Research ArticleLUNG CANCER

Down-regulation of A20 promotes immune escape of lung adenocarcinomas

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Science Translational Medicine  07 Jul 2021:
Vol. 13, Issue 601, eabc3911
DOI: 10.1126/scitranslmed.abc3911

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A checkpoint for lung cancer

Inflammation is a driver of tumor development, and down-regulation or loss of genes required to control inflammation can be protumorigenic. One such gene that may serve as such a controller of inflammation is tumor necrosis factor alpha–induced protein 3 (TNFAIP3), also known as A20. Here, Breitenecker et al. demonstrated that loss of A20 was associated with reduced CD8+ T cell–mediated immune surveillance in both mouse models and in patients with lung cancer. Further, A20 loss was associated with increased tumor burden in mouse models, but these tumors were sensitive to immune checkpoint blockade therapies. Together, these findings suggest that A20 may be a checkpoint in the development of lung adenocarcinoma.

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