Research
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Scanned: 1729
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    CANCER    GENETICS   

Mca39-006

Somatic and Germline Telomere Biology in Sarcoma: Telomere Maintenance Is Acquired at Liposarcoma Dedifferentiation, and Genetically Longer Telomeres Are Associated With Liposarcoma Risk

Quote: Conclusion: Sarcoma telomere maintenance is histology-specific and mutually exclusive. In liposarcoma it is acquired at dedifferentiation through focal TERT amplification or ALT and identifies DDLPS with inferior survival.
Abstract: https://www.medrxiv.org/content/10.64898/2026.09.28.26364135v1
Full Text: https://www.medrxiv.org/content/10.64898/2026.09.28.26364135v1.full-text
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Search Authors: Minggui Pan Joyce Chi Maggie Yuxi Zhou Nam Bui Kristen Ganjoo, 
    GENETICS   

Mge39-002

Expanding clinical and variant spectrum of CBX1-related syndrome: Report of three novel cases

Abstract: https://www.medrxiv.org/content/10.64898/2026.09.28.26363820v1
Full Text: https://www.medrxiv.org/content/10.64898/2026.09.28.26363820v1.full-text
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Search Authors: Graciela Carrollo Shuhei Fujino Harrison Higgs Anita Kabahizi Randy Le Rachel Rabin John Pappas Amy Crunk Kara Ranguin Jeremie Mortreux span classnlm-collab data-hwp-idcollab-1AURAGEN consortium Marilyn Lackmy Carlos A Gadia Matthew Hoi Kin Chau Jill A Rosenfeld Xi Luo Kosuke Izumi, 
    PRIME    EXERCISE    GENETICS   

Mre39-005

Prehabilitative Exercise Mitigates Immobilization-Induced Atrophy Through Muscle Reserve Rather Than Resistance to Disuse: The PRE-EX Randomized Controlled Trial

Quote: Instead, immobilization elicited an extensive transcriptional response comprising more than 7000 differentially expressed genes, characterized by activation of inflammatory, proteolytic, stress, and denervation-associated programs together with suppression of mitochondrial and muscle-structural pathways. Network analysis further linked these coordinated molecular programs to disuse-related changes in muscle size, strength, and morphology.
Abstract: https://www.medrxiv.org/content/10.64898/2026.09.25.26363998v1
Full Text: https://www.medrxiv.org/content/10.64898/2026.09.25.26363998v1.full-text
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Search Authors: Casper Soendenbroe Sara D. Pedersen Leonard Pulevic Amanda El Khoury Helena L. Christiansen Frederik H. Linden S. Peter Magnusson Rene B. Svensson Peter Schjerling Michael Kjaer Abigail L. Mackey, 
    PRIME    AGING    GENETICS   

Nih392-009

DNA organization changes in Alzheimers disease, aging

Quote: The scientists found DNA folding differences between cells obtained from the two groups. Distant parts of the DNA sequence were close to each other more often in cells from people with Alzheimers than in cells from people without Alzheimers. And neighboring parts of the sequence were close together less often.
Article: https://nih.gov//news-events/nih-research-matters/dna-organization-changes-alzheimers-disease-aging
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    PRIME    GENETICS    HEART   

Sd395-002

Weak Sunlight Can Still Damage Your DNA, Scientists Warn

Comment: It isnt just sunlight, we are bombarded by cosmic rays even indoors, and many other factors killing millions of cells per second. (Most are blood cells) Yet thanks to evolution, most of us live into our 70s.
Article: https://www.sciencedaily.com//releases/2026/09/260930020324.htm
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See Also:
  • https://www.sciencealert.com/your-body-makes-4-million-cells-a-second-and-most-of-them-are-blood
  •     AGING    GENETICS    HEART   

    Sd395-013

    Alzheimers Risk Gene APOE4 May Have a Reversible Weakness

    Quote: The Alzheimers risk gene APOE4 may actively damage brain blood vessels and sabotage the cellular systems that remove harmful proteins. Researchers were able to reverse some of these effects in experiments, revealing promising new targets for Alzheimers, Parkinsons, and other neurodegenerative
    Article: https://www.sciencedaily.com//releases/2026/09/260930225450.htm
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      Javilk's Research Links Newsletter for Week 39
    Updated 10/03/2026-03:08:04 AM
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