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This study aimed to analyze the association between driver mutations and predictive markers for some anti–tumor agents in non–small cell lung cancer ( NSCLC ). A cohort of 785 Chinese patients with  NSCLC  who underwent resection from March 2016 to November 2017 in the First Affiliated Hospital of Guangzhou Medical University was investigated. The specimens were subjected to hybridization capture and sequence of 8 important  NSCLC ‐related driver genes. In addition, the slides were tested for  PD ‐L1, excision repair cross‐complementation group 1 ( ERCC 1), ribonucleotide reductase subunit M1 ( RRM 1), thymidylate synthase ( TS ) and β‐tubulin  III  by immunohistochemical staining. A total of 498 (63.4%) patients had at least 1 driver gene alteration. Wild‐type,  EGFR  rare mutation (mut),  ALK  fusion (fus),  RAS  mut,  RET  fus and  MET  mut had relatively higher proportions of lower  ERCC 1 expression.  EGFR  19del,  EGFR  L858R,  EGFR  rare mut,  ALK  fus,  HER 2 mut,  ROS 1 fus and  MET  mut were more likely to have  TS  low expression. Wild‐type,  EGFR  L858R,  EGFR  rare mut and  BRAF  mut were associated with lower β‐tubulin  III  expression. In addition, wild‐type,  RAS  mut,  ROS 1 fus,  BRAF  and  MET  mut had higher proportion of  PD ‐L1 high expression. As a pilot validation, 21 wild‐type patients with advanced  NSCLC  showed better depth of response and response rate to taxanes compared with pemetrexed/gemcitabine (31.2%/60.0% vs 26.6%/45.5%). Our study may aid in selecting the optimal salvage regimen after targeted therapy failure, or the chemo‐regimen where targeted therapy has not been a routine option. Further validation is warranted.

cancer science

Association between certain non–small cell lung cancer driver mutations and predictive markers for chemotherapy or programmed death‐ligand 1 inhibition