Activity of EGFR-tyrosine kinase and ALK inhibitors for EML4–ALK-rearranged non–small–cell lung cancer harbored coexisting EGFR mutation

BMC Cancer

Akihiko Miyanaga⁷  Kumi Shimizu⁷  Rintaro Noro⁷  Masahiro Seike⁷  Kazuhiro Kitamura⁷  Seiji Kosaihira⁷  Yuji Minegishi⁷  Takehito Shukuya⁴  Akinobu Yoshimura⁵  Masashi Kawamoto³  Shinichi Tsuchiya²  Koichi Hagiwara⁸  Manabu Soda⁶  Kengo Takeuchi¹  Nobuyuki Yamamoto⁴  Hiroyuki Mano⁶  Yuichi Ishikawa¹  Akihiko Gemma⁷ 

[1] Division of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan

[2] Division of Diagnostic Pathology, Nippon Medical School Hospital, Tokyo, Japan

[3] Department of Clinical Pathology, University Hospital, Mizonokuchi, Teikyo University School of Medicine, Kanagawa, Japan

[4] Division of Thoracic Oncology, Shizuoka Cancer Center, Shizuoka, Japan

[5] Department of Clinical Oncology, Tokyo Medical University Hospital, Tokyo, Japan

[6] Division of Functional Genomics, Jichi Medical University, Tochigi, Japan

[7] Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan

[8] Saitama Medical School Respiratory Organs Internal Medicine, Saitama, Japan

关键词: Lung cancer;    EGFR mutation;    EML4–ALK;   

Others  :  1079729
DOI  :  10.1186/1471-2407-13-262

 received in 2013-01-17, accepted in 2013-05-22,  发布年份 2013

【 摘 要 】

Background

The EML4–ALK (echinoderm microtubule-associated protein-like 4 gene and the anaplastic lymphoma kinase gene) fusion oncogene represents a novel molecular target in a small subset of non–small–cell lung cancers (NSCLCs). The EML4–ALK fusion gene occurs generally in NSCLC without mutations in epidermal growth factor receptor (EGFR) and KRAS.

Case presentation

We report that a case of EML4–ALK-positive NSCLC with EGFR mutation had a response of stable disease to both an EGFR tyrosine kinase inhibitor (EGFR-TKI) and ALK inhibitor.

Conclusions

We described the first clinical report of a patient with EML4–ALK-positive NSCLC with EGFR mutation that had a response of stable disease to both single-agent EGFR-TKI and ALK inhibitor. EML4–ALK translocation may be associated with resistance to EGFR-TKI, and EGFR signaling may contribute to resistance to ALK inhibitor in EML4–ALK-positive NSCLC.

【 授权许可】

   
2013 Miyanaga et al.; licensee BioMed Central Ltd.

【 图 表 】

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