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表皮生长因子受体酪氨酸激酶抑制剂的耐药机制及应对策略
引用本文:徐秋一,牟海波,徐农.表皮生长因子受体酪氨酸激酶抑制剂的耐药机制及应对策略[J].国际肿瘤学杂志,2012,39(5):355-359.
作者姓名:徐秋一  牟海波  徐农
作者单位:浙江大学医学院附属第一医院化疗科,杭州,310000
摘    要: 表皮生长因子受体(EGFR)酪氨酸激酶抑制剂(EGFR-TKI)对含有EGFR突变的非小细胞肺癌治疗效果较好,但仍有部分患者对酪氨酸激酶抑制剂(TKI)原发耐药,而对TKI治疗敏感的患者最终无法避免继发耐药导致肿瘤进展,其主要分子机制是T790M突变和MET扩增。研究新的靶向治疗药物及联合应用药物克服耐药是目前临床科研的主题。

关 键 词:  非小细胞肺  药物疗法  抗药性  肿瘤  

Mechanism and treatment associated with resistance to EGFR-TKI
XU Qiu-yi , MOU Hai-bo , XU Nong.Mechanism and treatment associated with resistance to EGFR-TKI[J].Journal of International Oncology,2012,39(5):355-359.
Authors:XU Qiu-yi  MOU Hai-bo  XU Nong
Institution:Department of Chemotherapy, First Affiliated Hospital,  Medical School of Zhejiang University, Hangzhou 310000, China
Abstract:Epidermal growth factor receptor tyrosine kinases inhibitor (EGFR-TKI) has impressive clinical efficacy in EGFR-mutant non-small cell lung cancer. However, there are still some patients with primary resistance to TKI. And most patients who initially respond to treatment eventually develop resistance to these drugs, which the main molecular mechanisms are T790M and MET amplification. The new targeted therapies and combination drugs to overcome drug resistance is the subject of clinical research.
Keywords:Cancer  non-small cell lung  Drug therapy  Drug resistance  neoplasm
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