医学
表皮生长因子受体
肺癌
后天抵抗
酪氨酸激酶
癌症研究
受体酪氨酸激酶
突变体
突变
机制(生物学)
表皮生长因子
癌症
肿瘤科
受体
内科学
生物
基因
遗传学
哲学
认识论
作者
Jordi Remón,Teresa Morán,Margarita Majem,Noemı́ Reguart,E. Dalmau,Diego Márquez-Medina,P. Lianes
标识
DOI:10.1016/j.ctrv.2013.06.002
摘要
The discovery of mutated oncogenes has opened up a new era for the development of more effective treatments for non-small cell lung cancer patients (NSCLC) harbouring EGFR mutations. However, patients with EGFR-activating mutation ultimately develop acquired resistance (AR). Several studies have identified some of the mechanisms involved in the development of AR to EGFR tyrosine kinase inhibitors (TKI) that can be potential therapeutic strategies, although in up to 30% of cases, the underlying mechanism of AR are still unexplained. In this review we aim to summarize the main mechanisms of AR to EGFR TKI and some clinical strategies that can be used in the daily clinical practice to overcome this resistance and try to prolong the outcomes in this subgroup of patients.
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