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ArticleOnline nowOpen access Affiliations & Notes 1Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, 02215, United States of America 2Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, 02115, United States of America 3Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, 02215, United States of America 4Department of Immunology, Harvard Medical School, Boston, MA, 02115, United States of America 5Systems,...
Abstract Ovarian cancer represents the most lethal gynecologic malignancy, with tumor metastasis being the primary contributor to patient mortality. EZH2, frequently overexpressed in various cancers, has been implicated in promoting metastatic progression through metabolic dysregulation. However, the mechanistic basis by which EZH2 reprograms cholesterol metabolism to facilitate ovarian cancer metastasis remains poorly defined.
Abstract Approved KRAS inhibitors have shown limited therapeutic benefit over standard chemotherapy in PDAC and often encounter acquired resistance due to additional genetic alterations. RAS and RB1 functionally antagonize each other, which explains why RB1 is rarely mutated in KRAS-driven tumors. In PDAC cells, CDK4/6 inhibition induced cellular senescence accompanied by partial apoptosis.
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