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In KMT2A-rearranged AML, integrative multi-omics analyses identified a six-gene lactylation-associated signature (PFN1, S100A6, CBR1, LDHB, LGALS1, and PRDX1) that distinguishes this high-risk subtype from cytogenetically normal AML and associates with immune infiltration and metabolic pathway activity, defining molecular subtypes with distinct immunometabolism dependencies and suggesting potential sensitivity to PI3K, MEK, and proteasome inhibitors in signature-high cases [194]

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