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G3BP2 confers venetoclax resistance by stabilizing ELF1-mediated MCL1 transcription in acute myeloid leukemia
Abstract Venetoclax is a promising treatment for acute myeloid leukemia (AML) patients, but resistance occurs following the upregulation of MCL1. The RNA-binding protein G3BP2 is upregulated in various solid tumors, and targeting G3BP2 has been shown to restore chemosensitivity. However, the role of G3BP2 in AML development and venetoclax resistance remains unknown. Herein, an integrated analysis revealed that G3BP2 confers venetoclax resistance and correlates with poor outcomes in AML.
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