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Background  The therapeutic efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in advanced  EGFR -mutant lung squamous cell carcinoma (SCC) patients remains uncertain. Furthermore, the factors underlying the responsiveness have not been fully investigated. We therefore investigated the link between genomic profiles and EGFR-TKI efficacy.    Material and Methods  We consecutively enrolled stage IV,  EGFR -mutant, and EGFR-TKI–treated patients with SCC. Patients with  EGFR  wild-type lung SCC and  EGFR -mutant lung adenocarcinoma were consecutively enrolled as controls, and next-generation sequencing (NGS) was performed.    Results  In total, 28  EGFR -mutant lung SCC, 41  EGFR -mutant lung adenocarcinoma, and 40  EGFR  wild-type lung SCC patients were included. Among the patients with  EGFR  mutations, shorter progression-free survival (PFS) was observed in SCC compared to adenocarcinoma (4.6  vs.  11.0 months, P<0.001). Comparison of the genomic profiles revealed that  EGFR -mutant SCC patients had similar mutation characteristics to  EGFR -mutant adenocarcinoma patients, but differed from those with  EGFR  wild-type SCC. Further exploration of  EGFR -mutant SCC revealed that mutations in  CREBBP  (P = 0.005),  ZNF217  (P = 0.016), and the Wnt (P = 0.027) pathway were negatively associated with PFS. Mutations in  GRM8  (P = 0.025) were associated with improved PFS.    Conclusions    EGFR -mutant lung SCC has a worse prognosis than  EGFR -mutant adenocarcinoma. Mutations in other genes, such as  CREBBP ,  ZNF217 ,  GRM8 , or Wnt that had implications on PFS raise the possibility of understanding mechanisms of resistance to EGFR-TKI in lung SCC, which will aid identification of potential beneficial subgroups of patients with  EGFR -mutant SCCs receiving EGFR-TKIs.

EGFR-Mutated Squamous Cell Lung Cancer and Its Association With Outcomes