Podcasts about altmetric

A research paper recently published in Aging, titled “Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging,” investigated how a human-relevant mutation in the PTPN6 gene, which encodes the immune and metabolic regulator SHP-1, affects immune and liver function during aging. Using mice carrying the mutation, the researchers found that older mutant mice had improved glucose tolerance and hepatic insulin sensitivity, but also developed liver abnormalities characterized by increased fibrosis and the accumulation of immune cells, particularly B lymphocytes and macrophages. Further analyses indicated that these age-related changes were driven primarily by altered immune activity rather than direct effects within liver cells. The findings identify SHP-1 as an important regulator of liver immune homeostasis and provide new insight into how immune-cell infiltration may contribute to age-related changes in the liver. DOI - https://doi.org/10.18632/aging.206413 Corresponding author - André Marette - andre.marette@criucpq.ulaval.ca Abstract video - https://www.youtube.com/watch?v=lyn__UY9Buk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206413 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, SHP-1/Ptpn6, B cell, macrophage, aging, Ptpn6Ala457Thr 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 — September 16, 2026 — A new #research paper was #published in Volume 18 of Aging on August 28, 2026, titled “Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging.” The study examines how a mutation affecting the immune and metabolic regulator SHP-1 reshapes liver function during aging, revealing that improved glucose metabolism can coexist with immune-cell accumulation and liver fibrosis. The research was led by first author Beisy Laborit Labrada from the Institut Universitaire de Cardiologie et de Pneumologie de Québec (CRIUCPQ), Université Laval, Québec, Canada. André Marette, from CRIUCPQ and the Department of Medicine at Université Laval, is the corresponding author. SHP-1, encoded by the PTPN6 gene, is a protein tyrosine phosphatase that helps regulate both immune responses and metabolic signaling. In immune cells, it generally restrains signaling pathways that control cellular activation, while in metabolic tissues it acts as a negative regulator of insulin signaling. This dual function places SHP-1 at an important intersection between immunity and metabolism, two systems that undergo substantial changes during aging. The study centered on a rare PTPN6Ala455Thr variant originally identified in a French-Canadian family with early-onset severe emphysema. The human mutation moderately reduces SHP-1 phosphatase activity. To investigate its longer-term effects, the researchers used mice carrying the corresponding Ptpn6Ala457Thr mutation and compared young adult mice at 5.6 months with older animals at 16–19 months. Unlike more severe SHP-1-deficient mouse models, these animals have lifespans comparable to wild-type mice, allowing the consequences of partial SHP-1 dysfunction to be examined across aging. Full press release - https://www.aging-us.com/news-room/human-relevant-ptpn6-mutation-reveals-complex-links-between-immunity-metabolism-and-liver-aging DOI - https://doi.org/10.18632/aging.206413 Corresponding author - André Marette - andre.marette@criucpq.ulaval.ca Abstract video - https://www.youtube.com/watch?v=lyn__UY9Buk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206413 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, SHP-1/Ptpn6, B cell, macrophage, aging, Ptpn6Ala457Thr 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

Scientific progress often begins with questioning assumptions that have shaped a field for decades. Few researchers embodied this approach as strongly as Dr. Mikhail “Misha” Blagosklonny, an oncologist and biogerontologist whose unconventional theories challenged traditional explanations of why organisms age. An essay published in Volume 18 of Aging titled “Misha Blagosklonny: a life of ideas,” reflects on Dr. Blagosklonny's life, scientific career, and contributions to the biology of aging. Full blog post - https://aging-us.org/2026/09/misha-blagosklonnys-ideas-reshaped-thinking-about-aging/ Paper DOI - https://doi.org/10.18632/aging.206412 Corresponding author - David Gems - david.gems@ucl.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206412 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail Blagosklonny To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — September 14, 2026 — A new #review was #published in Volume 18 of Aging on August 26, 2026, titled “Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging.” The review examines two biological processes strongly associated with aging—cellular senescence and somatic DNA mutations—and evaluates whether the evidence supports their causal contribution to age-related functional decline. The review was authored by Lucrezia A. Trastus and Fabrizio d'Adda di Fagagna from IFOM ETS – The AIRC Institute of Molecular Oncology in Milan, Italy. d'Adda di Fagagna is also affiliated with the Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (IGM-CNR) in Pavia, Italy. Both authors are corresponding authors. Aging involves many interconnected molecular and cellular changes, making it difficult to distinguish processes that actively drive deterioration from those that simply accompany it. Trastus and d'Adda di Fagagna assess cellular senescence and somatic mutations using necessity and sufficiency as key criteria for causal inference. For cellular senescence, the evidence for causality is comparatively strong. Senescent cells undergo stable proliferative arrest, which can impair tissue regeneration, particularly when stem cells are affected. Their influence can extend far beyond individual cells through the senescence-associated secretory phenotype (SASP), a complex secretory program that allows senescent cells to alter surrounding tissues and promote senescence in neighboring cells. Full press release - https://www.aging-us.com/news-room/evidence-for-cellular-senescence-as-a-driver-of-aging-stronger-than-for-somatic-mutations DOI - https://doi.org/10.18632/aging.206414 Corresponding authors - Lucrezia A. Trastus - lucrezia.trastus@ifom.eu, Fabrizio d'Adda di Fagagna - fabrizio.dadda@ifom.eu Abstract video - https://www.youtube.com/watch?v=XHTBAJHjRZU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206414 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, somatic mutations, DNA damage, SASP 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 — September 10, 2026 — A new #research paper was #published in Volume 18 of Aging on August 24, 2026, titled “Disruption of the insulin/IGF-1 signaling pathway in Caenorhabditis elegans dramatically increases male longevity and enhances reproductive health late in life.” The research was conducted by Rose S. Al-Saadi, Hannah B. Lewack and Patrick C. Phillips. Al-Saadi and Lewack contributed equally to the study. Al-Saadi and Phillips are from the Institute of Ecology and Evolution at the University of Oregon, while Lewack is affiliated with both the Institute of Ecology and Evolution at the University of Oregon and the Department of Molecular Biology at the University of California, San Diego. Phillips is the corresponding author. Insulin/IGF-1 signaling (IIS) is one of the best-established molecular pathways regulating longevity across animal species. In C. elegans, the gene DAF-2 encodes an insulin/IGF-1 receptor, and reducing its activity can substantially extend lifespan. However, most previous aging studies in this model have focused on hermaphrodites, leaving considerably less known about how males respond to interventions targeting the same pathway. To investigate these sex-specific effects, the researchers used an auxin-inducible degron system to selectively degrade the DAF-2 receptor throughout the body or within particular tissues. When DAF-2 was degraded throughout the body, the effect on male longevity was striking: median lifespan increased by 446%, compared with a 109% increase in hermaphrodites exposed to the same intervention. The age at which 10% of the population remained alive reached 106 days in treated males, compared with 15 days in controls. The authors describe this as one of the largest lifespan extensions reported in C. elegans—or any animal—from a single intervention. Full press release - https://www.aging-us.com/news-room/reduced-insulin-igf-1-signaling-dramatically-extends-male-lifespan-in-c-elegans DOI - https://doi.org/10.18632/aging.206411 Corresponding author - Patrick C. Phillips - pphil@uoregon.edu Abstract video - https://www.youtube.com/watch?v=zQ32BnBwEBI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206411 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Insulin/IGF-1 signaling, sex differences, Caenorhabditis elegans, reproductive health 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 — September 9, 2026 — A new #research paper was #published in Volume 18 of Aging on August 13, 2026, titled “Protective effects of three herbal extracts on mitochondrial dysfunction in VPS13C-knockdown SH-SY5Y cells: implications for Parkinson's disease.” The study was led by co-first authors Yih-Ru Wu and Chih-Hsin Lin from the Chang Gung Memorial Hospital, Chang Gung University College of Medicine in Taoyuan, Taiwan, and Pei-Syuan Huang from the School of Life Science at National Taiwan Normal University in Taipei, Taiwan. Corresponding authors I-Cheng Chen and Guey-Jen Lee-Chen are from the School of Life Science at National Taiwan Normal University. The paper identifies Wu, Lin, and Huang as equal contributors. Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized primarily by dysfunction and loss of dopaminergic neurons in the substantia nigra. Although its causes are complex, mitochondrial dysfunction and oxidative stress are important biological processes implicated in both sporadic and inherited forms of the disease. The researchers focused on VPS13C, also known as PARK23, a gene associated with a rare autosomal recessive form of early-onset parkinsonism. Loss of VPS13C function has previously been linked to impaired mitochondrial function. The study investigated three extracts used in traditional Chinese medicine: Uncaria rhynchophylla (UR), Gardenia jasminoides (GJ), and Scutellaria baicalensis (SB). Previous experimental studies have reported neuroprotective effects from these plants or their bioactive constituents in models relevant to PD. The researchers examined whether the extracts could protect cells against mitochondrial dysfunction associated with reduced VPS13C expression. Chemical analyses identified several potentially bioactive constituents in the extracts. UR contained rhynchophylline and isorhynchophylline; GJ contained geniposide and crocin; and SB contained several flavonoids, including baicalin, wogonoside, baicalein, wogonin, and oroxylin A. Across the concentrations initially tested, the three extracts maintained greater than 90% viability in SH-SY5Y cells after 24 hours, indicating low cytotoxicity under these experimental conditions. Full press release - https://www.aging-us.com/news-room/three-herbal-extracts-protect-mitochondrial-function-in-a-cellular-model-of-parkinsons-disease DOI - https://doi.org/10.18632/aging.206409 Corresponding authors - I-Cheng Chen - ichen@ntnu.edu.tw, Guey-Jen Lee-Chen - t43019@ntnu.edu.tw Abstract video - https://www.youtube.com/watch?v=kM8hO89d_9k Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206409 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Parkinson's disease, traditional Chinese medicine, VPS13C knockdown, mitochondrial dysfunction, oxidative stress 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

Dr. Falak Pahwa, Dr. Ranjan Kumar Nanda, and Mr. Ashish Gupta from the International Centre for Genetic Engineering and Biotechnology (ICGEB) in New Delhi, India, discuss their research paper, recently published in Volume 18 of Aging, titled “Host immunosenescence compromises Mycobacterium tuberculosis clearance.” Video interview - https://www.youtube.com/watch?v=bSaJaB751kM DOI - https://doi.org/10.18632/aging.206374 Corresponding author - Ranjan Kumar Nanda - ranjan@icgeb.res.in Abstract video - https://www.youtube.com/watch?v=isPD8ZmUjv8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206374 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, tuberculosis, immunosenescence, TFH cells, proteomics 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 — September 3, 2026 — A new #research paper was published in Volume 18 of Aging on August 12, 2026, titled “Indy reduction decreases aging-related dysbiosis in Drosophila.” The study was led by first author Danielle N. A. Lesperance from the University of Connecticut. Corresponding authors Blanka Rogina and Nichole A. Broderick are affiliated with the University of Connecticut Health and Johns Hopkins University, respectively. Broderick is also affiliated with the University of Connecticut. The Indy gene—short for “I'm not dead yet”—encodes a plasma membrane citrate transporter in Drosophila melanogaster. Previous research has shown that reducing Indy activity can extend lifespan and preserve metabolic and intestinal health in flies. Because aging is also associated with disruption of the gut microbiota, the researchers investigated whether changes in intestinal microbes contribute to the longevity effects associated with reduced Indy activity. The researchers compared control flies with Indy heterozygous flies under conventional conditions and axenic conditions, in which microbes were absent. They also examined bacterial load and microbiota composition and performed RNA sequencing of the midgut to investigate molecular pathways connecting Indy, the microbiota, intestinal homeostasis, and aging. Full press release - https://www.aging-us.com/news-room/indy-gene-reduction-linked-to-healthier-gut-microbiota-and-longer-lifespan-in-fruit-flies DOI - https://doi.org/10.18632/aging.206408 Corresponding authors - Blanka Rogina - Rogina@uchc.edu, and Nichole A. Broderick - nbroder1@jhu.edu Abstract video - https://www.youtube.com/watch?v=d0PfTj_Pg7U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206408 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Indy, host-microbe interactions, lifespan, Drosophila melanogaster 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 – September 1, 2026 – A new #review was published in Volume 17 of Oncotarget on August 28, 2026, titled “Emerging biomedical imaging applications of tumor-derived extracellular vesicles for premetastatic niche detection: Biological rationale, engineering strategies, and translational challenges.” The review was led by first author Omkar Dhaygude, who is affiliated with Johns Hopkins University. Corresponding authors Franck Housseau and John Michel are affiliated with Johns Hopkins University, with Housseau also affiliated with the Cancer Research Center of Lille in France. Extracellular vesicles (EVs) are membrane-enclosed particles released by cells that transport proteins, lipids, nucleic acids, metabolites, and other molecular cargo. In cancer, tumor-derived extracellular vesicles (TEVs) can influence the tumor microenvironment and distant tissues by promoting processes such as angiogenesis, extracellular matrix remodeling, inflammatory signaling, immune evasion, and stromal reprogramming. Of particular interest is the role of TEVs in establishing premetastatic niches—biological environments in distant organs that become permissive to metastatic cells before overt tumors are detectable. TEVs can carry organ-specific molecular signals, and their surface molecules may influence which tissues they reach. For example, previous experimental research has linked the integrins α6β4 and α6β1 with lung tropism, providing a biological rationale for using TEVs to direct imaging probes toward metastasis-prone organs. This possibility could address an important limitation of conventional cancer imaging. Computed tomography and other anatomical methods are designed primarily to detect established structural lesions, whereas premetastatic niches are characterized by earlier molecular and microenvironmental alterations. The authors therefore examine whether TEV-associated imaging could provide information about metastatic conditioning before conventional imaging can identify overt metastatic lesions. Full press release - https://www.oncotarget.com/news/pr/tumor-derived-extracellular-vesicles-show-promise-for-earlier-detection-of-metastatic-risk/ DOI - https://doi.org/10.18632/oncotarget.28916 Correspondence to - Franck Housseau - fhousse1@jhmi.edu, and John Michel - jmiche14@jhmi.edu Abstract video - https://www.youtube.com/watch?v=0zygNvj4_YY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28916 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, lung metastases, cancer imaging, theranostic, premetastatic niches, extra-cellular vesicles 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

Why do we age? For decades, one of the dominant explanations has been that cells and tissues gradually accumulate molecular damage until they can no longer function normally. DNA mutations, damaged proteins, mitochondrial dysfunction, epigenetic alterations, and other forms of cellular wear have all been proposed as major drivers of aging. But another theory offers a very different possibility: some aspects of aging may result not from biological systems breaking down, but from developmental programs continuing to operate after they are no longer beneficial. A research perspective published in Volume 18 of Aging titled “A brief history of the hyperfunction theory of aging and future directions,” traces the development of this idea and examines where the field may go next. The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting a new experiment, the paper combines historical analysis, evolutionary theory, experimental evidence, and the author's own perspective on how programmatic models could reshape aging research. Full blog post - https://aging-us.org/2026/09/developmental-programs-could-help-drive-the-aging-process/ DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.info Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – August 31, 2026 – A new #editorial was published in Volume 17 of Oncotarget on June 8, 2026, titled “Tumor infiltrating lymphocyte (TIL) therapy for treating the solid tumors: Challenges and future perspectives.” The editorial was led by first and corresponding author Bhartendra Sharma from Mahatma Gandhi University of Medical Sciences and Technology, Jaipur, Rajasthan, India, along with co-authors Sukhbir Kaur, Vikas Sharma and Sanjay Soni. Tumor-infiltrating lymphocyte (TIL) therapy is a form of adoptive cellular therapy that uses immune cells naturally present within tumors to attack cancer. Unlike chimeric antigen receptor (CAR) T-cell therapy, which genetically modifies a patient's T cells to recognize specific tumor antigens and has achieved its greatest success in hematological malignancies, TIL therapy has shown potential in several types of solid tumors. The approach has a history spanning more than four decades. Steven Rosenberg first isolated TILs from a mouse tumor in 1982, and subsequent experiments demonstrated antitumor effects when TILs were combined with cyclophosphamide and interleukin-2 (IL-2). In 1988, Rosenberg and colleagues reported favorable clinical outcomes after administering TIL therapy to patients with metastatic melanoma. Full press release - https://www.oncotarget.com/news/pr/tumor-infiltrating-lymphocyte-therapy-offers-a-promising-approach-for-treating-solid-tumors/ DOI - https://doi.org/10.18632/oncotarget.28883 Correspondence to - Bhartendra Sharma - bhartendrasharma@mgumst.org Intro video - https://www.youtube.com/watch?v=QAr_R4WCJfk Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28883 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, tumor infiltrating lymphocytes, solid tumors, adoptive cellular therapy, immunotherapy 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 – August 28, 2026 – A new #research paper was published in Volume 17 of Oncotarget on August 19, 2026, titled “Incidence of KRAS G12C mutations in genitourinary malignancies; emerging target in precision medicine.” The study was led by first author Kelly Crane from the Department of Urology at SUNY Upstate Medical University. The corresponding author is K. R. Seetharam Bhat, who is affiliated with the Department of Urology at SUNY Upstate Medical University and Upstate Urology at MVHS. KRAS is one of the most extensively studied oncogenes in cancer, and the G12C variant has become clinically important following the development of mutation-specific inhibitors. Although KRAS G12C-targeted therapy is established in other malignancies, its frequency and genomic characteristics in genitourinary cancers have remained less well defined. To address this gap, the researchers performed comprehensive genomic profiling of 13,654 tumor specimens from patients with metastatic disease, including 1,453 renal clear cell carcinomas, 3,879 urothelial bladder carcinomas, and 8,322 prostate acinar adenocarcinomas. Tumor mutational burden, microsatellite instability, and PD-L1 expression were also evaluated. Across the full cohort, KRAS alterations were detected in 367 tumors, or 2.7%, while KRAS G12C was identified in only 25 tumors, representing approximately 0.2% of all specimens. No G12C variants were found among the renal clear cell carcinomas. In urothelial bladder carcinoma, 24 of 202 KRAS-altered tumors, or 12%, carried G12C, while only one of 158 KRAS-altered prostate tumors contained the variant. Full press release - https://www.oncotarget.com/news/pr/kras-g12c-mutation-identified-as-a-rare-potential-target-in-genitourinary-cancers/ DOI - https://doi.org/10.18632/oncotarget.28912 Correspondence to - K. R. Seetharam Bhat - bhatkuls@upstate.edu Abstract video - https://www.youtube.com/watch?v=me9HXtnDmp4 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28912 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, KRAS mutation, genitourinary malignancy, precision medicine, emerging target To learn more about the journal, 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 — August 26, 2026 — A new #review was #published in Volume 18 of Aging on August 10, 2026, titled “Metformin at the convergence of aging and longevity.” The review was authored by Jarra Manneh, May Alasmar and Nady El Hajj from the College of Health and Life Sciences at Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar. Corresponding author Nady El Hajj is also affiliated with the College of Science and Engineering at Hamad Bin Khalifa University, Doha, Qatar. Metformin has been used for decades as a first-line treatment for type 2 diabetes, but increasing interest in geroscience has raised a broader question: could this widely used metabolic drug also influence the biological processes that drive aging? The review brings together evidence from cellular studies, animal models, human observational research, and clinical trials examining how metformin interacts with multiple hallmarks of aging. A central mechanism involves AMP-activated protein kinase (AMPK), a major cellular energy sensor. By inhibiting mitochondrial complex I and altering cellular energy balance, metformin can activate AMPK, triggering downstream effects that include suppression of mechanistic target of rapamycin (mTOR) signaling, increased autophagy and mitochondrial biogenesis, and reduced oxidative stress. Metformin also improves insulin sensitivity and reduces hepatic gluconeogenesis, connecting its established metabolic effects with nutrient-sensing pathways involved in aging biology. Full press release - https://www.aging-us.com/news-room/metformin-emerges-as-a-promising-candidate-at-the-intersection-of-aging-and-longevity DOI - https://doi.org/10.18632/aging.206407 Corresponding author - Nady El Hajj - nelhajj@hbku.edu.qa Abstract video - https://www.youtube.com/watch?v=5Ws-x8e1klI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206407 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, metformin, AMPK, mTOR, epigenetic modifications To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – August 25, 2026 – A new precision oncology paper was #published in Volume 17 of Oncotarget on August 14, 2026, titled “Systematic methodological flaws in DNA contamination assessment of mRNA vaccines: A critical analysis of Achs et al. (2025).” The article was led by first and corresponding author Kevin McKernan from Medicinal Genomics, Beverly, Massachusetts, along with co-authors David J. Speicher from Cyrus Scientific Inc, Hamilton, Ontario, Canada, and Jessica Rose from Brownstone Institute, Austin, Texas. Rather than presenting a new experimental vaccine analysis, the paper critically examines the methodology used by Achs et al. in a 2025 study that reported no excessive residual DNA impurities in COVID-19 mRNA vaccines. McKernan and colleagues argue that several methodological choices in that study could systematically underestimate residual DNA and therefore limit its suitability for regulatory safety assessment. One major concern involves how quantitative PCR results were converted from DNA copy numbers into mass. Achs et al. used full-length plasmid molecular weight in their calculations even though their own sequencing data suggested much shorter median DNA fragment sizes. The critique argues that this approach requires fragmentation-correction factors because random DNA breakage can disrupt qPCR target regions and reduce the number of detectable amplicons. Without such correction, the authors contend that residual DNA mass may be underestimated. The paper also highlights the importance of primer and amplicon design. Achs et al. used qPCR targets with substantially different amplicon lengths, including shorter kanamycin-resistance targets and longer spike-encoding targets. Because the reported median DNA fragment sizes were approximately 130–201 base pairs, longer amplicons would be less likely to remain intact after fragmentation. The authors therefore argue that this design could preferentially reduce detection of spike-associated DNA relative to shorter plasmid regions. DOI - https://doi.org/10.18632/oncotarget.28913 Correspondence to - Kevin McKernan - Kevin.McKernan@medicinalgenomics.com Abstract video - https://www.youtube.com/watch?v=xSWS3HDQUus Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28913 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, mRNA vaccines, DNA contamination, qPCR; plasmid DNA, RNA:DNA hybrids 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

Pancreatic cancer remains one of the most difficult cancers to treat, in part because mutations in the KRAS gene are extraordinarily common in pancreatic ductal adenocarcinoma (PDAC). These mutations keep growth-promoting signals switched on, allowing cancer cells to proliferate and survive. Although drugs targeting certain KRAS mutations have emerged in recent years, they work against only a subset of mutant forms, leaving a need for strategies capable of targeting a broader range of KRAS-driven cancers. A research paper published in Volume 17 of Oncotarget, titled “The anticancer effects of PCAIs in pancreatic cancer cells involve MAPK and PI3K/AKT pathways hyperactivation,” investigated a class of experimental compounds known as polyisoprenylated cysteinyl amide inhibitors, or PCAIs. Rather than simply shutting down signaling pathways normally associated with cancer growth, the researchers uncovered a more unexpected effect: PCAIs pushed some of these pathways into unusually high activity while simultaneously promoting oxidative stress, disrupting cell structure, and triggering cancer cell death. Full blog post - https://www.oncotarget.org/2026/08/24/experimental-compounds-push-cancer-promoting-pathways-into-overdrive-in-pancreatic-cancer-cells/ 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 — August 24, 2026 — A new research paper was published in Volume 18 of Aging on August 8, 2026, titled “Investigating POLG-driven modulation of cancer stemness: a pilot study in breast cancer cells.” The study was led by first author Chiara Chinigò from the Italian National Research Center on Aging (IRCCS INRCA), Cosenza, Italy. Corresponding authors Federica Sotgia and Michael P. Lisanti are affiliated with the University of Salford, United Kingdom, and Lunella Biotech in Ottawa, Canada, with Lisanti additionally affiliated with the Institute of Mental Health Research at the University of Ottawa and The Royal Ottawa Hospital, and Université Laval in Québec. Breast cancer stem cells (CSCs) are a small population of tumor cells with self-renewal and differentiation capabilities that are associated with tumor progression, metastasis, and therapy resistance. These cells rely heavily on mitochondrial biogenesis and oxidative metabolism, making mitochondrial function a potential metabolic vulnerability. The researchers focused on mitochondrial DNA polymerase gamma (POLG), the enzyme responsible for mitochondrial DNA (mtDNA) replication and repair. POLG contains a catalytic subunit encoded by POLG1 and an accessory subunit encoded by POLG2. Using estrogen receptor-positive MCF-7 breast cancer cells, the researchers genetically silenced POLG1 and POLG2 to determine whether disrupting mtDNA maintenance would affect cancer stemness. POLG1 knockdown reduced mtDNA content by approximately 80%, while POLG2 knockdown produced an approximately 70% reduction. Both interventions impaired mitochondrial function, lowering the mtDNA-encoded respiratory-chain protein MTCO2, mitochondrial membrane potential, respiration, and ATP production. Full press release - https://www.aging-us.com/news-room/targeting-polg-reduces-breast-cancer-stemness-through-mitochondrial-dysfunction DOI - https://doi.org/10.18632/aging.206406 Corresponding authors - Federica Sotgia - fsotgia@gmail.com (ORCiD: 0000-0003-2826-4529), Michael P. Lisanti - michaelp.lisanti@gmail.com (ORCiD: 0000-0003-2034-1382) Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206406 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, breast cancer, cancer stem cells, cancer metabolism, POLG, mitochondrial DNA To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

A #Research paper recently #Published in Volume 18 of Aging, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b,” examines whether the senolytic PROTAC 753b can slow age-related intervertebral disc degeneration (IDD) in mice. Long-term systemic treatment with 753b reduced key features of disc degeneration in 22-month-old male mice, including matrix breakdown, loss of disc aggrecan, age-related structural changes, and inflammatory markers such as IL-6 and TNFα. These benefits, however, were not observed in female mice, highlighting potential sex-based differences in the role of cellular senescence in IDD and the response to senolytic therapies. DOI - https://doi.org/10.18632/aging.206394 Corresponding author - Nam Viet Vo - nvv1@pitt.edu Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — August 12, 2026 — A new #research paper was #published in Volume 18 of Aging on July 27, 2026, titled “Transcriptomic aging clock analysis identifies key genes in opioid dependence.” The study was led by first author Hai Duc Nguyen from the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University. The corresponding author is Woong-Ki Kim, who is affiliated with the Division of Microbiology, Tulane National Biomedical Research Center, Tulane University, and the Department of Microbiology and Immunology at Tulane University School of Medicine. Opioid dependence is a chronic and relapsing condition associated with substantial health and societal burdens. Chronic opioid exposure can affect neuronal signaling, immune function, metabolism, and other biological processes, yet the molecular mechanisms underlying dependence remain incompletely understood. Increasing evidence also suggests that substance use disorders may be associated with molecular changes related to aging, raising questions about how chronic opioid exposure interacts with age-dependent processes in the brain. To investigate these relationships, the researchers conducted an in silico study integrating three complementary approaches: RNA sequencing-based transcriptomic profiling, transcriptomic aging-clock modeling, and analysis of previously published genome-wide association studies (GWAS). The transcriptomic analysis used a publicly available brain RNA-seq dataset containing 42 samples—21 healthy controls and 21 individuals with opioid dependence—while the genetic analysis incorporated findings from six independent GWAS. Full press release - https://www.aging-us.com/news-room/transcriptomic-aging-clock-reveals-age-related-molecular-patterns-in-opioid-dependence DOI - https://doi.org/10.18632/aging.206405 Corresponding author - Woong-Ki Kim - wkim6@tulane.edu Abstract video - https://www.youtube.com/watch?v=7VwU0mFGkbg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206405 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, opioids, GWAS, transcriptomic clock To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Colorectal cancer does not develop in isolation. Cancer cells exist within a complex tumor microenvironment made up of fibroblasts, immune cells, blood vessels, and extracellular matrix. Increasing evidence suggests that these surrounding cells and structures can influence whether tumors grow, regress, or evade the immune system. A research paper published in Volume 17 of Oncotarget, titled “Microenvironmental CTHRC1 has a pro-tumorigenic role in colorectal cancer,” investigated the role of collagen triple helix repeat containing 1 (CTHRC1), a secreted protein found in cancer-associated stroma. Full blog post - https://www.oncotarget.org/2026/08/10/cthrc1-in-the-tumor-microenvironment-drives-colorectal-cancer-growth-in-mouse-study/ DOI - https://doi.org/10.18632/oncotarget.28878 Correspondence to: Sergey Ryzhov - Sergey.Ryzhov@mainehealth.org; Volkhard Lindner- Volkhard.Lindner@mainehealth.org; Michaela R. Reagan - Michaela.Reagan@mainehealth.org Abstract video - https://www.youtube.com/watch?v=gTbYy6vGd7E Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28878 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Cthrc1, CRC, colorectal cancer, subcutaneous tumor model, immune analysis To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – August 10, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on August 7, 2026, titled “Delayed growth of SK-ES-1 Ewing sarcoma tumor xenografts is associated with reduced Trk and IGF1R pathway markers.” The study was led by first author Bruna Almeida dos Santos and corresponding author Caroline Brunetto de Farias, primarily affiliated with the Federal University of Rio Grande do Sul and the National Science and Technology Institute for Children's Cancer Biology and Pediatric Oncology (INCT BioOncoPed), with de Farias also affiliated with the Children's Cancer Institute (ICI) in Brazil. The research team investigated whether targeting tropomyosin receptor kinase (Trk) and related signaling pathways could interfere with Ewing sarcoma growth. Ewing sarcoma is an aggressive cancer that primarily affects children and adolescents and can arise in bone or soft tissue. Although modern multimodal treatments have substantially improved outcomes for patients with localized disease, the prognosis remains considerably poorer for metastatic or relapsed Ewing sarcoma. This has driven efforts to identify molecular pathways that could provide additional therapeutic targets. One potential target involves the Trk family of receptor tyrosine kinases. TrkA, TrkB, and TrkC are encoded by the NTRK1, NTRK2, and NTRK3 genes, respectively, and regulate intracellular signaling pathways involved in cell survival, differentiation, and growth. Previous work from the research group showed that TrkA and TrkB are expressed in Ewing sarcoma and that blocking these receptors can reduce tumor-cell proliferation. Full press release - https://www.oncotarget.com/news/pr/trk-and-igf1r-related-signaling-linked-to-delayed-ewing-sarcoma-growth/ DOI - https://doi.org/10.18632/oncotarget.28911 Correspondence to - Caroline Brunetto de Farias - cbfarias@zielbiosciences.com Abstract video - https://www.youtube.com/watch?v=ZG-vhYfHjuw Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28911 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Ewing sarcoma, K252a, Trk, NTRK, insulin-like growth factor 1 receptor To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — August 10, 2026 — A new #essay was #published in Volume 18 of Aging on August 6, 2026, titled “Misha Blagosklonny: a life of ideas.” The article was written by Aging Editorial Board member David Gems from the Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, United Kingdom, along with Aging Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen, the Netherlands. Rather than presenting new experimental findings, the essay examines the life, scientific contributions, and lasting influence of Mikhail (“Misha”) Blagosklonny, whose ideas had a major influence on modern thinking about the biological mechanisms of aging. Dr. Blagosklonny was trained as a physician and experimental scientist before building an influential career in oncology and aging research after moving to the United States. His work combined cancer biology with theoretical biogerontology, leading to the proposal that aging is driven not primarily by the passive accumulation of molecular damage, but by developmental and growth-related programs that continue beyond their beneficial period. Through what he described as conceptual research, Misha synthesized evidence from diverse experimental studies to generate new hypotheses about aging and reinterpret existing biological observations. A central theme of the essay is Dr. Blagosklonny's development of the hyperfunction theory of aging. Building on observations that persistent activation of the mechanistic target of rapamycin (mTOR) pathway can drive cellular senescence, he proposed that many features of aging arise from the continued activity of biological programs that promote growth and reproduction earlier in life. Rather than viewing aging as an adaptive genetic program, Misha argued that it represents a quasi-program—a genetically determined continuation of normal developmental processes that become harmful later in life. This framework provided a mechanistic explanation linking evolutionary concepts such as antagonistic pleiotropy with molecular pathways that regulate growth, metabolism, and cellular senescence. Full press release - https://www.aging-us.com/news-room/misha-blagosklonnys-scientific-legacy-continues-to-shape-modern-aging-research DOI - https://doi.org/10.18632/aging.206412 Corresponding author - David Gems - david.gems@ucl.ac.uk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206412 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, hyperfunction, programmatic theory, disposable soma 2, quasi-program, biogerontology, evolutionary physiology, Mikhail Blagosklonny To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — August 6, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 24, 2026, titled “A brief history of the hyperfunction theory of aging and future directions.” The article was written by João Pedro de Magalhães from the Genomics of Ageing and Rejuvenation Lab, Department of Inflammation and Ageing, College of Medicine and Health, University of Birmingham, United Kingdom. Rather than presenting new experimental findings, the perspective examines the historical development of the hyperfunction theory of aging, reviews evidence supporting programmatic mechanisms of aging, and discusses future directions for understanding why organisms age and how aging might eventually be modified. For decades, most aging research has been dominated by the idea that aging results primarily from the gradual accumulation of molecular damage, including DNA damage, oxidative stress, mitochondrial dysfunction, and protein deterioration. In contrast, the hyperfunction theory proposes that aging is driven largely by developmental and growth programs that continue operating beyond their beneficial period. Rather than being intentionally programmed, aging is viewed as a consequence of biological pathways that promote growth and reproduction early in life but become harmful when they continue later in adulthood. The perspective traces the historical roots of these ideas from early theories proposed in the nineteenth century through Clive McCay's pioneering caloric restriction experiments and George Williams' concept of antagonistic pleiotropy. Particular attention is given to the contributions of the late Mikhail Blagosklonny, whose hyperfunction theory proposed that aging results from “quasi-programs”—developmental processes that fail to switch off after their normal biological role has ended. The author argues that this framework provides a mechanistic explanation linking evolutionary theory with many biological features of aging. Full press release - https://www.aging-us.com/news-room/hyperfunction-theory-offers-a-new-perspective-on-why-we-age Paper DOI - https://doi.org/10.18632/aging.206403 Corresponding author - João Pedro de Magalhães - jp@senescence.info Abstract video - https://www.youtube.com/watch?v=VwC6aJoUUQo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206403 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, antagonistic pleiotropy, longevity, programmatic aging, quasi-program To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

In this episode of the Longevity & Aging Series (S4, E5), Dr. Kan Cao of the Department of Cell Biology and Molecular Genetics at the University of Maryland joins host Dr. Yuan Zhao to discuss the research paper she co-authored in Volume 18 of Aging, titled “Methylene blue protects hair follicle stem cells from oxidative and metabolic stress to enhance hair regeneration.” Interview video - https://www.youtube.com/watch?v=2Por-Wh3AWo DOI - https://doi.org/10.18632/aging.206376 Corresponding author - Kan Cao - kcao@umd.edu Longevity & Aging Series - https://www.aging-us.com/longevity About Dr. Yuan Zhao - https://www.qmul.ac.uk/sbbs/staff/yuan-zhao.html Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206376 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, methylene blue, minoxidil, HFSCs, Wnt/β-catenin, GLP-1 RA To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — August 5, 2026 — A new #research paper was #published in Volume 18 of Aging on July 23, 2026, titled “Adipo-neuroinflammation, cognitive impairment and surrogate markers of cardiovascular risk in patients with Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD).” The study was led by co-first authors Gaetano Pacinella from the University of Palermo, and the Internal Medicine and Stroke Care Ward, Policlinico “P. Giaccone”, Palermo, and Alessandro Del Cuore from the same institutions. Gaetano Pacinella also served as the corresponding author. Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease, is increasingly recognized as a systemic condition that extends beyond the liver. People with MASLD have an elevated risk of cardiovascular disease, cognitive decline, and other metabolic complications, yet the biological mechanisms connecting these conditions remain incompletely understood. In this study, researchers investigated whether lipocalin-2 (LCN2), a protein involved in inflammatory and metabolic signaling, is associated with early vascular dysfunction, cognitive impairment, and cardiovascular risk in patients with MASLD. Full press release - https://www.aging-us.com/news-room/fatty-liver-disease-linked-to-early-cardiovascular-and-cognitive-changes DOI - https://doi.org/10.18632/aging.206397 Corresponding author - Gaetano Pacinella - gaetano.pacinella@unipa.it Abstract video - https://www.youtube.com/watch?v=CrqTayKl8KI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206397 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, metabolic dysfunction, cardiovascular risk, lipocalin-2, cognitive impairment, endothelial dysfunction To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Heart failure remains one of the leading causes of hospitalization among older adults worldwide. During episodes of acute decompensated heart failure (ADHF), excess fluid builds up in the lungs and body, making breathing difficult and increasing the risk of serious complications. Although intravenous loop diuretics such as furosemide are the standard treatment for relieving congestion, many patients continue to experience persistent inflammation, ongoing cardiac remodeling, and worsening heart function despite therapy. A research paper published in Volume 18 of Aging titled “Effects of intravenous furosemide plus small-volume hypertonic saline solutions on inflammatory, remodelling markers and epigenetics signatures of patients with congestive acute decompensated heart failure (ADHF),” investigated whether combining intravenous furosemide with small volumes of hypertonic saline solution (HSS) could improve biological markers associated with heart failure compared with furosemide alone. Full blog post - https://aging-us.org/2026/08/hypertonic-saline-plus-furosemide-improves-heart-failure-biomarkers-in-randomized-trial/ DOI - https://doi.org/10.18632/aging.206364 Corresponding author - Antonino Tuttolomondo - bruno.tuttolomondo@unipa.it Abstract video - https://www.youtube.com/watch?v=EG65XlcDJ3U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206364 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, heart failure, acute decompensated heart failure, furosemide, hypertonic saline solution To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — August 3, 2026 — A new #research paper was #published in Volume 18 of Aging on July 17, 2026, titled “Selective targeting of cancer and senescence via shared metabolic shifts extends lifespan of old mice.” The study was led by first author Zachery R. Robinson, and corresponding author and Aging editorial board member Irina M. Conboy, both from the Department of Bioengineering and QB3 Institute, University of California, Berkeley. The researchers developed a new combination therapy that selectively targets both cancer cells and senescent cells by exploiting metabolic vulnerabilities shared by these two cell types. In laboratory studies and aged mice, the treatment selectively eliminated senescent cells and reduced cancer cell viability while improving physical performance and extending lifespan without significant toxicity to healthy tissues. Cancer and aging are closely linked. As people age, senescent cells accumulate throughout the body. Although these cells no longer divide, they remain metabolically active and release inflammatory molecules known as the senescence-associated secretory phenotype (SASP), which contributes to chronic inflammation, tissue dysfunction, and tumor progression. Existing therapies such as the BCL-2/BCL-xL inhibitor navitoclax (ABT-263) can eliminate both cancer cells and senescent cells but require doses that frequently cause thrombocytopenia, a potentially serious reduction in platelet counts that has limited their clinical use. Full press release - https://www.aging-us.com/news-room/new-drug-combination-targets-cancer-and-senescent-cells-while-extending-lifespan-in-old-mice DOI - https://doi.org/10.18632/aging.206399 Corresponding author - Irina M. Conboy - irina@generationlab.co Abstract video - https://www.youtube.com/watch?v=7p5JMvy9Twg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206399 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, cancer, metabolic shift, ATP To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — July 30, 2026 — A new #research perspective was #published in Volume 18 of Aging on July 16, 2026, titled “Towards integration of healthspan strategies into the Italian National Health Service.” The article was led by co-first authors Nicola Marino, affiliated with the AEON Foundation and the Women's Brain Foundation, and Matteo Fiore from the University of Bologna, with both serving as corresponding authors. Rather than presenting new clinical trial results, the authors propose a prevention-focused framework for the staged, evidence-based evaluation and integration of healthspan strategies into Italy's National Health Service (Servizio Sanitario Nazionale, SSN) to help address the challenges of an aging population. Italy has one of the oldest populations in the world. Although life expectancy has continued to increase, many older adults spend a substantial portion of those additional years living with chronic disease, disability, or reduced physical and cognitive function. The authors describe this mismatch as the lifespan–healthspan divide and argue that healthcare systems should increasingly focus not only on helping people live longer, but also on extending the years they remain healthy and functionally independent. To address this challenge, the authors outline the concept of longevity medicine, describing it as a prevention-oriented, life-course framework rather than a new medical specialty. The approach integrates principles from geroscience, preventive medicine, and personalized healthcare with the goal of identifying age-related risks earlier and promoting healthy aging before chronic diseases and functional limitations accumulate. At the same time, the paper emphasizes that many emerging tools—including biological-age biomarkers, multi-omic profiling, wearable sensor data, and artificial intelligence-based risk stratification—remain exploratory and should not be adopted routinely until they demonstrate clear clinical utility, cost-effectiveness, and meaningful benefits for patients. Full press release - https://www.aging-us.com/news-room/italy-proposes-a-healthspan-focused-framework-for-healthy-aging DOI - https://doi.org/10.18632/aging.206402 Corresponding authors - Nicola Marino - marino@aeonfoundation.eu, and Matteo Fiore - matteo.fiore@auslromagna.it Abstract video - https://www.youtube.com/watch?v=uc1tGVfiHMw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206402 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, preventive, longevity, national health system, health span, biomarkers To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Nutrition plays a critical role in cancer care, yet it is often overlooked. Many patients experience weight loss, muscle wasting, treatment-related side effects, and changes in appetite that can affect their ability to tolerate therapy and maintain quality of life. Although nutrition specialists can help manage these challenges, access to specialized nutritional care remains limited in many healthcare settings. An editorial published in Volume 17 of Oncotarget, titled “Artificial intelligence in nutritional oncology: From isolated screening tools to agentic intervention systems,” explores how advances in artificial intelligence (AI) could help address this gap. The editorial was written by Arnab Sarkar and corresponding author Yashbir Singh-Wolkenhauer, who is affiliated with the Department of Radiology, Mayo Clinic, Rochester, Minnesota. Rather than presenting new clinical trial data, the authors outline a future vision in which AI systems move beyond isolated tasks to continuously support nutritional care throughout a patient's cancer journey. Full blog post - https://www.oncotarget.org/2026/07/28/artificial-intelligence-could-transform-nutrition-care-for-cancer-patients/ DOI - https://doi.org/10.18632/oncotarget.28874 Correspondence to - Yashbir Singh-Wolkenhauer - singh.yashbir@mayo.edu Abstract video - https://www.youtube.com/watch?v=sVKhRSr5xaY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28874 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, artificial intelligence To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — July 27, 2026 — A new #research paper was #published in Volume 18 of Aging on July 13, 2026, titled “Slowing intervertebral disc aging in mice through long-term systemic treatment with the senolytic BCL-2/BCL-xL proteolysis targeting chimera (PROTAC) 753b.” The study was led by first author Peter G. Alexander from the Ferguson Laboratory for Spine Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, and corresponding author Nam Viet Vo from the same institution. Intervertebral disc degeneration is a leading cause of chronic low back pain and disability. As discs age, they lose important structural components, become less able to absorb mechanical stress, and accumulate senescent cells—dysfunctional cells that stop dividing but continue releasing inflammatory molecules that contribute to tissue degeneration. Senolytic therapies, which selectively eliminate these cells, have emerged as a promising strategy to slow age-related diseases. In this study, researchers evaluated PROTAC 753b, a next-generation senolytic designed to target the anti-apoptotic proteins BCL-2 and BCL-xL while reducing the platelet toxicity associated with earlier drugs in this class. The researchers treated 16-month-old male and female mice with PROTAC 753b for six months and evaluated their intervertebral discs at 22 months of age using histology, molecular analyses, and measurements of inflammatory markers. The treatment significantly improved several measures of intervertebral disc health in aged male mice, preserving the extracellular matrix protein aggrecan and reducing matrix metalloproteinase (MMP)-mediated aggrecan breakdown, a hallmark of disc degeneration. In contrast, female mice showed little overall improvement, revealing a sex-specific response to treatment. Full press release - https://www.aging-us.com/news-room/senolytic-protac-slows-age-related-intervertebral-disc-degeneration-in-male-mice DOI - https://doi.org/10.18632/aging.206394 Corresponding author - Nam Viet Vo - nvv1@pitt.edu Abstract video - https://www.youtube.com/watch?v=t0z4MULDr1A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206394 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, intervertebral disc aging, cellular senescence, senolytic, anti-apoptosis, PROTAC-753b To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — July 23, 2026 — A new #research paper was #published in Volume 18 of Aging on July 8, 2026, titled “TM4SF1 is a surface marker of senescent pancreatic β-cells.” The study was led by first author Ana Beathriz Leite Lorente from Joslin Diabetes Center and Harvard Medical School, and São Paulo State University (UNESP), Brazil, and corresponding author Cristina Aguayo-Mazzucato from Joslin Diabetes Center and Harvard Medical School. Type 2 diabetes is characterized by insulin resistance and the progressive loss of pancreatic β-cell function. With aging and metabolic stress, senescent β-cells accumulate within the pancreas, producing less insulin while releasing inflammatory signals that contribute to disease progression. Although eliminating these dysfunctional cells has emerged as a promising therapeutic strategy, a major challenge has been identifying markers that distinguish senescent β-cells from healthy cells with sufficient precision. This study identifies transmembrane 4 L six family member 1 (TM4SF1) as a highly selective surface marker of senescent β-cells, providing a promising candidate for the future development of more selective therapies for type 2 diabetes. In this study, the researchers searched for cell-surface proteins that specifically identify senescent β-cells. Using RNA sequencing, flow cytometry, immunofluorescence, and analyses of both mouse and human pancreatic tissue, they compared TM4SF1 with the previously established senescence marker urokinase-type plasminogen activator receptor (uPAR/PLAUR). Their findings showed that TM4SF1 is expressed predominantly in senescent β-cells while exhibiting much lower expression in non-senescent β-cells and other tissues, making it a more β-cell-specific surface marker than uPAR. Full press release - https://www.aging-us.com/news-room/new-surface-marker-could-advance-precision-therapies-for-type-2-diabetes DOI - https://doi.org/10.18632/aging.206398 Corresponding author - Cristina Aguayo-Mazzucato - Cristina.aguayo-mazzucato@joslin.harvard.edu Abstract video - https://www.youtube.com/watch?v=tNbFKdleTJo Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206398 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescent β-cell, type 2 diabetes, transmembrane 4 l six family member 1, urokinase-type plasminogen activator receptor To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – July 22, 2026 – A new #PrecisionOncology paper was #Published in Volume 17 of Oncotarget on July 21, 2026, titled “WIN-MTB-2024017 – WIN International Molecular Tumor Board: A 48-year-old female with multiple primary cancers.” The study was led by Oncotarget Editor-in-Chief, Dr. Wafik S. El-Deiry, from the Worldwide Innovative Network (WIN) Association – WIN Consortium and Legorreta Cancer Center at Brown University. Patients who develop multiple primary cancers face unique diagnostic and treatment challenges because each tumor may have distinct biological characteristics requiring different therapeutic approaches. Advances in genomic profiling and precision oncology now enable clinicians to better distinguish between independent tumors and recurrent disease while identifying molecular alterations that may guide individualized treatment strategies. This case report demonstrates how an international molecular tumor board integrated comprehensive genomic data with multidisciplinary expertise to develop personalized recommendations for a patient with an exceptionally complex cancer history. The case describes the clinical journey of a 48-year-old woman carrying a germline BRCA1 mutation who developed multiple primary cancers over nearly two decades, including breast cancer, basal cell carcinoma of the skin, high-grade serous ovarian carcinoma, colon cancer, and small bowel adenocarcinoma. During this time, she underwent multiple surgeries, chemotherapy regimens, targeted therapy with the PARP inhibitor niraparib, and extensive molecular testing to characterize each malignancy. Full press release - https://www.oncotarget.com/news/pr/international-molecular-tumor-board-explores-personalized-treatment-strategies-for-a-patient-with-multiple-primary-cancers/ DOI - https://doi.org/10.18632/oncotarget.28899 Correspondence to - Wafik S. El-Deiry - wafik_el-deiry@brown.edu Abstract video - https://www.youtube.com/watch?v=4KIDbmq6ui8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28899 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, precision oncology, molecular tumor board To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — July 21, 2026 — A new #research paper was #published in Volume 18 of Aging on July 6, 2026, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.” The study was authored by Yash Flora, Dhriti Shastri, Kathryn R. DeLeo, and K. Adam Bohnert from the Department of Biological Sciences, Louisiana State University. Aging is accompanied by the gradual decline of many cellular structures that help maintain healthy tissues and organs. Among these are peroxisomes, which play essential roles in breaking down toxic molecules and metabolizing lipids, and mitochondria, which generate most of the cell's energy. Although these organelles work closely together, little has been known about how changes in one influence the aging of the other. This new study reveals that preserving peroxisomes helps maintain healthier mitochondria and extends lifespan in the nematode Caenorhabditis elegans, providing new insight into how communication between cellular organelles influences aging. In this study, the researchers investigated the function of PRX-11, a peroxisomal protein involved in peroxisome division. Previous work from the group showed that reducing PRX-11 activity prevents the age-related degradation of peroxisomes through a process known as pexophagy and increases lifespan. The new study explored why preserving peroxisomes produces these beneficial effects and found that maintaining peroxisomes also preserves mitochondrial health during aging. The researchers found that animals with reduced PRX-11 activity retained long, interconnected mitochondrial networks that resembled those seen in young adults, whereas normal aging was associated with progressive mitochondrial fragmentation. These preserved mitochondria also accumulated less calcium, generated lower levels of oxidative stress, maintained higher ATP-to-ADP ratios, and were associated with improved locomotor function in older animals. Together, these findings indicate that preventing age-related peroxisome loss supports multiple aspects of mitochondrial function during aging. Full press release - https://www.aging-us.com/news-room/preserving-peroxisomes-helps-maintain-mitochondrial-health-and-extend-lifespan-in-c-elegans DOI - https://doi.org/10.18632/aging.206395 Corresponding author - K. Adam Bohnert - bohnerta@lsu.edu Abstract video - https://www.youtube.com/watch?v=fbcqBsP90CY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206395 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular aging, lifespan, pexophagy, mitochondrial tubulation, inter-organelle crosstalk To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Coordinating both hands is something most people take for granted. Everyday activities such as buttoning a shirt, preparing a meal, driving, or using a knife and fork all depend on the brain's ability to precisely control movements on both sides of the body. As people age, however, these tasks often become more difficult, especially when they require both hands to perform different movements at the same time. A research paper published in Volume 18 of Aging titled “Age-specific relationship between the modulation of brain dynamics in response to task demands and bimanual performance,” investigated how aging affects the brain's ability to adapt to increasingly complex hand-coordination tasks. The study was led by first author Sara Magalhães Ferreira from Hasselt University, with corresponding author Koen Cuypers from Hasselt University and KU Leuven. Full blog - https://aging-us.org/2026/07/brain-flexibility-is-linked-to-hand-coordination-during-aging/ DOI - https://doi.org/10.18632/aging.206363 Corresponding author - Koen Cuypers - koen.cuypers@uhasselt.be Abstract video - https://www.youtube.com/watch?v=3TbcGFCZV9s Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206363 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, bimanual coordination, Bimanual Tracking Task, BOLD variability, task modulation To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

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 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

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 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 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

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