BUFFALO, NY – February 14, 2025 – A new #review was #published in Oncotarget, Volume 16, on February 12, 2025, titled “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.”

Authors Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, and Antonin Marchais from the Gustave Roussy Cancer Campus analyzed recent studies on a gene called SETDB1, which may play a key role in osteosarcoma, a type of bone cancer that mostly affects teenagers and young adults. Their review highlights how SETDB1 helps cancer cells grow, resist treatment, and avoid the immune system. Because of this, blocking SETDB1 could be a promising new way to treat osteosarcoma.

Osteosarcoma is a fast-growing bone cancer that is usually treated with surgery and chemotherapy. However, if the cancer spreads or returns, treatment options are very limited. Scientists are searching for new ways to stop this disease, and recent studies have found that osteosarcoma cells often have extra copies of the SETDB1 gene. This seems to make the cancer more aggressive and harder to treat.

“Whole exome sequencing of osteosarcoma samples from both diagnosis and relapses has highlighted several factors, including SETDB1, that are amplified in the most aggressive forms of the disease.”

SETDB1 is involved in epigenetics, meaning it affects how genes are turned on and off without changing the DNA itself. The review explains that SETDB1 helps tumors hide from the immune system, making it difficult for the body to fight the cancer naturally. The researchers believe that blocking SETDB1 could help the immune system recognize and attack osteosarcoma cells. Some experimental drugs that target SETDB1 are already being tested in the lab.

The review also describes how SETDB1 influences key cancer pathways, such as Wnt signaling, which helps cancer cells grow, and epithelial-mesenchymal transition (EMT), a process that allows cancer to spread. The authors suggest that combining SETDB1-blocking drugs with immunotherapy or radiation could be an effective new strategy for treating osteosarcoma.

Another key finding is that SETDB1 may help cancer cells become resistant to chemotherapy, making treatment less effective. This means that drugs targeting SETDB1 could not only slow cancer growth but also make existing treatments work better.

While more research is needed, this review brings attention to SETDB1 as a potential treatment target. Scientists hope that a deeper understanding of SETDB1 will lead to new therapies that improve survival rates for osteosarcoma patients.

DOI - https://doi.org/10.18632/oncotarget.28688

Correspondence to - Antonin Marchais - antonin.marchais@gustaveroussy.fr, and Maria Eugenia Marques Da Costa - jenny.marquescosta@gustaveroussy.fr

Video short - https://www.youtube.com/watch?v=f9WgaDoEubs

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).

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SETDB1 Amplification Identified as a Potential Target for New Osteosarcoma Treatment

In this episode, Ji Li discusses her book, At the Frontier of God’s Empire with Chloë Starr. The book tells the story of French missionary Alfred Caubrière who before his murder in 1948 left behind some 800 letters to his family, as well as 13 volumes of transcripts of everyday conversations in the local dialect among villagers in Santaizi, Manchuria. The episode discusses the life of Caubrière and especially his experience of the weeks-long siege of Santaizi church by the Boxer Rebels in 1900, as well as his depictions of the lives and beliefs of local Catholics.

Ji Li,  At the Frontier of God’s Empire: A Missionary Odyssey in Modern China

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

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Aging-US

PAI-1 Deficiency Protects Aging Female Mice from Muscle and Bone Loss

In this special episode of the Yale University Press podcast, Jennifer Banks, Senior Executive Editor in Religion and the Humanities, talks with Anthony T. Kronman about his latest book, True Conservatism: Reclaiming Our Humanity in an Arrogant Age.

Jennifer Banks in Conversation with Anthony T. Kronman

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

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Keywords - aging, Trf1, metabolism, leaner, fat, telomeres

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TRF1 Protein Loss Reduces Body Fat and Improves Metabolic Health in Mice Without Shortening Telomeres

TRF1 Protein Loss Reduces Fat and Improves Metabolic Health in Mice Without Shortening Telomeres

Lauren Jackson is a religion columnist for the New York Times where she is the associate editor and writer for The Morning, the Times's flagship daily newsletter. Over the past year, she has been deeply involved in reporting on belief. Lauren developed 'Believing,' a project that explores how we experience religion and spirituality in contemporary times. Lauren's thought-provoking columns delve into the complexities of faith, spirituality, and society. In this episode of The Leader’s Way, Lauren discusses the powerful transformation that is possible when we turn our attention to the people around us, attending to hyper-local needs, longings, and joys within our own community.

Host: Brandon Nappi
Guest: Lauren Jackson

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69: Believing with Lauren Jackson

BUFFALO, NY — November 3, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 10 of Aging-US was #published on October 20, 2025, titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model.”

In this study, led by first author Vivien Hoof and corresponding author Thomas Hentrich from Saarland University, Germany, researchers investigated how excess alpha-synuclein—a protein linked to Parkinson’s disease—affects gene activity in different brain regions and the gut. They found that early, region-specific gene disruptions may contribute to the appearance of disease, with some effects also detected in the gut. These early molecular changes could serve as biomarkers for Parkinson’s and point to new directions for treatment.

Alpha-synuclein accumulates in the brains of individuals with Parkinson’s disease and other age-related neurological conditions known as synucleinopathies. To better understand this process, the research team used a genetically modified rat model that overexpresses human alpha-synuclein. They studied gene expression in the striatum, cortex, and cerebellum—three key brain regions involved in movement and cognition—and analyzed how these changes evolved with age. 

“Transcriptomic analyses were performed on gene and transcript level of striatal, frontocortical, and cerebellar tissue in 5- and 12-month-old transgenic (BAC SNCA) and wild type rats […]”

The results showed that gene alterations appeared earlier and were more pronounced in young rats, particularly in the striatum and cortex, before any visible signs of disease manifested. This early disruption challenges the common belief that gene alterations gradually increase with age and suggests that early-life molecular changes may be critical in disease development.

The researchers also found that many gene expression changes were unique to individual brain regions. However, they identified a set of genes that were consistently affected across all brain regions and the gut. This suggests that the disease may begin to affect the entire body—not just the brain—long before symptoms become noticeable.

Several of the shared genes are involved in synaptic signaling and inflammation—processes known to be altered in Parkinson’s. Others are linked to dopamine production and neuronal plasticity, indicating potential early efforts by the brain to compensate for the harmful effects of the alpha-synuclein buildup.

Overall, this study provides a detailed view of how alpha-synuclein affects gene networks early in the disease process. Understanding these changes may help identify biomarkers and develop targeted therapies before irreversible brain damage occurs.

DOI - https://doi.org/10.18632/aging.206331

Corresponding author - Thomas Hentrich - thomas.hentrich@uni-saarland.de

Abstract video - https://www.youtube.com/watch?v=Yl6AfVchkb0

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Keywords - aging, alpha-synuclein, transgenic rat model, different brain regions, transcriptome analysis

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Alpha-Synuclein Triggers Early Gene Expression Changes in Parkinson’s Disease Model

What do we do with our pain? It’s an important spiritual question, and one that Brandon Nappi explores with James Kimmel, Jr., JD, on this episode of Within, a contemplative segment of The Leader's Way Podcast, that explores the convergence of mental health, art, and spirituality through authentic conversations across traditions about personal and collective transformation. James Kimmel is a violence researcher, psychiatry professor, and author who explores the science of revenge, addiction, forgiveness, and violence. A breakthrough scholar, James first identified compulsive revenge-seeking as an addiction. He made the study of revenge and forgiveness his life's work after nearly committing a mass shooting as a teenager. 

 

Host: Brandon Nappi 

Guest: James Kimmel 

 

Instagram: @theleadersway.podcast berkeleydivinity.yale.edu/podcast 

 

You can support our work at https://tinyurl.com/support-transforming-leaders 

70: On Revenge with James Kimmel

BUFFALO, NY — November 5, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on September 10, 2025, titled “Longitudinal associations of epigenetic aging with cognitive aging in Hispanic/Latino adults from the Hispanic Community Health Study/Study of Latinos.”

In this study led by Myriam Fornage, from The University of Texas Health Science Center at Houston, researchers found that faster biological aging, measured by DNA-based epigenetic clocks, is associated with greater cognitive decline and higher risk of mild cognitive impairment (MCI) in Hispanic/Latino adults. The results highlight the potential of epigenetic clocks to track changes in brain health over time, helping improve early detection and monitoring of age-related cognitive problems.

Cognitive decline and dementia are major public health concerns, especially among aging populations. In this study, researchers followed 2671 Hispanic/Latino adults (average age 57; 66% women) over a seven-year period. They measured each participant’s biological age using epigenetic clocks and assessed their cognitive performance at two time points.

“We evaluated the associations of 5 epigenetic clocks and their between-visit change with multiple measures of cognitive aging that included a global and domain-specific cognitive function score at each visit, between-visit change in global and domain-specific cognitive function score, and MCI diagnosis at visit 2 (V2).”

Epigenetic clocks estimate biological age based on DNA chemical modifications, called methylation, that accumulate with age. The study evaluated five different clocks, including newer models like GrimAge and DunedinPACE, which are designed to more accurately reflect health-related aging.

The researchers found that individuals with faster biological aging showed lower cognitive function and higher probability of developing MCI over time. Among the five clocks studied, newer models such as GrimAge and DunedinPACE showed the strongest associations with memory, processing speed, and overall brain health. These findings suggest that tracking changes in biological age over time may be more effective than relying on a single measurement to identify those at risk for cognitive impairment.

Importantly, the associations between biological aging and cognitive decline remained significant even after accounting for other known risk factors such as education, language preference, and cardiovascular health. This supports the idea that epigenetic clocks capture unique biological processes that influence brain aging. The study also found that the impact of changes in biological age over time was comparable to that of APOE4, a well-established genetic risk factor for Alzheimer’s disease.

Overall, this is the first large-scale study to examine these associations in a Hispanic/Latino population, a group that is underrepresented in aging research. By identifying early biological signs of brain aging, this work highlights the potential of epigenetic clocks as tools for routine health assessments. Monitoring changes in these biological markers could help detect individuals at risk for cognitive decline and guide timely interventions to preserve brain health.

DOI - https://doi.org/10.18632/aging.206317

Corresponding author - Myriam Fornage - Myriam.Fornage@uth.tmc.edu

Abstract video - https://www.youtube.com/watch?v=kG0Y-F_sods

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Epigenetic Aging Linked to Cognitive Decline in Hispanic/Latino Adults

Prostate cancer is one of the most common cancers in men. While treatment options have improved, advanced stages of the disease remain difficult to manage. One promising approach involves a process called ferroptosis. This is a type of programmed cell death that relies on iron and lipid oxidation to kill cancer cells by damaging specific fats in their outer membrane. These fats are especially vulnerable in environments with normal oxygen levels.

However, many prostate tumors grow in low-oxygen areas of the body, a condition known as hypoxia, where ferroptosis becomes less effective. A recent study, titled “Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer,” and published on Oncotarget (Volume 16), explores how oxygen-poor environments help prostate cancer cells resist treatment and what strategies could help overcome this resistance.

Full blog - https://www.oncotarget.org/2025/11/06/how-low-oxygen-shields-prostate-cancer-from-ferroptosis-therapies/

Paper DOI - https://doi.org/10.18632/oncotarget.28750

Correspondence to - Noel A. Warfel - warfelna@arizona.edu, and Shailender S. Chauhan - shailenderc@arizona.edu

Abstract video - https://www.youtube.com/watch?v=xFypDT4ALmc

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Keywords - cancer, hypoxia, lipid droplets, ferroptosis, resistance, prostate

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Oncotarget

How Low Oxygen Shields Prostate Cancer from Ferroptosis Therapies

BUFFALO, NY - November 10, 2025 – A new #research paper was #published in Oncotarget (Volume 16) on November 6, 2025, titled “Anti-DNA virus agent cidofovir - loaded green synthesized cerium oxide nanoparticles (Nanoceria): Nucleic acids (DNA and RNA) binding affinity and cytotoxicity effects.”

In this study, led by Nahid Shahabadi from Razi University in Kermanshah, researchers developed an environmentally friendly approach to enhance the performance of cidofovir, a drug used to treat infections caused by DNA viruses. The work responds to the growing need for therapies that are safer, more effective, and better targeted.

The research team developed a new compound by loading cidofovir onto green-synthesized cerium oxide nanoparticles (nanoceria), known as CDV-CeO2 NPs. This method combines the drug’s antiviral and anticancer properties with the biological activity of nanoceria, which is known for its antioxidant, anti-inflammatory, and tumor-targeting effects. To avoid toxic chemicals, the nanoparticles were synthesized using quince fruit peel extract, making the process more sustainable and suitable for medical applications.

Laboratory experiments showed that the CDV-CeO2 nanoparticles were significantly more effective at killing breast cancer cells than either cidofovir or cerium oxide nanoparticles alone. At the highest tested concentration, the new compound destroyed more than 97% of cancer cells, compared to 72% with cidofovir alone and 50% with nanoparticles alone. These findings suggest that the combined formulation enhances anticancer activity and may allow for lower drug doses with fewer side effects.

To understand how these nanoparticles interact with genetic material, the team studied their binding to DNA and RNA, two key molecules involved in cancer development and viral replication. CDV-CeO2 nanoparticles showed strong binding affinity through two mechanisms: groove binding, which fits into natural curves of the genetic molecule strands, and intercalation, which inserts between base pairs. The nanoparticles formed stable complexes that responded to temperature, indicating reliable interactions in biological systems.

“The novelty of this work lies in the innovative green synthesis method, the dual-functional therapeutic application, and the enhanced biological activity of the CDV-CeO2 NPs, which collectively position these nanoparticles as promising candidates for future cancer and antiviral therapies.”

This research presents a potential new strategy for improving drug targeting and delivery using green nanotechnology. The approach could lead to more effective treatments for diseases such as breast cancer and infections caused by human papillomavirus (HPV) and other DNA viruses. However, further research, including animal and clinical studies, is needed to confirm the safety and long-term effectiveness of this treatment.

Overall, this study represents a significant step toward combining natural materials with nanomedicine to create more efficient therapies. If supported by future research, CDV-CeO2 nanoparticles could offer a new generation of dual-action treatments.

DOI - https://doi.org/10.18632/oncotarget.28774

Correspondence to - Nahid Shahabadi - nahidshahabadi@yahoo.com

Abstract video - https://www.youtube.com/watch?v=Il9CsfgO2mU

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Eco-Friendly Nanoparticles Improve Cidofovir’s Anticancer and Antiviral Effects

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

SETDB1 Amplification Identified as a Potential Target for New Osteosarcoma Treatment

Oncotarget Podcast