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miR-196b-TLR7/8 Signaling Axis Regulates Innate Immune Signaling and Myeloid Maturation in DNMT3A-Mutant AML.

Holly A GamlenJennifer S Romer-SeibertMichael E LawlerAmanda M VersaceMelanie L GoetzYang FengOlga A GuryanovaNeil PalmisianoSara E Meyer
Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2022)
DNMT3A loss-of-function mutations cause miRNA locus-specific hypomethylation and overexpression important for mutant DNMT3A-mediated pathogenesis and clinical outcomes. Specifically, the overexpression of miR-196b in DNMT3A-mutant AML creates a novel therapeutic vulnerability by controlling sensitivity to TLR7/8-directed therapies.
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