ATM Regulates Differentiation of Myofibroblastic Cancer-Associated Fibroblasts and Can Be Targeted to Overcome Immunotherapy Resistance

Investigators identified ataxia-telangiectasia (ATM) mutated as a central regulator of the myofibroblastic cancer-associated fibroblast (myoCAFs) phenotype. Differentiating myofibroblasts in vitro and myoCAFs cultured ex vivo displayed activated ATM signaling, and targeting ATM genetically or pharmacologically could suppress and reverse differentiation.