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Description
Mechanistic modeling of the MAT2ASRFPARN axis reveals a SAM-independent pathway that stabilizes SRF, drives glycolysis through PI3K/AKT activation, and promotes osteosarcoma progression, highlighting MAT2A as a therapeutic target.
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TP53 is the most frequently mutated gene in high-grade serous ovarian cancer, and the majority of these mutations result in overexpression of mutant p53
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