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BUFFALO, NY - May 21, 2025 – A new #review was #published in Volume 16 of Oncotarget on May 19, 2025, titled “Advancements in bladder cancer treatment: The synergy of radiation and immunotherapy." Researchers from the University of California, Irvine, led by Nazmul Hasan, reviewed recent clinical and scientific advances in combining radiation therapy with immunotherapy for bladder cancer. The article summarizes growing evidence that this combined approach may strengthen the immune response and improve long-term disease control. This strategy is especially important for patients who are not candidates for surgery or who respond poorly to conventional treatments. Bladder cancer is a serious and frequent condition, particularly affecting older men. Traditional treatments—surgery, chemotherapy, and radiation—can be effective, but they often fail to prevent cancer reappearance in advanced cases. The review explores how combining radiation and immunotherapy could improve outcomes by helping the immune system detect and destroy cancer cells more effectively. Radiation therapy destroys cancer cells and triggers the release of tumor signals that attract immune cells. Immunotherapy, including drugs like pembrolizumab and nivolumab, helps the immune system work better by blocking proteins that allow cancer to evade detection. Used together, these treatments may produce a stronger, more widespread anti-tumor effect, even at distant sites not directly targeted by radiation. The review discusses several clinical trials that support this approach. One phase II study reported that combining radiation with the immunotherapy drug durvalumab led to promising survival rates and manageable side effects. Another trial in Australia tested pembrolizumab with radiation and chemotherapy, resulting in high tumor control and extended patient survival. However, the review also points out that other trials showed serious side effects when high doses or multiple immunotherapy drugs were used at once. "Joshi et al. performed a phase II study to determine the safety and efficacy of combining radiation therapy with durvalumab, a PD-L1 inhibitor, in patients who were ineligible for surgery or cisplatin-based chemotherapy." While the combination approach is promising, the authors emphasize that more research is needed to refine this treatment strategy. One major challenge is determining which patients are most likely to benefit. Future studies should focus on identifying reliable biomarkers, such as tumor mutation burden or immune activity, to guide personalized treatment plans. This review highlights the potential of combining radiation and immunotherapy to improve outcomes for bladder cancer patients. With continued research and careful treatment design, this approach could offer new treatment options for those facing aggressive or hard-to-treat forms of the disease. DOI - https://doi.org/10.18632/oncotarget.28723 Correspondence to - Nazmul Hasan - nhasan1@hs.uci.edu Video short - https://www.youtube.com/watch?v=AxrZhIUXrOQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28723 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, bladder cancer, immunotherapy, radiation, microenvironment, abscopal 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

Scientists have engineered small, targeted proteins that can penetrate brain cancer cells and prevent them from invading healthy tissue, offering a promising new approach to treating glioblastoma multiforme (GBM), one of the deadliest forms of brain cancer. This strategy was developed by researchers at the University of Nevada, Reno, and published recently in Oncotarget. The Challenge of Treating Glioblastoma Multiforme Glioblastoma is an aggressive and fast-growing brain tumor that infiltrates healthy brain tissue, making complete surgical removal nearly impossible. Standard treatments like chemotherapy and radiation can slow its growth but rarely prevent it from returning. One major reason for this invasiveness is a group of enzymes known as matrix metalloproteinases (MMPs), which break down surrounding tissue to allow cancer cells to spread. Among these, MMP-9 plays a particularly important role in driving tumor progression and resisting existing therapies. Attempts to block MMPs using small-molecule drugs have failed in clinical trials due to problems like poor selectivity and harmful side effects. Researchers have been searching for safer, more targeted methods to interfere with these enzymes and limit glioblastoma's spread. The Study: Engineered Proteins to Inhibit Tumor Invasion In the study called “Effect of TIMPs and their minimally engineered variants in blocking invasion and migration of brain cancer cells,” researchers Elham Taheri and Maryam Raeeszadeh-Sarmazdeh investigated tissue inhibitors of metalloproteinases (TIMPs), which are natural blockers of MMPs, and their engineered modified versions made to work better. Specifically, the team studied TIMP-1, TIMP-3, along with two engineered molecules, mTC1 and mTC3, in laboratory cell models of GBM. Full blog - https://www.oncotarget.org/2025/05/21/engineered-proteins-show-promise-in-stopping-glioblastoma-invasion/ Paper DOI - https://doi.org/10.18632/oncotarget.28691 Correspondence to - Maryam Raeeszadeh-Sarmazdeh - maryamr@unr.edu Video short - https://www.youtube.com/watch?v=tdBlkOX50D8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28691 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, TIMP minimal variants, glioblastoma multiforme (GBM), brain cancer, MMP inhibitors 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

In this #episode of the Longevity & Aging Series, Dr. Shubhankar Suman from the Department of Oncology at Georgetown University Medical Center joins host Dr. Evgeniy Galimov to discuss a #research paper he co-authored in Volume 17, Issue 1 of Aging (Aging-US), titled: “Senolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in Apc1638N/+ mice.” DOI - https://doi.org/10.18632/aging.206183 Corresponding author - Shubhankar Suman - ss2286@georgetown.edu Author interview - https://www.youtube.com/watch?v=ClLO0ERwC0M Video short - https://www.youtube.com/watch?v=M_WEht4vy4w Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206183 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence-associated secretory phenotype, senolytic agent, carcinogenesis, inflammation, β-catenin To learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - May 14, 2025 – A new #review paper was #published in Volume 16 of Oncotarget on May 9, 2025, titled “Relationship between ABO blood group antigens and Rh factor with breast cancer: A systematic review and meta-analysis." A comprehensive study, led by first authors Rahaf Alchazal from Yarmouk University and Khaled J. Zaitoun from Johns Hopkins University School of Medicine and Jordan University of Science and Technology, examined the potential link between blood type and breast cancer. The research team conducted a systematic review and meta-analysis of 29 previously published studies, involving more than 13,000 breast cancer patients and over 717,000 controls. “Researchers searched for studies on breast cancer patients and ABO blood groups across four major databases: PubMed, Scopus, Web of Science, and Google.“ Breast cancer is the most common cancer among women worldwide. Identifying risk factors is vital for early detection and prevention. While many studies have explored lifestyle and genetic causes, this analysis focused on the ABO blood group system. By pooling global data, the researchers found that blood type A was the most common among breast cancer patients and was significantly associated with an 18% increased risk compared to type O. The study did not find a significant association between breast cancer and blood types B, AB, or Rh factor. Although the results do not prove causation, they point to a biological pattern worth further investigation. Blood group antigens are proteins found on the surface of cells, including breast tissue. These molecules may influence how cancer develops and spreads by interacting with the immune system or affecting cell behavior. This meta-analysis is the most extensive review to date on this topic, based on studies conducted across Asia, Europe, Africa, and the Americas. While previous research found unclear conclusions, this large-scale evaluation provides stronger evidence for a possible connection between blood type A and breast cancer risk. Researchers note that regional differences, genetic diversity, and study quality may affect individual results. Nevertheless, the overall trend supports considering blood type A as a potential risk marker. This insight could help shape screening guidelines, encouraging earlier or more frequent checkups for women with this blood type. Further research is needed to understand why blood type A may play a role in cancer development. Future studies may explore genetic mechanisms, immune responses, and other biological pathways. These efforts could lead the way for more personalized cancer prevention and care strategies. DOI - https://doi.org/10.18632/oncotarget.28718 Correspondence to - Khaled J. Zaitoun - kzaitou1@jh.edu Video short - https://www.youtube.com/watch?v=BQFVtreaetI Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28718 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, breast cancer, cancer risk factors, blood group antigens, tumor To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — May 14, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 10, 2025, titled “Impact of Factor Xa inhibitors on cardiovascular events in older patients with nonvalvular atrial fibrillation.” In this study, first author Masahiko Takahashi and corresponding author Keisuke Okawa led a research team from Kagawa Prefectural Central Hospital and Hyogo Medical University that investigated whether Factor Xa inhibitors (Xa-Is)—a type of blood thinner—can reduce the risk of heart-related complications in patients over 80 with nonvalvular atrial fibrillation (NVAF). The study found that patients using Xa-Is experienced significantly fewer cardiovascular problems than those on other anticoagulants. This finding is especially relevant, as older adults face a high risk of both stroke and heart disease. Atrial fibrillation is a common heart rhythm disorder, particularly in the elderly, that increases the risk of blood clots, heart failure, and stroke. Anticoagulants are often prescribed to prevent clots, but not all types have the same effects on heart health. This study focused on comparing Xa-Is—specifically rivaroxaban, apixaban, and edoxaban—with commonly used drugs such as warfarin and dabigatran. Researchers followed more than 1,000 patients aged 80 and above for up to five years to assess the long-term impact of these medications on cardiovascular outcomes. Patients who used Xa-Is had significantly lower rates of heart failure, artery disease, and cardiovascular death. The risk of cardiovascular problems in the Xa-I group was less than half that of those on non-Xa-I medications. These benefits remained even after adjusting for factors like age, existing heart conditions, and kidney function. Additionally, stroke and all-cause death rates were notably lower in the Xa-I group. “Xa-Is may be useful for not only anticoagulation but also the prevention of cardiovascular events in very old patients with NVAF.” What makes Xa-Is different, according to the researchers, is their ability to inhibit a specific biological pathway—known as Factor Xa–PAR2—that contributes to inflammation, fibrosis, and damage in blood vessels and heart tissue. This effect extends beyond their traditional role in preventing blood clots. Although the study was conducted at a single medical center in Japan, its rigorous design and long follow-up period enhance the reliability of the findings for real-world clinical decision-making. While further studies, especially across multiple centers, are needed to confirm the full range of benefits, this study strongly suggests that Xa-Is may offer broader cardiovascular protection for very old patients. The findings could influence how clinicians choose blood thinners for elderly individuals with atrial fibrillation, potentially improving both survival and quality of life in this growing population. DOI - https://doi.org/10.18632/aging.206238 Corresponding author - Keisuke Okawa - k-ookawa@chp-kagawa.jp Video short - https://www.youtube.com/watch?v=YtbYpfVDVDI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206238 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Factor Xa inhibitor, atrial fibrillation, older patient, cardiovascular events To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Werner syndrome is a rare condition marked by accelerated aging. A recent study, featured as the cover paper in Aging (Aging-US), Volume 17, Issue 4, led by researchers at the University of Oslo and international collaborators, suggests that nicotinamide adenine dinucleotide (NAD+), a vital molecule involved in cellular energy production, may be key to understanding this disease and developing future strategies to manage it. Understanding Werner Syndrome Werner syndrome (WS) is a rare genetic condition that causes people to age more quickly than normal. By their 20s or 30s, individuals with WS often show signs typically associated with older age, such as cataracts, hair loss, thinning skin, and heart disease. This premature aging is caused by mutations in the WRN gene, which normally helps repair DNA and protect cells from damage. While the WRN gene's role in maintaining genetic stability is well understood, the reasons behind the rapid decline of cells in WS patients are still not fully clear. The Study: Investigating NAD+ in Werner Syndrome Nicotinamide adenine dinucleotide levels naturally decline with age. In the study titled “Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation,” researchers investigated whether this decline is more severe in people with WS and whether restoring NAD+ levels could help slow the aging process in these patients. Full blog - https://aging-us.org/2025/05/fighting-premature-aging-how-nad-could-help-treat-werner-syndrome/ Paper DOI - https://doi.org/10.18632/aging.206236 Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.no Video short - https://www.youtube.com/watch?v=WpRpi8TYPfU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206236 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferation To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - May 9, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on May 8, 2025, titled “METTL3 promotes oral squamous cell carcinoma by regulating miR-146a-5p/SMAD4 axis." In this study, researchers Jayasree Peroth Jayaprakash, Pragati Karemore, and Piyush Khandelia from the Birla Institute of Technology and Science, India, discovered that a molecule called METTL3 contributes to the development and spread of oral squamous cell carcinoma (OSCC). The study shows that METTL3 increases the levels of a small RNA molecule called miR-146a-5p, which blocks SMAD4, a key tumor-suppressing gene. These findings help explain why oral cancers are difficult to treat and may offer a new target for more effective therapies. Oral squamous cell carcinoma is a common and aggressive cancer affecting the mouth and throat. It has a high death rate, mainly due to late detection, treatment resistance, and the cancer's ability to invade nearby tissues. In this study, the researchers focused on METTL3, an enzyme that adds chemical tags known as m6A marks to RNA, which change how genetic information is used by cells. They found that METTL3 is unusually active in OSCC cells, causing an increase in miR-146a-5p. This molecule, in turn, blocks the function of SMAD4, which helps control how cells grow and die in our bodies. “METTL3, the primary m6A RNA methyltransferase, is significantly upregulated in OSCC cells leading to increased global m6A levels.” When METTL3 was reduced or chemically blocked, miR-146a-5p levels dropped and SMAD4 levels increased. This shift slowed the growth of cancer cells, increased their death, and made them less likely to spread. When researchers reintroduced miR-146a-5p or lowered SMAD4 levels again, the cancer-promoting behavior returned. These results show that the METTL3–miR-146a-5p–SMAD4 pathway plays a key role in OSCC. The findings open up new possibilities for treatment. Drugs that block METTL3 or miR-146a-5p or that restore SMAD4 could slow or stop tumor growth. One such drug, STM2457, which targets METTL3, has already shown promise in lab studies. As research progresses, targeting this molecular pathway may offer a new strategy in treating OSCC. This discovery improves our understanding of how OSCC develops and avoids the body's defenses. By interfering with this newly discovered pathway, future treatments may become more successful, improving survival rates and quality of life for people with this disease. DOI - https://doi.org/10.18632/oncotarget.28717 Correspondence to - Piyush Khandelia - piyush.khandelia@hyderabad.bits-pilani.ac.in Video short - https://www.youtube.com/watch?v=o5XuDlcIma8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28717 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ 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

A recent #study from Assiut University Hospital in Egypt, published in #Oncotarget, presents a promising strategy for patients with metastatic #colorectalcancer (mCRC). The #research introduces a gentler yet effective maintenance therapy that may extend survival, enhance quality of life, and offer a more accessible treatment option for mCRC patients worldwide. The Challenge of Treating Metastatic Colorectal Cancer Colorectal cancer is one of the most common causes of cancer-related deaths worldwide. When it spreads to other parts of the body—a stage known as mCRC—it becomes much more difficult to treat. At this stage, clinicians often use strong drug combinations like FOLFOX or CAPOX, which mix chemotherapy drugs to stop cancer growth. FOLFOX combines three drugs given intravenously, while CAPOX includes two of the same drugs, with one taken as a pill. While effective, these treatments can cause serious side effects. For example, one of the main drugs, oxaliplatin, can lead to nerve damage, making it painful or difficult to use the hands and feet. Fatigue, diarrhea, and other issues are also common. Over time, these side effects may force clinicians to stop or adjust the treatment, even if it is working. That is where maintenance therapy comes in. After the cancer is controlled, clinicians often switch to a gentler treatment plan to keep it from returning. The challenge is finding a therapy that continues to work without causing too many side effects, especially in places where access to expensive or intensive treatments is limited. Full blog - https://www.oncotarget.org/2025/05/07/panitumumab-and-low-dose-capecitabine-a-promising-maintenance-therapy-for-metastatic-colorectal-cancer/ Paper DOI - https://doi.org/10.18632/oncotarget.28687 Correspondence to - Doaa A. Gamal - doaaalygamaal@gmail.com Video short - https://www.youtube.com/watch?v=wuPSS0EdK-8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28687 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, Panitumumab, maintenance, colorectal cancer, Capecitabine About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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 — May 1, 2025 — A new #research paper was #published in Aging (Aging-US) on April 2, 2025, as the #cover of Volume 17, Issue 4, titled “Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.” In this study, the team led by first author Sofie Lautrup and corresponding author Evandro F. Fang, from the University of Oslo and Akershus University Hospital in Norway, discovered that cells from people with Werner syndrome (WS)—a rare genetic disorder that causes premature aging—have low levels of a molecule called NAD+ in their mitochondria. This molecule is essential for energy production, cellular metabolism, and maintaining cell health. The researchers also found a potential way to improve cell function in WS patients, pointing to new directions for treating age-related decline and other premature aging disorders. Werner syndrome leads to signs of aging much earlier than normal, including problems such as cataracts, hair loss, and atherosclerosis by age 20 to 30. The team found that when the WRN gene is missing or damaged, cells cannot maintain healthy NAD+ levels in their mitochondria. As a result, the cells age more quickly and stop growing properly. When the researchers boosted NAD+ levels using nicotinamide riboside (a vitamin B3 compound) the affected stem cells and skin cells from patients showed less aging and improved mitochondrial activity. “Interestingly, only 24 h treatment with 1 mM nicotinamide riboside (NR), an NAD+ precursor, rescued multiple pathways in the WRN−/− cells, including increased expression of genes driving mitochondrial and metabolism-related pathways, as well as proliferation-related pathways.” The study also found that the WRN gene helps regulate other important genes that control how NAD+ is made in the body. Without WRN, this system becomes unbalanced, which affects how cells function, grow, and respond to stress. Although adding more NAD+ helped some cells look healthier, it could not completely fix the growth problems in other types of lab-grown cells. This suggests that while NAD+ supplementation is beneficial, it cannot fully replace the essential functions of the WRN gene. These findings offer new insights into the biological mechanisms of aging and reinforce the therapeutic potential of targeting NAD+ metabolism in age-related and genetic diseases. Future studies will aim to better understand how subcellular NAD+ regulation interacts with mutations like those seen in WS. Finally, this research supports ongoing efforts to develop NAD+-based treatments that could slow cellular aging and improve quality of life for patients with premature aging conditions. DOI - https://doi.org/10.18632/aging.206236 Corresponding author - Evandro F. Fang - e.f.fang@medisin.uio.no Video short - https://www.youtube.com/watch?v=WpRpi8TYPfU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206236 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner syndrome, premature aging, NAD+, mitochondria, proliferation To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

In this #episode of the Longevity & Aging Series, Dr. Stephen Vatner from the Department of Cell Biology and Molecular Medicine at Rutgers New Jersey Medical School, joins host Dr. Evgeniy Galimov to discuss a #research perspective he co-authored in Volume 16, Issue 22 of Aging (Aging-US), titled “Brown adipose tissue enhances exercise performance and healthful longevity.” DOI - https://doi.org/10.18632/aging.206179 Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu Author interview - https://www.youtube.com/watch?v=-DE4H2DtSZg Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14 To learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — April 23, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 18, 2025, titled “Epigenetic and accelerated age in captive olive baboons (Papio anubis), and relationships with walking speed and fine motor performance.” In this study, led by Sarah J. Neal from The University of Texas MD Anderson Cancer Center, researchers examined how the epigenetic age of baboons—a measure of biological aging based on DNA methylation—compared to their actual age (chronological age) and whether it related to signs of aging like slower walking or reduced hand coordination. While many baboons showed a mismatch between their epigenetic and chronological ages, these differences did not consistently align with physical performance measures. Researchers analyzed blood samples from 140 captive olive baboons (Papio anubis) to determine whether these primates, like humans, show signs of “age acceleration”—a condition where epigenetic age surpasses chronological age. The results revealed that about a quarter of the baboons exhibited accelerated aging, while another quarter showed signs of slower aging, known as “age deceleration.” “We found that epigenetic age was strongly correlated with chronological age, and that approximately 27% of the sample showed age acceleration and 28% showed age deceleration." The scientists then investigated whether these differences were reflected in physical indicators such as walking speed or fine motor skills. To do this, researchers measured walking speed by tracking how quickly baboons moved between points in their enclosures and assessed fine motor skills using a simple task that involved picking up small objects. Older baboons did tend to walk more slowly and perform worse on tasks requiring dexterity, patterns also seen in aging humans. However, these changes were more closely related to chronological age than epigenetic age. Two different methods were used to measure the gap between epigenetic and chronological age. Each method produced slightly different outcomes, highlighting the complexity of defining age acceleration. In one analysis, the oldest baboons appeared to age more slowly epigenetically, possibly reflecting selective survival, where only the healthiest individuals live into old age. This research is among the first to classify baboons based on their epigenetic aging rate and investigate how this links to real-world signs of aging. Although the findings did not provide clear evidence that epigenetic age acceleration leads to physical decline, they point to the importance of DNA methylation as a biomarker in aging research. Because baboons share many biological similarities with humans, these findings help refine how researchers measure aging and assess potential early warning signs of decline. Continued studies in baboons and other primates may improve our understanding of how epigenetic aging influences health and longevity—and could help develop better tools for predicting age-related decline in humans. DOI - https://doi.org/10.18632/aging.206223 Corresponding author - Sarah Neal - SJNeal@MDAnderson.org Video short - https://www.youtube.com/watch?v=EFfRMFbAMqk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206223 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

A new study from the Sidney Kimmel Comprehensive Cancer Center and Johns Hopkins University School of Medicine, published in Oncotarget, reveals that the gene p53, long known as the “guardian of the genome,” may be even more powerful than previously thought. By studying it in non-cancerous human cells, researchers discovered how p53 stops risky cell growth and uncovered two new potential targets for cancer therapy. Understanding p53: The Genome's Guardian Against Cancer The p53 gene is one of the most important natural defenses our body has against cancer. When functioning properly, p53 detects damage in a cell's DNA and either stops the cell from dividing or pushes it to self-destruct. This process helps prevent potentially dangerous mutations from spreading. However, many cancers find ways to silence or mutate p53, allowing uncontrolled growth and resistance to treatments. Studying p53 in a clear and accurate way has long been a challenge. Most cancer cell models used in research already carry numerous genetic mutations, which can mask or alter how p53 truly functions. To fully understand this vital tumor-suppressing gene, scientists needed a model that closely resembled healthy, genetically stable human cells—yet could still be maintained and studied over time in the laboratory. The Study: Exploring p53 in Normal and Cancer Cell Models Researchers Jessica J. Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J. Munoz, and Fred Bunz explored p53 activity using a uniquely suitable cell line: hTERT-RPE1. These non-cancerous human cells are immortalized using telomerase, meaning they continue dividing like cancer cells, but without the chaotic mutations seen in tumors. This makes them an excellent model for studying how p53 operates in near-normal conditions. Full blog - https://www.oncotarget.org/2025/04/22/new-insights-into-p53-a-powerful-genes-role-in-cancer-therapy/ Paper DOI - https://doi.org/10.18632/oncotarget.28690 Correspondence to - Fred Bunz - fredbunz@jhmi.edu Video short - https://www.youtube.com/watch?v=Psxj3ctbTuk Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28690 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, p53, ionizing radiation, immortalized cells, ALDH3A1, NECTIN4 About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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

The Times Higher Education recently reported that Bluesky has overtaken X in hosting posts related to new academic research. And yet many Medical Affairs teams aren't equipped to maximize the potential of this emerging resources. Here we speak with Mike Taylor, Head of Data Insights, at Altmetric, and Carlos Areia, Senior Data Scientist at Altmetric about the uses of Bluesky in comparison with exiting social media platforms, and how Medical Affairs can leverage this resource for insights, KOL identification/mapping, data dissemination and more. 

BUFFALO, NY — April 16, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 12, 2025, titled “DNA methylation entropy is a biomarker for aging.” Researchers Jonathan Chan, Liudmilla Rubbi, and Matteo Pellegrini from the University of California, Los Angeles, led a study that discovered a new way to measure changes in DNA that can help predict a person's age. This method focuses on how random certain chemical tags on DNA become over time. The team compared this new measurement, called methylation entropy, to existing methods and found it performed just as well—or even better. These findings support the idea that changes in our epigenetic information are closely linked to aging and could offer new tools for studying age-related diseases. The study focused on DNA methylation, a process where chemical marks are added to DNA and help control which genes are turned on or off. Scientists have traditionally measured average methylation levels to estimate biological age using “epigenetic clocks.” This study, however, takes a different approach. The researchers used buccal swabs (cells from inside the cheek) from 100 individuals between ages 7 and 84 and applied targeted bisulfite sequencing techniques to measure methylation entropy across 3,000 regions of the genome. Entropy in this context reflects how disordered or varied the methylation patterns are at certain sites on the DNA. The researchers discovered that as people age, the entropy of methylation at many locations changes in a reproducible way. Sometimes it increases, reflecting more random patterns, and sometimes it decreases, showing more uniformity. These shifts are not always tied to how much methylation is happening, which suggests entropy provides new information beyond what traditional methods can offer. To test how well this new metric could predict age, the team used both statistical and machine learning models. They found that methylation entropy predicted age as accurately as traditional methods, and the best results came from combining entropy with other measurements like average methylation and a method called CHALM. These combined models were able to estimate age with an average error of just five years. "[...] methylation entropy is measuring different properties of a locus compared to mean methylation and CHALM, and that loci can become both more or less disordered with age, independently of whether the methylation is increasing or decreasing with age." This research supports the growing theory that aging is partly caused by a gradual loss of epigenetic information—the biological “instructions” that help keep our cells working properly. This insight also connects with recent studies suggesting that restoring this lost information might reverse some signs of aging. While more research is needed to study methylation entropy in other tissues, this work points to a more precise and powerful way to measure biological aging, which could influence the future of aging-related treatments and therapies. Read the full paper: DOI: https://doi.org/10.18632/aging.206220 Corresponding author: Matteo Pellegrini - matteope@gmail.com Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206220 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords: entropy, DNA methylation, aging, epigenetics, epigenetic clocks To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Breast cancer survivors are living longer than ever, thanks to research and medical advances, but new studies suggest that some treatments may come with a hidden cost: accelerated aging. A recent study, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors,” published in Aging (Aging-US), reveals that breast cancer and its treatments may speed up biological aging, with effects lasting up to a decade post-diagnosis. Breast Cancer and Aging Breast cancer is one of the most common cancers among women worldwide. Medical advancements have dramatically improved survival rates, making it one of the most treatable forms of cancer. Yet, many survivors report lasting symptoms like fatigue, memory issues, and reduced vitality that resemble accelerated aging. This pattern has led scientists to investigate whether treatments for breast cancer might be contributing to biological age acceleration. Full blog - https://aging-us.org/2025/04/breast-cancer-treatments-hidden-impact-accelerated-aging-among-survivors/ Paper DOI - https://doi.org/10.18632/aging.206218 Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org Video short - https://www.youtube.com/watch?v=cfuyzVyDeHY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206218 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, accelerated aging, PhenoAge, breast cancer, survivors Visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Paula Cilleros-Holgado from Pablo de Olavide University discusses a #research paper she co-authored that was #published in Volume 17, Issue 2 of Aging (Aging-US), entitled “Mitochondrial dysfunction, iron accumulation, lipid peroxidation, and inflammasome activation in cellular models derived from patients with multiple sclerosis.” DOI - https://doi.org/10.18632/aging.206198 Corresponding author - José Antonio Sánchez-Alcázar - jasanalc@upo.es Video interview - https://www.youtube.com/watch?v=wIV0lAHPA_M Abstract Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Despite advancements in managing relapsing active illness, effective treatments for the irreversible progressive decline in MS remain limited. Research employing skin fibroblasts obtained from patients with neurological disorders revealed modifications in cellular stress pathways and bioenergetics. However, research using MS patient-derived cellular models is scarce. In this study, we collected fibroblasts from two MS patients to investigate cellular pathological alterations. We observed that MS fibroblasts showed a senescent morphology associated with iron/lipofuscin accumulation and altered expression of iron metabolism proteins. In addition, we found increased lipid peroxidation and downregulation of antioxidant enzymes expression levels in MS fibroblasts. When challenged against erastin, a ferroptosis inducer, MS fibroblasts showed decreased viability, suggesting increased sensitivity to ferroptosis. Furthermore, MS fibroblasts presented alterations in the expression levels of autophagy-related proteins. Interestingly, these alterations were associated with mitochondrial dysfunction and inflammasome activation. These findings were validated in 7 additional patient-derived cell lines. Our findings suggest that the underlying stress phenotype of MS fibroblasts may be disease-specific and recapitulate the main cellular pathological alterations found in the disease such as mitochondrial dysfunction, iron accumulation, lipid peroxidation, inflammasome activation, and pro-inflammatory cytokine production. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206198 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, multiple sclerosis, iron accumulation, lipid peroxidation, inflammasome, mitochondrial dysfunction To learn more about Aging (Aging-US), please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Despite decades of research, treatment for osteosarcoma has remained largely unchanged, especially for patients whose cancer spreads or returns. However, a growing body of evidence, summarized in the review “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types,” published in Oncotarget, highlights the gene regulator SETDB1 as a potential key player in cancer progression, immune system evasion, and resistance to therapy. Targeting this protein may offer a new direction for developing more effective treatments. Understanding Osteosarcoma Osteosarcoma is a rare but aggressive bone cancer that primarily affects teenagers and young adults. While current treatments like surgery and chemotherapy can help some patients, outcomes are much worse for those with relapsed or advanced disease. One of the reasons osteosarcomas are so difficult to treat is their complex and unstable genetics. Unlike cancers with well-defined mutations, osteosarcomas involve chaotic DNA rearrangements, making it difficult to identify precise drug targets. Adding to the challenge, the immune system often fails to recognize these cancer cells, limiting the success of immunotherapy. Full blog - https://www.oncotarget.org/2025/04/09/targeting-setdb1-a-new-strategy-for-treating-osteosarcoma/ Paper DOI - https://doi.org/10.18632/oncotarget.28688 Correspondence to - Antonin Marchais - antonin.marchais@gustaveroussy.fr, and Maria Eugenia Marques Da Costa - jenny.marquescosta@gustaveroussy.fr Video short - https://www.youtube.com/watch?v=f9WgaDoEubs Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28688 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, SETDB1, cancer epigenetics, tumor immunogenicity, mesenchymal differentiation in osteosarcoma About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — April 7, 2025 — A new #research paper was #published in Aging (Aging-US) on March 18, 2025, in Volume 17, Issue 3, titled “Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness.” Researchers from the University of Arkansas for Medical Sciences, led by first author Ana Resende-Coelho and corresponding authors Melda Onal and Maria Almeida, investigated why bones become less responsive to exercise as people age. They studied two well-known aging-related cellular changes: oxidative stress (a buildup of harmful molecules inside cells) and reduced autophagy (a slowdown in the cell's ability to clean out and recycle damaged parts) to determine whether these could explain the decline in bone strength. Their findings revealed that these changes alone are not enough to account for the reduced bone-building response seen with aging. Physical activity is known to strengthen bones by creating mechanical stress, which activates bone cells like osteocytes to promote new bone formation. However, this process becomes less effective with age, increasing the risk of bone loss and fractures in older adults. The study aimed to uncover why this response weakens over time by focusing on specific age-related changes inside bone-forming cells. “The bone response to loading is less effective with aging, but the cellular and molecular mechanisms responsible for the impaired mechanoresponsiveness remain unclear.” The research team used a well-established mouse model in which pressure was applied to the tibia, simulating the effects of exercise. As expected, bones from older mice showed a weaker response compared to those of younger mice. However, when the researchers examined younger mice genetically modified to have either high oxidative stress or impaired autophagy, as seen in aging, their bones still responded normally to mechanical loading. The researchers also found that damage to the bone's osteocyte network, a system of cells that helps sense and respond to mechanical forces, did not prevent a healthy bone-building response in mice with autophagy deficiencies. This challenges the long-standing idea that deterioration of this cell network is a main cause of age-related bone decline. These results are significant because they eliminate two widely suspected causes of the aging skeleton's reduced responsiveness to exercise. While oxidative stress and autophagy dysfunction are common in older bone, they are not solely responsible for its reduced ability to grow stronger under physical stress. The authors suggest that future studies should explore other possible factors, such as changes in energy metabolism or how bone cells communicate. Overall, this study shows that bone aging is more complex than previously thought. Protecting bone health in older adults may require new strategies that go beyond targeting oxidative stress or autophagy. DOI - https://doi.org/10.18632/aging.206213 Corresponding authors - Melda Onal - MOnal@uams.edu, and Maria Almeida - schullermaria@uams.edu Video short - https://www.youtube.com/watch?v=fHQhA6rOaDc Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206213 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Atg7, tibia compressive loading, Sod2, Osx1-Cre, osteocytes Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - April 8, 2025 – A new #editorial was #published in Oncotarget, Volume 16, on April 4, 2025, titled “Deep learning-based uncertainty quantification for quality assurance in hepatobiliary imaging-based techniques." Dr. Yashbir Singh from Mayo Clinic and his colleagues discussed how artificial intelligence (AI) can improve liver imaging by recognizing when it might be wrong. This approach, called “uncertainty quantification,” helps clinicians better detect liver cancer and other diseases by pointing out areas in medical scans that need a second look. The authors explain how these AI tools could make imaging results more accurate and reliable, which is especially important when diagnosing serious conditions like liver tumors. Liver and bile duct imaging is difficult because of the organ's complex structure and differences in image quality. Even skilled radiologists can struggle to identify small or hidden tumors, especially in patients with liver damage or scarring. The editorial explains how new AI models not only read medical images but also measure their own confidence. When the AI system is unsure, it can alert clinicians to take a closer look. This extra layer of information can reduce missed diagnoses and improve early detection of liver cancer. One of the most advanced tools described in the editorial is called AHUNet (Anisotropic Hybrid Network). This AI model works with both 2D and 3D images and can highlight which parts of a scan it is most confident about. It performed well when measuring the entire liver and showed how its confidence dropped when scanning smaller or multiple lesions. This feature helps clinicians know when more testing or review is needed. The authors also looked at other AI models used in liver imaging. Some tools were able to analyze liver fat using ultrasound images and give clinicians both a result and a confidence score. Others improved the speed and accuracy of liver magnetic resonance imaging (MRI) scans, helping to create clear images in less time. These advancements could help hospitals work faster and provide better care. The editorial highlights how this technology can be especially helpful in smaller clinics. If they do not have liver specialists, they could still use AI systems that flag uncertain results and send them to larger centers for review. Such an approach could improve care in rural or less-resourced areas. “Radiology departments should develop standardized reporting templates that incorporate uncertainty metrics alongside traditional imaging findings.” By using AI tools that know when to second-guess themselves, clinicians may soon have more reliable methods for detecting liver cancer and monitoring liver disease. The authors suggest that uncertainty-aware AI may soon become a vital part of everyday medical imaging, supporting faster and more accurate decisions in liver disease care. DOI: https://doi.org/10.18632/oncotarget.28709 Correspondence to: Yashbir Singh — singh.yashbir@mayo.edu Video short - https://www.youtube.com/watch?v=Zm0QASQ_YSI Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28709 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords: cancer, deep learning, uncertainty quantification, radiology, hepatobiliary imaging 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 Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY - April 4, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on March 27, 2025, titled “Imipridones ONC201/ONC206 + RT/TMZ triple (IRT) therapy reduces intracranial tumor burden, prolongs survival in orthotopic IDH-WT GBM mouse model, and suppresses MGMT." Researchers from Brown University, led by first author Lanlan Zhou and corresponding author Wafik S. El-Deiry, have shown that combining a new class of drugs called imipridones with standard glioblastoma treatments significantly improves outcomes in mice. The study tested ONC201 and its analog ONC206 in combination with radiation therapy and the chemotherapy drug temozolomide (TMZ), a regimen referred to as IRT. This triple therapy slowed tumor growth and extended survival in a mouse model of glioblastoma, offering a potential new strategy for one of the most aggressive and treatment-resistant brain cancers. Glioblastoma is a fast-growing brain tumor with a poor prognosis and limited treatment options. Standard care typically includes surgery, radiation, and TMZ, but most patients still face a short life expectancy. While ONC201 and ONC206 are currently being studied in clinical trials as single agents, there has been limited information on how they interact with standard therapies. This study is the first to show that both drugs work synergistically with radiation and TMZ, strengthening their overall effects. The results showed that in both laboratory-grown tumor cells and mice, the triple therapy significantly slowed cancer cell growth, reduced tumor size, and prolonged survival compared to using any single or double treatment. Mice treated with IRT lived an average of 123 days, with some surviving more than 200 days—far longer than the 44 to 103 days observed with other treatment combinations. In addition to directly killing tumor cells, ONC201 and ONC206 lowered the expression of MGMT, a protein that helps tumors resist chemotherapy, making the treatment more effective. The researchers also found that the triple therapy reshaped the tumor environment. It decreased levels of harmful molecules that promote tumor growth and immune evasion while increasing signals that activate the immune system. This dual action—directly attacking tumors and boosting immune responses—adds to the potential impact of this treatment approach. “Overall, our preclinical findings support further exploration of the ONC201 and ONC206 IRT regimen as a potential treatment for GBM and diffuse gliomas with H3K27M mutations.” While these findings are based on preclinical mouse models, they offer strong support for advancing this triple therapy to clinical trials. ONC201 and ONC206 are promising due to their ability to cross the blood-brain barrier and enhance the effects of standard treatment. This combination could lead to more effective therapies for glioblastoma and other hard-to-treat brain tumors. DOI - https://doi.org/10.18632/oncotarget.28707 Correspondence to - Wafik S. El-Deiry - wafik@brown.edu Video short - https://www.youtube.com/watch?v=Q_mXy8mana0 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28707 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ 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

Could a class of drugs that clear aging cells also help treat Alzheimer's disease? A recent study, featured as the cover for Aging (Volume 17, Issue 3), titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer's disease,” suggests they might—and with remarkable precision. Understanding Alzheimer's Disease Alzheimer's disease is a progressive neurological disorder that gradually steals memory, independence, and a person's sense of identity. A defining feature of Alzheimer's is the buildup of amyloid-β (Aβ) plaques—sticky protein clumps that interfere with communication between brain cells. This disruption is closely linked to changes in a group of enzymes called cholinesterases, especially acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes normally play a vital role in regulating neurotransmitters critical for memory, learning, and cognitive function. In Alzheimer's, however, their behavior changes significantly, particularly when they interact with Aβ plaques. The Study: Exploring Senolytics for Alzheimer's Enzyme Inhibition A research team from Dalhousie University in Canada looked into whether senolytic compounds—a class of drugs that eliminate damaged, aging cells often referred to as “zombie” cells—could also target the harmful forms of cholinesterase enzymes found in Alzheimer's disease. Their goal was to see if these compounds could selectively inhibit the disease-associated versions of AChE and BChE, without affecting the healthy forms that are essential for normal brain function. Full blog - https://aging-us.org/2025/04/senolytic-compounds-show-promise-in-targeted-alzheimers-treatments/ DOI - https://doi.org/10.18632/aging.206227 Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca Video short - https://www.youtube.com/watch?v=CJQFpG9Jn6Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, β-amyloid, acetylcholinesterase, butyrylcholinesterase, cholinesterase inhibitors About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — April 1, 2025 — A new #research paper was #published in Aging (Aging-US) on March 29, 2025, as the #cover of Volume 17, Issue 3, titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer's disease.” In this study, a research team from Dalhousie University, led by Sultan Darvesh, discovered that certain anti-aging compounds, known as senolytics, can block harmful brain enzymes linked to Alzheimer's disease (AD) without affecting healthy ones. Senolytics are compounds that help clear out damaged or “zombie” cells that build up with age and contribute to inflammation and tissue dysfunction. This work provides new insight into how AD-related damage can be precisely targeted, leading the way for safer treatments that protect memory and brain health in older adults. Alzheimer's disease is one of the most common causes of memory loss and dementia. A hallmark of the disease is the buildup of sticky protein clumps in the brain, known as amyloid-beta plaques. Two enzymes—acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)—are found near these plaques. While these enzymes play important roles in brain function, they can also contribute to AD progression when they attach to plaques. Drugs that target these enzymes are already used to help with memory, but they often block both harmful and healthy forms, which can cause unwanted side effects. To investigate a better solution, researchers tested six compounds that are known for their anti-aging or brain-boosting properties. They wanted to know if these compounds could block only the harmful AChE and BChE enzymes forms linked to Alzheimer's disease. Using brain tissue samples from AD patients and enzyme activity assays, they discovered that compounds such as dasatinib and nintedanib, both senolytics, were able to block the forms of AChE and BChE associated with amyloid-beta plaques. These compounds did not affect normal brain enzymes, though. “We show that the selected senolytics and nootropic inhibit ChEs associated with plaques but not the enzymes associated with normal neural elements.” The study also used computer modeling to explore how these compounds interact with the enzymes. The models showed that the enzymes change shape when near plaques, making them easier for certain compounds to target. This change may explain how the drugs can selectively affect only the diseased areas of the brain. While not all compounds worked equally well, the findings offer a new strategy for treating AD. By focusing on the differences between healthy and diseased enzyme forms, researchers may be able to design more precise and effective therapies. This selective approach could improve memory, reduce inflammation, and avoid the side effects of AD's current treatments. In summary, this research opens new possibilities for treating Alzheimer's disease in a more targeted way. It also highlights how discoveries in aging and brain health can work together to create better therapies for neurodegenerative diseases. DOI - https://doi.org/10.18632/aging.206227 Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca Video short - https://www.youtube.com/watch?v=CJQFpG9Jn6Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

A young woman beat leukemia; however, nine years later, she faced a different blood cancer. This rare twist, reported recently in Oncotarget, reveals an unexpected risk of bone marrow transplants and opens new questions about long-term outcomes and donor screening. Bone Marrow Transplant Bone marrow transplants, also known as hematopoietic stem cell transplants, are often lifesaving for patients with blood cancers like leukemia. These transplants replace a patient's damaged bone marrow with healthy cells from a donor, giving the body a fresh start. While this treatment can be remarkably effective, it comes with complex risks. Relapse of the original cancer is the most feared outcome. But in very rare cases, a different threat emerges; a cancer formed from the donor's cells. This condition, called donor cell–derived hematologic neoplasm (DCHN), occurs in less than 1% of cases, and it can emerge years after a transplant. The Case Report Dr. Aleksandra Mroczkowska-Bękarciak and Dr. Tomasz Wróbel from Wroclaw Medical University in Poland recently published a new DCHN case report, titled “A case report of donor cell–derived hematologic neoplasms 9 years after allogeneic hematopoietic cell transplantation,” in Volume 16 of Oncotarget. Full blog - https://www.oncotarget.org/2025/03/26/when-the-cure-becomes-the-cause-a-rare-case-of-cancer-from-donor-cells/ Paper DOI - https://doi.org/10.18632/oncotarget.28686 Correspondence to - Aleksandra Mroczkowska-Bękarciak - omroczkowska@interia.pl Video short - https://www.youtube.com/watch?v=G2zd0UqWzeE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28686 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, hematology, donor cell-derived hematologic neoplasms, genetics About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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

In this installment of the Longevity & Aging Series, Dr. Julia Sidorova from the Department of Laboratory Medicine and Pathology at the University of Washington (Seattle, WA) joined host Dr. Evgeniy Galimov to discuss her co-authored research paper from Volume 16, Issue 20 of Aging (Aging-US), titled “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.” DOI - https://doi.org/10.18632/aging.206132 Corresponding Author - Julia M. Sidorova - julias@uw.edu Video interview - https://www.youtube.com/watch?v=3yn8O-JA6GE Abstract Werner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206132 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Believe it or not, the field of Kardashian studies can inform the ways Medical Affair professionals identify and understand influencers and influence in the space of science communications. Here we talk with Mike Taylor, Head of Data Insights at Altmetric, and Carlos Areia, Senior Data Scientist at Altmetric about making sense of what is otherwise certainly nonsense. 

Traditional metrics like downloads and citations have long been the standard for measuring research impact. But with advancements in AI and sentiment analysis, medical publication professionals can now uncover deeper insights—how research is perceived, discussed, and acted upon.In this episode, guest host Dr. Carrie Brubaker is joined by Julia Mutygullina and Carlos Areia of Digital Science to explore how sentiment analysis is transforming medical communications. Tune in as they discuss how AI-driven insights go beyond numbers to reveal the quality and emotional tone of engagement, helping publication professionals understand real-world impact.To join ISMPP, visit our website at https://www.ismpp.org/ This Special Edition Topic episode is generously sponsored by Digital Science. Altmetric, part of Digital Science, is pleased to now have clinical guidelines as an attention source. Find out more here.

Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity. Understanding How Scientists Measure Aging at the DNA Level Aging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person's actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers. The Study: Investigating the Impact of Environmental Pollutants on Aging A research team led by first author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, conducted an exposome-wide association study to examine how different environmental pollutants affect epigenetic aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they analyzed blood and urine samples from 2,346 adults aged 50 to 84. The study measured 64 environmental chemicals, including heavy metals, pesticides, plastics, and tobacco-related compounds, to identify potential links to accelerated aging. The study titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey,” was published in Aging on February 11, 2025. Full blog - https://aging-us.org/2025/03/how-environmental-chemicals-may-accelerate-biological-aging/ Paper DOI - https://doi.org/10.18632/aging.206201 Corresponding author - Andres Cardenas - andresca@stanford.edu Video short - https://www.youtube.com/watch?v=WcL-K399a7M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206201 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Radiation therapy or radiotherapy, is a common treatment for cancer, but its effectiveness differs across patients. A recent study published as the cover for Volume 17, Issue 2 of Aging explored why this happens. The findings provide valuable insights, particularly for brain cancers like glioblastoma (GBM) and low-grade gliomas (LGG). Understanding Glioblastoma and Low-Grade Gliomas Glioblastoma and LGG are both brain tumors, but they behave in very different ways. GBM is highly aggressive, with most patients surviving only 12 to 18 months, even with surgery, chemotherapy, and radiation therapy. LGG, on the other hand, grows more slowly, and many patients live for decades with proper care. Despite their differences, LGG and GBM are biologically linked. Some LGG tumors eventually transform into GBM, making early treatment decisions critical. Given radiation therapy's effectiveness in GBM, it has often been assumed that LGG patients would also benefit from it. However, a new study titled “Variability in radiotherapy outcomes across cancer types: a comparative study of glioblastoma multiforme and low-grade gliomas” challenges this assumption. Full blog - https://aging-us.org/2025/03/how-radiation-therapy-affects-tumors-glioblastoma-vs-low-grade-gliomas/ Paper DOI - https://doi.org/10.18632/aging.206212 Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dk Video short - https://www.youtube.com/watch?v=j91rzDJHXTE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206212 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cancer, biomarkers, radiotherapy, GBM, LGG, survival About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Imagine if a single blood test could tell clinicians in real time how successful a cancer surgery has been. A recent study from the University of Brasília, published in Oncotarget, suggests that such an approach might soon be possible. By tracking changes in cell-free DNA (cfDNA) levels before, during, and after colorectal cancer (CRC) surgery, researchers have found a potential new way to monitor tumor removal and predict patient outcomes. Cell-Free DNA and Colorectal Cancer Surgery Cell-free DNA consists of tiny fragments of genetic material that are released into the bloodstream when cells break down. In healthy individuals, these fragments come from normal cell turnover, but in cancer patients, some of this DNA originates from tumor cells. cfDNA detection has been used to track cancer progression and treatment response in diseases like lung, breast, and CRC. What had not been investigated until now was how cfDNA levels fluctuate during cancer surgery itself. Since surgery is the primary treatment for CRC, understanding how cfDNA levels change during surgical intervention could provide valuable insights into whether the tumor has been fully removed and how the patient's body reacts to the procedure. The Study: Measuring Cell-Free DNA in Real-Time In the study, titled “Assessment of cfDNA release dynamics during colorectal cancer surgery,” led by first author Mailson Alves Lopes and corresponding author Fabio Pittella-Silva, scientists analyzed ​​blood plasma samples from 30 CRC patients at three critical time points—before, during, and after surgery. Using highly sensitive genetic tests, they measured changes in cfDNA concentration to determine whether surgery had a direct impact on its release. The goal was to check whether cfDNA could serve as a biomarker for evaluating surgical effectiveness and predicting the probability of cancer recurrence. Full blog - https://www.oncotarget.org/2025/02/26/how-a-simple-blood-test-could-predict-colorectal-cancer-surgery-success/ Paper DOI - https://doi.org/10.18632/oncotarget.28681 Correspondence to - Fabio Pittella-Silva - pittella@unb.br Video short - https://www.youtube.com/watch?v=jC5_xqIrbtA Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28681 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, colorectal cancer, cfDNA, surgery About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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 — February 24, 2025 — A new #researchpaper was #published in Aging (Aging-US) on January 22, 2025, in Volume 17, Issue 1, titled “EpiAge: a next-generation sequencing-based ELOVL2 epigenetic clock for biological age assessment in saliva and blood across health and disease.” The research team, experts from both industry (EpiMedTech Global, HKG Epitherapeutics Ltd) and academic institutions (McGill University, Oxford University, University of Catania, and the Research Institute-IRCCS), led by first author David Cheishvili and corresponding author Moshe Szyf, have developed EpiAgePublic, a new method to estimate biological age using only three key DNA sites in the ELOVL2 gene, a well-known marker of aging. Unlike traditional methods that require analyzing thousands of DNA regions, this approach simplifies the process while maintaining accuracy. Their findings show that EpiAgePublic performs as well as, or even better than, more complex models in predicting biological age in diverse populations. Biological age measures how fast or slow a person's body is aging. It can be different from chronological age and is influenced by genetics, lifestyle, and health conditions. Understanding biological aging can help researchers and clinicians identify age-related diseases like Alzheimer's disease and develop anti-aging treatments. However, many existing biological age tests rely on expensive and complicated processes. The EpiAgePublic model overcomes these challenges with a simple yet powerful approach. The study analyzed data from over 4,600 individuals across different health conditions, including Alzheimer's disease and HIV. It confirmed that EpiAgePublic accurately tracks aging patterns and can identify factors such as chronic illness or stress that accelerate the aging process. Importantly, the researchers demonstrated that the test works well using saliva samples, offering a convenient and non-invasive alternative to blood-based tests. This makes it easier to conduct epigenetic age testing in both clinical and research settings. “The simplicity and precision of epiAgePublic, designed for compatibility with next-generation sequencing (NGS) technologies, mark a significant step forward in the field of epigenetic research.” The ability to measure epigenetic aging with a quick and cost-effective test has significant implications for healthcare, longevity research, and personalized medicine. This method could be used in hospitals, wellness clinics, and longevity studies to track aging and evaluate the effectiveness of anti-aging interventions. It may also help clinicians detect early signs of aging-related diseases, allowing for better preventive care. Finally, the study's findings highlight the advantages of next-generation sequencing in epigenetic research, leading the way for more precise and accessible aging diagnostics. Future research will explore how this model can be expanded to other health conditions and used in routine medical practice. DOI - https://doi.org/10.18632/aging.206188 Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.com Author interview - https://www.youtube.com/watch?v=NA8Vctks0gY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206188 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

In the Season 3 premiere of the Longevity & Aging Series, Dr. Yu-Xuan Lyu from Southern University of Science and Technology (Shenzhen, China) joins host Dr. Evgeniy Galimov to discuss his co-authored research paper, featured as the cover for Aging (Aging-US) Volume 16, Issue 20, titled “Longevity biotechnology: bridging AI, biomarkers, geroscience, and clinical applications for healthy longevity.” #aging #author #interview #series #biotechnology #ai #artificialintelligence #longevity #healthspan #lifespan #oa #openscience #peerreview #journal #publication #publishing #meded #agingshort #video DOI - https://doi.org/10.18632/aging.206135 Corresponding authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dk Video interview - https://www.youtube.com/watch?v=VUfNxWdBV5k Video short - https://www.youtube.com/watch?v=Hpfe5WJ5g7I Abstract The recent unprecedented progress in ageing research and drug discovery brings together fundamental research and clinical applications to advance the goal of promoting healthy longevity in the human population. We, from the gathering at the Aging Research and Drug Discovery Meeting in 2023, summarised the latest developments in healthspan biotechnology, with a particular emphasis on artificial intelligence (AI), biomarkers and clocks, geroscience, and clinical trials and interventions for healthy longevity. Moreover, we provide an overview of academic research and the biotech industry focused on targeting ageing as the root of age-related diseases to combat multimorbidity and extend healthspan. We propose that the integration of generative AI, cutting-edge biological technology, and longevity medicine is essential for extending the productive and healthy human lifespan. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biotechnology, artificial intelligence, healthy longevity About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — February 19, 2025 — A new #research paper was #published by Aging (Aging-US) on January 6, 2025, in Volume 17, Issue 1, titled “The profile of oxidative stress markers (arachidonic and linoleic acid derivatives) in patients with benign prostatic hyperplasia in relation to metabolic syndrome.” A team of researchers, led by first author Weronika Ratajczak and corresponding author Olimpia Sipak from Pomeranian Medical University, examined how inflammation and metabolic health contribute to benign prostatic hyperplasia (BPH), a common condition that causes prostate enlargement in aging men, leading to urinary problems. Their findings suggest that inflammatory-related molecules in the blood may play a key role in BPH development, especially in men with metabolic syndrome—a group of conditions including obesity, high blood sugar, and high cholesterol. BPH affects millions of men as they age, making urination more difficult and sometimes painful. While age and hormonal changes are known factors, the precise causes of prostate enlargement remain unclear. This study provides new evidence that inflammation, especially lipid-derived inflammatory markers, may be a driving factor behind BPH, particularly in those with poor metabolic health. The research team analyzed blood samples from 219 men, including 144 with BPH and 75 without, measuring markers related to inflammation and oxidative stress. The results showed that men with BPH had significantly higher levels of pro-inflammatory molecules such as 12S-HETE and 5-HETE while having lower levels of anti-inflammatory substances like lipoxin A4. The imbalance was even more pronounced in men with both BPH and metabolic syndrome, indicating a possible link between poor metabolic health and worsening prostate conditions​. “Furthermore, there is mounting evidence that links the onset of inflammation with the development of prostate diseases, including benign prostatic hyperplasia and prostate cancer.” Metabolic dysfunction and chronic inflammation may not only contribute to BPH development but also exacerbate its severity. Monitoring metabolic health could play a role in reducing the risk of prostate enlargement. Future research is needed and may focus on whether anti-inflammatory treatments or lifestyle changes—such as improved diet, weight management, and exercise—could help slow the progression of BPH or reduce its symptoms​. DOI - https://doi.org/10.18632/aging.206187 Corresponding author - Olimpia Sipak - olimpiasipak-szmigiel@wp.pl Video short - https://www.youtube.com/watch?v=O0VMvqaVsUs Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206187 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, benign prostatic hyperplasia (BPH), metabolic syndrome (MetS), lipid markers, inflammation, fatty acids derivatives About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Dr. Moshe Szyf from EpiMedTech Global in Singapore discusses a research paper he co-authored that was published in Volume 17, Issue 1 of Aging (Aging-US), entitled “EpiAge: a next-generation sequencing-based ELOVL2 epigenetic clock for biological age assessment in saliva and blood across health and disease.” DOI - https://doi.org/10.18632/aging.206188 Corresponding author - Moshe Szyf - moshe.szyf@epimedtech.com Video interview - https://www.youtube.com/watch?v=NA8Vctks0gY Video transcript - https://www.aging-us.com/interviews/epiage-ngs-based-elovl2-epigenetic-clock-for-biological-age-assessment Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206188 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic clock, elovl2, next-generation sequencing, EpiAge, Alzheimer's disease About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Imagine a simple topical treatment that could help aging skin heal faster, reducing recovery time from wounds and even improving skin quality. Scientists may have found exactly that. A recent study, published in Aging, reveals that a compound called ABT-263 can eliminate aging cells in the skin, boosting its ability to regenerate. Understanding How Aging Affects Skin Healing Aging affects the skin's structure and function, leading to a reduced ability to heal from wounds. Scientists have long suspected that senescent cells, also known as “zombie cells,” play a major role in this decline. These cells stop dividing but refuse to die, accumulating in tissues and releasing inflammatory molecules that impair the body's natural repair processes. Various studies have explored senolytics, a class of drugs designed to eliminate these aging cells and restore tissue function. While these drugs have shown promise in treating diseases like osteoporosis and fibrosis, their impact on skin regeneration and wound healing has been less studied. A new study titled “Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing” now suggests that a topical application of the senolytic ABT-263 could significantly improve wound healing in older individuals. Full blog - https://aging-us.org/2025/02/a-new-approach-to-healing-aging-skin-insights-from-senolytic-research/ Paper DOI - https://doi.org/10.18632/aging.206165 Corresponding author - Daniel S. Roh - droh@bu.edu Video short - https://www.youtube.com/watch?v=AKS7sZyEChg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206165 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senolytic, senescence, wound healing, ABT-263 About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

For years, breast cancer has been classified as either HER2-positive or HER2-negative, determining whether a patient could receive HER2-targeted therapies like trastuzumab (Herceptin). However, a growing body of research suggests a middle category—HER2-low breast cancer—which has led to important changes in how clinicians approach treatment. A recent review published in Oncotarget, titled “Evolving Concepts in HER2-Low Breast Cancer: Genomic Insights, Definitions, and Treatment Paradigms,” explores what this means for both patients and clinicians​. Full blog - https://www.oncotarget.org/2025/02/12/her2-low-breast-cancer-a-new-understanding/ Paper DOI - https://doi.org/10.18632/oncotarget.28680 Correspondence to - Andrew A. Davis - aadavis@wustl.edu Video short - https://www.youtube.com/watch?v=dn54UrHCUNQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28680 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, breast cancer, HER2-low, genomics About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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

Emerging research suggests that a specific type of body fat may play an important role in healthy aging and physical performance. Researchers from Rutgers New Jersey Medical School explore this topic in a recent research perspective published in Aging (Aging-US). Their work discusses new findings and emerging ideas about the role of brown adipose tissue (BAT), commonly known as brown fat. Understanding Brown Fat The human body contains different types of fat. The most common is white adipose tissue (WAT), which primarily stores excess calories. When present in large amounts, WAT contributes to health problems like obesity, type 2 diabetes, and cardiovascular disease as a result of its role in metabolic imbalance. In contrast, BAT serves a more dynamic role. Instead of storing energy, BAT burns calories to generate heat through a process called thermogenesis, powered by its high concentration of mitochondria—the energy-producing structures in cells. While BAT is abundant in newborns to help regulate body temperature, it persists in smaller amounts in adults, particularly around the neck, shoulders, and spine. According to the research perspective, titled “Brown Adipose Tissue Enhances Exercise Performance and Healthful Longevity” brown fat's role extends beyond thermoregulation. The authors suggest that BAT can significantly improve metabolic health, enhance physical performance, and promote healthful longevity. Full blog - https://aging-us.org/2025/02/the-hidden-power-of-brown-fat-a-new-ally-in-healthy-aging/ Paper DOI - https://doi.org/10.18632/aging.206179 Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14 About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

An unexpected link between KLRG1 and PD-1, two key immune system proteins, was revealed in a study recently published in Oncotarget. This discovery could help explain why some cancer immunotherapy treatments are less effective for certain patients and lead to new therapeutic strategies. How the Immune System Fights Cancer The immune system is a powerful defense mechanism against cancer, with CD8 T cells acting as the primary soldiers. These specialized immune cells identify and destroy tumor cells. However, cancer can cleverly evade this attack by manipulating immune checkpoints—natural “breaks” on the immune system that prevent it from overreacting and damaging healthy tissue. One of the most studied checkpoints is PD-1 (Programmed Death-1), a receptor on T cells that acts as an “off switch” when activated by tumor cells. This mechanism suppresses the immune response, allowing cancer to grow without control. In response, researchers have developed treatments called PD-1 inhibitors, which block this “off switch” and keep T cells active. The Study: Investigating KLRG1 and PD-1 in Tumor-Fighting T Cells In the study titled “Anti-correlation of KLRG1 and PD-1 expression in human tumor CD8 T cells,” Dr. Steven A. Greenberg from Harvard Medical School analyzed publicly available gene expression data from various cancer types, including lung cancer, melanoma, and colorectal cancer. His goal was to identify immune-related proteins that could complement existing therapies, such as PD-1 inhibitors. Full blog - https://www.oncotarget.org/2025/01/28/a-new-approach-for-cancer-treatment-the-surprising-relationship-between-klrg1-and-pd-1/ Paper DOI - https://doi.org/10.18632/oncotarget.28679 Correspondence to - Steven A. Greenberg - sagreenberg@bwh.harvard.edu Video short - https://www.youtube.com/watch?v=PME2xfyYN18 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28679 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, immunotherapy, KLRG1 About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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- January 28, 2025 – A new #research paper was #published in Volume 16, Issue 22 of Aging (Aging-US) on December 20, 2024, titled, “Impaired renal transporter gene expression and uremic toxin excretion as aging hallmarks in cats with naturally occurring chronic kidney disease.” This study, led by researchers Qinghong Li, James A. Holzwarth, Bethany Smith, Sonia Karaz, Mathieu Membrez, Vincenzo Sorrentino, Stacie Summers, Julie Spears, and Eugenia Migliavacca from Nestlé Purina Research and Oregon State University, explores how aging affects kidney function in cats with chronic kidney disease (CKD). The researchers found that older cats have lower levels of important kidney transporter genes, which usually help remove harmful waste products from the blood. These findings could help veterinarians better understand CKD in aging cats and offer insights that may be relevant to human kidney health. "Chronic kidney disease (CKD) is a naturally occurring kidney disease common in both geriatric cats and older people. Despite differing etiology, both species share many pathophysiological similarities, including chronic tubulointerstitial inflammation and fibrosis." Older cats with CKD struggle to filter toxins from their bloodstream effectively. In this study, the researchers analyzed kidney samples from two cat cohorts aged 6 to 21 years. The cohort number one included 41 colony cats: 28 control and 13 CKD cats. The cohort number two had 30 privately owned cats with 10 control and 20 CKD cats. They discovered that certain transporter genes, such as OAT1, OAT4, OATP4C1 and ABCC2, were significantly decreased in cats with CKD compared to healthy cats. The research team also found increased levels of harmful toxins in the blood of cats with CKD. Even healthy older cats had higher toxin levels compared to younger cats, showing that aging itself might contribute to declining kidney function. Monitoring kidney transporters levels and toxin buildup may help detect the disease early and improve treatment options. The researchers highlight the importance of regular veterinary check-ups to catch kidney problems early and keep cats healthier for longer. Because cats and humans share similar kidney health challenges, studying feline CKD can provide valuable insights into human kidney disease and aging. Continued research is essential to develop treatments that may improve kidney function in aging cats and potentially benefit humans as well. DOI - https://doi.org/10.18632/aging.206176 Corresponding author - Qinghong Li - qinghong.li@rd.nestle.com Video short - https://www.youtube.com/watch?v=WuEP9PXtx2A Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206176 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, trimethylamine N-oxide, indoxyl sulfate, OAT1, OATP4C1, ABCC2 About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

“We illustrate our strategy in brain and liver tissue, demonstrating how cell-type specific epigenetic clocks from these tissues can improve tissue-specific estimation of chronological and biological age.” Aging affects everyone differently. There are two types of aging: chronological aging, which refers to the number of years a person has lived, and biological aging, which reflects how well the body is functioning based on cellular changes. A recent study published as the cover for Volume 16, Issue 22 of Aging reports a new discovery that could revolutionize the way we understand aging and its impact on health. Understanding Biological Age Biological age reflects how well the body is aging and can vary based on lifestyle, genetics, and environmental factors. Traditionally, scientists estimate it using epigenetic clocks, which measure DNA methylation, chemical changes that occur over time. Until recently, these clocks could only provide general estimates by analyzing entire tissues, meaning they could not distinguish how different cell types aged within those tissues. A recent study titled “Cell-type Specific Epigenetic Clocks to Quantify Biological Age at Cell-Type Resolution” aims to change that. Full blog - https://aging-us.org/2025/01/how-scientists-are-measuring-aging-at-the-cellular-level/ Paper DOI - https://doi.org/10.18632/aging.206184 Corresponding author - Andrew E. Teschendorff - andrew@sinh.ac.cn Video short - https://www.youtube.com/watch?v=FjJa5U2-AqQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206184 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, DNA methylation, epigenetic clocks, cell-type deconvolution, biological aging, Alzheimer's disease, obesity About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- January 16, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 2, 2024, entitled “Less frequent skin ulcers among patients with Werner syndrome treated with pioglitazone: findings from the Japanese Werner Syndrome Registry.” Scientists from Chiba University in Japan and other institutions have discovered that the drug pioglitazone, commonly used to treat diabetes, may help prevent painful skin ulcers in people with Werner syndrome. Werner syndrome is a rare genetic condition that causes people to age faster than normal, leading to early gray hair, cataracts, and other age-related health problems. One of the most serious complications is skin ulcers, which affect nearly 70% of people with the disorder and can lead to severe pain, infections, and even amputations. The study, led by first author Kazuto Aono and corresponding author Masaya Koshizaka, looked at 51 patients with Werner syndrome from the Japanese Werner Syndrome Registry. Over half of the patients had skin ulcers, and those with ulcers were generally older and had higher blood pressure. The research team found that patients who took pioglitazone were much less likely to have ulcers, even after accounting for age. The research suggests that pioglitazone's ability to reduce inflammation helps wounds heal faster and prevents ulcers from forming. However, since the drug can cause side effects, like weaker bones, scientists recommend further studies to explore safer options, such as creams or gels made from pioglitazone that can be applied directly to the skin. “Nanostructured hybrid materials loaded with pioglitazone are also being developed for clinical use and may be useful as wound dressings for ulcer treatment.” Although the study shows promising results, the authors emphasize that more long-term studies are needed to confirm how effective the treatment is besides the exploration of other factors, like diet and exercise, that may also help reduce the ulcers. In conclusion, this study presents pioglitazone as a potential option to prevent skin ulcers in Werner syndrome patients. While further studies are needed, these findings provide hope for better treatments. DOI - https://doi.org/10.18632/aging.206161 Corresponding author - Masaya Koshizaka - overslope@chiba-u.jp Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206161 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner syndrome, skin ulcer, metformin, pioglitazon, progeroid syndrome About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Scientists have discovered that a genetic variant called KIT M541L may play an important role in a rare immune disorder known as #mastocytosis. The findings may help explain why some #patients develop more severe forms of the disease. Understanding Mastocytosis Mastocytosis is a condition where the body produces too many mast cells. These cells are part of the immune system and help the body fight infections, but in excess, they release chemicals that can cause itching, swelling, and even serious organ damage. There are two main types of mastocytosis. The first is cutaneous mastocytosis, which mostly affects the skin. The second is systemic mastocytosis, a more serious form where mast cells build up in internal organs like the liver, spleen, and bone marrow. The disease is linked to mutations in the KIT gene, which regulates mast cell growth. The most studied mutation is KIT D816V, but recent research has highlighted another variant, KIT M541L. The Study: Impact of KIT M541L Variant A team of researchers at the National Institutes of Health (NIH), led by first author Luisa N. Dominguez Aldama and corresponding author Melody C. Carter, aimed to better understand the prevalence and impact of the KIT M541L genetic variant in mastocytosis patients. The study published in Oncotarget on July 22, 2024, titled “Prevalence and impact of the KIT M541L variant in patients with mastocytosis,” examined the presence of the KIT M541L gene variant in 100 patients with mastocytosis, both adults and children, alongside 500 healthy individuals. By comparing these two groups, the researchers wanted to see if there was a relation between the KIT M541L variant and mastocytosis severity. Full blog - https://www.oncotarget.org/2025/01/15/mastocytosis-key-insights-into-kit-m541l-gene-mutation/ Paper DOI - https://doi.org/10.18632/oncotarget.28614 Correspondence to - Melody C. Carter - mcarter@niaid.nih.gov Video short - https://www.youtube.com/watch?v=zpiBbSfkTX4 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28614 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, mastocytosis, KIT M541L, KIT D816V, adults, pediatrics About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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- January 14, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on November 26, 2024, entitled “When do the pathological signs become evident? Study of human mesenchymal stem cells in MDPL syndrome.” Researchers from the University of Rome Tor Vergata, Fondazione Policlinico Tor Vergata, Roma Tre University, and Meyer Children's Hospital IRCCS have identified early cellular changes associated with Mandibular Hypoplasia, Deafness, Progeroid Features, and Lipodystrophy (MDPL) syndrome, a rare genetic aging disorder caused by a mutation in the POLD1 gene. MDPL leads to fat loss, distinct facial features, and metabolic disturbances. This study aimed to better understand how MDPL progresses at the cellular level. MDPL syndrome is extremely rare, with only a few documented cases worldwide, making it difficult to study. To investigate the disease, researchers Spitalieri Paola, Guerrieri Lara, Murdocca Michela, Di Cesare Silvia, Maccaroni Serena, Pecorari Rosalba, Nardone Anna Maria, Candi Eleonora, Colasuonno Fiorella, Gori Giulia, Traficante Giovanna, Novelli Giuseppe, and Sangiuolo Federica, converted skin cells from three female MDPL patients and two healthy donors into human induced pluripotent stem cells (hiPSCs). These hiPSCs were then transformed into mesenchymal stem cells (MSCs), cells that can form tissues like bone and fat, which are primarily affected in MDPL syndrome. The study revealed that MSCs from MDPL patients exhibited signs of premature aging much earlier than expected. The cells had irregular shapes, grew at a slower rate, and showed higher levels of cellular stress. “These cells differentiate with lower efficiency, proliferate more slowly and have abnormal mitochondrial activity with increased production of ROS. Furthermore, the telomeres show evident shortening.” All the findings suggest that aging-related changes may occur long before patients display visible symptoms of the disease. This highlights the need for early diagnosis and intervention, which could delay or even prevent the most debilitating effects of MDPL syndrome. In summary, this study offers new perspectives on the initial cellular impacts of MDPL, opening the door for the creation of novel treatments. The findings highlight the potential for personalized therapies and emphasize the critical role of lab-created hiPSCs in advancing research on rare genetic diseases and age-related conditions. DOI - https://doi.org/10.18632/aging.206159 Corresponding author - Sangiuolo Federica - sangiuolo@med.uniroma2.it Video short - https://www.youtube.com/watch?v=DLXD2ztPTm0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206159 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, MDPL syndrome, MSCs, hiPSCs, POLD1 gene About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- January 8, 2025 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 18, 2024, entitled “Brown adipose tissue enhances exercise performance and healthful longevity.” Researchers from Rutgers New Jersey Medical School, Dorothy E. Vatner, Jie Zhang, and Stephen F. Vatner, evaluated the role of brown adipose tissue (BAT), a special type of fat that burns calories to generate heat, in improving exercise endurance and supporting healthy aging. Unlike regular white fat, which stores energy, brown fat helps the body stay warm and boosts metabolism. According to the authors, this process may also help protect against health conditions such as obesity, diabetes, and cardiovascular disease. This research perspective highlights key findings from multiple studies on BAT. While most studies have shown that exercise regulates BAT activation and increases BAT density, relatively few have demonstrated that BAT itself can directly increase exercise performance. One notable example involves RGS14 knockout mice, a genetically modified group known for their longer lifespan. When BAT from these mice was transplanted into regular mice, the recipients displayed improved running endurance just three days after the transplant. In contrast, brown fat from non-modified mice took much longer to produce similar improvements. These findings highlight the unique properties of BAT in enhancing physical performance. The researchers emphasized also that BAT improves blood circulation and reduces cellular stress, which may help combat age-related muscle loss, fatigue, and metabolic decline. The authors suggest that treatments designed to mimic the benefits of brown fat could lead to innovative approaches for improving energy levels, maintaining a healthy weight, and supporting heart health. “​​In view of the ability of BAT to mediate healthful longevity and enhance exercise performance, it is likely that a pharmaceutical analog of BAT will become a novel therapeutic modality.” In conclusion, continued research on this topic may lead to the development of promising new therapies that help older adults live more active lives while reducing the risk of chronic age-related conditions. DOI - https://doi.org/10.18632/aging.206179 Corresponding author - Stephen F. Vatner - vatnersf@njms.rutgers.edu Video short - https://www.youtube.com/watch?v=n1DvuR7owJQ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206179 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brown adipose tissue, white adipose tissue, healthful longevity, exercise, regulator of G protein signaling 14 About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- January 7, 2025 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 9, 2024, entitled “Nuclear lipid droplets: a novel regulator of nuclear homeostasis and ageing.” In this article, Dr. Konstantinos Palikaras from the National and Kapodistrian University of Athens and Dr. Nektarios Tavernarakis from the University of Crete explore how tiny fat droplets, known as nuclear lipid droplets (nLDs), accumulate in the nucleus of cells as we age. Unlike regular lipid droplets, which store energy in the cytoplasm, these nuclear droplets may weaken the nucleus by disrupting critical cellular processes. The authors suggest that excessive buildup of nLDs could lead to nuclear instability and may be linked to metabolic conditions such as fatty liver disease, obesity-related disorders, and premature aging. This highlights the potential role of nLDs in cellular aging and age-related diseases. Previous research by the authors using Caenorhabditis elegans (C. elegans), a model organism commonly used to study aging, revealed the role of ATGL-1, an enzyme that regulates fat storage in the nucleus. When functioning properly, ATGL-1 helps maintain a healthy lipid balance. However, when it becomes inactive or overwhelmed, fat droplets build up around the nuclear lamina, making it more difficult for the cell to function properly. “These findings establish excessive nuclear lipid deposition as a key hallmark of aging, with profound implications for nuclear processes such as chromatin organization, DNA repair, and gene regulation.” The authors emphasize that lifestyle interventions, such as caloric restriction and better insulin regulation, can significantly reduce harmful nLD buildup, reinforcing the role of healthy metabolism in slowing cellular aging. They also call for further studies to understand how nLDs behave in human experimental models, particularly in patients with conditions like metabolic syndrome and progeria. A deeper understanding of these processes could lead to treatments designed to preserve cell health and delay age-related diseases. In summary, by presenting nuclear lipid droplets as potential therapeutic targets, this research perspective presents a new path for exploring treatments aimed at combating age-related diseases driven by lipid dysregulation. DOI - https://doi.org/10.18632/aging.206175 Corresponding authors - Konstantinos Palikaras - palikarask@med.uoa.gr, and Nektarios Tavernarakis - tavernarakis@imbb.forth.gr Video short - https://www.youtube.com/watch?v=vuSLuDk8Xjk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206175 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, ATGL-1, HLH-30/TFEB, lipid droplet, non-linear optical phenomena, nucleus About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Would you take a test to find out your cancer risk? At-home genetic testing makes it easy, but experts warn that these tests may create more harm than good. A New Approach to Genetic Testing Genetic testing has traditionally been performed under the supervision of healthcare providers, with genetic counseling to help patients navigate their results. This approach ensures that individuals receive proper guidance, reducing the emotional and practical challenges of interpreting complex genetic information. In September 2023, the United States Food and Drug Administration (FDA) approved a new test called the Invitae Common Hereditary Cancers Panel. This test checks for changes in 48 genes linked to hereditary cancers, including breast, ovarian, and Lynch syndrome-related cancers. What makes it different is that it can be ordered online and taken at home with no doctor required. While the convenience of these tests is appealing, health experts have raised serious concerns. An editorial titled “Pitfalls and Perils from FDA-Approved Germ-line Cancer Predisposition Tests,” authored by Dr. Wafik S. El-Deiry, Editor-in-Chief of Oncotarget, and Dr. Eli Y. Adashi, both from Brown University, highlights the potential risks of using these tests without professional guidance. Full blog - https://www.oncotarget.org/2025/01/03/the-hidden-risks-of-at-home-genetic-cancer-tests/ Paper DOI - https://doi.org/10.18632/oncotarget.28677 Correspondence to - Wafik S. El-Deiry - wafik@brown.edu Video short - https://www.youtube.com/watch?v=DjKpiBNDWHo Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28677 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, cancer predisposition, germline, marketing authorization, hereditary cancer, direct to consumer About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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

The p53 protein, often called the “guardian of the genome,” is crucial for preventing cancer by repairing damaged DNA or triggering cell death in cells that cannot be repaired. However, in about half of all cancers, the p53 gene is mutated, making the protein ineffective. A groundbreaking study has introduced PG3, a new compound that restores tumor suppression without relying on p53, offering a new option to treat resistant cancers. Published in Oncotarget on September 17, 2024, the study titled “Integrated stress response (ISR) activation and apoptosis through HRI kinase by PG3 and other p53 pathway-restoring cancer therapeutics,” introduces PG3, a small molecule with a completely new approach to treating cancer. This groundbreaking research was conducted by Dr. Xiaobing Tian and Oncotarget Editor-in-Chief Dr. Wafik S. El-Deiry from Brown University. The researchers tested PG3 on cancer cell lines with various p53 mutations, as well as on cells that lacked p53 entirely. Full blog - https://www.oncotarget.org/2024/12/18/a-new-path-to-tumor-suppression-the-promise-of-pg3/ Paper DOI - https://doi.org/10.18632/oncotarget.28637 Correspondence to - Wafik S. El-Deiry - wafik@brown.edu Video short - https://www.youtube.com/watch?v=eBp_UGrkii8 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28637 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, mutant p53, integrated stress response (ISR), ATF4, HRI, ClpP About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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 - December 11, 2024 – A #news feature on the #research paper “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition” by Rackear et al. was #published in Oncotarget's Volume 15 on November 22, 2024, titled “Advancements in cell-penetrating monoclonal antibody treatment." This new publication by Sai Pallavi Pradeep and Raman Bahal from the Department of Pharmaceutical Sciences at the University of Connecticut highlights significant advancements in monoclonal antibody (mAb) therapies. The focus is on the 3E10 antibody, originally derived from autoimmune mouse studies in systemic lupus erythematosus. Unlike traditional mAbs, which struggle to reach intracellular targets, this cell-penetrating antibody targets cancer cells by addressing a major limitation of current therapies. By targeting RAD51, a key intracellular protein involved in DNA repair, the 3E10 antibody shows great promise for cancer treatment, particularly in cancers with defective DNA repair pathways. mAbs have already changed the landscape of cancer therapy, offering treatments that are more targeted and have fewer side effects compared to chemotherapy. However, current therapies are limited since mAbs only target proteins on the surface of cancer cells. This research pushes the boundaries by demonstrating how 3E10 antibodies can penetrate cells and access their internal molecules. This unique capability expands the potential of mAb therapies and targeted cancer treatments. Different humanized versions of the 3E10 antibody were created and carefully tested. Some versions were particularly effective at blocking RAD51, while others showed promise for carrying other therapeutic molecules like genetic material into the cancer cells. This flexibility means that 3E10 could be used to treat different cancer types and deliver various therapeutic molecules directly into tumor cells. This progress offers exciting new possibilities for treating cancer tumors that are resistant to conventional therapies. In conclusion, the 3E10 antibody's dual function—targeting DNA repair pathways and delivering therapeutic molecules—positions it as a transformative tool in cancer research and targeted cancer treatments. DOI - https://doi.org/10.18632/oncotarget.28674 Correspondence to - Raman Bahal - raman.bahal@uconn.edu Video short - https://www.youtube.com/watch?v=3uMdPvThFHA Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28674 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, monoclonal anti-bodies, cell penetration, nucleic acid delivery, 3E10 About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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 Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY - December 9, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on November 22, 2024, entitled “Computed tomography-based radiomics and body composition model for predicting hepatic decompensation." Mayo Clinic researchers Yashbir Singh, John E. Eaton, Sudhakar K. Venkatesh, and Bradley J. Erickson have developed an innovative AI tool to predict hepatic decompensation in individuals with primary sclerosing cholangitis (PSC). PSC is a chronic disease that damages the bile ducts and can lead to liver failure. Hepatic decompensation marks a critical stage of advanced liver disease, and clinicians have long faced challenges in predicting who is at risk. The Mayo Clinic's new AI tool addresses this gap by combining body fat and muscle composition data with insights extracted from computed tomography (CT) scans using computational radiomics. By analyzing these tissues, the AI model identifies patterns linked to an increased risk of liver failure. The study involved 80 PSC patients, including 30 with hepatic decompensation, 30 without, and 20 patients in an external validation set. The AI model achieved impressive results, correctly identifying at-risk patients with 97% accuracy. By recognizing these risks early, clinicians may be able to intervene sooner and improve patient outcomes. While the study focused on PSC, the team emphasized the broader implications of their work. “It may hold promise for the detection of other PSC-related complications, such as cholangiocarcinoma, as well as applications in more prevalent chronic liver diseases like non-alcoholic fatty liver disease (NAFLD).” This non-invasive, data-driven approach offers a powerful way to assess health risks and provide more tailored treatments. Despite the promising findings, the researchers acknowledge the limitations of the study, which include a limited sample size and a single-center design. “However, further research is necessary to validate our findings on a large-scale, independent dataset, ensuring the robustness and generalizability of the model.” In conclusion, this study shows how detailed information from CT scans can help clinicians predict severe liver problems in patients with PSC. By identifying hidden patterns in the images, they can better understand risks and create personalized treatment plans. This approach could improve care for PSC and other long-term liver diseases. DOI - https://doi.org/10.18632/oncotarget.28673 Correspondence to - Bradley J. Erickson - bje@mayo.edu Video short - https://www.youtube.com/watch?v=QCekNtYni4w Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28673 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, radiomics, body composition, machine learning, primary sclerosing cholangitis, computer tomography About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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 - December 4, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on November 22, 2024, entitled “B7-H4: A potential therapeutic target in adenoid cystic carcinoma." Researchers Luana Guimaraes de Sousa and Renata Ferrarotto from The University of Texas MD Anderson Cancer Center made an important discovery about adenoid cystic carcinoma (ACC), a rare and aggressive cancer of the secretory glands. The study found that B7-H4, an inhibitory immune checkpoint, helps ACC tumors avoid attacks from the immune system. This discovery could lead to new treatments for ACC, which currently has very limited options for patients, especially when the cancer spreads to other organs. ACC is known for behaving in two distinct ways. The aggressive form, called ACC-I, spreads quickly to organs like the liver and lungs and leads to a short survival time of approximately three years. The less aggressive form, ACC-II, grows more slowly and often allows patients to live much longer, sometimes over 20 years. However, treatment options for both forms are limited, and once the cancer spreads, it becomes difficult to treat. The study showed that the protein B7-H4 is found at high levels in the aggressive ACC-I tumors. This protein blocks immune cells from entering the tumor, allowing the cancer to grow without being attacked by the immune system. Patients with high levels of B7-H4 in their tumors were found to have worse survival outcomes. To explore possible treatments, the researchers tested a new drug called AZD8205, designed to specifically target and block B7-H4. In preclinical tests on mice, the drug showed remarkable success. Tumors derived from patients shrank in every case, and in many cases of aggressive ACC, the tumors disappeared completely. Importantly, the drug had little effect on less aggressive ACC-II tumors, which have lower levels of B7-H4. This shows that the treatment is highly specific to tumors with high B7-H4 levels. These results have already led to clinical trials that are testing similar drugs in patients with ACC. “These trials represent attractive, rationale therapeutic opportunities for patients facing this rare, aggressive, and chemo-refractory disease, for which no systemic therapy is currently available.” In conclusion, this discovery represents a significant breakthrough in ACC research, identifying B7-H4 as a crucial factor in cancer growth and immune evasion. By leading the way for personalized treatments, it offers promising new therapeutic options and the potential for improved outcomes for ACC patients. DOI - https://doi.org/10.18632/oncotarget.28661 Correspondence to - Renata Ferrarotto - rferrarotto@mdanderson.org Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28661 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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

“Precision medicine is an innovative approach to disease prevention and treatment that considers differences in people's genes, injuries, environments, and lifestyles to target the right therapies to the right patients at the right time.” Could a deeper understanding of one of the deadliest lung cancers lead to more effective treatments? Recent research offers a promising way forward, aiming to improve patient outcomes and provide clinicians with valuable insights. Small Cell Lung Cancer (SCLC) is a particularly aggressive form of lung cancer. It spreads fast and does not always respond well to conventional therapies such as chemotherapy. Although SCLC accounts for around 15% of all lung cancer cases, survival rates are extremely low. Only less than 5% of patients live more than five years after diagnosis. These alarming statistics highlight the critical need for new treatments. A team of researchers from the Federal University of Ceará, working together with collaborators from Argentina and Spain, may have found part of the solution. Full blog - https://www.oncotarget.org/2024/12/04/small-cell-lung-cancer-advancing-precision-medicine-with-biomarker-research/ Paper DOI - https://doi.org/10.18632/oncotarget.28660 Correspondence to - Fabio Tavora - fabio.tavora@argospatologia.com Author interview - https://www.youtube.com/watch?v=bJO2MD8AXkY Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28660 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, DLL3, pathology, biomarkers, qupath, small cell carcinoma About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). 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