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Background  The majority of non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor ( EGFR ) mutation eventually develop resistance to EGFR tyrosine kinase inhibitors (TKIs). Minimal information exists regarding genetic alterations in rebiopsy samples from Asian NSCLC patients who develop acquired resistance to EGFR-TKIs.    Methods  We retrospectively reviewed the medical records of patients with NSCLC harboring  EGFR  mutations who had undergone rebiopsies after developing acquired resistance to EGFR-TKIs. We analyzed 27 practicable samples using a tumor genotyping panel to assess 23 hot-spot sites of genetic alterations in nine genes ( EGFR ,  KRAS ,  BRAF ,  PIK3CA ,  NRAS ,  MEK1 ,  AKT1 ,  PTEN , and  HER2 ), gene copy number of  EGFR ,  MET ,  PIK3CA ,  FGFR1 , and  FGFR2 , and  ALK ,  ROS1 , and  RET  fusions. Additionally, 34 samples were analyzed by commercially available  EGFR  mutation tests.    Results  Sixty-one patients underwent rebiopsy. Twenty-seven samples were analyzed using our tumor genotyping panel, and 34 samples were analyzed for  EGFR  mutations only by commercial clinical laboratories. Twenty-one patients (34 %) had  EGFR  T790M mutation. Using our tumor genotyping panel,  MET  gene copy number gain was observed in two of 27 (7 %) samples. Twenty patients received continuous treatment with EGFR-TKIs even after disease progression, and 11 of these patients had T790M mutation in rebiopsy samples. In contrast, only 10 of 41 patients who finished EGFR-TKI treatment at disease progression had T790M mutation. The frequency of T790M mutation in patients who received continuous treatment with EGFR-TKIs after disease progression was significantly higher than that in patients who finished EGFR-TKI treatment at disease progression (55 % versus 24 %,  p  = 0.018).    Conclusions  The frequency of T790M mutation in this study was lower than that in previous reports examining western patients. These results suggest that continuous treatment with EGFR-TKI after disease progression may enhance the frequency of  EGFR  T790M mutation in rebiopsy samples.    Electronic supplementary material  The online version of this article (doi:10.1186/s12885-016-2902-0) contains supplementary material, which is available to authorized users.

bmc cancer

Frequency of EGFR T790M mutation and multimutational profiles of rebiopsy samples from non-small cell lung cancer developing acquired resistance to EGFR tyrosine kinase inhibitors in Japanese patients