Podcasts about ny october

BUFFALO, NY — October 27, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 17, 2025, titled “Depletion of the TRF1 telomere-binding protein leads to leaner mice with altered metabolic profiles.” In this study led by first author Jessica Louzame Ruano and corresponding author Maria A. Blasco from the Spanish National Cancer Centre (CNIO), researchers investigated the role of TRF1, a protein known for protecting telomeres, in regulating whole-body metabolism. The results suggest that TRF1 influences metabolic health through mechanisms unrelated to its known function in telomere maintenance. Obesity and metabolic disorders are major health concerns, especially as people age. To explore TRF1's role beyond telomere protection, the research team studied both normal mice and genetically modified mice that lacked TRF1. Mice without TRF1 remained leaner over time, resisted fat accumulation, and showed healthier blood sugar and insulin levels compared to normal mice. Importantly, these benefits occurred without any detectable shortening of telomeres. The leaner body composition in TRF1-deficient mice was not due to reduced food intake or increased physical activity. Instead, the fat loss appeared to result from biological changes in how energy was processed and stored. Male mice without TRF1 gained less weight and had lower LDL cholesterol levels, even on a high-fat diet. Female mice showed milder effects, reflecting known sex-based differences in susceptibility to diet-induced obesity. This highlights the importance of including both sexes in metabolic research. “Major metabolic pathways related with energy production and regulation of metabolism homeostasis were also found downregulated in Trf1-deficient mice.” Gene expression analysis in the liver revealed shifts in several key pathways. Genes related to fat production, energy generation, and muscle growth were downregulated, while genes linked to inflammation and cholesterol synthesis were upregulated. The mice also showed signs of higher energy expenditure and a shift from using fat to protein as an energy source, possibly due to their reduced fat reserves. However, some older mice developed mild liver stress, including fibrosis and DNA damage, suggesting a possible long-term trade-off. Overall, this study expands the understanding of how telomere-related proteins influence more than just cellular aging. By identifying a connection between TRF1 and metabolism, the research opens new possibilities for targeting TRF1 or its pathways to address obesity and related conditions. Still, further studies are needed to clarify how TRF1 affects fat development and whether similar effects occur in humans. DOI - https://doi.org/10.18632/aging.206320 Corresponding author - Maria A. Blasco — mblasco@cnio.es Abstract video - https://www.youtube.com/watch?v=7AG3TBgDZIw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206320 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Trf1, metabolism, leaner, fat, telomeres To learn more about the journal, visit 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

BUFFALO, NY — October 23, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 11, 2025, titled “Roles of plasminogen activator inhibitor-1 in aging-related muscle and bone loss in mice.” In this study led by first author Takashi Ohira and corresponding author Hiroshi Kaji from Kindai University Faculty of Medicine, researchers found that female mice lacking the gene for plasminogen activator inhibitor-1 (PAI-1) were protected from age-related muscle weakness and bone thinning. This suggests that PAI-1 could be a potential target for future treatments to reduce frailty in aging populations. As the global population continues to age, more people are affected by conditions such as sarcopenia and osteoporosis. These disorders involve the progressive loss of skeletal muscle mass and bone density, leading to reduced mobility, a greater risk of falls, and a lower quality of life. To investigate the role of PAI-1 in aging, researchers compared young (6-month-old) and aged (24-month-old) male and female mice, with and without the PAI-1 gene. They found that PAI-1 levels increased with age in both sexes. However, only female mice lacking the PAI-1 gene experienced a significant reduction in age-related muscle and bone loss. Female mice without PAI-1 maintained stronger grip strength and greater muscle mass in their lower limbs. They also showed less cortical bone loss in their femurs and tibias. In contrast, male mice did not experience the same benefits, despite also showing increased levels of PAI-1 with age. These results suggest that PAI-1 contributes to aging-related decline in a sex-specific manner. “The present study found that lower limb muscle mass, gastrocnemius and soleus muscle tissue weights, and grip strength were significantly lower in 24-month-old male and female wild-type mice than in their 6-month-old counterparts.” PAI-1 plays key roles in blood clotting, inflammation, and cellular senescence—a process in which aging cells release harmful molecules that affect nearby tissues. One of these molecules, interleukin-6 (IL-6), is a major driver of inflammation. The researchers found that aged female mice lacking PAI-1 had lower IL-6 levels in both muscle and blood, suggesting that PAI-1 may contribute to muscle and bone loss by promoting inflammation. These protective effects were also not associated with changes in muscle protein turnover or reductions in fibrous tissue, reinforcing the idea that PAI-1's impact is likely driven by inflammatory signaling. This study highlights PAI-1 as a promising therapeutic target for slowing or preventing age-related declines in muscle and bone health, particularly in women. Since postmenopausal women are especially vulnerable to osteoporosis and frailty, a better understanding of how PAI-1 contributes to aging could lead to new strategies for maintaining strength and mobility in later life. Further research is needed to explore how PAI-1 interacts with other age-related biological changes and why its effects differ between sexes. DOI - https://doi.org/10.18632/aging.206318 Corresponding author - Hiroshi Kaji - hkaji@med.kindai.ac.jp Abstract video - https://www.youtube.com/watch?v=hg4qKf-oO2I Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit 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/@Aging-US 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 — October 21, 2025 — A new #editorial was #published in Aging-US on October 13, 2025, titled “Longevity clinics: between promise and peril.” In this editorial, Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), reviews the rapid rise of longevity clinics worldwide. Longevity clinics have emerged globally in response to increasing demand for personalized, preventive healthcare. Located in countries such as the United States, Switzerland, and the United Arab Emirates, these centers offer advanced diagnostic services, including genomic testing, advanced imaging, and multi-omics profiling. Their goal is to extend healthspan—the number of years a person lives in good health—through customized lifestyle interventions, nutritional guidance, and, in some cases, experimental therapies. “Longevity clinics embody an important vision: healthcare is personalized, preventive, and engaged.” Although the concept of proactive aging care is attractive, the editorial raises serious concerns about the scientific and ethical foundations of these clinics. Many operate outside conventional medical systems and lack connections to academic geroscience. This disconnection allows them to market expensive interventions without sufficient clinical validation. Program costs can range from €10,000 to over €100,000 per year, limiting access to wealthy individuals while leaving out populations most at risk for premature aging. Despite these challenges, Dr. Demaria notes that longevity clinics may contribute meaningfully to innovation. By collecting extensive, long-term health data from clients, these clinics have the potential to identify early biomarkers of aging and detect signs of age-related diseases. Unlike traditional clinical trials, which are limited in scope and duration, longevity clinics track a wide range of health data over time. When paired with artificial intelligence tools, this information could help advance the science of healthy aging. However, several risks remain. Many clinics lack standardized protocols, and the tools they use, such as biological age calculators or hormone therapies, often lack accuracy or clear clinical value. Without proper guidelines, clients may receive advice that is confusing or not scientifically supported. This can reduce public trust in the broader field of longevity research. To ensure these clinics contribute positively to health innovation, the editorial outlines different key steps: greater collaboration with academic researchers, the adoption of standardized protocols, increased transparency, and work toward regulatory clarity. Broader access must also be considered by developing scalable and more affordable models, possibly through partnerships with public health systems. Ultimately, longevity clinics represent both a major opportunity and a serious concern. If integrated responsibly with science, policy, and public health, they could support a shift toward personalized, preventive healthcare. Without this alignment, however, they risk reinforcing inequality and weakening the credibility of the science behind aging. DOI - https://doi.org/10.18632/aging.206330 Corresponding author - Marco Demaria — m.demaria@umcg.nl Abstract video - https://www.youtube.com/watch?v=Bt84xBdii0s To learn more about the journal, visit 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

BUFFALO, NY – October 20, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on October 16, 2025, titled “Widespread folate receptor expression in pediatric and adolescent solid tumors – opportunity for intraoperative visualization with the novel fluorescent agent pafolacianine.” In this study, led by first author Ashley C. Dodd from Ann & Robert H. Lurie Children's Hospital and corresponding author Timothy B. Lautz from the same institution and Northwestern University Feinberg School of Medicine, researchers discovered that folate receptor beta (FRβ) is widely expressed in various pediatric and adolescent solid tumors. This finding highlights FRβ as a promising target for improving the accuracy of tumor surgery using a fluorescent imaging agent known as pafolacianine. Pediatric cancers are often challenging to remove completely during surgery, particularly when tumors spread or form small metastases. Fluorescence-guided surgery is a method that helps surgeons better identify tumors during operations using special imaging dyes. However, commonly used dyes such as indocyanine green are not tumor-specific and rely on general features of blood vessel permeability, limiting their precision. In this study, researchers investigated the potential of pafolacianine, a next-generation dye that targets folate receptors, for pediatric use. Folate receptors are proteins commonly found on the surface of cancer cells. Pafolacianine is already FDA-approved for adults with ovarian and lung cancers due to its ability to bind these receptors and highlight tumors during surgery. The research team analyzed tissue samples from 13 young patients diagnosed with various cancers, including Wilms tumor, osteosarcoma, synovial sarcoma, rhabdomyosarcoma, Ewing sarcoma, and neuroblastoma. The results showed that FRα was predominantly absent, whereas FRβ was present in 100% of the tumor samples. Notably, FRβ appeared both on the tumor cells and in the surrounding tumor microenvironment but showed little to no expression in normal tissue, making it an excellent candidate for targeted imaging. “In this study, we performed immunohistochemistry staining on slides obtained from a range of pediatric patients with solid tumors.” This consistent expression of FRβ in pediatric tumors is a significant and novel finding. Earlier studies primarily linked FRβ to immune cells called tumor-associated macrophages. This study reveals that FRβ is also expressed directly on tumor tissue, which could help surgeons better distinguish cancer from healthy tissue during procedures. Based on these results, the team has launched a clinical trial to evaluate pafolacianine in children undergoing surgery for metastatic lung tumors. If successful, this method could make pediatric cancer surgery safer and more effective. Overall, this study suggests that targeting FRβ with pafolacianine could serve as a tumor-agnostic imaging strategy, applicable across a wide range of pediatric solid tumors. This represents a potential advancement in real-time surgical imaging and a step forward in pediatric cancer care. DOI - https://doi.org/10.18632/oncotarget.28772 Correspondence to - Timothy B. Lautz - TLautz@luriechildrens.org Abstract video - https://www.youtube.com/watch?v=0its0QkOcwM 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

BUFFALO, NY — October 17, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 8, 2025, titled, “Runx1 overexpression induces early onset of intervertebral disc degeneration.” In this study, led by first author Takanori Fukunaga from Emory University School of Medicine and corresponding author Hicham Drissi from Emory and the Atlanta VA Medical Center, researchers found that the Runx1 gene, when overactive in spinal disc cells, can accelerate age-related degeneration of the intervertebral discs. The findings offer new insight into the genetic factors that drive disc aging and suggest possible directions for treating chronic back pain. Intervertebral discs cushion the spine and support movement. Their deterioration is a major cause of lower back pain, especially with aging. At the center of each disc is the nucleus pulposus (NP), a gel-like core that contains proteins such as collagen and aggrecan, which help retain water and maintain structure. As people age, NP cells often lose their function, contributing to disc breakdown. Using a genetically modified mouse model, the researchers activated Runx1 specifically in NP cells. These mice developed signs of disc degeneration by five months of age, which is much earlier than normal. The overexpression of Runx1 led to the loss of healthy NP cells, an increase in abnormal cell types, and damage to disc structure. Levels of essential proteins like aggrecan and type II collagen decreased, while type X collagen increased, signaling unhealthy tissue changes. “To achieve NP-specific postnatal overexpression of Runx1, we crossed Krt19CreERT mice with Rosa26-Runx1 transgenic mice previously generated in our laboratory.” A key finding was that Runx1 overactivity did not kill cells directly. Instead, it caused premature cellular aging, known as senescence. Senescent cells lose the ability to repair tissue, creating an environment that accelerates degeneration. Markers of senescence were significantly elevated in the affected discs. The researchers also observed a dose-dependent response. The more Runx1 was activated, the more severe the degeneration was. This suggests that targeting Runx1 may be a promising strategy to prevent or slow disc aging. Overall, this study highlights the genetic and cellular processes that contribute to intervertebral disc degeneration, a leading cause of disability. By identifying Runx1 as a potential driver of early disc aging, the research opens new opportunities for intervention and treatment of degenerative spine conditions. DOI - https://doi.org/10.18632/aging.206316 Corresponding author - Hicham Drissi - hicham.drissi@emory.edu Abstract video - https://www.youtube.com/watch?v=BPwWbVBPIUM Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206316 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - cell senescence, aging, Runx1, nucleus pulposus, intervertebral disc degeneration 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/@Aging-US 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

Brent Morin and Adam Ray make their 7th appearance together with Rick on TYSO.

BUFFALO, NY – October 14, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on October 13, 2025, titled “Treatment of glioblastoma with tumor-specific amplitude-modulated radiofrequency electromagnetic fields.” The study, led by Hugo Jimenez from Wayne State University School of Medicine, Karmanos Cancer Institute, introduces a novel treatment approach for glioblastoma, an aggressive and often treatment-resistant brain cancer. The findings open a new potential path for patients who currently have limited therapeutic options. The approach uses a device developed by TheraBionic that delivers extremely low levels of radiofrequency electromagnetic fields, tuned to frequencies associated with glioblastoma. In laboratory experiments, this therapy significantly slowed the growth of multiple glioblastoma cell lines. It was especially effective against tumor stem cells, which are known to resist standard treatments and drive cancer reappearance. Researchers also found that the treatment's effects depend on a calcium channel in tumor cells known as Cav3.2 (CACNA1H). When this channel was blocked, the therapy lost its effectiveness, highlighting the channel's essential role in how tumor cells respond to the signal. The therapy also disrupted the process of cell division by interfering with the mitotic spindle, a structure critical for cell replication. This disruption was associated with changes in the expression of genes that regulate cell division, particularly those involved in the “Mitotic Roles of Polo-Like Kinase” pathway. These effects were specific to tumor-targeted frequencies, as non-matching signals had no measurable impact. The study also includes data from two patients with difficult-to-treat brain tumors who received the therapy through compassionate use. One patient with recurrent glioblastoma showed signs of clinical and radiographic improvement after one month of treatment. Another patient with oligodendroglioma tolerated the therapy well and had stable disease during follow-up imaging. Neither patient experienced serious side effects, further supporting the safety of the therapy. “There was evidence of clinical and radiological benefit in a 38-year-old patient with recurrent GB and evidence of safety and feasibility in a 47-year-old patient with oligodendroglioma.” This is the first study to demonstrate that tumor-specific radiofrequency therapy can suppress both tumor growth and cancer stem cells in glioblastoma. Similar results had previously been observed in liver and breast cancers. These findings contribute to the growing body of evidence supporting a new class of systemic, non-toxic cancer therapies. Further clinical trials will be crucial to confirm these results and fully assess the potential of this approach for treating brain cancer. DOI - https://doi.org/10.18632/oncotarget.28770 Correspondence to - Hugo Jimenez - hugo.jimenez@wayne.edu Abstract video - https://www.youtube.com/watch?v=uxYnWcNKYfg Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28770 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, oncology, amplitude-modulated radiofrequency electromagnetic fields, glioblastoma, TheraBionic, CACNA1H, Cav3.2 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 — October 14, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 30, 2025, titled, “Glycocalyx-targeted therapy prevents age-related muscle loss and declines in maximal exercise capacity.” In this study, led by Daniel R. Machin from the University of New Mexico School of Medicine and the University of Utah, researchers found that protecting a fragile layer lining blood vessels, known as the glycocalyx, can prevent muscle deterioration and help maintain physical performance during aging. They also discovered that a supplement containing high-molecular-weight hyaluronan (HMW-HA), a key component of the glycocalyx, enabled older mice to preserve muscle mass and exercise capacity. These findings suggest that targeting the glycocalyx may offer a new approach to reduce frailty and support mobility in older adults. As this layer degrades with age, it contributes to cardiovascular and muscular decline by impairing blood flow and vascular health. The study examined how preserving the glycocalyx using a therapy called Endocalyx™ affects physical function in aging mice. Researchers first studied genetically modified mice lacking Has2, the enzyme responsible for producing HMW-HA. These mice had a thinner glycocalyx, reduced exercise performance, and lower mitochondrial function in their muscles, even though muscle size remained normal. This indicated that glycocalyx damage alone can directly impair physical performance. The team then gave older mice a diet containing Endocalyx™ for 10 weeks. Compared to untreated controls, these mice maintained muscle mass and performed better on treadmill tests. Notably, the treated mice did not show the typical age-related decline in muscle strength and endurance. While the supplement did not fully restore youthful performance, it significantly slowed physical deterioration, suggesting a protective benefit. In contrast, untreated older mice lost both body mass and muscle volume during the same period. “Taken together, these findings provide direct evidence of a role for HMW-HA in the modulation of exercise capacity.” This research builds on prior evidence that the glycocalyx is essential for healthy blood vessel function. Since muscle health depends on proper blood flow and oxygen delivery, restoring the glycocalyx may help maintain strength and mobility with age. While more research is needed to confirm these results in humans, the findings point to a potential therapeutic approach to promote healthier aging. DOI - https://doi.org/10.18632/aging.206313 Corresponding author - Daniel R. Machin — dmachin@salud.unm.edu Abstract video - https://www.youtube.com/watch?v=S7HjCeXT8fU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206313 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, glycocalyx, hyaluronan 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

BUFFALO, NY — October 9, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 22, 2025, titled, “The impact of long-term social housing on biconditional association task performance and neuron ensembles in the anterior cingulate cortex and the hippocampal CA3 region of aged rats.” The research team led by Anne M. Dankert from Providence College and University of North Carolina, Chapel Hill, showed that aged rats who lived in socially enriched environments throughout life retained better memory and cognitive flexibility than those housed alone. This study highlights the importance of social interaction in protecting the aging brain. Cognitive decline, such as memory loss and reduced problem-solving ability, affects many people over the age of 65. While many factors contribute to age-related cognitive decline, this study suggests that one key factor may be surprisingly simple: long-term social connection. To explore how social interaction might influence memory performance and brain activity, the researchers designed a study using rats as a model for aging in humans. “Cognitive decline and changes in neuronal activity are hallmarks of aging.” They compared three groups of rats: young adults, aged rats housed alone, and aged rats housed socially in groups. All groups had access to the same physical enrichment, such as exercise and stimulating objects, but only some experienced lifelong social companionship. The team tested these animals on a complex memory challenge known as the biconditional association task, which requires animals to make context-based decisions—an ability that typically declines with age. The results showed that aged rats living in social groups performed just as well as young adults on the memory task, while those housed alone showed significant impairments. Socially housed rats also made fewer working memory errors and required less effort to complete cognitive tasks, suggesting not only better performance but more efficient brain function. These benefits were not observed in aged rats who received only environmental enrichment without social interaction. Brain imaging revealed additional differences between the groups. Socially housed aged rats showed increased activity in the hippocampus, particularly in the CA3 region, which plays a key role in forming and separating memories. In contrast, aged rats that lived alone had lower activity in this region, which may explain their poorer performance. Interestingly, socially housed rats also showed reduced overactivity in the anterior cingulate cortex—a brain area involved in attention and decision-making—suggesting a more balanced and efficient neural response. This research provides new insight into how lifelong social experiences shape brain health during aging. While earlier studies have shown that physical activity and cognitive stimulation help preserve cognitive function, this study identifies social interaction as an independent and powerful protective factor. The findings are consistent with human studies showing that older adults who remain socially active tend to experience slower cognitive decline and stronger brain function. Overall, these results emphasize that brain aging is not inevitable but may be influenced by our social environments. This research suggests that fostering lifelong social connections could be a critical, low-cost strategy to protect memory and mental flexibility in older adults. DOI - https://doi.org/10.18632/aging.206310 Corresponding author - Anne M. Dankert - adankert@unc.edu Abstract video - https://www.youtube.com/watch?v=poNnPz1ti6Q https://www.aging-us.com/ MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – October 8, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on October 6, 2025, titled “ACTM-838, a novel systemically delivered bacterial immunotherapy that enriches in solid tumors and delivers IL-15/IL-15Rα and STING payloads to engage innate and adaptive immunity in the TME and enable a durable anti-tumor immune response.” In this study, led by first author Kyle R. Cron and corresponding author Akshata R. Udyavar, researchers from Actym Therapeutics developed a new form of bacterial immunotherapy called ACTM-838. This treatment safely delivers immune-activating proteins directly to solid tumors. The approach may offer a new option for cancer patients whose solid tumors are resistant to current immunotherapies. Solid tumors often suppress the immune system, making it difficult for treatments like immune checkpoint inhibitors to work effectively. ACTM-838 was designed to overcome this challenge by targeting phagocytic immune cells within the tumor microenvironment (TME). Once inside the tumor, the therapy delivers two immune-stimulating components: IL-15/IL-15Rα and a modified version of STING. Both are known to activate the body's innate and adaptive immune responses. This combination of immune-stimulating proteins helps shift the TME from immune-suppressive to immune-permissive, enabling the body's natural defenses to fight the cancer. “STACT is a modular, genetically engineered live attenuated S. Typhimurium bacterial platform that enables tissue-specific localization and cell-targeted delivery of large, multiplexed payloads via systemic administration.” The study highlights how ACTM-838, built on a specially modified strain of Salmonella Typhimurium, safely targets tumors and avoids healthy tissue after intravenous injection. This targeted delivery reduces the risk of side effects while ensuring the immune-boosting agents reach their intended location. Importantly, ACTM-838 also showed significantly reduced inflammatory toxicity compared to its parent bacterial strain, which had previously presented challenges in clinical use. In preclinical tests, ACTM-838 shrank tumors and prevented their recurrence after treatment. Mice that were cured of tumors resisted re-injection with cancer cells, suggesting the development of long-lasting immune memory. The therapy also showed strong synergy with anti-PD1 drugs, a widely used class of cancer treatments, further improving outcomes in both treatment-resistant and responsive tumor models. Researchers also found that ACTM-838 changed the composition of immune cells within the tumor. It increased beneficial cells like cytotoxic T-cells and antigen-presenting macrophages, while reducing suppressive cell types such as regulatory T-cells and exhausted T-cells. These effects were confirmed through genetic analysis and cellular studies, pointing to a broad and coordinated immune response. This study offers proof-of-concept that live bacterial therapy can safely and effectively deliver gene-based immune modulators directly to tumors. With ACTM-838 now being tested in a Phase I clinical trial, the findings offer a new direction for cancer treatment strategies that activate the body's own immune system, particularly in difficult-to-treat cases where other therapies fail. DOI - https://doi.org/10.18632/oncotarget.28769 Correspondence to - Akshata R. Udyavar - akshata.udyavar@pfizer.com Abstract video - https://www.youtube.com/watch?v=fr5OR3tvC_I 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 — October 7, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on August 27, 2025, titled, “Deregulated miR-145 and miR-27b in Hutchinson-Gilford progeria syndrome: implications for adipogenesis.” In this study, led by first author Felix Quirin Fenzl and corresponding author Karima Djabali from the Technical University of Munich (TUM), researchers identified that miR-145-5p and miR-27b-3p interfere with the formation of fat cells in children with Hutchinson-Gilford progeria syndrome (HGPS), a rare and fatal premature aging disorder. Their findings help explain why patients often experience fat loss and related metabolic complications and suggest new potential therapeutic strategies. Hutchinson-Gilford progeria syndrome is a genetic condition that causes rapid aging in children, often leading to early death due to heart disease. Although affected children appear healthy at birth, they soon develop signs of accelerated aging, including hair loss, stiff joints, and a significant reduction in fat tissue. While certain treatments can slow disease progression, many aspects, such as the loss of fat tissue, remain poorly understood. “Overall, this study provides the first comprehensive miRNA profiling of HGPS and control fibroblasts across different stages of cellular senescence.” This study focused on how microRNAs—tiny molecules that help regulate gene expression—contribute to the disease. To explore this, the researchers used skin-derived stem cells from both healthy individuals and HGPS patients. When they transformed these cells into fat cells, the HGPS-derived stem cells formed significantly fewer fat cells. This difference was linked to unusually high levels of miR-145-5p and miR-27b-3p. These molecules were found to silence important genes required for fat cell growth and function. When the researchers blocked these microRNAs, fat cell formation improved. The team also examined fat tissue from a mouse model of HGPS. Similar to the human cells, these mice showed increased levels of miR-145-5p and miR-27b-3p and impaired fat development. These results confirm that these two microRNAs play a central role in the loss of fat tissue seen in the disease. Importantly, reducing their activity could become a promising therapeutic strategy for restoring fat tissue in affected individuals. Although further research is needed before developing treatments, this study represents a step forward in understanding the molecular causes of lipodystrophy, a condition in which the body cannot form healthy fat tissue, in HGPS. It also opens the door for future therapies that could improve quality of life and health outcomes for patients. In the long term, similar approaches might benefit people with other metabolic diseases, such as obesity or diabetes, where fat cell function is also disrupted. DOI - https://doi.org/10.18632/aging.206309 Corresponding authors - Karima Djabali — djabali@tum.de Abstract video - https://www.youtube.com/watch?v=b0ksC3cvdZ0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206309 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Hutchinson-Gilford progeria syndrome (HGPS), progerin, microRNAs, adipogenesis 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

BUFFALO, NY — October 3, 2025 — A new #research perspective was #published in Volume 17, Issue 9 of Aging-US on August 26, 2025, titled “Analysis of the current state of frailty indexes and their implementation for aging intervention studies.” In this work, led by first author Oliver G. Frost from Loughborough University alongside corresponding authors Abdelhadi Rebbaa and Amit Sharma, from the Lifespan Research Institute, the authors explore growing concerns about the lack of standardization in how frailty is measured in rodent aging studies, which may limit the development of effective interventions targeting age-related decline. Frailty, a key indicator of deteriorating health in older adults, is increasingly assessed in preclinical models using frailty indexes (FIs). These indexes quantify health deficits, such as reduced mobility, cognitive decline, or physical weakness. However, this perspective highlights that FI methodologies vary significantly across studies, from the selection of parameters to the cut-off thresholds used, resulting in inconsistent outcomes that affects reproducibility and translational value. The authors reviewed 18 rodent studies and found substantial variation in how frailty is defined and measured. Some FIs rely on clinical observations, such as appearance or beahaviour, while others focus on physical performance metrics like grip strength or locomotion. In several cases, applying different FIs to the same group of animals produced contradictory results, underscoring the importance of harmonized protocols. To illustrate these issues, the researchers applied an 8-item FI to mice of different ages and found that even young mice were sometimes scored as frail, depending on the scoring method and reference values. This finding emphasizes the need for consistent baselines and controlled environments, especially when comparing across studies. The authors recommend using each animal as its own baseline in longitudinal studies, a strategy that enhances reliability without adding significant cost. “Sex as a biological variable in FIs is an important consideration, as there is a known difference between male and female frailty onset and progression.” The authors also discuss emerging automated tools, such as video-based open-field testing, which can reduce observer bias and improve reproducibility. In the future, broader health indicators, such as cognition, circadian rhythms, social behavior, and body composition, may further enhance frailty assessments. Overall, this work underscores the urgent need for standardized, transparent, and reproducible methods for evaluating frailty in preclinical aging studies. Improved consistency in frailty scoring will better inform the development of healthspan-extending therapies and enhance the translational relevance of animal models. DOI - https://doi.org/10.18632/aging.206307 Corresponding authors - Abdelhadi Rebbaa - rebbaa@gmail.com, and Amit Sharma - amit.sharma@sens.org Abstract video - https://www.youtube.com/watch?v=eha3XA9LyWA Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206307 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, frailty, rodents, frailty index, phenotype 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

BUFFALO, NY - October 1, 2025 – Oncotarget is proud to announce that its Editor-in-Chief, Wafik S. El-Deiry, MD, PhD, FACP, will chair the WIN Symposium as the Oncology Track of the Advancing Precision Medicine (APM) Annual Conference held October 3–4, 2025, at the Pennsylvania Convention Center in Philadelphia. The WIN Consortium annual symposium featured as the Oncology Track of the APM Annual Conference 2025 unites global leaders in oncology, translational science, and precision medicine. This year's program features keynote lectures, multi-track sessions– WIN Symposium, Multi-Omics Integration and Precision Medicine Outside of Oncology– and networking opportunities designed to accelerate the translation of research into clinical practice. Highlights include: --A keynote at opening of the WIN Symposium in Philadelphia by William G. Kaelin, Jr., MD — 2019 Nobel Laureate. --Other luminaries in Oncology are speaking, including AACR President Lillian Siu, MD and AACR President-Elect Keith Flaherty, MD along with internationally recognized leaders in precision oncology. --A world-class precision oncology molecular tumor board and oral presentations from the most competitive abstracts are part of the program. --Multi-omics and disease-specific tracks spanning oncology, neurology, cardiovascular disease, rare disease, and infectious disease. --Opportunities for collaboration among scientists, clinicians, industry innovators, and policymakers. Registration is still open. Attendance is free for students, academic/government/non-profit participants, healthcare providers, and investors. The event provides CME credits. For full program details, visit the APM Annual Conference website. About WIN Consortium: WIN Consortium is a non-profit association headquartered in France. WIN was the first consortium that assembled all stakeholders of cancer care, from academia, industry, and patient advocates to work together across the globe. The WIN network assembles 34 world-class academic medical centers, industries, research organizations and patient advocates spanning 18 countries and 5 continents, aligned to launch trials to bolster Precision Oncology across the world. It was also the first organization to launch a N-of-One study using transcriptomics in addition to genomics to inform therapeutic choice in the WINTHER study. WIN is the organizer of the WIN symposia in Precision Oncology. 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

BUFFALO, NY — October 1, 2025 — A new #research paper #featured as the #cover of Volume 17, Issue 9 of Aging-US was published on August 21, 2025, titled “Sex-specific longitudinal reversal of aging in old frail mice.” The study, led by first author Cameron Kato and corresponding author and Aging-US Editorial Board Member Irina M. Conboy from the University of California, Berkeley, reports that a combination of oxytocin and an Alk5 inhibitor (OT+A5i) significantly extended both lifespan and healthspan in frail, elderly, male mice. These rejuvenating effects were not seen in female mice, highlighting key biological differences between the sexes in their response to aging therapies. The researchers tested a dual-drug approach targeting two biological pathways that change with age. Oxytocin, a hormone that declines with aging and supports tissue repair, was combined with an Alk5 inhibitor that blocks the TGF-beta pathway. TGF-beta becomes overactive with age and contributes to chronic inflammation and tissue damage. In this study, frail mice at 25 months of age—roughly equivalent to 75 human years—were treated regularly with the OT+A5i combination. Male mice receiving the therapy lived over 70% longer than untreated controls and showed significant improvements in physical endurance, agility, and memory. According to hazard ratio analysis, the treated males were nearly three times less likely to die at any given time than untreated males. “Treatment of old frail male mice with OT+A5i resulted in a remarkable 73% life extension from that time, and a 14% increase in the overall median lifespan.” The therapy also reduced “biological noise” in circulating blood proteins—an established marker of aging—bringing those levels back to a more youthful state. Short-term benefits, were seen in both sexes, however, after four months of continuous treatment, only the male mice showed sustained improvement in systemic protein balance. Female mice did not experience significant gains in lifespan or healthspan, though middle-aged females did show improved fertility after treatment. These results underscore the importance of understanding sex-specific biology when developing treatments for aging. While the reasons for these differences remain unclear, the findings provide a new model for studying and designing longevity therapies. Oxytocin is already FDA-approved, and Alk5 inhibitors are currently in clinical trials, suggesting that this approach could be translated to humans. With strong results in aged and frail male animals, OT+A5i appears to be a promising candidate for improving late-life health and survival. DOI - https://doi.org/10.18632/aging.206304 Corresponding author - Irina M. Conboy - irina@generationlab.co Abstract video - https://www.youtube.com/watch?v=bpWxDd7hHhM Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206304 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, lifespan, healthspan, Alk5 inhibitor, oxytocin, sex-specific differences 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

Craig takes his shoes off to talk about stuff with Rick Glassman. Watch video here: https://youtu.be/fIwvlt93zsM

This week on Toon'd In!, Jim Cummings welcomes the electric and ever-animated Ryan Drummond! Beloved by fans around the world as the original voice of Sonic the Hedgehog in the iconic Sonic Adventure series, Ryan brings a whirlwind of energy, talent, and behind-the-scenes stories from his dynamic career in voiceover, theater, and beyond.In this lively and nostalgic episode, Ryan opens up about stepping into the role of Sega's blue blur at a pivotal moment in gaming history, what it was like bringing attitude and heart to one of pop culture's most recognizable characters, and how his love of performing has taken him from sound booths to Broadway stages.Jim and Ryan geek out over the evolution of Sonic, the challenges of voicing fast-paced characters, and the unique bond that forms between a voice actor and a global fanbase. With laughter, insight, and a few unexpected impressions, Ryan reminds us why voice actors are the unsung heroes behind our favorite characters—and why Sonic will always be more than just a game.

Rhett & Link from (Mythical Pod and Mythical Kitchen) and their wonder holes take their shoes off.

Cristina Mariani takes her shoes off to talk with Rick. Watch on YouTube: https://youtu.be/dp7lTlHNCWY?si=qA1E4oeZ8LD0pLbB

Kevin Nealon (Saturday Night Live, Happy Gilmore, The Larry Sanders Show, Weeds, Hiking with Kevin) takes his shoes off and becomes BFFs with Rick Glassman.

The AC is broken and it's HOT. Ian Fidance and Rick Glassman take their shoes AND pants off (to put on shorts). WATCH ON YOUTUBE HERE: https://youtu.be/nUs7QYaZvpw

Blaine Anderson is a professional dating coach and match maker.

Dax Flame takes his shoes off AGAIN and talks with Rick Glassman about stuff.

Veronika Slowikowska, of Tires and the Nevermind Podcast, makes her first TYSO appearance and she and Rick meet for the first time. And let's just say they "podcast," during a sleepover, if you know what I mean. ;)

Jerrod Carmichael makes his first TYSO appearance and boy are our arms tired! Check out the follow up to Emmy Award Winning "Rothaniel," his newest stand up special, "Jerrod Carmichael: Don't Be Gay." On HBO here: https://www.hbomax.com/movies/jerrod-carmichael-dont-be-gay/797f6457-02b4-4309-8996-998dcf203d0d

Lisa takes her shoes off with Rick. Don't believe me? Hahahaha oooooookay...

Love on the Spectrum's Abbey Romeo & David Isaacman take their shoes off. With them are Abbey's mom, Christine and TYSO House Musician, George Krikes. Songs, laughs, and more on this episode of Take Your Shoes Off! Watch on YouTube here: https://youtu.be/x7xFg5bgOhQ

BUFFALO, NY- October 31, 2024 – A new #research paper was #published as the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20, entitled, “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity.” This paper summarizes recent advances in healthspan biotechnology discussed at the 2023 Aging Research and Drug Discovery Meeting (ARDD), where leading experts reviewed breakthroughs in artificial intelligence (AI), biomarkers, aging clocks, geroscience, and clinical trials that support healthier, longer lives. The authors present a comprehensive view of how these technologies are shaping research and industry approaches to aging, focusing on targeting aging itself to reduce multiple age-related diseases and extend the healthy years of life. With people living longer, addressing age-related health issues is more critical than ever. Traditional healthcare often treats age-related diseases individually, overlooking aging as a core issue. Longevity biotechnology seeks to change this by combining AI with biomarker analysis to detect early signs of aging, enabling targeted interventions that not only delay disease but also promote longer, healthier lives. Led by corresponding authors Yu-Xuan Lyu from Southern University of Science and Technology Shenzhen; Alex Zhavoronkov from Insilico Medicine AI Limited, Masdar City, Abu Dhabi; Morten Scheibye-Knudsen and Daniela Bakula from the Center for Healthy Aging, University of Copenhagen, this research synthesizes the potential of AI to identify precise biomarkers of aging, supporting the development of "aging clocks"—tools that use biological data to estimate a person's biological age and health risks. These tools help clinicians tailor prevention and treatment to individual needs. Additionally, AI speeds up the discovery of drugs that target primary aging drivers, such as cellular damage and decreased cellular energy, offering the potential to slow, prevent, or even reverse certain effects of aging and enhance quality of life. “The fusion of AI with biomarker research has markedly revolutionized the way biomarkers are identified and validated in the field of ageing.” This approach not only promises to slow, prevent, or even reverse certain effects of aging but also emphasizes the potential for AI-driven methods to extend healthspans. In conclusion, the authors emphasize the need for continued investment in AI-driven therapies and biomarker research, which hold the potential to redefine aging care and improve health outcomes as people grow older. 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 short - https://www.youtube.com/watch?v=Hpfe5WJ5g7I 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 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- October 30, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on October 11, 2024, entitled “Initiation of tumor dormancy by the lymphovascular embolus.” Researchers Yin Ye, Justin Wang, Michael G. Izban, Billy R. Ballard, and Sanford H. Barsky from Meharry Medical College in Nashville, TN, and Scripps Mercy Hospital in San Diego, CA, uncovered critical mechanisms that lead to tumor dormancy in breast cancer. This study sheds light on how certain cancer cells can remain dormant for years before potentially reawakening as metastatic tumors. Using breast cancer patient-derived organoids and tumor samples, the research team discovered that tumor dormancy in breast cancer can be triggered by specific signaling changes within small cell clusters, called tumor emboli, which detach from the primary tumor and travel through the bloodstream. These emboli can remain inactive, sometimes for years, before reawakening in other parts of the body. Key changes include reduced activity of mTOR, a metabolic regulator, and structural shifts in E-cadherin, a molecule involved in cell adhesion. This study also suggests these changes are regulated by the PI3K pathway and occur within the unique three-dimensional structure of tumor spheroids, shedding light on the interactions within dormant cell clusters. As a conclusion, this work not only identifies mTOR and E-cadherin as key components in maintaining dormancy but also offers a promising roadmap for future therapies. By targeting these pathways, there may be potential to keep cancer cells in a dormant state, reducing the risk of late-stage recurrence and improving patient outcomes. DOI - https://doi.org/10.18632/oncotarget.28658 Correspondence to - Sanford H. Barsky - sbarsky@mmc.edu Video short - https://www.youtube.com/watch?v=z6ex7Yl8r5Q Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28658 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, dormancy, lymphovascular embolus, mTOR, E-cadherin proteolysis 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- October 29, 2024 – A new #casereport was #published in Oncotarget's Volume 15 on October 11, 2024, entitled “Complete response to encorafenib plus binimetinib in a BRAF V600E-mutant metastasic malignant glomus tumor.” As highlighted in the abstract, glomus tumors (GT) are rare mesenchymal neoplasms originating in dermal arteriovenous structures involved in thermoregulation. While generally benign, some can exhibit malignant features, leading to aggressive behavior, metastasis, and limited response to standard chemotherapy. The identification of the BRAF V600E mutation in certain malignant GT cases offers a promising therapeutic target. In their paper, researchers Marta Arregui, Antonio Calles, María del Mar Galera, Ana Gutiérrez, Carlos López-Jiménez, Carolina Agra, Adriana Fernández, Natalia Gutiérrez, María de Toro and Rosa Álvarez from Gregorio Marañón University Hospital and Fundación Jiménez Díaz University Hospital in Madrid, Spain, document a remarkable clinical and metabolic response in a case of metastatic BRAF V600E-mutated glomangiosarcoma treated with the combination of encorafenib and binimetinib. They report on a 45-year-old male patient with stage IV malignant GT carrying a BRAF V600E mutation, who was treated systemically with encorafenib and binimetinib. This approach led to a swift clinical and radiological improvement. “To our knowledge, our patient represents the first reported case of a metastatic malignant GT successfully treated with BRAF and MEK inhibitors, achieving a long-lasting complete morpho-metabolic response.” DOI - https://doi.org/10.18632/oncotarget.28654 Correspondence to - Carlos López-Jiménez - clopezjimenez@atbsarc.org Video short - https://www.youtube.com/watch?v=xjbj3Iu16P4 Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28654 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, malignant glomus tumor, glomangiosarcoma, BRAF V600E, agnostic treatment, targeted therapy 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- October 29, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science) Volume 16, Issue 19 on October 14, 2024, entitled “Integrating cardiovascular risk biomarkers in the context of inflammaging.” Cardiovascular diseases (CVD) remain the leading cause of death worldwide, accounting for nearly one-third of all global mortalities. Risk assessment for CVD has traditionally focused on well-known factors linked to atherosclerosis, including demographics, lifestyle choices like smoking and physical activity, and conditions such as diabetes, hypertension, and obesity. Biomarkers, such as non-HDL cholesterol, have also played a key role in identifying those at risk. However, significant residual cardiovascular risk persists despite managing these established risk factors, suggesting additional, unaddressed contributors to cardiovascular health. In their paper, researchers Jacopo Sabbatinelli, Matilde Sbriscia, Fabiola Olivieri, and Angelica Giuliani from Università Politecnica delle Marche and IRCCS INRCA in Ancona, Italy, explore how integrating specific cardiovascular biomarkers could help assess this residual inflammatory risk, particularly in the context of aging-related inflammation, or “inflammaging.” The biomarkers investigated—high-sensitivity C-reactive protein (hs-CRP), high-sensitivity cardiac troponin (hs-cTn), and natriuretic peptides—serve as valuable indicators of both inflammatory burden and early cardiovascular risk. In conclusion, the authors demonstrate that combining markers of chronic inflammation with cardiac health indicators offers a more complete understanding of cardiovascular risk and reveals the impact of aging-related inflammation, or “inflammaging,” on heart health. Researchers suggest that this approach opens new avenues for targeted interventions in aging populations. DOI - https://doi.org/10.18632/aging.206136 Corresponding author - Jacopo Sabbatinelli - j.sabbatinelli@staff.univpm.it Video short - https://www.youtube.com/watch?v=yJJXbwHj6hs Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206136 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cardiovascular disease, inflammaging, cardiac biomarkers, residual inflammatory risk 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

Qool DJ Marv Live at Dumbo House Brooklyn NY - October 27 2024 - Mauve ---     https://www.sohohouse.com/en-us/houses/dumbo-house     +    Artwork: https://www.artbyycolemanburney.com/      ---    https://www.youtube.com/channel/UC5gQLsodBsCys1_3Zbm83vg        https://podcasts.apple.com/gb/podcast/qool-dj-marv-aural-memoirs-and-buttamilk-archives/id269880758        https://music.apple.com/us/artist/qool-dj-marv/1558418894        https://www.instagram.com/qooldjmarv/        https://qooldjmarv.bandcamp.com/album/sound-paths-v-1        https://tidal.com/browse/artist/23883666        https://www.mixcloud.com/qooldjmarv/        https://open.spotify.com/artist/48vhJ2d1hVaFHf6gqXeTm0?si=fWO0N456QeWRMWLUtqe4Yg        https://twitter.com/qooldjmarv        https://www.threads.net/@qooldjmarv        https://www.facebook.com/MarvJColeman/        https://soundcloud.com/qooldjmarv    

BUFFALO, NY- October 24, 2024 – 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 19 on October 3, 2024, entitled “A new model and precious tool to study molecular mechanisms of macrophage aging.” As highlighted in the abstract, the accumulation of senescent cells, marked by a senescence-associated secretory phenotype (SASP), plays a role in chronic inflammation and age-related diseases (ARD). During aging, macrophages can develop a senescent-like phenotype with altered functions, promoting the buildup of senescent cells. In the context of aging and ARD, controlling the resolution of inflammation and preventing chronic inflammation—particularly by targeting macrophages—should be a priority. In their paper, researchers Rémy Smith, Kévin Bassand, Ashok Dussol, Christophe Piesse, Eric Duplus, and Khadija El Hadri from Sorbonne Université in Paris and Université Sorbonne Paris Nord in Bobigny, France, developed an in vitro model of murine peritoneal macrophage aging. Using this model, they demonstrated that chronic treatment with CB3, a thioredoxin-1 mimetic anti-inflammatory peptide, completely prevents the increase of p21CIP1 and allows day 14 macrophages to maintain their proliferative activity. "We describe a new model of macrophage aging with a senescence-like phenotype associated with inflammatory, metabolic and functional perturbations.” DOI - https://doi.org/10.18632/aging.206124 Corresponding authors - Eric Duplus - eric.duplus@sorbonne-universite.fr, and Khadija El Hadri - khadija.zegouagh@sorbonne-universite.fr Video short - https://www.youtube.com/watch?v=LfN78LR-CYU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206124 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, macrophage, inflammation, senescence, thioredoxin-1 mimetic peptide 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- October 23, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on October 11, 2024, entitled, “Gene regulatory network and signalling pathway rewiring: How blood cancer cells shift their shapes to evade drug treatment.” As highlighted in the paper, Acute Myeloid Leukemia (AML) is a complex and diverse disease caused by multiple mutations in genes that regulate transcription and growth. These mutations lead to extensive rewiring of the gene regulatory network (GRN), which alters the identity of hematopoietic stem and progenitor cells, ultimately blocking normal myeloid differentiation. A key feature of AML is the presence of mutations in growth factor receptor and signaling genes, such as FLT3, KIT, and RAS. Notably, FLT3 is one of the most commonly mutated genes in AML, with around 25% of cases showing an internal tandem duplication (ITD) that causes the receptor to remain constantly active. In their paper, researchers Constanze Bonifer and Peter N. Cockerill from the Institute of Cancer and Genomic Sciences at the University of Birmingham, UK, and the Murdoch Children's Research Institute, Royal Children's Hospital in Melbourne, Australia, discuss recent publications from their group addressing this issue through a multi-omics study. The authors investigated how gene regulatory networks (GRNs) in FLT3-ITD patients were rewired compared to normal cells and in response to FLT3 inhibitor treatment. Several key findings stood out, including: 1) Mapping of open chromatin regions revealed that patients initially responsive to FLT3 inhibition showed significant rewiring of their GRNs, forming new connections between transcription factors (TFs) and target genes, while non-responsive patients did not; 2) Chromatin immunoprecipitation (ChIP) experiments showed that drug treatment led to the loss of binding of RUNX1, the master regulator of hematopoiesis, and the MAP-Kinase (MAPK)-inducible TF AP-1; 3) Disruption of AP-1 binding via a dominant-negative version of the TF (dnFOS) also abolished RUNX1 binding at hundreds of sites, indicating that RUNX1 binding is AP-1 dependent; and 4) Inhibition of both AP-1 and RUNX1 led to a pronounced cell cycle block. “In summary, drugs that target individual signalling pathways in AML often fail to stop proliferation malignant growth, due to the wide variety, redundancy and cross talk between multiple pathways regulating and differentiation.” DOI - https://doi.org/10.18632/oncotarget.28662 Correspondence to - Constanze Bonifer - constanze.bonifer@mcri.edu.au Video short - https://www.youtube.com/watch?v=5c_uT6aE36A Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28662 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, acute myeloid leukemia, gene regulatory networks, aberrant growth factor signaling, transcription, RUNX1/AP-1 axis 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

BUFFALO, NY- October 22, 2024 – 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 19 on September 26, 2024, entitled, “Use of the senolytics dasatinib and quercetin for prevention of pelvic organ prolapse in a mouse animal model.” Pelvic organ prolapse is a common condition among women in the U.S., with a 13% estimated risk of requiring surgery by age 80. Senolytic agents like dasatinib and quercetin (D+Q) target age-related cellular senescence and reduce senescent cell activity in various disease processes. In their paper, researchers Erryn Tappy, Haolin Shi, Jessica Pruszynski, and Maria Florian-Rodriguez from the University of Texas Southwestern Medical Center, Department of Obstetrics and Gynecology in Dallas, utilized a mouse model of pelvic organ prolapse, Fibulin-5 knockout (Fbln-5-/-) mice, to assess the ability of D+Q to prevent development of prolapse. The D+Q injections administered did not result in significant differences in prolapse development but did reduce cellular senescence markers in Fbln-5-/- mice. This suggests senolytic agents may help mitigate the role of cellular senescence in tissue dysfunction associated with prolapse. The researchers suggest that further studies are needed to determine optimal timing, dosage, and delivery of senolytics for prolapse prevention. "This study represents one of the first to evaluate the impact of senolytic agents D+Q on the clinical development of pelvic organ prolapse and expression of proteins associated with cellular senescence in a mouse model.” DOI - https://doi.org/10.18632/aging.206120 Corresponding author - Maria Florian-Rodriguez - Maria.Florian-Rodriguez@UTSouthwestern.edu Video short - https://www.youtube.com/watch?v=kTQfjhubx_4 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206120 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, pelvic organ prolapse, cellular senescence, senolytic agents, animal model 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

Qool DJ Marv Live on the deck at Dumbo House Brooklyn NY - October 20 2024 - ...Before it Gets Cold --- https://www.sohohouse.com/en-us/houses/dumbo-house + Image: https://www.coreybarksdale.com/index.html ---     https://www.youtube.com/channel/UC5gQLsodBsCys1_3Zbm83vg        https://podcasts.apple.com/gb/podcast/qool-dj-marv-aural-memoirs-and-buttamilk-archives/id269880758        https://music.apple.com/us/artist/qool-dj-marv/1558418894        https://www.instagram.com/qooldjmarv/        https://qooldjmarv.bandcamp.com/album/sound-paths-v-1        https://tidal.com/browse/artist/23883666        https://www.mixcloud.com/qooldjmarv/        https://open.spotify.com/artist/48vhJ2d1hVaFHf6gqXeTm0?si=fWO0N456QeWRMWLUtqe4Yg        https://twitter.com/qooldjmarv        https://www.threads.net/@qooldjmarv        https://www.facebook.com/MarvJColeman/        https://soundcloud.com/qooldjmarv    

BUFFALO, NY- October 21, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition.” As highlighted in the abstract, monoclonal antibody therapies for cancer have shown extraordinary clinical success in recent years. However, these strategies are primarily limited to targeting specific cell surface antigens, despite many disease targets being located intracellularly. In their paper, researchers Madison Rackear, Elias Quijano, Zaira Ianniello, Daniel A. Colón-Ríos, Adam Krysztofiak, Rashed Abdullah, Yanfeng Liu, Faye A. Rogers, Dale L. Ludwig, Rohini Dwivedi, Franziska Bleichert, and Peter M. Glazer from the Departments of Therapeutic Radiology and Genetics at Yale University School of Medicine, Gennao Bio, and the Department of Molecular Biophysics and Biochemistry at Yale University report on the humanization of the full-length, nucleic acid-binding monoclonal lupus-derived autoantibody 3E10, which exhibits a novel mechanism for cell penetration and tumor-specific targeting. The authors compare humanized variants of 3E10 and demonstrate that cell uptake relies on the nucleoside transporter ENT2. They also find that faster cell uptake and superior in vivo tumor targeting are associated with higher affinity nucleic acid binding. “We show that one human variant retains the ability of the parental 3E10 to bind RAD51, serving as a synthetically lethal inhibitor of homology-directed repair in vitro.” DOI - https://doi.org/10.18632/oncotarget.28651 Correspondence to - Peter M. Glazer - peter.glazer@yale.edu Video short - https://www.youtube.com/watch?v=sTHjJ0Qq0YQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28651 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, 3E10, cell penetration, nucleic acid binding, nucleic acid delivery, RAD51 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- October 17, 2024 – 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 19 on September 18, 2024, entitled, “Fibroblast growth factor 21 inversely correlates with survival in elderly population – the results of the Polsenior2 study.” As noted in the abstract, fibroblast growth factor 21 (FGF21) is a liver-secreted hormone involved in regulating lipid, glucose, and energy metabolism. Its serum concentration increases with age and is elevated in various diseases. FGF21 is currently being investigated for its potential as a biomarker and therapeutic target. In their paper, Polish researchers Gabriela Handzlik, Aleksander J. Owczarek, Andrzej Więcek, Małgorzata Mossakowska, Tomasz Zdrojewski, Anna Chudek, Magdalena Olszanecka-Glinianowicz, and Jerzy Chudek from the Medical University of Silesia in Katowice, the International Institute of Molecular and Cell Biology in Warsaw, and the Medical University of Gdansk aimed to assess the prognostic value of FGF21 in an older, population-based cohort from the PolSenior2 study. The researchers report that in a sub-analysis of 3,512 individuals aged 60 and older, stratified into tertiles based on FGF21 levels, the survival estimate was worse in participants with middle and high FGF21 levels compared to those in the lowest tertile. These findings were supported by univariable Cox regression analysis, where participants in the middle and high FGF21 tertiles, after adjusting for age, had a 1.43-fold (HR 1.31; 95% CI, 1.05–1.62) and 2.56-fold (HR 1.94; 95% CI, 1.59–2.37) increased risk of mortality, respectively, compared to the lowest tertile. In multivariable Cox regression analysis, the highest FGF21 levels were independently associated with increased mortality (HR 1.53; 95% CI, 1.22–1.92), regardless of co-morbidities and blood parameters. "These results indicate that higher serum FGF21 concentration is an independent predictor of all-cause mortality in the general population of older adults.” DOI - https://doi.org/10.18632/aging.206114 Corresponding author - Gabriela Handzlik - ghandzlik@sum.edu.pl Video short - https://www.youtube.com/watch?v=QkPrI68nbLE Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206114 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, fibroblast growth factor 21, survival, population-based study, 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@IMPACTJOURNALS.COM

BUFFALO, NY- October 16, 2024 – A new #review was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Molecular chaperones: Guardians of tumor suppressor stability and function.” As highlighted in the abstract of this paper, "tumor suppressor" describes a diverse set of genes typically involved in suppressing metastasis, but which can lead to tumorigenesis when loss-of-function mutations occur. Despite the varied structures and functions of tumor suppressor proteins, many share a common regulatory mechanism—they are "clients" of molecular chaperones, and they rely on an intracellular network of chaperones and co-chaperones to maintain their stability. Mutations in tumor suppressors that disrupt proper chaperoning prevent cells from maintaining sufficient protein levels for normal physiological function. In their review, researchers Jennifer A. Heritz, Sarah J. Backe, and Mehdi Mollapour from SUNY Upstate Medical University and New York VA Health Care in Syracuse, New York, discuss the role of molecular chaperones Hsp70 and Hsp90 in maintaining the stability and functional integrity of tumor suppressors. They also detail the contributions of co-chaperones prefoldin, HOP, Aha1, p23, FNIP1/2, and Tsc1, as well as the chaperonin TRiC, to tumor suppressor stability. “Overall, it is clear that oncogenesis can result from the dysregulation of tumor suppressor stabilization by chaperones.” DOI - https://doi.org/10.18632/oncotarget.28653 Correspondence to - Mehdi Mollapour - mollapom@upstate.edu Video short - https://www.youtube.com/watch?v=V5OFjeqaH3A Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28653 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, molecular chaperone, tumor suppressor, renal cell carcinoma, Birt-Hogg-Dubé (BHD) syndrome, TSC syndrome 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- October 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on October 12, 2024, entitled, “A proteomics approach to study mouse long bones: examining baseline differences and mechanical loading-induced bone formation in young-adult and old mice.” As noted in the abstract, bone mass declines with age, and the anabolic effects of skeletal loading decrease. While much research has focused on gene transcription, how bone ages and loses its mechanoresponsiveness at the protein level remains unclear. In their paper, researchers Christopher J. Chermside-Scabbo, John T. Shuster, Petra Erdmann-Gilmore, Eric Tycksen, Qiang Zhang, R. Reid Townsend, and Matthew J. Silva from Washington University School of Medicine and Washington University in St. Louis, Missouri, describe how they developed a novel proteomics approach and conducted paired mass spectrometry and RNA-seq analyses on tibias from young-adult (5-month) and old (22-month) mice. The researchers report the first correlation estimate between the bone proteome and transcriptome (Spearman ρ = 0.40). While this is consistent with findings from other tissues, it suggests that only a relatively low amount of variation in protein levels is explained by variation in transcript levels. Of the 71 shared targets that differed with age, eight were associated with bone mineral density in previous GWAS, including the understudied targets Asrgl1 and Timp2. Using complementary RNA in situ hybridization, the researchers confirmed that Asrgl1 and Timp2 showed reduced expression in osteoblasts/osteocytes in aged bones. Additionally, they found evidence of reduced TGF-beta signaling with aging, particularly Tgfb2. The researchers also identified proteomic changes following mechanical loading, noting that at the protein level, bone differed more with age than with loading, and aged bone exhibited fewer loading-induced changes. "Overall, our findings underscore the need for complementary protein-level assays in skeletal biology research.” DOI - https://doi.org/10.18632/aging.206131 Corresponding author - Christopher J. Chermside-Scabbo - ccherms@wustl.edu Video short - https://www.youtube.com/watch?v=xm6o7gWH8p4 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206131 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, bone, mechanical loading, proteomics, RNA-seq/transcriptomics 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- October 11, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Transplant or no transplant for TP53 mutated AML.” As highlighted in this editorial, TP53 mutations (mut) occur in 10–15% of acute myeloid leukemia (AML) cases, commonly associated with therapy-related AML (t-AML) and complex cytogenetics (CG). TP53-mut AML is inherently resistant to conventional chemotherapies and continues to show a poor prognosis, even with venetoclax-based therapies. Allogeneic hematopoietic stem cell transplant (allo-HCT) remains a potential curative option, though only 10–15% of patients receive it. In a recent study, allo-HCT was the only variable significantly improving survival, despite only 16% of patients successfully bridging to it. In their editorial, researchers Talha Badar, Moazzam Shahzad, Ehab Atallah, Mark R. Litzow, and Mohamed A. Kharfan-Dabaja from the Division of Hematology-Oncology and Blood and Marrow Transplantation and Cellular Therapy Program at Mayo Clinic (Jacksonville, Florida) evaluated the outcomes of TP53-mutated AML patients based on data from the Consortium of Myeloid Malignancies and Neoplastic Diseases (COMMAND). The study found a “dismal” survival rate of 8.5 months, with no significant difference among treatment types, and allo-HCT was the only variable associated with improved survival. The authors also report on the “better long-term outcomes” when allo-HCT was performed during Complete Remission 1 (CR1) in previous observations. They acknowledge the limitations of their retrospective analysis, including selection bias, data heterogeneity from participating institutions, and the lack of complete molecular data prior to allo-HCT that might have influenced the results. Nevertheless, the findings are encouraging and suggest that allo-HCT improves long-term outcomes in this poor prognostic disease, where effective therapies remain limited. “In summary, this study reported improved survival when allo-HTC was performed in CR1 versus after later lines of therapy.” DOI - https://doi.org/10.18632/oncotarget.28652 Correspondence to - Talha Badar - badar.talha@mayo.edu Video short - https://www.youtube.com/watch?v=OQue9gbqsxE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28652 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, AML, TP53 mutation, allogeneic stem cell transplant 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- October 9, 2024 – A new #review was #published in Oncotarget's Volume 15 on September 30, 2024, entitled, “Zika virus and brain cancer: Can Zika be an effective treatment for brain cancer? A systematic review.” As highlighted in the introduction of this review, many studies have identified oncolytic viruses as a promising new class of therapeutic agents for central nervous system (CNS) tumors, particularly glioblastomas (GBM). Zika virus (ZIKV) proteins, specifically targeting certain stem cells, have shown promising results in both in vitro and animal model studies. In their review, researchers Mateus Gonçalves de Sena Barbosa, Beatriz Rodrigues Messias, Rafael Trindade Tatit, Maycon Cristian Gomes de Paula, Valdecir Boeno Spenazato Júnior, Maria Gabriella Borges Braga, Caio Vinícius Marcolino Santos, Luiza D'Ottaviano Cobos, Vinícius Otávio da Silva, Eberval Gadelha Figueiredo, Nicollas Nunes Rabelo, and Bipin Chaurasia from Atenas University Center, Passos; University of Israelita de Ciências da Saúde Albert Einstein; University of Sapucaí Valley; Atenas University Center, Sete Lagoas; Nove de Julho University, Campus Vergueiro; José do Rosário Vellano University, Alfenas; School of Medicine-University of São Paulo (FMUSP), Hospital das Clínicas/FMUSP; and Neurosurgery Clinic in Birgunj, evaluated the efficacy and safety of using ZIKV for treating CNS tumors. Data from in vivo studies were extracted and assessed for bias using the Robins-I tool, evaluating factors such as selection, performance, detection, attrition, and reporting bias. The 14 studies demonstrated that ZIKV reduced cell viability, inhibited the growth and proliferation of glioma stem cells (GSCs), and decreased Bcl2 expression, potentially enhancing chemotherapy and radiotherapy effects. ZIKV caused cytopathic effects, induced tumor cell damage, showed oncolytic properties, and selectively killed GSCs safely. This ultimately led to significant tumor remission and improved long-term survival through an enhanced T-cell response. “Although current evidence suggests ZIKV as a promising treatment for CNS tumors and may improve survival when combined with surgery and radiotherapy.” DOI - https://doi.org/10.18632/oncotarget.28647 Correspondence to - Bipin Chaurasia - trozexa@gmail.com Video short - https://www.youtube.com/watch?v=JINORGdqAO4 Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28647 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, Zika, neurotropism, glioblastoma, glioma, brain tumor 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- October 8, 2024 – 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 18 on September 18, 2024, entitled, “Determinants of cerebral blood flow and arterial transit time in healthy older adults.” This research paper highlights that brain health deteriorates with age, particularly in terms of cerebral blood flow (CBF) and arterial transit time (ATT), key markers of brain vascular health. This decline can impair cognitive function and limit independence in later life—an issue that will affect many as the global population continues to age rapidly. In their paper, researchers Jack Feron, Katrien Segaert, Foyzul Rahman, Sindre H. Fosstveit, Kelsey E. Joyce, Ahmed Gilani, Hilde Lohne-Seiler, Sveinung Berntsen, Karen J Mullinger, and Samuel J. E. Lucas from the University of Birmingham, University of Agder, and University of Nottingham aimed to identify modifiable determinants of CBF and ATT in healthy older adults (n = 78, aged 60–81 years). They also investigated the relationship between CBF, ATT, and cognitive function in older adults. The researchers hypothesized that markers of superior general health—such as higher cardiorespiratory fitness, handgrip strength, and grey matter volume, or lower age, BMI, and blood pressure—would be associated with greater CBF and shorter ATT. Results from multiple linear regressions revealed that a higher BMI was associated with lower global cerebral blood flow (CBF) (β = −0.35, P = 0.008) and longer global arterial transit time (ATT) (β = 0.30, P = 0.017). Additionally, global ATT increased with age (β = 0.43, P = 0.004), while higher cardiorespiratory fitness was linked to longer ATT in the parietal (β = 0.44, P = 0.004) and occipital (β = 0.45, P = 0.003) regions. However, neither global nor regional CBF or ATT were associated with processing speed, working memory, or attention. “In conclusion, preventing excessive weight gain may help attenuate age-related declines in brain vascular health.” DOI - https://doi.org/10.18632/aging.206112 Corresponding author - Jack Feron - j.feron@bham.ac.uk Video short - https://www.youtube.com/watch?v=QpS4kK273os Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206112 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts 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

Your favorite podcast is back after a summer hiatus! Small business coach & retreat leader, Desha Peacock, and holistic interior designer, Christine Martin kick start season 2 with reflections, intentions, and a very special invitation for you.  Be part of the magic unfolding! Shownotes 0:00   Intro 0:42  The Good Abode 1:48 Kicking off Season 2: we're back! 2:32 Desha's summer reflection; taking a marketing break & the hospitality dream 5:08 More than manifestation 5:48 The expansion of She DESIGNS 8:13 The thread of resilience  10:23 Our first LIVE event: She DESIGNS Mini Retreat Oct. 18-20 12:28 The magic of Long Story Short space  13:56 Panelists: highlighting 3 women small business owners : -Jilan Glorfield, hospitality entrepreneur & owner of Long Story Short -Estefany, Perez, co founder of Flowers Atelier -Bibbe Hansen, creator, actress, artist 14:37 The retreat activities: intentional candle making, oil painting sequencing, meal sharing 15:14 Where to sign up 16:28 Outro   Check out our first LIVE event! Join our She DESIGNS Mini Retreat at Long Story Short in Hudson, NY -October 18-20, 2024  -3 posts left for the retreat; claim your spot now! Or, join us for the LIVE Podcast Panel 4-7pm October 19  Tickets available!   Theme song for season 2: Resilient   Join our community! Follow this podcast and share with a friend! In the world of podcasts, reviews are everything! Please rate and review this episode on your favorite platform. Follow us on Instagram and let us know what you'd like for us to cover and any nominations for guests   Live your life by design. 

Learn how to connect to higher realms and your own spiritual gifts. In this special episode of Dropping In we join four world renowned spiritual teachers. Psychic medium John Holland, author and angel communicator Radleigh Valentine, psychic and cosmic coach Dougall Fraser and spirit medium, teacher and holistic healer Maureen Hancock talk about working in the spiritual realms and share tips on how you can enhance your own gifts. Recorded during a recent Facebook live, these four gifted practitioners give you a taste of what you will experience at the upcoming Answers from the Light workshop at the Omega Institute in Rhinebeck, NY October 25 to the 27th. Learn how to connect to angels, guides, and loved ones from spiritual realms during this 3-day event. Reserve your space today at eomega.org/light. Learn more about your ad choices. Visit megaphone.fm/adchoices

BUFFALO, NY- October 30, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on March 24, 2023, entitled, “Neutrophil PAD4: how does it function in cancer beyond promoting NETosis?” Expansion of pathologically activated immune suppressive myeloid cells called myeloid-derived suppressor cells (MDSC) is one of the hallmarks of cancer. In most tumor types, MDSC are represented primarily by pathologically activated neutrophils (PMN-MDSC). In this new editorial, researchers Laura Garcia-Gerique and Yulia Nefedova from the Wistar Institute discussed their team's recent study identifying a novel mechanism by which neutrophil PAD4 promotes cancer progression. “Using several transplantable and genetically engineered mouse models, we demonstrated that tumor growth was accompanied by significantly elevated enzymatic activity of neutrophil PAD4 [10]. To further clarify the role of PAD4 in tumor progression, we utilized PAD4fl/fl MRP8Cre mice with targeted deletion of PAD4 in myeloid cells, primarily neutrophils.” PMN-MDSC originate in the bone marrow and migrate to various sites including tumor tissues and premetastatic niches. These cells have a relatively short lifespan (less than 48 hours) and, therefore, are continually replaced from the bone marrow. Tumor-infiltrating PMN-MDSC possess a potent suppressive activity as they are able to inhibit both antigen-specific immune responses of T cells and non-specific anti-CD3/CD28-stimulated responses. As a result, a highly immunosuppressive environment is created in tumors, which prevents their rejection via immunological mechanisms. In addition, PMN-MDSC employ non-immunological mechanisms to facilitate tumor progression, including angiogenesis, remodeling of extracellular matrix, and production of cytokines. In patients with solid tumors, levels of MDSC in circulation and tumor tissues have been positively associated with a poor response to the therapy in many types of cancer and represent an independent indicator of poor outcomes. However, many of the details about how PMN-MDSC support cancer progression, and thus approaches for therapeutically targeting these cells, remain enigmatic. “Taken together, our study identified a new mechanism responsible for transcriptional regulation of neutrophil migration and a new mechanism by which neutrophil PAD4 is contributing to tumor progression. PAD4 inhibitors are in development and may enter early phase clinical trials in the future.” DOI - https://doi.org/10.18632/oncotarget.28369 Correspondence to - Yulia Nefedova - ynefedova@wistar.org Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28369 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PAD4, PMN-MDSC, neutrophils, neutrophil migration 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. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget 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/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY- October 25, 2023 – A new editorial perspective was published in Oncotarget's Volume 14 on March 24, 2023, entitled, “Genetic modifiers of p53: opportunities for breast cancer therapies.” Each day our cells encounter a wide range of genomic damage and the p53 protein arbitrates decisions of cell cycle arrest to allow repair of DNA or promote elimination of cells with malignant potential through apoptosis. In this new editorial perspective, researchers Prabin Dhangada Majhi, Aman Sharma and D. Joseph Jerry from the University of Massachusetts, Pioneer Valley Life Sciences Institute and Rays of Hope Center for Breast Cancer Research discuss TP53 mutations. The prevalence of TP53 mutations in nearly all tumors emphasizes its role as a formidable barrier that must be breached to allow oncogenic transformation. Inherited mutations in TP53 are also the primary genetic lesions found in Li-Fraumeni Syndrome (LFS), a familial cancer predisposition characterized by tumors in many tissues. However, tissues are not all equally vulnerable to disruptions in p53 function. Among women with inherited mutations in TP53, breast cancer is by far the most common tumor (Figure 1). Somatic mutations in TP53 are also prevalent in sporadic breast cancers, especially in the triple-negative subtype. The proportion rises to nearly 50% of breast cancers that exhibit impaired function of the p53 pathway based on gene expression signatures as a surrogate biomarker of p53 activity. Therefore, the breast epithelium appears to be uniquely sensitive to alterations in p53 function. “Genomewide association studies (GWAS) have identified over 300 polymorphisms that contribute to breast cancer risk [38–41]. These provide a rich resource of candidate polymorphisms that may modify the consequences of mutations in TP53.” DOI - https://doi.org/10.18632/oncotarget.28387 Correspondence to - D. Joseph Jerry - jjerry@vasci.umass.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28387 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, p53, Li-Fraumeni syndrome, genetic modifiers, breast cancer, DNA repair 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. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget 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/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY- October 23, 2023 – A new research paper was published in Oncotarget's Volume 14 on October 19, 2023, entitled, “Apoptotic cells may drive cell death in hair follicles during their regression cycle.” Intravital microscopy in live mice has shown that the elimination of epithelial cells during hair follicle regression involves supra-basal cell differentiation and basal cell apoptosis through synergistic action of TGF-β (transforming growth factor) and mesenchymal-epithelial interactions. In this process the basal epithelial cells are not internally committed to death and the mesenchymal dermal papilla (DP) plays an essential role in death induction. Given that DP cells are not necessary for completion of the cycle, only for its initiation, it is still an open question as to the mechanism that leads to the propagation of apoptosis towards the regenerative stem cell population. In their new study, researchers Bradley D. Keister, Kailin R. Mesa and Krastan B. Blagoev from the National Science Foundation, The Jane Coffin Childs Memorial Fund for Medical Research, Yale School of Medicine, Johns Hopkins University, Bulgarian Academy of Sciences, and Sorbonne Université performed a quantitative analysis of the length of hair follicles to investigate their regression cycle. “In this paper we introduced a mathematical model of the hair follicle regression cycle that postulates that the regression is initiated by the dermal papilla, but that this signal affects only the cells adjacent to it.” The data are consistent with a propagation mechanism driven by apoptotic cells inducing apoptosis in their neighboring cells. The observation that the apoptosis slows down as the apoptotic front approaches the stem cells at the end of the follicle is consistent with a gradient of a pro-survival signal sent by these stem cells. An experiment that can falsify this mechanism is proposed. “In conclusion, hair follicle regression may be governed by cell-cell induced programmed cell death, which slows down as the stem cell compartment is approached and does not affect the stem cell compartment from which the growth phase is initiated. The class of models introduced here can be used to describe the renewal kinetics of other stem cell niches like the intestinal stem cell niche [18].” DOI - https://doi.org/10.18632/oncotarget.28529 Correspondence to - Krastan B. Blagoev - kblagoev@nsf.gov Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28529 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, hair follicle, stem cells, regression cycle, mathematical model, analysis 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. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget 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/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY- October 19, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on October 19, 2023, entitled, “GLS2 shapes ferroptosis in hepatocellular carcinoma.” In their new editorial, researchers Sawako Suzuki, Divya Venkatesh, Tomoaki Tanaka, and Carol Prives from Columbia University discuss ferroptosis regulation of GLS2 as a potential therapeutic strategy against liver diseases. “More than a decade has passed since our group (1) as well as Hu et al., (2) identified glutaminase (GLS2) as a p53 target gene that promotes the tricarboxylic acid cycle (TCA) via α-ketoglutarate (αKG) and lowers oxidative stress via increasing glutathione (GSH) [1, 2].” Two years after this Dixon et al., [3] described a form of cell death they named ferroptosis which is caused by iron-mediated lipid peroxidation. Then, three years later, Gao et al., reported that GLS2 but not GLS1 is an inducer of ferroptosis in human cancer cells [4]. Ferroptosis had first been shown to be regulated by p53 via repression of SLC7A11 [5]. The circle was closed by a study from the Murphy group who reported that a cancer-related nonsynonymous mutation in p53 (P47S) is correlated with failure to either activate GLS2 expression or produce ferroptosis [6]. “Our recent study (Suzuki et al.) [7] has validated the ability of GLS2 to promote ferroptosis in murine models.” DOI - https://doi.org/10.18632/oncotarget.28526 Correspondence to - Carol Prives - clp3@columbia.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28526 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, ferroptosis, hepatocellular carcinoma, GLS2, p53, tumor suppression 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. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget 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/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY- October 18, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on April 14, 2023, entitled, “The nuclear envelope and metastasis.” In their new editorial, researchers Emily Hansen and James M. Holaska from Rowan University discuss nuclear morphology — one of the basic visual criteria used by pathologists to diagnose breast cancer. Immunofluorescence staining of the nuclear structural proteins lamin B and emerin was recommended as an effective diagnostic tool for both thyroid and breast cancer, suggesting nuclear structure is intimately tied to malignant transformation. But what role nuclear morphology plays in cancer transformation and progression remains unclear. “The most likely explanation for why cancer cells present with distinct nuclear morphology is thought to be related to the most likely route of cancer spread: the vasculature.” For a tumor to metastasize, cancer cells need to enter and exit the blood and lymphatic vessels by squeezing through extremely small gaps in the endothelium, most of which are 1.2–2 µm in diameter. While the cytoplasm is very flexible and the cytoskeleton can rearrange to fit through openings as narrow as 1 µm, the nuclear diameter (10–20 µm) and its considerable stiffness (2–10x stiffer than the cytoplasm) represent physical barriers to this process. “Thus, to enable metastasis, cancer cells must also increase their nuclear malleability.” Studies have shown that nuclear softening is associated with tumor aggressiveness and metastasis. Although nuclear softening is one of the ‘hallmarks of cancer' it remains poorly understood. Nuclear shape and stiffness are governed by a complex set of structural proteins that serve as both scaffolds and signaling proteins to influence almost all aspects of nuclear function. The best studied nucleostructural proteins are lamins, which are frequently downregulated in cancer. However, it is difficult to ascertain whether specific functional consequences are due to lamins or due to displacement of lamin-interacting proteins upon lamin loss. For example, nuclear size and shape is also governed by emerin, which binds to lamins at the nuclear envelope (NE) and upon lamin loss is retained in the endoplasmic reticulum. Like lamins, emerin is frequently mutated in cancer, with mutations in its transmembrane and actin-binding domains. “We found that in breast cancer, emerin expression in tumor tissue is significantly correlated to survival time [16]. These data suggest emerin plays a central role in pathogenic transformation and progression of malignant breast tissue.” DOI - https://doi.org/10.18632/oncotarget.28375 Correspondence to - James M. Holaska - holaska@rowan.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28375 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, emerin, metastasis, mechanotransduction, breast cancer, nucleoskeleton 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. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget 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/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Gubernatorial Candidate, Rep. Lee Zeldin of NY, talks about the shooting that happened outside of his home last night related to gang violence; a bullet fell 30 ft. from his 16 year old daughters who were sitting at the table doing homework. See omnystudio.com/listener for privacy information.