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晚期非小细胞肺癌靶向治疗的研究进展

姜文丽 黄才国

姜文丽, 黄才国. 晚期非小细胞肺癌靶向治疗的研究进展[J]. 药学实践与服务, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
引用本文: 姜文丽, 黄才国. 晚期非小细胞肺癌靶向治疗的研究进展[J]. 药学实践与服务, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
JIANG Wenli, HANG Caiguo. Research progress on target therapy of advanced non-small cell lung cancer[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
Citation: JIANG Wenli, HANG Caiguo. Research progress on target therapy of advanced non-small cell lung cancer[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004

晚期非小细胞肺癌靶向治疗的研究进展

doi: 10.3969/j.issn.1006-0111.2016.04.004
基金项目: 国家自然科学基金面上项目(41576160,81473239)

Research progress on target therapy of advanced non-small cell lung cancer

  • 摘要: 生物标志物检测使得许多晚期非小细胞肺癌(NSCLC)患者获益。近年来,针对表皮生长因子受体(EGFR)和间变性淋巴瘤激酶(ALK)突变呈阳性的NSCLC患者,以吉非替尼、厄洛替尼、阿法替尼为代表的表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)和以克唑替尼为代表的ALK-TKI取得了卓越的疗效。但是,大多数第一代EGFR-TKI和ALK-TKI的疗效因为不可避免的继发性耐药而被减弱。目前,第三代EGFR-TKI正是基于第二代EGFR-TKI的耐药机制研发而成。除此之外,还有许多针对其他突变位点的晚期NSCLC维持治疗的靶向抑制剂。遗憾的是,针对突变比例最大的K-RAS突变,尚无疗效确切的靶向药物。因此,基于肿瘤驱动基因突变机制的探索和靶向药物的开发是目前NSCLC的研究热点。
  • [1] Chen W, Zheng R, Baade PD, et al. Cancer statistics in China, 2015[J]. CA Cancer J Clin, 2016,66(2):115-132.
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    [4] Banno E, Togashi Y, Kobayashi Y, et al. Afatinib is especially effective against non-small cell lung cancer carrying an EGFR exon 19 deletion[J]. Anticancer Res, 2015,35(4):2005-2008.
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    [9] Vacondio F, Carmi C, Galvani E, et al. Long-lasting inhibition of EGFR autophosphorylation in A549 tumor cells by intracellular accumulation of non-covalent inhibitors[J]. Bioorg Med Chem Lett, 2013, 23(19):5290-5294.
    [10] Giordano P, Manzo A, Montanino A, et al. Afatinib:An overview of its clinical development in non-small-cell lung cancer and other tumors[J]. Crit Rev Oncol Hematol, 2016, 97:143-151.
    [11] Kato T, Yoshioka H, Okamoto I, et al. Afatinib versus cisplatin plus pemetrexed in Japanese patients with advanced non-small cell lung cancer harboring activating EGFR mutations:Subgroup analysis of LUX-Lung 3[J]. Cancer Sci, 2015, 106(9):1202-1211.
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    [13] Janne PA, Yang JC, Kim DW, et al. AZD9291 in EGFR inhibitor-resistant non-small-cell lung cancer[J]. N Engl J Med, 2015, 372(18):1689-1699.
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    [17] Chong CR, Janne PA. The quest to overcome resistance to EGFR-targeted therapies in cancer[J]. Nat Med, 2013,19(11):1389-1400.
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    [19] Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer[J]. Nature, 2007, 448(7153):561-566.
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    [22] Lukas RV, Hasan Y, Nicholas MK, et al. ROS1 rearranged non-small cell lung cancer brain metastases respond to low dose radiotherapy[J]. J Clin Neurosci, 2015,22(12):1978-1979.
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  • 收稿日期:  2016-01-26
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晚期非小细胞肺癌靶向治疗的研究进展

doi: 10.3969/j.issn.1006-0111.2016.04.004
    基金项目:  国家自然科学基金面上项目(41576160,81473239)

摘要: 生物标志物检测使得许多晚期非小细胞肺癌(NSCLC)患者获益。近年来,针对表皮生长因子受体(EGFR)和间变性淋巴瘤激酶(ALK)突变呈阳性的NSCLC患者,以吉非替尼、厄洛替尼、阿法替尼为代表的表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKI)和以克唑替尼为代表的ALK-TKI取得了卓越的疗效。但是,大多数第一代EGFR-TKI和ALK-TKI的疗效因为不可避免的继发性耐药而被减弱。目前,第三代EGFR-TKI正是基于第二代EGFR-TKI的耐药机制研发而成。除此之外,还有许多针对其他突变位点的晚期NSCLC维持治疗的靶向抑制剂。遗憾的是,针对突变比例最大的K-RAS突变,尚无疗效确切的靶向药物。因此,基于肿瘤驱动基因突变机制的探索和靶向药物的开发是目前NSCLC的研究热点。

English Abstract

姜文丽, 黄才国. 晚期非小细胞肺癌靶向治疗的研究进展[J]. 药学实践与服务, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
引用本文: 姜文丽, 黄才国. 晚期非小细胞肺癌靶向治疗的研究进展[J]. 药学实践与服务, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
JIANG Wenli, HANG Caiguo. Research progress on target therapy of advanced non-small cell lung cancer[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
Citation: JIANG Wenli, HANG Caiguo. Research progress on target therapy of advanced non-small cell lung cancer[J]. Journal of Pharmaceutical Practice and Service, 2016, 34(4): 301-304,333. doi: 10.3969/j.issn.1006-0111.2016.04.004
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