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EML4-ALK融合基因抑制剂耐药机制的研究进展 被引量：5

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摘要 随着对肿瘤发病机制认识的不断深入，近年来肺癌的分子靶向治疗已经成为全世界的研究热点之一。2003年，美国食品及药物管理局（FDA）首先确立了表皮生长因子受体酪氨酸激酶抑制剂（epidermal growth factor receptor tyrosine kinase inhibitors，EGFR—TKI）在晚期非小细胞肺癌（NSCLC）中的治疗地位；2004年，EGFR敏感突变相继被发现，
作者 张会娟 张晓彤 张力
机构地区 中国医学科学院北京协和医学院北京协和医院呼吸科
出处 《中华病理学杂志》 CAS CSCD 北大核心 2012年第12期862-864,共3页 Chinese Journal of Pathology
关键词 基因抑制剂 耐药机制 晚期非小细胞肺癌 受体酪氨酸激酶抑制剂 美国食品及药物管理局 分子靶向治疗 表皮生长因子 EGFR
分类号 R734.2 [医药卫生—肿瘤]
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参考文献17

  • 1Ou SH. Crizotinib : a novel and first-in-class muhitargeted tyrosine kinase inhibitor for the treatment of anaplastic lymphoma kinase rearranged non-small cell lung cancer and beyond. Drug Des Devel Ther, 2011,5 : 471-485.
  • 2Doebele RC, Pilling AB, Aisner DL, et al. Mechanisms of resistance to crizotinib in patients with ALK gene rearranged non- small cell lung cancer. Clin Cancer Res, 2012,18 (5): 1472- 1482.
  • 3Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EMIA-ALK fusion gene in non-small-cell lung cancer. Nature, 2007,448(7153): 561-566.
  • 4Sasaki T, Rodig S J, Chirieac LR, et al. The biology and treatment of EMIA-ALK non-small cell lung cancer. Eur J Cancer, 2010,46(10) : 1773-1780.
  • 5Lin E, Li L, Guan Y, et al. Exon array profiling detects EMIA- ALK fusion in breast, colorecta|, and non-small cell lung cancers. Mol Cancer Res, 2009, 7 (9) : 1466-1476.
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同被引文献57

  • 1任学群,李宜雄,陈善正,胡国潢,应娇茜,李劲东,裴海平,陈志康,汤恢焕,吕新生.胰十二指肠切除术后胰瘘的危险因素[J].中国普通外科杂志,2006,15(10):772-776. 被引量：45
  • 2Jemal A, Siegel R,Ward E,et al. Cancer statistics. CA Cancer JClin, 2006,56(2) : 106-130.
  • 3Mok TS, Wu YL, Thongprasert S, et al. Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Engl J Med, 2009,361(10) : 947-957.
  • 4Zhou C, Wu YL, Chen G, et al. Erlotinib versus chemotherapy asfirst-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer ( OPTIMAL, CTONG-0802 ):a multicentre, open-label, randomised, phase 3 study. LancetOncol, 2011,12(8) :735-742.
  • 5Sun Y,Shi Y, Zhang L, et al. A randomized, double-blind phaseIE study of icotinib versus gefitinib in patients with advanced non-small cell lung cancer ( NSCLC ) previously treated withchemotherapy ( ICOGEN ). J Clin Onco, 2011, 29 ( Suppl ):[abstr 7522].
  • 6Soda M, Choi YL, Enomoto M, et al. Identification of thetransforming EML4-ALK fusion gene in non-small-cell lungcancer. Nature, 2007 , 448(8) : 561-566.
  • 7Hom L, Pao W. EML4-ALK: honing in on a new target in non-small-cell lung cancer. J Clin Oncol, 2009, 27(26) :4232-4235.
  • 8Soda M, Takada S,Takeuchi K, et al. A mouse model for EML4-ALK-positive lung cancer. Proc Natl Acad Sci USA, 2008, 105(50) ; 19893-19897.
  • 9Shaw AT, Yeap BY, Solomon BJ, et al. Effect of crizotinib oroverall survival in patients with advanced non-small-cell lun!cancer harbouring ALK gene rearrangement: a retrospectiveanalysis. Lancet Oncol, 2011,12( 11 ) : 1004-1012.
  • 10Zhang X, Zhang S, Yang X,et al. Fusion of EML4 and ALK ifassociated with development of lung adenocarcinomas lackingEGFR and KRAS mutations and is correlated with ALKexpression. Mol Cancer, 2010,9:188.

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中华病理学杂志
2012年 第12期

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