达布拉芬尼
曲美替尼
突变
癌症研究
MEK抑制剂
肺癌
V600E型
桑格测序
医学
癌症
威罗菲尼
黑色素瘤
肿瘤科
激酶
生物
内科学
MAPK/ERK通路
基因
遗传学
转移性黑色素瘤
作者
Katsutoshi Seto,Junichi Shimizu,Katsuhiro Masago,Mitsugu Araki,Ryohei Katayama,Yukari Sagae,Shiro Fujita,Yoshitsugu Horio,Eiichi Sasaki,Hiroaki Kuroda,Kenichi Okubo,Yasushi Okuno,Toyoaki Hida
标识
DOI:10.1016/j.cancergen.2022.05.001
摘要
Purpose The present study clarified the sensitivity of the BRAF tyrosine kinase inhibitor mechanism in patients with BRAF compound mutation and predicted the sensitivity using molecular dynamics simulation. Methods We examined 16 BRAF tumors with p.V600E-positive non-small-cell lung cancer. Results One patient (6.2%) had a BRAF p.V600E and p.K601_W604 compound mutation with a good clinical response to dabrafenib and trametinib. Molecular dynamics simulation also complemented the effect. Conclusions The combination of a genetic analysis and computational simulation model may help predict the sensitivity for dabrafenib in cases with a rare BRAF compound mutation. The construction of a genomic and simulation fused database is important for the development of personalized medicine in this field.
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