EGFR exon 21 L858R as an acquired resistance mechanism to nivolumab in a lung cancer patient originally driver gene-negative.

ABSTRACT: The use of immune checkpoint inhibitors targeting PD-1 and PD-L1 in advanced non-small cell lung cancer (NSCLC) has been one of the most significant improvements in recent years. However the resistance mechanisms of immune checkpoint inhibitors require further investigation. Herein we attempted to determine the possible resistance mechanism of nivolumab in a male smoker with advanced adenosquamous carcinoma. After experiencing disease progression on systematic chemotherapy, he was administered nivolumab as a result of high PD-L1 expression. Larger panel gene detection was performed after the failure of nivolumab treatment to investigate the possible resistance mechanism and a new EGFR exon 21 L858R mutation was detected. After a achieving a response with gefitinib, the patient suffered a r

SUBMITTER: Xia C 

PROVIDER: S-EPMC6501009 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature