Increased BRAF copy number in lung adenocarcinoma

被引:8
|
作者
Sasaki, Hidefumi [1 ]
Maekawa, Masahiko [2 ]
Tatematsu, Tsutomu [1 ]
Okuda, Katsuhiro [1 ]
Moriyama, Satoru [1 ]
Yano, Motoki [1 ]
Fujii, Yoshitaka [1 ]
机构
[1] Nagoya City Univ, Grad Sch Med Sci, Dept Oncol Immunol & Surg, Nagoya, Aichi 4678601, Japan
[2] GSP Lab Inc, Kawasaki, Kanagawa 2120032, Japan
基金
日本学术振兴会;
关键词
BRAF; lung cancer; adnocarcinoma; copy number; V600E; IMPROVED SURVIVAL; MEK INHIBITION; SOLID TUMORS; CANCER; MUTATIONS; MELANOMA; DABRAFENIB; FEATURES; PATIENT; GENOME;
D O I
10.3892/ol.2014.2719
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Point mutation of the BRAF gene is a genetic event that occurs in a subset of lung adenocarcinoma cases. For example, BRAF V600E is a driver mutation that can be effectively targeted using selective BRAF and/or MEK inhibitors. The present study hypothesized that an increase in BRAF copy number may be correlated with certain clinicopathological features of lung adenocarcinoma in Japanese patients. The BRAF gene copy number was analyzed using quantitative polymerase chain reaction amplifications in 29 surgically treated lung adenocarcinoma cases without EGFR or Kras mutations from Nagoya City University Hospital (Nagoya, Japan). Seven BRAF-mutant cases were included. Increased BRAF gene copy number was identified in three lung adenocarcinoma patients (10.3%), all of which exhibited the V600E mutation. Using fluorescence in situ hybridization with BRAF-specific and chromosome 7 centromeric probes, increased copy number status was associated with gene amplification or gain of chromosome 7. Although increased BRAF copy number was correlated with BRAF V600E mutations, numerical changes in BRAF copy number were rare and mild in lung adenocarcinoma, resulting in no significant difference in pathological tumor status or tumor stage.
引用
收藏
页码:709 / 712
页数:4
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