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

Holly A Gamlen Jennifer S Romer-Seibert Michael E Lawler Amanda M Versace Melanie L Goetz Yang Feng Olga A Guryanova Neil Palmisiano Sara 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.

Keyphrases

dna methylation
acute myeloid leukemia
innate immune
toll like receptor
wild type
inflammatory response
immune response
cell proliferation
gene expression
climate change
dendritic cells
bone marrow
nuclear factor
genome wide association study