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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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Participants 283 patients 65 years with VB12 deficiency were randomly assigned to oral (n=140) or IM (n=143) treatment arm

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