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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
引用本文:王笑影,张新. 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[J]. 国际呼吸杂志, 2011, 31(8): 630-636. DOI: 10.3760/cma.j.issn.1673-436X.2011.008.017
作者姓名:王笑影  张新
作者单位:复旦大学附属中山医院呼吸科,上海,200322
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...

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

Mechanism and reverse of acquired resistance of non-small cell lung cancer to epidermal growth factor receptor-tyrosine kinase inhibitor
WANG Xiao-ying,ZHANG Xin. Mechanism and reverse of acquired resistance of non-small cell lung cancer to epidermal growth factor receptor-tyrosine kinase inhibitor[J]. International Journal of Respiration, 2011, 31(8): 630-636. DOI: 10.3760/cma.j.issn.1673-436X.2011.008.017
Authors:WANG Xiao-ying  ZHANG Xin
Abstract:Epidermal 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.
Keywords:Non-small cell lung cancer  Epidermal growth factor receptor-tyrosine kinase inhibitor  Acquired resistance  T790M mutation  MET amplification
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