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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

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

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

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

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

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

Efforts to improve metabolic health through dietary interventions often come with trade-offs. Some approaches that reduce obesity or extend lifespan in laboratory models can also negatively affect other tissues, including bone. One example is sulfur amino acid restriction (SAAR), a diet low in methionine and lacking cysteine that has repeatedly shown strong anti-obesity effects in animal studies. However, despite these promising metabolic benefits, SAAR has also been associated with reduced bone mineral density, weaker bones, and increased marrow fat accumulation. This has led researchers to ask whether the metabolic benefits of SAAR can be separated from its harmful skeletal effects. A new research paper was published in Volume 18 of Aging-US, titled “D, L-Buthionine-(S, R)-sulfoximine recapitulates the anti-obesity effects of sulfur amino acid restriction without the associated deleterious effects on bone in male mice.” The researchers investigated whether those metabolic benefits could be achieved without the same harmful effects on bone. The study was led by first author Naidu B. Ommi and corresponding author Sailendra N. Nichenametla from the Orentreich Foundation for the Advancement of Science Inc., in collaboration with Dwight A. L. Mattocks from the same institution and Mark C. Horowitz from the Yale University School of Medicine. Full blog - https://aging-us.org/2026/05/glutathione-pathway-may-hold-the-key-to-safer-anti-obesity-interventions/ Paper DOI - https://doi.org/10.18632/aging.206358 Corresponding author - Sailendra N. Nichenametla - snichenametla@orentreich.org Abstract video - https://www.youtube.com/watch?v=0adFA_b-q1Q Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206358 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - bone, aging, methionine, glutathione, redox 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

Aging has long been linked to a range of biological processes, including cellular senescence, epigenetic changes, and chronic tissue remodeling. Yet, these explanations often describe what happens during aging rather than why certain age-related diseases, such as fibrosis, continue to progress over time. In conditions like idiopathic pulmonary fibrosis (IPF), a key question remains: what drives the persistent activation of cells that should normally return to a resting state after injury? Increasing attention has turned to the interaction between cellular signaling pathways and epigenetic regulation as a potential explanation. Understanding how these processes work together to control gene expression and cell behavior is becoming an important focus in uncovering the mechanisms behind age-related disease. A new research paper was published in Volume 18 of Aging-US, titled “P38 MAPK is involved in epigenetic regulation of fibrotic genes in replication induced senescence in lung fibroblasts.” The study was led by first author Shan Zhu and corresponding author Yan Y. Sanders from the Department of Biomedical and Translational Sciences, Eastern Virginia Medical School (Macon & Joan Brock Virginia Health Sciences at Old Dominion University), in collaboration with Jennifer Q. Zhou, Kan Wang, and Ming-lei Guo from the same institution. Full blog - https://aging-us.org/2026/04/p38-mapk-driven-epigenetic-regulation-identified-as-a-key-mechanism-in-lung-fibrosis/ Paper DOI - https://doi.org/10.18632/aging.206357 Corresponding author - Yan Y Sanders - sandery@odu.edu Abstract video - https://www.youtube.com/watch?v=yP0CwWMUhnY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206357 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, fibroblast activation, p38 MAPK, lung fibrosis, H4K16Ac 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 — April 23, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 7, 2026, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer's disease neurodegeneration.” The study was led by first and corresponding author Linda K. McEvoy from the Kaiser Permanente Washington Health Research Institute, in collaboration with a multidisciplinary team of researchers across leading institutions in the United States and Europe. In this study, the researchers examined whether epigenetic measures of biological aging are associated with structural brain changes linked to aging and Alzheimer's disease. Using data from 1,196 older women enrolled in the Women's Health Initiative Memory Study, they analyzed five widely used epigenetic clocks and compared them with MRI-derived measures obtained approximately eight years later. The findings revealed a clear distinction between different aspects of aging. None of the epigenetic clocks were associated with accelerated brain aging as measured by the SPARE-BA index, a composite MRI marker of brain age. However, one specific clock—AgeAccelGrim2—was significantly associated with the Alzheimer's Disease Pattern Similarity Score (AD-PS), a validated imaging biomarker linked to increased risk of dementia. Further analyses suggested that this association was largely driven by epigenetic signatures related to smoking exposure. In particular, a DNA methylation marker reflecting cumulative smoking history was linked to reduced frontal and temporal lobe volumes—regions commonly affected in age-related neurodegeneration. Notably, no significant associations were observed with hippocampal or entorhinal cortex volumes, areas more directly implicated in early Alzheimer's pathology. “Taken together with prior findings, these results suggest that measures of epigenetic and brain age acceleration capture different aspects of biological aging, and that AgeAccelGrim2 is predictive of neurodegenerative changes associated with smoking that increase risk of dementia.” The study highlights the complexity of biological aging and underscores that not all aging biomarkers reflect the same underlying processes. While epigenetic clocks are increasingly used to estimate biological age, their relationship with brain structure appears to depend on the specific pathways they capture—particularly those influenced by environmental exposures such as smoking. Overall, these findings provide important insight into how molecular measures of aging relate to neuroimaging markers of brain health. By distinguishing between general brain aging and disease-related neurodegeneration, this work helps refine the use of epigenetic biomarkers in aging research and may support future efforts to identify individuals at risk for cognitive decline. 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

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 17, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 3, 2026, titled “Modeling premature aging in yeast via the expression of Progerin.” The study was led by first author Zachery R. Belak from the University of Saskatchewan, and corresponding author Troy A.A. Harkness from the University of Saskatchewan and the University of Alberta. The team developed a yeast-based model to study premature aging by expressing Progerin, the toxic protein responsible for Hutchinson–Gilford Progeria Syndrome. Using genetically engineered yeast cells, they compared the effects of Progerin with its normal counterpart, Lamin A, to better understand how protein accumulation impacts cellular aging. Their findings show that Progerin expression leads to slower cell growth, increased genome instability, and a significant reduction in chronological lifespan. In contrast, Lamin A did not produce the same harmful effects, highlighting the specific role of Progerin in driving premature aging phenotypes. The study also demonstrates that Progerin accumulates in aging mother cells and remains more stable than Lamin A, suggesting a mechanism by which damaged or toxic proteins are retained during the aging process. These observations mirror what has been reported in human cells, reinforcing the relevance of this model system. “Taken together, expression of Progerin in yeast cells mimics what is observed in human cells, establishing yeast as a powerful model to discover genetic mechanisms driving premature and normal aging.” Overall, the researchers present a practical and efficient model for studying the biological mechanisms underlying premature aging. Their work provides a valuable platform for testing new strategies aimed at reducing toxic protein accumulation and improving cellular health during aging. DOI - https://doi.org/10.18632/aging.206367 Corresponding author - Troy AA. Harkness - taharkne@ualberta.ca Abstract video - https://www.youtube.com/watch?v=VYQKAJjgIb8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206367 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Hutchinson-Gilford Progeria Syndrome, yeast, Progerin, Lamin A, premature aging 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 – 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

BUFFALO, NY — April 15, 2026 — A new #research paper was #published in Volume 18 of Aging-US on March 30, 2026, titled “A manually curated gene–phenotype catalogue for progeroid syndromes and premature aging.” The study was led by Nuša Likar and Tanja Kunej from the University of Ljubljana, Slovenia. The researchers developed a comprehensive, manually curated catalogue integrating data from 84 scientific publications and the OMIM database. The resulting resource systematically organizes genetic and clinical information on progeroid syndromes, linking 144 genes to 56 syndromes and 160 distinct clinical entities, making it one of the most extensive datasets in this field to date. Using genome–phenome association analysis and protein–protein interaction networks, the study reveals the complex genetic and phenotypic heterogeneity underlying premature aging disorders. The findings highlight strong enrichment in genome maintenance and DNA repair pathways, reinforcing their central role in aging biology. The catalogue also demonstrates how single genes, such as LMNA, can be associated with multiple syndromes, illustrating the pleiotropic nature of genetic variants in progeroid conditions and their broader relevance to human aging mechanisms. “Overall, this study provides a reference resource and framework to support future research into premature aging syndromes and their broader implications for understanding physiological aging.” Overall, the authors present a valuable framework for improving the classification, diagnosis, and study of rare premature aging disorders. Their work not only advances understanding of progeroid syndromes but also offers important insights into the biological processes that drive normal human aging. DOI - https://doi.org/10.18632/aging.206366 Corresponding author - Tanja Kunej - tanja.kunej@bf.uni-lj.si Abstract video - https://www.youtube.com/watch?v=Ov6Saz34ZpE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206366 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, premature aging, progeroid syndromes, DNA repair, LMNA gene 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, E3), Dr. Ricardo Costeira of King's College London joins host Dr. Yuan Zhao of Queen Mary University of London to discuss a research paper he co-authored in Volume 17, Issue 12 of Aging-US, titled “Theobromine is associated with slower epigenetic ageing.” DOI - https://doi.org/10.18632/aging.206344 Corresponding authors - Ramy Saad - ramy.saad@kcl.ac.uk, and Jordana T. Bell - jordana.bell@kcl.ac.uk Video interview - https://www.youtube.com/watch?v=in0z_QApqWQ Longevity & Aging Series - https://www.aging-us.com/longevity About Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Abstract video - https://www.youtube.com/watch?v=S0P1USM8L6E Abstract Theobromine, a commonly consumed dietary alkaloid derived from cocoa, has been linked to extended lifespan in model organisms and to health benefits in humans. We examined associations between circulating levels of theobromine intake, measured using serum metabolomics, and blood-based epigenetic markers of biological ageing in two European human population-based cohorts. Serum theobromine levels were significantly associated with reduced epigenetic age acceleration, as measured by GrimAge (p < 2e-7) and DNAmTL (p < 0.001) in 509 individuals from the TwinsUK cohort, and both signals replicated in 1,160 individuals from the KORA cohort (p = 7.2e-08 and p = 0.007, respectively). Sensitivity analyses including covariates of other cocoa and coffee metabolites suggest that the effect is specific to theobromine. Our findings indicate that the reported beneficial links between theobromine intake on health and ageing extend to the molecular epigenetic level in humans. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206344 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, theobromine, epigenetic aging, DNA methylation, metabolomics, nutrition To learn more about the journal, 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 Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl 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 – April 13, 2026 – A new #review was #published in Volume 17 of Oncotarget on March 31, 2026, titled “Cancer without borders: Policy frameworks for oncology care in humanitarian and conflict settings.” The study—led by corresponding author Pragnesh Parmar, along with Gunvanti Rathod from AIIMS Bibinagar, Telangana, India—brings together evidence from peer-reviewed studies, global health reports, and case examples from regions such as Gaza, Sudan, and Ukraine to examine the structural, ethical, and policy barriers limiting access to cancer care in humanitarian settings. Their findings show that oncology services are often excluded from emergency health priorities, resulting in delayed diagnosis, treatment interruptions, and reduced access to palliative care. The review further highlights that disrupted infrastructure, legal constraints, and fragmented policies disproportionately impact vulnerable populations—including women, children, and the elderly—who often present with advanced disease stages due to delays in care. “Addressing cancer in humanitarian contexts is not merely a technical challenge but a moral imperative.” The authors conclude that integrating oncology into humanitarian response frameworks is essential to ensure equitable access to care and improve outcomes for displaced populations. They emphasize the need for coordinated global strategies, including cross-border care models, tele-oncology, and policy reform, to address this critical gap in global health systems. 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

Aging has long been attributed to a range of biological processes, including DNA damage, telomere shortening, and mitochondrial dysfunction. Yet, these frameworks often describe downstream consequences rather than a single unifying cause. Despite decades of research, a central question remains unresolved: what ultimately determines lifespan across species? Increasing attention has turned to cellular energy metabolism—particularly pathways responsible for rapid ATP generation—as a potential key driver. Understanding how these metabolic changes unfold over time, and how they influence survival, regeneration, and disease, remains a major challenge in aging biology. A new research perspective published in Volume 18 of Aging-US introduces a unifying concept in aging biology, titled “A decline in glycolytic ATP production is the fundamental mechanism limiting lifespan; species with an optimal rate of decline over time survived.” Full blog - https://aging-us.org/2026/04/decline-in-glycolytic-atp-production-proposed-as-a-fundamental-mechanism-limiting-lifespan/ Paper DOI - https://doi.org/10.18632/aging.206356 Corresponding author - Akihiko Taguchi - taguchi@fbri.org Abstract video - https://www.youtube.com/watch?v=rA23radaoqI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206356 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - hypothesis, aging, glycolytic ATP production, lifespan, Heterocephalus glaber 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 – April 10, 2026 – A new #editorial perspective was #published in Volume 17 of Oncotarget on April 8, 2026, titled “Oncotarget: Past, Present and Future: Trends in the publishing industry.” Authored by the Scientific Integrity Office at Oncotarget, the editorial comprehensively analyzes the journal's evolving approach to scientific integrity. It addresses historical challenges in scholarly publishing and discusses the necessity of modern image forensics tools to meet the most rigorous standards of scientific integrity. The Scientific Integrity Office describes how advances in digital technologies—particularly image forensics tools such as ImageTwin and analytical platforms like Argos—have transformed the ability to detect problematic data and analyze the quality of published research. The editorial emphasizes that the lack of adequate image tools in the “pre-tools” era limited journals' ability to detect image-related issues, underscoring the importance of recent technological advancements. It also highlights that Argos provides a good opportunity to obtain a more objective picture across different journals in both the pre- and post-tools era. Looking forward, Oncotarget advocates indexes for broader adoption of independent analytical and AI-based tools in journal evaluation. In the public interest, it also encourages open discussion of how indexes select, deselect, and reevaluate journals. DOI - https://doi.org/10.18632/oncotarget.28852 Correspondence to - Scientific Integrity Office - scientificintegrityoffice@impactjournals.com Introduction video - https://www.youtube.com/watch?v=hgxvr2Q_ZPM Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28852 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - Scientific Integrity, Academic Publishing, Open Access, Peer Review, Research 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

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 this study, titled “Plant-based dietary patterns are associated with slower epigenetic aging,” the researchers examined whether plant-based dietary patterns are linked to biological aging in large, diverse U.S. populations. Using data from the Atherosclerosis Risk in Communities (ARIC) Study and National Health and Nutrition Examination Survey (NHANES), they analyzed several versions of plant-based diet scores that reflect higher intake of plant foods and lower intake of animal products, as well as distinctions between healthy and less healthy plant-based foods. They then compared these dietary patterns with DNA methylation-based “epigenetic clocks,” which estimate biological age, including GrimAge2, PhenoAge, and HannumAge. The results showed that greater adherence to overall plant-based diets, provegetarian diets, and especially healthy plant-based diets was consistently associated with slower epigenetic aging, meaning participants appeared biologically younger than their chronological age. In contrast, diets higher in less healthy plant-based foods did not show the same benefits. The findings suggest that diets emphasizing whole plant foods and limiting animal products may help slow biological aging at the molecular level. 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 – April 7, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 31, 2026, 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.” Led by first author Maryam Aleid from Imam Abdulrahman Bin Faisal University, and corresponding author Dhai Almuteri from King Fahad Specialist Hospital, the researchers evaluated 13 randomized controlled trials involving 9,850 patients to assess the efficacy and safety of PD-1 and PD-L1 inhibitors as adjuvant therapy following tumor resection. The analysis demonstrated that immune checkpoint inhibitors significantly improved key clinical outcomes, including disease-free survival and distant metastasis-free survival. However, no clear improvement in overall survival was observed across studies. The study also identified a reduction in recurrence and metastasis risk, supporting the role of these therapies in early-stage cancer management. At the same time, variability across tumor types suggests that benefits may differ depending on cancer subtype and patient population. “Adjuvant PD-1 and PD-L1 inhibitors improve disease-free and distant metastasis-free survival in selected patients with high-risk solid tumors.” In terms of safety, the findings highlight an increased incidence of adverse events associated with PD-1/PD-L1 inhibitors, including fatigue, nausea, pruritus, and hypothyroidism, emphasizing the importance of careful monitoring during treatment. The authors conclude that while PD-1/PD-L1 inhibitors offer meaningful benefits in reducing recurrence and metastasis in high-risk solid tumors, the clinical benefit must be balanced against higher toxicity rates. Future research is needed to refine patient selection, evaluate long-term survival outcomes, and better understand differences across tumor types to optimize the use of these therapies in clinical practice. 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

Androgen receptor (AR) signaling has long been the central driver of prostate cancer progression and the primary target of therapies for advanced disease. Yet, a significant subset of tumors either fail to respond or develop resistance, often by switching to AR-independent programs that resemble basal or stem cell-like states. Understanding what drives these aggressive, therapy-resistant phenotypes is a critical challenge in oncology. A research paper, titled “CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer” was published in Volume 17 of Oncotarget by a multi-institutional team of researchers, identifies a key molecular regulator of this process and reveals how it promotes tumor progression. Full blog - https://www.oncotarget.org/2026/04/07/creb5-a-master-regulator-of-stem-cell-like-programs-in-prostate-cancer-progression/ Paper DOI - https://doi.org/10.18632/oncotarget.28826 Correspondence to - Emmanuel S. Antonarakis - anton401@umn.edu, Justin Hwang - jhwang@umn.edu Abstract video - https://www.youtube.com/watch?v=Zywrj5hV4ho Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28826 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, prostate cancer, CREB5, basal-like, stem cell-like, AP-1 transcription factors 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 – April 6, 2026 – A new #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.” Led by first and corresponding author Kayode Ahmed from The University of Texas MD Anderson Cancer Center, and Juan E. Núñez-Ríos from Universidad Panamericana, the study uses bibliometric network analysis to map how glioma classification research has evolved across clinical, molecular, and social domains. The authors analyzed Web of Science data using direct citation networks and applied main path analysis, key route analysis, and K-core analysis to identify influential papers, critical routes, and densely connected thematic clusters. The network comprised 46,204 nodes and 231,432 arcs, highlighting the prominent role of DNA methylation profiling in molecular biomarker-based classification models. The authors also found that advanced imaging and molecular techniques were key drivers of the field, while the subset of glioma classification studies that incorporate social factors remained relatively scarce. Their analysis, therefore, points not only to the major intellectual structure of the literature but also to a thematic gap in how social determinants are represented in glioma classification research. “Through quantitative network analysis complemented by narrative interpretation, we uncovered patterns and substructures that offer deep insights into the evolving research landscape.” The authors conclude that their framework offers a more integrative view of glioma classification research than approaches centered only on citation counts or h-index–style metrics. By identifying the evolutionary logic of the field and the limited but notable presence of social factors, the study suggests future glioma classification models may benefit from incorporating clinical, molecular, and social dimensions more explicitly. 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

BUFFALO, NY – March 31, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 27, 2026, titled “The SCD1 inhibitor aramchol interacts with regorafenib and metformin to kill tumor cells.” Led by Michael R. Booth, Laurence Booth, and Jane L. Roberts from Virginia Commonwealth University, with corresponding author Paul Dent from the same institution and John M. Kirkwood from the University of Pittsburgh Cancer Institute, the study examines how aramchol interacts with regorafenib and metformin to kill tumor cells, particularly patient-derived uveal melanoma (UM) cells and cholangiocarcinoma cells. The authors report that aramchol, regorafenib, and metformin interact to enhance tumor cell killing, with the strongest effects seen when metformin is added to aramchol plus regorafenib. In patient-derived UM cells and LD-1 cholangiocarcinoma cells, the three-drug combination increased autophagosome formation and autophagic flux, while knockdown of Beclin1, ATG5, or LAMP2 reduced autophagosome and autolysosome formation and lowered cell killing. The study also found that BID contributes to the lethal response, supporting a multifactorial mechanism involving macroautophagy and death-receptor signaling. “Our data demonstrates that UM cells are killed by treatment with aramchol plus regorafenib plus metformin via enhanced autophagic flux and that this combination may have the potential to control UM tumors that have metastasized to the liver.” The authors also note that while SCD1 knockdown increased baseline tumor cell death, it did not replicate the full anticancer effects of aramchol, suggesting additional molecular targets contribute to its activity. They emphasize the need for further in vivo studies to evaluate the therapeutic potential of this combination in metastatic uveal melanoma, particularly in liver-targeted disease. 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

Colorectal cancer (CRC) ranks among the most common and lethal cancers worldwide, accounting for approximately 10% of all cancer diagnoses. While advances in prevention and treatment have improved outcomes, predicting which patients will survive remains a complex challenge—one that depends on an intricate interplay between molecular biology and clinical factors. A research paper, titled “Machine learning-based survival prediction in colorectal cancer combining clinical and biological features” was published in Volume 16 of Oncotarget by an international team of researchers, demonstrating how machine learning can integrate these two domains to achieve highly accurate survival predictions. The team's investigation demonstrates that combining clinical features—such as pathological stage, age, and lymph node status—with biological markers—including the E2F8 gene and hsa-miR-495-3p—can significantly improve the ability to predict patient survival. Full blog - https://www.oncotarget.org/2026/03/25/predicting-colorectal-cancer-survival-how-machine-learning-combines-clinical-and-biological-clues/ Paper DOI - https://doi.org/10.18632/oncotarget.28783 Correspondence to - Lucas M. Vieira - lvieira@health.ucsd.edu Abstract video - https://www.youtube.com/watch?v=cy7UL5ZUKuI Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28783 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, colorectal cancer, machine learning, feature selection, non-coding RNAs, genes 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 – March 24, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 17, 2026, titled “CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer.” Led by corresponding authors Emmanuel S. Antonarakis and Justin Hwang from the Department of Medicine and the Masonic Cancer Center at the University of Minnesota – Twin Cities, the study examines how CREB5 shapes basal-like and stem cell-like transcriptional states in prostate cancer. The authors note that about 30–40% of advanced prostate cancers harbor basal-like transcriptional programs, and that stem cell-like tumors are a major mechanism of resistance to androgen receptor-targeted therapies. Using transcriptomic analyses of primary prostate cancer and castration-resistant prostate cancer cohorts (n = 493 and 208), the authors found that CREB5 expression strongly correlates with basal-like gene signatures and stem cell-like transcriptional programs. CREB5 was also shown to interact with AP-1 transcription factors and bind regulatory elements of AP-1 genes, suggesting a mechanistic role in promoting these aggressive tumor states. Functional experiments demonstrated that CREB5 overexpression enhances colony formation and tumor growth, supporting its role in tumor progression. “Taken together, this study indicates that CREB5 enhances PC tumor progression through genes that are associated with SCL traits.” Mechanistically, the study shows that CREB5 regulates transcriptional programs linked to tumor progression and stem cell-like features, positioning it as a central driver of aggressive prostate cancer phenotypes. The findings also suggest that CREB5 activity may already be present in primary tumors, potentially contributing to later therapy resistance and disease progression. The authors conclude that targeting CREB5-regulated transcriptional programs could represent a future strategy for addressing androgen receptor-independent prostate cancer. Further studies are needed to determine how disrupting CREB5 or its downstream pathways may improve therapeutic responses in advanced disease. DOI - https://doi.org/10.18632/oncotarget.28826 Correspondence to - Emmanuel S. Antonarakis - anton401@umn.edu, Justin Hwang - jhwang@umn.edu Abstract video - https://www.youtube.com/watch?v=Zywrj5hV4ho Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28826 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, prostate cancer, CREB5, basal-like, stem cell-like, AP-1 transcription factors 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 treatment has long been a battle of attrition—surgery, radiation, and chemotherapy have saved countless lives, but for patients with advanced or refractory malignancies, the options remain limited. In recent years, however, a new approach has emerged that harnesses the power of the patient's own immune system to seek and destroy cancer cells with unprecedented precision. An editorial perspective, titled “CAR-T therapy: Trailblazing CAR(ing) in cancer treatment.” published in Volume 17 of Oncotarget by researchers Uzma Saqib, Monika Pandey, and Krishnan Hajela from the School of Life Sciences, Devi Ahilya Vishwavidyalaya, Indore, India, provides an overview of this revolutionary therapeutic strategy. The paper presents the current state of CAR-T therapy, its clinical successes, and the formidable challenges that remain before it can fulfill its transformative potential. Full blog - https://www.oncotarget.org/2026/03/10/car-t-cell-therapy-a-revolutionary-approach-to-cancer-treatment/ Paper DOI - https://doi.org/10.18632/oncotarget.28836 Correspondence to - Krishnan Hajela - hajelak@gmail.com Abstract video - https://www.youtube.com/watch?v=T4hbwPToVKI Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28836 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, CAR-T therapy, therapeutic approaches 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