer, and in patients with a history of oral contraceptive use. Reduced TRAIL-R2 expression was also associated with advanced tumor stage and several clinicopathological features linked to more aggressive disease. The researchers observed a strong inverse relationship between promoter methylation and TRAIL-R2 expression, suggesting that epigenetic silencing may contribute directly to loss of this important apoptotic receptor. Tumors with reduced TRAIL-R2 activity may become less susceptible to programmed cell death, potentially allowing cancer cells to survive and progress. Full press release - https://www.oncotarget.net/2026/06/24/trail-r2-silencing-linked-to-more-aggressive-breast-cancer/ DOI - https://doi.org/10.18632/oncotarget.28891 Correspondence to - Asia Asiaf - asiaf29@cukashmir.ac.in, and Showkat Ahmad Ganie - showkatganie@kashmiruniversity.ac.in Abstract video - https://www.youtube.com/watch?v=BvhkOYLTJUY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28891 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, TRAIL-R2/DR5, promoter methylation, breast cancer biomarkers, tumor suppressor gene, apoptotic signalling pathways To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
As people live longer, maintaining mental well-being has become an increasingly important part of healthy aging. While regular physical activity is known to support both physical and psychological health, many older adults face barriers that make traditional exercise programs difficult to sustain. Researchers have therefore been exploring new approaches that combine physical activity with enjoyment, social interaction, and cognitive engagement. A review published in Volume 18 of Aging titled “What are the effects of exergames on the mood states of older people? A systematic review of experimental studies, impacts on mental health and recommendations,” examined whether exergames—video games that require physical movement to play—can improve mood and mental health in older adults. The study was led by authors from the Laboratory of Sport and Exercise Psychology, Human Movement Sciences Graduate Program, College of Health and Sport Science of the Santa Catarina State University (UDESC) in Florianópolis, Brazil. Full blog - https://aging-us.org/2026/06/do-exergames-improve-mood-and-mental-well-being-in-older-adults/ DOI - https://doi.org/10.18632/aging.206361 Corresponding author - Alexandro Andrade - alexandro.andrade.phd@gmail.com Abstract video - https://www.youtube.com/watch?v=mNBh_alqVRI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206361 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, electronic games, older adults, BRUMS, mental health, physical activity To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 18, 2026 — A new #research paper was #published in Volume 18 of Aging on May 26, 2026, titled “Early-life determinants of cardiometabolic outcomes and accelerated biological ageing in Colombia.” The study was led by first and corresponding author Juan Carlos Rivillas from the Department of Epidemiology and Biostatistics, MRC Centre for Environment and Health, School of Public Health, Imperial College London, United Kingdom. Experiences during childhood can shape health for decades. Adverse childhood experiences (ACEs), such as emotional abuse, domestic violence, food insecurity, poor health, and forced displacement, have long been linked to chronic disease. However, less is known about how these early-life hardships may influence biological aging itself. In this study, researchers examined whether childhood adversity is associated with cardiometabolic disease and accelerated biological aging among older adults in Colombia. The investigators analyzed data from 3,385 adults aged 60 years and older who participated in the nationally representative SABE-Colombia study. Five forms of childhood adversity experienced before age 15 were evaluated: emotional abuse, domestic violence, poor childhood health, food scarcity, and forced migration related to Colombia's armed conflict. Biological aging was estimated using the Klemera-Doubal Method for Biological Age, a biomarker-based measure that compares biological age with chronological age. Full press release - https://aging-us.net/2026/06/18/childhood-adversity-may-leave-lasting-biological-scars-decades-later/ DOI - https://doi.org/10.18632/aging.206384 Corresponding author - Juan Carlos Rivillas - j.rivillas-garcia20@imperial.ac.uk Abstract video - https://www.youtube.com/watch?v=5w6vgFzjcNQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206384 Keywords - aging, adverse childhood experiences, forced childhood migration, biological ageing, cardiometabolic outcomes, life course epidemiology To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – June 17, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on June 8, 2026, titled “DHHC3 interferes with antitumor immunity in melanoma cells.” The study was led by first author and corresponding author Chandan Sharma and corresponding author Martin E. Hemler from the Department of Cancer Immunology and Virology at the Dana-Farber Cancer Institute. Melanoma is one of the most aggressive forms of skin cancer and is highly influenced by interactions between tumor cells and the immune system. Although modern immunotherapies have transformed treatment for many patients, researchers continue to search for molecular mechanisms that enable tumors to evade immune attack and continue growing. In this study, researchers investigated DHHC3, a protein acyltransferase that regulates protein palmitoylation and helps maintain cellular redox balance. Previous studies had linked elevated DHHC3 expression to poor outcomes in several cancers, but its role in melanoma and anti-tumor immunity remained unclear. To explore this question, the team used CRISPR gene editing to eliminate DHHC3 expression in B16F10 melanoma cells. Loss of DHHC3 caused a marked increase in oxidative stress and cellular senescence, as demonstrated by elevated TXNIP expression, increased reactive oxygen species levels, and enhanced expression of senescence-associated markers. Full press release - https://www.oncotarget.net/2026/06/17/protein-linked-to-melanoma-growth-may-suppress-the-bodys-natural-anti-tumor-immune-response/ DOI - https://doi.org/10.18632/oncotarget.28880 Correspondence to - Martin E. Hemler - martin_hemler@dfci.harvard.edu, and Chandan Sharma - csharma@mgh.harvard.edu Abstract video - https://www.youtube.com/watch?v=QQhP2VhzKSE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28880 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, oxidative stress, DHHC3, anti-cancer immunity, palmitoylation, melanoma To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Prostate cancer is the most commonly diagnosed cancer among men and remains a leading cause of cancer-related death worldwide. While age, family history, and genetics are well-established risk factors, researchers have increasingly focused on the role of metabolic health in prostate cancer progression. Obesity, insulin resistance, type 2 diabetes, and chronic inflammation have all been associated with more aggressive disease, but the molecular mechanisms connecting these conditions to prostate cancer remain incompletely understood. A research paper titled “Epigenetic dysregulation and biological function of PDX1 in prostate cancer” was published in Volume 17 of Oncotarget. In this study, the researchers investigated whether a gene best known for regulating pancreatic function may also play an important role in prostate tumor biology. The study was led by first author Tayo A. Adeyika and corresponding author Bernard Kwabi-Addo from Howard University, Washington, DC. Full blog - https://www.oncotarget.org/2026/06/16/pdx1-may-link-metabolic-dysfunction-to-prostate-cancer-progression/ DOI - https://doi.org/10.18632/oncotarget.28854 Correspondence to - Bernard Kwabi-Addo - bkwabi-addo@howard.edu Abstract video - https://www.youtube.com/watch?v=itYVsyXJJoE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28854 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PDX1, DNA methylation prostate cancer, shRNA knockdown, over-expression, glucose To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 16, 2026 — A new #research paper was #published in Volume 18 of Aging on May 22, 2026, titled “Systemic cancer risk profile in neovascular age-related macular degeneration: insights into shared aging-related mechanisms from a nationwide population-based study.” The study was led by first author Hyeong Min Kim and corresponding author Hyewon Chung from Konkuk University College of Medicine and Konkuk University Medical Center in Seoul, Republic of Korea. Neovascular age-related macular degeneration (nAMD) is one of the leading causes of severe vision loss in older adults. Although the disease primarily affects the retina, researchers increasingly recognize that it may reflect broader biological processes associated with aging, including chronic inflammation, vascular dysfunction, and immune dysregulation. These same mechanisms have also been implicated in the development of several cancers, raising questions about whether the two conditions may be biologically connected. To explore this possibility, investigators analyzed data from the Korean National Health Insurance Service, one of the world's largest population-based healthcare databases. The study included 334,091 individuals aged 50 years and older, including 83,742 patients with nAMD and 250,349 matched controls without the disease. Participants were followed for up to 10 years, allowing researchers to evaluate both overall cancer incidence and risks for specific cancer types. The analysis revealed that individuals with nAMD had a modest but statistically significant increase in overall cancer risk compared with matched controls. However, the increased risk was not observed across all cancers. Instead, patients with nAMD showed elevated risks for several specific malignancies, including thyroid, kidney, pancreatic, lung, bladder, and prostate cancers, while no significant associations were found for many other cancer types. Full press release - https://aging-us.net/2026/06/16/common-aging-mechanisms-may-link-vision-loss-disorder-to-increased-risk-of-certain-cancers/ DOI - https://doi.org/10.18632/aging.206383 Corresponding author - Hyewon Chung - hchung@kuh.ac.kr Abstract video - https://www.youtube.com/watch?v=hViOqGLYr1Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206383 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, neovascular age-related macular degeneration, cancer, population cohort, polygenic risk, shared susceptibility To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging chosen as the “Editors' Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases. This exploratory randomized controlled trial, titled “Short-term responsiveness of DNA methylation–based aging biomarkers to a multimodal intervention comprising exercise and dietary guidance involving daily consumption of yogurt containing Bifidobacterium longum BB536: an exploratory randomized controlled trial,” investigated whether a 12-week lifestyle intervention combining exercise, dietary guidance, and daily consumption of yogurt containing Bifidobacterium longum BB536 could influence biological aging. The researchers found a significant slowing of the DNA methylation-based pace of aging measure DunedinPACE in overweight men aged 50 and older, suggesting that feasible lifestyle changes may be associated with short-term improvements in selected epigenetic aging biomarkers. DOI - https://doi.org/10.18632/aging.206386 Corresponding author - Yukihiro Hishida - yukihiro-hishida639@morinagamilk.co.jp Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206386 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, DNA methylation clock, DunedinPACE, Multicomponent lifestyle intervention, Bifidobacterium longum BB536 To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – June 15, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on June 5, 2026, titled “A randomized double-blind placebo-controlled phase I/II clinical trial of a human papillomavirus therapeutic vaccine, PepCan, for reducing head and neck squamous cell carcinoma recurrence.” The study was led by first author Emily Bivens and corresponding author Mayumi Nakagawa from the University of Arkansas for Medical Sciences, Little Rock. Head and neck squamous cell carcinoma (HNSCC) remains a major clinical challenge. Even after surgery, radiation, and chemotherapy successfully eliminate detectable disease, many patients experience recurrence within the following years. Researchers have therefore been exploring whether immunotherapy-based approaches can help strengthen anti-tumor immune responses and reduce the risk of cancer returning. In this study, investigators evaluated PepCan, an experimental therapeutic vaccine designed to stimulate immune responses against human papillomavirus type 16 (HPV 16). Unlike preventive HPV vaccines that aim to stop infection before it occurs, therapeutic vaccines are intended to activate the immune system against existing HPV-related disease. PepCan contains four HPV 16 E6 peptides combined with a Candida-derived immune-stimulating adjuvant. Full press release - https://www.oncotarget.net/2026/06/15/hpv-therapeutic-vaccine-shows-safety-but-uncertain-benefit-in-preventing-head-and-neck-cancer-recurrence/ DOI - https://doi.org/10.18632/oncotarget.28892 Correspondence to - Mayumi Nakagawa - mnakagawa@uams.edu Abstract video - https://www.youtube.com/watch?v=oh0MNrrPGhw Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28892 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, human papillomavirus, head and neck cancer, therapeutic vaccine, adjuvant, clinical trial To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 11, 2026 — A new #meetingreport was #published in Volume 18 of Aging on May 14, 2026, titled “Foundations of Gerophysics.” The report was led by corresponding authors Maximilian Unfried and Brian K. Kennedy from the National University of Singapore. Aging is often studied through biology, genetics, and medicine. Yet despite tremendous advances, many fundamental questions remain unanswered: Why do organisms age at different rates? Why does resilience decline over time? And can the trajectory of aging be predicted before disease develops? Researchers participating in the inaugural Global Conference on Gerophysics explored whether answering these questions may require integrating biology with the quantitative principles of physics. Held in Singapore on March 5–6, 2025, the conference brought together 160 researchers from physics, biology, computation, and medicine and featured 31 speakers from institutions around the world. The meeting focused on developing a predictive and testable science of aging by applying concepts from dynamical systems, thermodynamics, network theory, stochastic processes, and artificial intelligence to biological aging. Full press release - https://aging-us.net/2026/06/11/physics-meets-aging-researchers-lay-the-foundations-of-gerophysics/ DOI - https://doi.org/10.18632/aging.206378 Corresponding authors - Maximilian Unfried - unfried@nus.edu.sg, and Brian K. Kennedy - bkennedy@nus.edu.sg Abstract video - https://www.youtube.com/watch?v=hgsA8EhjF0U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206378 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - gerophysics, geroscience, aging biology, longevity, complex systems, theoretical physics To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 10, 2026 — A new #research paper was #published in Volume 18 of Aging on May 18, 2026, titled “Transcriptional programs diverge in aging mouse and human skeletal muscle.” The study was led by co-first authors Charles D. Hwang and Siti Rahmayanti and corresponding author Indranil Sinha from Brigham and Women's Hospital, Harvard University. Aging is widely associated with the gradual loss of muscle mass, strength, and physical function. Much of what scientists know about these changes comes from studies in laboratory mice, which are frequently used to investigate the biological mechanisms of aging and to identify potential therapeutic targets. However, an important question remains: how closely do aging-related changes in mouse muscle reflect what actually occurs in humans? To address this question, researchers performed a detailed comparison of gene expression patterns in skeletal muscle from young and old mice and humans. The team analyzed RNA sequencing data from mouse gastrocnemius muscle and compared it with transcriptomic data from healthy young and older adults obtained through the National Institute on Aging's GESTALT study. The results revealed substantial differences between the two species. Despite both mice and humans experiencing age-related muscle decline, fewer than 5% of significantly altered biological pathways were shared between them. Many of the genetic programs that changed with aging in mice showed little resemblance to those observed in human skeletal muscle. Full press release - https://aging-us.net/2026/06/10/aging-muscle-follows-different-genetic-programs-in-mice-and-humans/ DOI - https://doi.org/10.18632/aging.206382 Corresponding author - Indranil Sinha - isinha@bwh.harvard.edu Abstract video - https://www.youtube.com/watch?v=CYKh4X1w8H0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206382 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - hypoxia, angiogenesis, aging, skeletal muscle, regeneration To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Why do some people appear to age faster than others, even when they are the same age? Researchers increasingly believe that chronological age tells only part of the story. Biological age attempts to capture how well the body's systems are functioning and may provide a more meaningful picture of overall health. A research paper on this topic was published in Volume 18 of Aging titled “Blood biochemical and gut microbiotic neural network models forecasting human biological age.” In the study, Russian researchers explored whether information from routine blood tests and the gut microbiome could be used to estimate biological age. Full blog - https://aging-us.org/2026/06/blood-tests-and-gut-bacteria-may-help-reveal-your-biological-age/ DOI - https://doi.org/10.18632/aging.206360 Corresponding author - Alexey Moskalev - amoskalev@med.ru Abstract video - https://www.youtube.com/watch?v=wg3YEwXMKWY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206360 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biological age, blood biochemistry, gut microbiome, neural network To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – June 8, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on June 3, 2026, titled “The anticancer effects of PCAIs in pancreatic cancer cells involve MAPK and PI3K/AKT pathways hyperactivation.” The study was led by first author Kweku Ofosu-Asante and corresponding author Nazarius S. Lamango from the Florida A&M University College of Pharmacy and Pharmaceutical Sciences, Institute of Public Health in Tallahassee, Florida. Pancreatic ductal adenocarcinoma is among the deadliest forms of cancer, due in large part to the high frequency of KRAS mutations that drive tumor growth and resistance to treatment. Although targeted therapies have recently been developed for specific KRAS mutations, many patients continue to have limited treatment options, highlighting the need for broader strategies capable of targeting multiple KRAS-driven cancers. In this study, researchers investigated a class of experimental compounds known as polyisoprenylated cysteinyl amide inhibitors (PCAIs), which were originally designed to disrupt abnormal KRAS signaling. Using pancreatic cancer cell lines carrying KRAS mutations, the team explored how these compounds affect cancer cell survival, migration, invasion, and the molecular pathways that regulate tumor growth. Full press release - https://www.oncotarget.com/news/pr/experimental-compounds-trigger-cancer-cell-death-in-kras-driven-pancreatic-cancer/ DOI - https://doi.org/10.18632/oncotarget.28879 Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu Abstract video - https://www.youtube.com/watch?v=asbhjME7rFQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28879 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCAIs, PDAC, MAPK, PI3K/AKT, KRAS To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 5, 2026 — A new #review was #published in Volume 18 of Aging on May 15, 2026, titled “Blue period – features of senescence 30 years after beta-galactosidase.” The review was led by first author Chisaka Kuehnemann and corresponding author Christopher D. Wiley from Tufts University. Cellular senescence has emerged as one of the most important biological processes linked to aging and age-related disease. Senescent cells stop dividing in response to stress or damage, yet they remain metabolically active and release a variety of signaling molecules that can influence surrounding tissues. Over the past three decades, evidence has increasingly shown that the accumulation of these cells contributes to chronic inflammation, tissue dysfunction, and many degenerative conditions associated with aging. In this review, the authors examine how the field has evolved since the landmark discovery of senescence-associated beta-galactosidase (SA-β-gal) in 1995. That finding provided one of the first practical methods for identifying senescent cells and helped establish that these cells accumulate in aging tissues. Since then, researchers have identified numerous additional characteristics of senescence and developed new approaches to study their role in health and disease. The review highlights several major features now recognized as hallmarks of senescent cells. These include stable proliferative arrest, increased lysosomal activity, secretion of inflammatory and signaling molecules collectively known as the senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, alterations in nuclear architecture, accumulation of metals and lipofuscin, and enhanced survival despite exposure to cellular stress. Full press release - https://aging-us.net/2026/06/05/thirty-years-after-the-discovery-of-sa-%ce%b2-gal-researchers-revisit-the-hallmarks-of-cellular-senescence/ DOI - https://doi.org/10.18632/aging.206380 Corresponding author - Christopher D. Wiley - christopher.wiley@tufts.edu Abstract video - https://www.youtube.com/watch?v=lfMPJF6No7M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206380 Keywords - aging, senescence, biomarkers, SASP, cell death To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Cancer is increasingly recognized as a major global health challenge, yet for people living through war, displacement, and humanitarian crises, access to even basic oncology services can be difficult or impossible. While emergency responses typically focus on trauma care, infectious diseases, and immediate survival needs, cancer care remains largely absent from many humanitarian health programs. A review paper on this topic was published in Volume 17 of Oncotarget titled “Cancer without borders: Policy frameworks for oncology care in humanitarian and conflict settings.” The study was led by first and corresponding author Pragnesh Parmar, with Gunvanti Rathod as co-author, both from AIIMS Bibinagar, Telangana, India. Full blog - https://www.oncotarget.org/2026/06/03/cancer-care-often-overlooked-in-humanitarian-crises/ Paper DOI - https://doi.org/10.18632/oncotarget.28856 Correspondence to - Pragnesh Parmar - drprag@gmail.com; (ORCID: orcid.org/0000-0002-8402-8435) Abstract video - https://www.youtube.com/watch?v=zXlhIBZyJ6Q Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28856 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, cancer care, humanitarian crisis, tele-oncology, global health policy, oncology triage To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — June 3, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 15, 2026, titled “Extracellular vesicles released by senescent myoblasts affect recipient cells via miRNA-target interactions.” The study was led by first author Michael Kamal from the Department of Kinesiology at McMaster University and corresponding author Gianni Parise from the same university. As people age, skeletal muscle gradually loses strength, size, and regenerative capacity. Scientists have increasingly linked these changes to cellular senescence—a state in which damaged cells permanently stop dividing but remain metabolically active. These senescent cells release a complex mixture of signaling molecules known as the senescence-associated secretory phenotype (SASP), which can influence neighboring cells and contribute to tissue dysfunction. In this study, the researchers investigated whether extracellular vesicles (EVs)—tiny membrane-bound particles released by cells—play a role in this process. Specifically, they examined EVs released by senescent muscle precursor cells, known as myoblasts, and analyzed the microRNAs (miRNAs) carried within these vesicles. The team found that senescent myoblasts released factors that impaired normal muscle cell development. When healthy muscle cells were exposed to signals from senescent cells, the resulting muscle fibers became significantly smaller and displayed increased expression of genes associated with cellular stress and senescence. Further analysis revealed that EVs released by senescent myoblasts carried a distinct set of miRNAs. The researchers identified 22 significantly altered miRNAs, including several previously linked to cellular senescence, such as miR-34a, miR-34b, miR-34c, and miR-22. The study also identified miR-301a-3p as a potentially novel senescence-associated miRNA. Full press release - https://aging-us.net/2026/06/03/senescent-muscle-cells-send-molecular-messages-that-may-contribute-to-age-related-muscle-decline/ DOI - https://doi.org/10.18632/aging.206379 Corresponding author - Gianni Parise - pariseg@mcmaster.ca Abstract video - https://www.youtube.com/watch?v=HKBbraYg8ew Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206379 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, extracellular vesicles, myoblasts, miRNA, multi-omics To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY — May 27, 2026 — A new #research paper was #published in Volume 18 of Aging-US on May 8, 2026, titled “The mediating role of DNA methylation clocks in associations of race, ethnicity, education, income, and occupation with mortality: findings from NHANES 1999-2002.” The study was led by first and corresponding author Hanyang Shen from the Department of Epidemiology and Population Health at Stanford University. In this study, the authors investigated whether DNA methylation aging biomarkers—often called epigenetic aging clocks—may help explain how social inequalities become biologically embedded and contribute to differences in mortality risk. Social factors such as race, ethnicity, educational attainment, household income, and occupation have long been associated with disparities in health outcomes and life expectancy. However, the biological mechanisms linking these social exposures to long-term disease risk and mortality remain incompletely understood. Using nationally representative data from 2,402 adults in the U.S. National Health and Nutrition Examination Survey (NHANES) 1999–2002 linked to mortality follow-up data through 2019, the researchers examined thirteen different DNA methylation biomarkers alongside traditional clinical and behavioral risk factors. The study evaluated whether these epigenetic aging measures mediated associations between social stratification factors and all-cause mortality. The findings showed that several DNA methylation clocks significantly mediated the relationship between social disadvantage and mortality risk. Among all biomarkers examined, GrimAge2 consistently demonstrated the strongest mediation effects, accounting for up to 52% of mortality disparities in some occupational comparisons. DunedinPoAm, a pace-of-aging biomarker, also demonstrated substantial mediation effects across multiple socioeconomic categories. Importantly, the mediation effects observed for several DNA methylation biomarkers frequently exceeded those of traditional clinical risk factors measured in the study, including C-reactive protein and cholesterol-related markers. The results suggest that epigenetic aging measures may capture the cumulative biological effects of multiple social, environmental, behavioral, and physiological stressors simultaneously. “Among all the 13 DNA methylation biomarkers available in NHANES, GrimAge2 consistently exhibited the strongest positive mediation capturing the social disparities on mortality up to 52% (95%CI: 26%-128%), followed by the DunedinPoAm.” Full press release - https://aging-us.net/2026/05/27/dna-methylation-clocks-may-help-explain-how-social-inequality-influences-mortality/ DOI - https://doi.org/10.18632/aging.206377 Corresponding author - Hanyang Shen - hyshen@stanford.edu Abstract video - https://www.youtube.com/watch?v=XObIyirTJok Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206377 Keywords - aging, race and ethnicity, social position, epigenetic aging, mediation analysis, mortality disparities To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Cancer immunotherapy has transformed the treatment landscape for many advanced cancers over the past decade. Drugs targeting the PD-1 and PD-L1 pathways are now widely used across several tumor types, helping the immune system recognize and attack cancer cells more effectively. However, researchers are still working to understand how beneficial these therapies may be when used earlier in the disease course, particularly after surgery in patients with high-risk solid tumors. A research paper on this topic was published in Volume 17 of Oncotarget titled “Efficacy and safety of PD-1/ PD-L1 inhibitors as adjuvants in the treatment of patients with solid cancers: A systematic review and meta-analysis of randomized controlled trials.” Full blog - https://www.oncotarget.org/2026/05/20/immune-checkpoint-inhibitors-may-improve-outcomes-in-high-risk-solid-tumors/ Paper DOI - https://doi.org/10.18632/oncotarget.28855 Correspondence to - Dhai Almuteri - d.almuteri@qu.edu.sa Abstract video - https://www.youtube.com/watch?v=4Ce07bHfjB4 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28855 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PD-1, PD-L1, adjuvant immunotherapy, solid tumor To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Each month, we will highlight a paper published in Aging-US chosen as the “Editors' Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases. __________ In the research paper, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer's disease neurodegeneration,” researchers investigated whether epigenetic clocks of biological aging are associated with MRI markers of brain aging and Alzheimer's disease-related neurodegeneration in 1,196 older women. While none of the five epigenetic clocks examined were linked to accelerated overall brain aging, one measure (AgeAccelGrim2) was associated with MRI patterns related to neurodegeneration. The findings suggest this relationship was largely driven by DNA methylation markers linked to smoking history and changes in frontal and temporal brain regions rather than areas typically affected early in Alzheimer's disease. Overall, the study indicates that epigenetic aging and brain aging may reflect different aspects of the aging process, while highlighting the potential role of smoking-related biological aging in increasing dementia risk. DOI - https://doi.org/10.18632/aging.206369 Corresponding author - Linda K. McEvoy - linda.k.mcevoy@kp.org Abstract video - https://www.youtube.com/watch?v=kZiRjlKnnsI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206369 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic clocks, brain age, biological aging, smoking, frontal lobe To learn more about the journal, please visit https://www.Aging-US.com and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM
Glioma research has evolved rapidly over the past decade, driven by breakthroughs in molecular biology, imaging technologies, and computational tools. Today, clinicians can classify tumors with far greater precision than ever before, using genetic mutations, epigenetic markers, and advanced diagnostic frameworks. Yet, despite this progress, an important question remains: are we truly capturing the full picture of what shapes patient outcomes? Traditionally, glioma classification has focused on what can be measured in the tumor itself—its histology, molecular profile, and biological behavior. While these factors are undeniably critical, they may not fully explain why patients with similar tumors can experience very different clinical trajectories. Increasingly, researchers are beginning to recognize that broader influences—particularly social and environmental factors—may also play a role. Understanding how these different layers of information connect is becoming an important challenge in neuro-oncology. A review was published in Volume 17 of Oncotarget on March 31, 2026, titled “Bibliometric mapping of glioma classification research through main path, key route, and K-core analyses.” The study was led by first and corresponding author Kayode Ahmed from The University of Texas MD Anderson Cancer Center, in collaboration with Juan E. Núñez-Ríos from Universidad Panamericana. Full blog - https://www.oncotarget.org/2026/05/05/mapping-the-hidden-structure-of-glioma-research-what-are-we-missing/ Paper DOI - https://doi.org/10.18632/oncotarget.28851 Correspondence to - Kayode Ahmed - kmahmed@mdanderson.org Abstract video - https://www.youtube.com/watch?v=v8h2z3eEMFM Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28851 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, glioma research, social network analysis, socio-clinical domains, web of science, networks To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
Cancer has long been understood through a variety of biological frameworks, including genetic mutations, dysregulated signaling pathways, and uncontrolled cell proliferation. Yet, these models often capture the visible consequences of disease rather than the deeper metabolic dependencies that sustain tumor survival. Despite major advances in targeted therapies, a central challenge remains: what underlying mechanisms make cancer cells vulnerable to treatment, and how can these vulnerabilities be exploited more effectively? Increasing attention has shifted toward cellular metabolism—particularly lipid regulation and energy-sensing pathways such as AMPK—as critical determinants of tumor behavior. Scientists are now taking a closer look at how metabolism works together with stress responses like autophagy—and how this connection could be used to develop better cancer treatments. A new research paper was published in Volume 17 of Oncotarget, titled “The SCD1 inhibitor aramchol interacts with regorafenib and metformin to kill tumor cells.” The study was led by first author Michael R. Booth and corresponding author Paul Dent from Virginia Commonwealth University, in collaboration with Laurence Booth and Jane L. Roberts from Virginia Commonwealth University and John M. Kirkwood from the University of Pittsburgh Cancer Institute. Full blog - https://www.oncotarget.org/2026/04/21/scd1-inhibition-strategy-shows-potent-synergy-with-regorafenib-and-metformin-in-tumor-cell-killing/ Paper DOI - https://doi.org/10.18632/oncotarget.28861 Correspondence to - Paul Dent - paul.dent@vcuhealth.org Abstract video - https://www.youtube.com/watch?v=lmX_c2e_-HY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28861 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, macroautophagy, ER stress, aramchol, regorafenib, BID To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
BUFFALO, NY – April 15, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 31, 2026, titled “Epigenetic dysregulation and biological function of PDX1 in prostate cancer.” The study was led by first author Tayo A. Adeyika and corresponding author Bernard Kwabi-Addo from Howard University, Washington, DC. The team explored the role of the pancreatic and duodenal homeobox 1 (PDX1) gene in prostate cancer, with a focus on its epigenetic regulation and biological function. Their analysis identified PDX1 as differentially hypermethylated in prostate cancer tissues compared to normal prostate samples, alongside a paradoxical increase in protein expression in tumor tissues. Experiments in prostate cancer cell lines showed that PDX1 overexpression significantly enhanced cell proliferation and migration, while knockdown of PDX1 suppressed these tumor-associated behaviors. These findings point to a clear role for PDX1 in promoting aggressive cancer phenotypes. The work further shows that PDX1 regulates key metabolic, inflammatory, and epithelial–mesenchymal transition (EMT) pathways, including genes such as INSR, IGF1R, TWIST1, and SNAI1. Notably, these effects were more pronounced under high-glucose conditions, suggesting a link between metabolic state and prostate cancer progression. “Overall, our findings suggest that PDX1 plays a tumor-promoting role in human PCa cells by influencing expression of metabolites in insulin, inflammatory, and epithelial-mesenchymal transition (EMT) signaling pathways.” The authors conclude that PDX1 may represent a potential therapeutic target, particularly in the context of metabolic disorders such as obesity and diabetes, which are known to influence prostate cancer risk and progression. Their findings provide new insight into the interplay between epigenetics, metabolism, and tumor biology in prostate cancer. DOI - https://doi.org/10.18632/oncotarget.28854 Correspondence to - Bernard Kwabi-Addo - bkwabi-addo@howard.edu Abstract video - https://www.youtube.com/watch?v=itYVsyXJJoE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28854 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PDX1, DNA methylation prostate cancer, shRNA knockdown, over-expression, glucose To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM
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