[1] Soda M, Choi YL, Enomoto M, et al. Identification of the transforming EML4ALK fusion gene in nonsmallcell lung cancer[J]. Nature, 2007, 448(7153): 561566. DOI: 10.1038/nature05945.
[2] Shackelford RE, Vora M, Mayhall K, et al. ALKrearrangements and testing methods in nonsmall cell lung cancer: a review[J]. Genes Cancer, 2014, 5(1/2): 114.
[3] Pan Y, Zhang Y, Li Y, et al. ALK, ROS1 and RET fusions in 1139 lung adenocarcinomas: a comprehensive study of common and fusion patternspecific clinicopathologic, histologic and cytologic features[J]. Lung Cancer, 2014, 84(2): 121126. DOI: 10.1016/j.lungcan.2014.02.007.
[4] 董江萍. FDA批准克里唑替尼及其基因测试法治疗晚期非小细胞肺癌[J]. 药物评价研究, 2011, 34(5): 402.
[5] Solomon BJ, Mok T, Kim DW, et al. Firstline crizotinib versus chemotherapy in ALKpositive lung cancer[J]. N Engl J Med, 2014, 371(23): 21672177. DOI: 10.1056/NEJMx150034.
[6] Shaw AT, Kim DW, Nakagawa K, et al. Crizotinib versus chemotherapy in advanced ALKpositive lung cancer[J]. N Engl J Med, 2013, 368(25): 23852394. DOI: 10.1056/NEJMoa1214886.
[7] Camidge DR, Bang YJ, Kwak EL, et al. Activity and safety of crizotinib in patients with ALKpositive nonsmallcell lung cancer: updated results from a phase 1 study[J]. Lancet Oncol, 2012, 13(10): 10111019. DOI: 10.1016/S14702045(12)703443.
[8] Solomon BJ, Mok T, Kim DW, et al. Firstline crizotinib versus chemotherapy in ALKpositive lung cancer[J]. N Engl J Med, 2014, 371(23): 21672177. DOI: 10.1056/NEJMoa1408440.
[9] 穆晶, 吴卫华, 蔡毅然, 等. ALK阳性并克唑替尼治疗有效肺鳞状细胞癌临床病理分析[J]. 临床和实验医学杂志, 2015 (11): 919922. DOI: 10.3969/j.issn.16714695.2015.011.018.
[10] Shaw AT, Ou SH, Bang YJ, et al. Crizotinib in ROS1rearranged nonsmallcell lung cancer[J]. N Engl J Med, 2014, 371(21): 19631971. DOI: 10.1056/NEJMoa1406766.
[11] Heuckmann JM, BalkeWant H, Malchers F, et al. Differential protein stability and ALK inhibitor sensitivity of EML4ALK fusion variants[J]. Clin Cancer Res, 2012, 18(17): 46824690. DOI: 10.1158/10780432.CCR113260.
[12] Katayama R, Shaw AT, Khan TM, et al. Mechanisms of acquired crizotinib resistance in ALKrearranged lung cancers[J]. Sci Transl Med, 2012, 4(120): 120ra17. DOI: 10.1126/scitranslmed.3003316.
[13] Perez CA, Velez M, Raez LE, et al. Overcoming the resistance to crizotinib in patients with nonsmall cell lung cancer harboring EML4/ALK translocation[J]. Lung Cancer, 2014, 84(2): 110115. DOI: 10.1016/j.lungcan.2014.02.001.
[14] Ou SH, Ahn JS, De Petris L, et al. Alectinib in Crizotinibrefractory ALKrearranged nonsmallcell lung cancer: a phase Ⅱ global study[J]. J Clin Oncol, 2016, 34(7): 661668. DOI: 10.1200/JCO.2015.63.9443.
[15] Ou SH, Jnne PA, Bartlett CH, et al. Clinical benefit of continuing ALK inhibition with crizotinib beyond initial disease progression in patients with advanced ALKpositive NSCLC[J]. Ann Oncol, 2014, 25(2): 415422. DOI: 10.1093/annonc/mdt572.
[16] Camidge DR, Kono SA, Flacco A, et al. Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment[J]. Clin Cancer Res, 2010, 16(22): 55815590. DOI: 10.1158/10780432.CCR100851.
[17] Zhang X, Zhang S, Yang X, et al. Fusion of EML4 and ALK is associated with development of lung adenocarcinomas lacking EGFR and KRAS mutations and is correlated with ALK expression[J]. Mol Cancer, 2010, 9: 188. DOI: 10.1186/147645989188.
[18] Sang J, Acquaviva J, Friedland JC, et al. Targeted inhibition of the molecular chaperone Hsp90 overcomes ALK inhibitor resistance in nonsmall cell lung cancer[J]. Cancer Discov, 2013, 3(4): 430443. DOI: 10.1158/21598290.CD120440.
[19] Sessa C, Shapiro GI, Bhalla KN, et al. Firstinhuman phase Ⅰ doseescalation study of the HSP90 inhibitor AUY922 in patients with advanced solid tumors[J]. Clin Cancer Res, 2013, 19(13): 36713680. DOI: 10.1158/10780432.CCR123404. |