Downregulation of anti-inflammatory A20 promotes immune escape of lung adenocarcinomas

We found that the potent anti-inflammatory enzyme A20 is a potent tumor suppressor and hence often downregulated in human and mouse lung adenocarcinoma. Comparison of gene expression profiles of A20 expressing versus A20 deficient lung tumor tissue samples revealed that loss of A20 enhanced the cellular response to interferons. This hypersensitivity to interferons was responsible to drive immune evasion of A20 deficient lung adenocarcinomas. , Overall design: KRASG12D mutated, p53 and A20 deficient tumors were induced in mice via inhalation with a Cre recombinase expressing adenovirus. After 10 weeks, tumors were macroscopically dissected and RNA was processed for RNAseq analysis.