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ALK and ROS1 concurrent with EGFR mutation in patients with lung adenocarcinoma

Authors Mao Y, Wu S

Received 26 January 2017

Accepted for publication 12 April 2017

Published 11 July 2017 Volume 2017:10 Pages 3399—3404


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Akshita Wason

Peer reviewer comments 2

Editor who approved publication: Dr XuYu Yang

Yanjiao Mao, Shixiu Wu

Department of Radiotherapy Oncology, Hangzhou Cancer Hospital, Hangzhou, People’s Republic of China

Purpose: The purpose of this study was to explore the frequencies of ALK and ROS1 fusion genes in EGFR-mutant lung adenocarcinoma patients and examine the therapeutic efficacies of EGFR-tyrosine kinase inhibitors (TKIs).
Materials and methods: A total of 421 EGFR-mutated patients taking EGFR-TKIs were examined for ALK and ROS1 fusion genes based on reverse transcription-polymerase chain reaction (RT-PCR). Progression-free survival (PFS) and overall survival (OS) were evaluated by the Kaplan–Meier method and compared by the log-rank test.
Results: The mutations of ALK rearrangement (n=10) and ROS1 rearrangement (n=3) were detected. All the patients received EGFR-TKIs, and eight took subsequent ALK/ROS1 inhibitor. PFS was longer in single EGFR mutants (n=408) than in EGFR/ALK or EGFR/ROS1 counterparts (n=13; 10.7 vs 6.6 months, P=0.004). No difference in OS existed between single EGFR and EGFR/ALK or EGFR/ROS1 mutants (21.0 vs 23.0 months, P=0.196). The median PFS of eight patients treated with ALK/ROS1 inhibitor was 6.0 months.
Conclusion: Concomitant ALK/ROS1 fusion genes occurred in 3.1% EGFR-mutated lung adenocarcinoma patients. Concomitant ALK/ROS1–EGFR mutations may influence the therapeutic efficacy of EGFR-TKIs.

Keywords: epidermal growth factor receptor, ALK, ROS1, lung adenocarcinoma, efficacy

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