换一批非小细胞肺癌对表皮生长因子受体酪氨酸激酶抑制剂获得性耐药的机制及逆转
Mechanism and reverse of acquired resistance of non-small cell lung cancer to epidermal growth factor receptor-tyrosine kinase inhibitor
摘要表皮生长因子受体酪氨酸激酶抑制剂在非小细胞肺癌的治疗中发挥了重要作用,但开始对此药敏感的患者经过6～12个月的治疗后多数会出现获得性耐药,成为其持续用药难以回避的治疗瓶颈.本文主要阐述T790M突变和MET扩增等非小细胞肺癌对表皮生长因子受体酪氨酸激酶抑制剂获得性耐药的机制及逆转耐药的新一代酪氨酸激酶抑制剂和其他靶向治疗药物的研究进展.
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abstractsEpidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) plays an important role in the treatment of non-small cell lung cancer. However,after EGFR-TKI therapy for six to twelve months, acquired resistance may occur in patients who are initially sensitive to it, which blocks the sustained medication. This article mainly reviews the mechanism of acquired resistance of non-small cell lung cancer to EGFR-TKI including T790M mutation and MET amplification and the progress on new generation tyrosine kinase inhibitor and other targeted agents.
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关键词
非小细胞肺癌表皮生长因子受体酪氨酸激酶抑制剂获得性耐药T790M突变MET扩增Non-small cell lung cancerEpidermal growth factor receptor-tyrosine kinase inhibitorAcquired resistanceT790M mutationMET amplification
医学主题词
酪氨酸(Tyrosine)癌, 非小细胞肺(Carcinoma, Non-Small-Cell Lung)受体, 表皮生长因子(Receptor, Epidermal Growth Factor)性(Sex)突变(Mutation)
分类号
R73（肿瘤学）
栏目名称
DOI
10.3760/cma.j.issn.1673-436X.2011.008.017
发布时间
2011-05-26（万方平台首次上网日期，不代表论文的发表时间）
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