已发表论文

表皮生长因子受体酪氨酸激酶抑制剂在切除后复发性肺腺鳞癌中的临床结果

 

Authors Fan L, Yang H, Yao F, Zhao Y, Gu H, Han K, Zhao H

Received 7 June 2016

Accepted for publication 27 August 2016

Published 6 January 2017 Volume 2017:10 Pages 239—245

DOI https://doi.org/10.2147/OTT.S114451

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 3

Editor who approved publication: Dr Samir Farghaly

Purpose: The therapeutic efficacy of targeted therapy for adenosquamous carcinoma (ASC) of the lung remains unclear and the role of epidermal growth factor receptor (EGFR) testing in patients with ASC also remains controversial. We aimed to analyze the efficacy of EGFR tyrosine kinase inhibitors (EGFR-TKIs) in ASC.
Methods: Clinical records of patients with ASC who received treatment with EGFR-TKIs between January 2006 and December 2014 at two institutions were retrospectively reviewed.
Results: A total of 27 EGFR mutation-positive patients with ASC who received TKI therapy were enrolled in this study. EGFR mutations included a deletion in exon 19 in 15 cases and a point mutation at codon 858 (L858R) in exon 21 in 12 cases. Among the 27 ASC patients who received treatment with EGFR-TKIs, nine had a partial response and 11 achieved stable disease, accounting for a disease control rate of 74.1% (20/27). The median postoperative overall survival (OS) of the EGFR-mutant patients who received TKI therapy was 39 months (95% confidence interval [CI]: 25.6–52.4). The median progression-free survival for EGFR mutation-positive patients was 15 months (95% CI: 12.9–17.1), and the median relapse OS was 19 months (95% CI: 0.9–37.1). In addition, the 3- and 5-year postoperative survival rate was 51.9% and 15.3%, respectively.
Conclusion: ASC patients harboring EGFR mutations had a good response to TKI therapy. Routine EGFR testing for ASCs was recommended. Further studies on TKI therapy versus chemotherapy alone for EGFR-mutant ASCs are required.
Keywords: adenosquamous carcinoma of the lung, epidermal growth factor receptor tyrosine kinase inhibitors, mutation, survival