EGFR, KRAS and ROS1 variants coexist in a lung adenocarcinoma patient

被引：31

作者：

Ju, Lixia ^{[1
]}

Han, Mingquan ^{[1
]}

Zhao, Chao ^{[2
]}

Li, Xuefei ^{[2
]}

机构：

[1] Tongji Univ, Dept Integrat Med, Shanghai Pulm Hosp, Sch Med, 507 Zheng Min Rd, Shanghai 200433, Peoples R China

[2] Tongji Univ, Dept Lung Canc & Immunol, Sch Med, Canc Inst,Med Ctr, Shanghai 200433, Peoples R China

来源：

LUNG CANCER | 2016年 / 95卷

基金：

中国国家自然科学基金;

关键词：

EGFR mutation; KRAS mutation; ROS1; Non-small cell lung cancer; TYROSINE-KINASE INHIBITORS; ALK REARRANGEMENT; CANCER; MUTATION; CRIZOTINIB; FUSIONS; MUTANT;

D O I：

10.1016/j.lungcan.2016.03.005

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The c-ros oncogene 1 (ROS1) fusion is almost mutually exclusive to epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK) or Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation in non-small cell lung cancer (NSCLC), and it is not seen in the literature for patients to exhibit three mutations. The present study reported a case of a 53-year-old male diagnosed with adenocarcinoma, exhibiting combined EGFR, KRAS mutations and ROS1 rearrangement. At the first line therapy, the patient was treated with crizotinib because of the KRAS mutation that is a known resistant factor of EGFR-TKI resistance, but no responsive. At the second line therapy, EGFR-TKI Icotinib revealed a good response until now. To the best of to our knowledge, this is the first case report of a patient with concurrent EGFR, KRAS mutations and ROS1 fusion. This patient had an excellent response to Icotinib but not crizotinib, suggesting that the EGFR mutation was the oncogenic driver but ROS1 fusion and KRAS mutation not. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

引用

页码：94 / 97

页数：4

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