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GAB2 couples genetic drivers and signaling networks in acute myeloid leukemia
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Journal Article
GAB2 couples genetic drivers and signaling networks in acute myeloid leukemia
2025
Overview
In acute myeloid leukemia (AML), leukemogenesis is typically driven by the sequential acquisition of distinct classes of mutations that collaborate to transform normal hematopoietic stem and progenitor cells. The founding and cooperating mutations in AML are often in signaling genes and form functional partnerships with each other, each addressing complementary aspects of malignant transformation. In this issue of the JCI, Kramer et al. elaborate on the molecular pathogenesis of AML. By using a mouse bone marrow model bearing the common AML-initiating mutations in DNA methyltransferase 3 a (ОММТЗА) and nucleophosmin 1 (NPM1), the work provides further evidence for the role of the signaling orchestrator GRB2associated-binding protein 2 (GAB2) in AML progression, positioning GAB2 as a potential therapeutic target.
Publisher
American Society for Clinical Investigation
Subject
