Activity of EGFR-tyrosine kinase and ALK inhibitors for EML4–ALK-rearranged non–small–cell lung cancer harbored coexisting EGFR mutation
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- 作者：Akihiko Miyanaga (1)
Kumi Shimizu (1)
Rintaro Noro (1)
Masahiro Seike (1)
Kazuhiro Kitamura (1)
Seiji Kosaihira (1)
Yuji Minegishi (1)
Takehito Shukuya (7)
Akinobu Yoshimura (1) (8)
Masashi Kawamoto (2) (3)
Shinichi Tsuchiya (2)
Koichi Hagiwara (4)
Manabu Soda (5)
Kengo Takeuchi (6)
Nobuyuki Yamamoto (7)
Hiroyuki Mano (5)
Yuichi Ishikawa (6)
Akihiko Gemma (1) - 关键词：EML4–ALK ; EGFR mutation ; Lung cancer
- 刊名：BMC Cancer
- 出版年：2013
- 出版时间：December 2013
- 年：2013
- 卷：13
- 期：1
- 全文大小：375KB
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21. The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2407/13/262/prepub - 作者单位：Akihiko Miyanaga (1)
Kumi Shimizu (1)
Rintaro Noro (1)
Masahiro Seike (1)
Kazuhiro Kitamura (1)
Seiji Kosaihira (1)
Yuji Minegishi (1)
Takehito Shukuya (7)
Akinobu Yoshimura (1) (8)
Masashi Kawamoto (2) (3)
Shinichi Tsuchiya (2)
Koichi Hagiwara (4)
Manabu Soda (5)
Kengo Takeuchi (6)
Nobuyuki Yamamoto (7)
Hiroyuki Mano (5)
Yuichi Ishikawa (6)
Akihiko Gemma (1)
1. Department of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan
7. Division of Thoracic Oncology, Shizuoka Cancer Center, Shizuoka, Japan
8. Department of Clinical Oncology, Tokyo Medical University Hospital, 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. Saitama Medical School Respiratory Organs Internal Medicine, Saitama, Japan
5. Division of Functional Genomics, Jichi Medical University, Tochigi, Japan
6. Division of Pathology, The Cancer Institute, Japanese Foundation for Cancer Research, Tokyo, Japan - ISSN：1471-2407
文摘
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.