摘要
非小细胞肺癌(NCSLC)中15%~30%有gK-RASg突变,目前研究认为,其突变与表皮生长因子受体(EGFR)突变互相排斥,与EGFR酪氨酸激酶抑制剂(EGFR-TKIs)耐药正相关,但与C-225疗效无正相关关系,与NCSLC不良预后有关。现有许多研究探索法尼基转移酶抑制剂(Ftase抑制剂,FTIs)、RAF抑制剂、MAPK激酶(MEK)抑制剂来消除突变性K-RAS活性,改善临床疗效。
Mutated K-RAS is found in 15% - 30% NSCLC patients, the mutations of K-RAS and EGFR are mutually exclusive,K-RAS mutations have poor sensitivity to EGFR-TKIs. The response of C-225 is not restricted to mutated K-RAS, NSCLC patients with K-RAS mutations are associated with unfavorable prognosis. A number of different approaches such as Ftase inhibitors, RAF inhibitors, MEK inhibitors aimed at abrogating K-RAS activity to improve clinical response have been explored in clinical trials.
出处
《基础医学与临床》
CSCD
北大核心
2010年第2期212-214,共3页
Basic and Clinical Medicine