Targeting TMEM16A/ANO1 inhibits the progression of BRAF mutant(V600E)melanoma through the MEK/ERK and AKT signaling pathways  

作　　者：Meiyun Shi Jiahui Wang Xingyu Huang Linsu Liu Lutao Liu Na Zhou Xinqi Shan Huaqun Chen 

机构地区：[1]Jiangsu Key Laboratory for Molecular and Medical Biotechnology,College of Life Sciences,Nanjing Normal University,Nanjing,Jiangsu 210023,China

出　　处：《Genes & Diseases》2024年第6期5-7,共3页基因与疾病（英文）

摘　　要：The BRAF(V600E)mutation is common in malignant melanoma patients and drives constitutive activation of the MEK/ERK signaling pathway and cancer progression.1 To date,precision therapies targeting the BRAF/MEK/ERK pathway,including BRAF inhibitor(BRAFi)monotherapy using vemurafenib(VMF)and dabrafenib and combination therapy using dabrafenib and the MEKi trametinib,have been developed and have led to great advances in malignant melanoma therapy.

关 键 词：MEK/ERK V600E BRAF 

分 类 号：R739.5[医药卫生—肿瘤]