Open AccessFirst‐generation EGFR tyrosine kinase inhibitor therapy in 106 patients with compound EGFR ‐mutated lung cancer: a single institution's clinical practice experience
Author(s) -
Yu Xiangyang,
Zhang Xuewen,
Zhang Zichen,
Lin Yongbin,
Wen Yingsheng,
Chen Yongqiang,
Wang Weidong,
Zhang Lanjun
Publication year - 2018
Publication title -
cancer communications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.119
H-Index - 53
ISSN - 2523-3548
DOI - 10.1186/s40880-018-0321-0
Subject(s) - t790m , lung cancer , mutation , medicine , oncology , exon , point mutation , tyrosine kinase inhibitor , epidermal growth factor receptor , gefitinib , tyrosine kinase , cancer , cancer research , biology , genetics , gene , receptor
Background The antitumour efficacy of tyrosine kinase inhibitors (TKIs) in lung cancer patients with compound epidermal growth factor receptor ( EGFR ) mutations has not been resolved. Our study summarizes a single institutional experience of first‐generation TKI therapy for lung cancers with compound EGFR mutations. Methods A total of 106 consecutive patients with tumours bearing compound EGFR mutations were identified between January 2012 and May 2016; all patients received first‐generation TKI therapy. Deletions in exon 19 and the L858R point mutation in exon 21 were considered common mutations; T790M was considered separately because of its association with TKIs resistances. Any other mutation was defined as a rare mutation. Patients were divided as follows: double common mutations (group A); common plus T790M mutations (group B); common plus rare mutations (group C); double rare mutations (group D); and rare plus T790M mutations (group E). A separate group of 115 consecutive patients with a single common mutation was created for comparative analysis (group F). Results The frequency of patients with compound EGFR was 2.9% (114/3925) and their response rate to first‐generation TKIs was 50.9%, which was not significantly different from group F (67.0%, P = 0.088). The progression‐free survival (PFS) of the 106 patients receiving TKI therapy was worse than that of group F (median, 9.1 vs. 13.0 months, respectively; P < 0.001). The PFS of the compound mutation group was shorter than that of the single common mutation group (median, 10.1 months in group A, P = 0.240; 9.1 months in group B, P < 0.001; 9.6 months in group C, P = 0.010; 6.5 months in group D, P = 0.048; 5.4 months in group E, P = 0.017). Patients with a co‐occurring mutation in exon 20 (excluding T790M) exhibited significantly worse PFS than the patients with other compound mutations or with a single common mutation (median, 6.5 vs. 9.1 vs. 13.0 months, respectively, P = 0.002). Conclusions There was significant heterogeneity among the compound EGFR mutations and their response to first‐generation TKIs. Individualized treatment in clinical practice should be considered for each case.