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G3BP2-Mediated Venetoclax Resistance via ELF1-Driven MCL1 Transcription in Acute Myeloid Leukemia: Mechanisms and Therapeutic Implications

MedXY Editorial Team•Jul 24, 2026•Clinical Updates
acute myeloid leukemiaELF1G3BP2MCL1venetoclax resistance

Highlights

  • G3BP2 upregulation in AML is linked to venetoclax resistance and poor clinical outcomes.
  • G3BP2 enhances AML cell survival by stabilizing ELF1 mRNA, which transcriptionally activates anti-apoptotic MCL1.
  • Pharmacologic inhibition of G3BP2 by C108 synergizes with venetoclax to overcome resistance, improving survival in AML preclinical models.
  • The G3BP2-ELF1-MCL1 axis represents a promising target for next-generation therapeutic strategies against AML.

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This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

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