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克唑替尼治疗ALK融合基因阳性的晚期非小细胞肺癌患者的疗效分析 被引量:7

Analysis of response to crizotinib in ALK-positive advanced NSCLC patients
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摘要 目的:探讨克唑替尼治疗中国 ALK 融合基因阳性的非小细胞肺癌(NSCLC)患者的疗效和安全性。方法:4名患者接受至少4周的克唑替尼(250 mg,q12h)治疗,以评价治疗后的近期疗效、生活质量、不良反应。结果12例患者口服克唑替尼治疗后,11例(91.67%)获得部分缓解,1例(8.33%)获得疾病稳定,客观缓解率为91.67%;在生活质量评估中,患者的疲乏、气短、睡眠等均得到改善;不良反应主要为消化道症状,其次是谷丙转氨酶升高(64.29%),视觉障碍(57.14%),大部分为1~2级。结论克唑替尼作为 ALK 融合基因阳性的 NSCLC 患者的靶向治疗,具有良好的疗效及安全性,不良反应轻微。 Objective To make a summary of efficacy and tolerability of crizotinib in Chinese EML4-ALK-posi-tive NSCLC patient. Method 14 NSCLC patients with positive ALK fusion gene were administered with crizotinib (250 mg, q12h) for at least 4 weeks, in which the efficacy and tolerability of crizotinib were evaluated. Result Among the 12 patients who were included in final analysis, 11 patients achieved partial remission (PR), one patient was with stable disease (SD, 8.33%). A statistically significant (P〈0.05) and clinically meaningful (≥10 points) im-provement from baseline was observed for patient-reported dyspnea, fatigue and global QOL. The most frequent ad-verse reactions were gastrointestinal disorders, elevated ALT (64.29% ), visual disorder (57.14% ), and which were mostly in grade 1-2. Conclusion As a target therapy for NSCLC, crizotinib demonstrates a high response rate, favor-able tolerability profile and significant improvement in patient-reported symptoms.
作者 郑明英 张力
出处 《癌症进展》 2015年第1期83-86,共4页 Oncology Progress
关键词 非小细胞肺癌 ALK 克唑替尼 non-small cell lung cancer ALK crizotinib
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参考文献22

  • 1Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012[J]. CA Cancer J Clin, 2012, 62(1): 10-29.
  • 2Lynch T J, Bell DW, Sordella R, et al. Activating muta- tions in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib [J]. N Engl J Med, 2004, 350(21): 2129-2139.
  • 3Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefi- tinib therapy[J]. Science, 2004, 304(5676): 1497-1500.
  • 4Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EML-4-ALK fusion gene in non-small cell lung cancer[J]. Nature, 2007, 448(7153): 561-566.
  • 5lnamura K, Takeuchi K, Togashi Y, et al. EML4-ALK lung cancers are characterized by rare other mutations, a TTF-1 cell lineage, an acinar histology, and young onset [J]. Mod Pathol, 2009, 22(4): 508-515.
  • 6Shaw AT, Yeap BY, Solomon B J, et al. Effect of crizo- tinib on overall survival in patients with advanced non- small-cell lung cancer harbouring ALK gene rearrange- ment: a retrospective analysis[J]. Lancet Oncol, 2011, 12 (11): 1004-1012.
  • 7Sun Y, Ren Y, Fang Z, et al. Lung adenocarcinoma from East Asian never-smokers is a disease largely defined by targetable oncogenic mutant kinases[J]. J Clin Oncol, 2010, 28(30): 4616-4620.
  • 8Zhang X, Zhang S, Yang X, et al. Fusion of EML4 and ALK is associated with development of lung adenocarci- nomas lacking EGFR and KRAS mutations and is corre- lated with ALK expression[J]. Mol Cancer, 2010, 9(1): 188.
  • 9Wong DW, Leung EL, So KK, et al. The EML4-ALK fu- sion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS[J]. Cancer, 2009, 115(8): 1723-1733.
  • 10Takahashi T, Sonobe M, Kobayashi M, et al. Clinico- pathologic features of non-small-cell lung cancer with EML4-ALK fusion gene[J]. Ann Surg Oncol, 2010, 17 (3): 889-897.

同被引文献59

  • 1葛均波,徐永健.内科学.北京:人民卫生出版社,2013:385-390.
  • 2Travis WD, BrambiUa E, MuUer-Hermelink HK eds. Pathology and genetics of tumors of the lung, pleura, thymus and heart World Health Organization classification of tumors. Lyon: IARC Press, 2004: 9-67.
  • 3Sasaki T, Rodig SJ, Chirieac LR, et al. The biology and treatment of EMIA- ALK non-small cell lung cancer. Eur J Cancer, 2010, 46 ( 10 ): 1773 - 1780.
  • 4Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature, 2007, 448(7153): 561-566.
  • 5Kwak EL, Bang YJ, Camidge DR, et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med, 2010, 363 (18): 1693-1703.
  • 6Cuijj, Tran-Dube M, Shen H, et al. Structure based drug design of crizotinib (PF-02341066), a potent and selective dual inhibitor of mesenchymal- epithelial transition factor (c-MET) kinase and anaplastic lymphoma kinase (ALK). J Med Chem, 2011, 54(18): 6342-6363.
  • 7Shaw AT, Yeap BY, Solomon BJ, et al. Impact of crizotinib on survival in patients with advanced, ALK-positive NSCLC compared with historical controls.J Clin Oncol, 2011, 29(15): 7507.
  • 8Kim DW, Alan MJ, Shi Y, et al. Results of a global phase II study with crizotinib in advanced ALK-positive non-smalllung cancer (NSCLC). J Clin Oncol, 2012, 30(15): 7533.
  • 9Shaw AT, Kim DW, Nakagawa K, et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med, 2013, 368(25): 2385-2394.
  • 10Sun HY, Ji FO,. A molecular dynamics investigation on the crizotinib resistance mechanism of C1156Y mutation in ALK. Biochem Biophys Res Commun, 2012, 423(2): 319-324.

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