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作 者:黄辉[1] 丁江华 Huang Hui;Ding Jianghua(Department of Clinical Medicine,Clinical Medicine School of Jiujiang University,Jiujiang 332000,China;Department of Hematology&Oncology,Affiliated Hospital of Jiujiang University,Jiujiang 332000,China)
机构地区:[1]九江学院医学院临床医学系,九江332000 [2]九江学院附属医院血液肿瘤科,九江332000
出 处:《国际肿瘤学杂志》2023年第9期569-573,共5页Journal of International Oncology
摘 要:成纤维细胞生长因子受体(FGFR)2基因融合是胆管癌发生的重要机制。靶向FGFR2的药物成为晚期胆管癌的主要治疗方法。以英菲替尼和培米替尼为代表的三磷酸腺苷竞争性FGFR抑制剂可有效延缓肿瘤进展,延长患者生存期,是FGFR2融合型晚期胆管癌患者的首选药物。然而,几乎所有经英菲替尼治疗的晚期胆管癌患者最终都产生耐药,需要联用其他药物治疗。福巴替尼可作为发生V564F突变的英菲替尼耐药性胆管癌患者的后线药物;对于丝裂原活化蛋白激酶(MAPK)信号通路异常激活所致英菲替尼耐药胆管癌患者,MAPK抑制剂与热休克蛋白90抑制剂可作为新的治疗选择。Fibroblast growth factor receptor(FGFR)2 gene fusion plays an important role in the patho⁃genesis of cholangiocarcinoma(CCA).The method of targeting FGFR2 has been listed as the major therapy for advanced CCA.Adenosine triphosphate(ATP)-competitive FGFR inhibitors,represented by infigratinib and pemigatinib,effectively delay tumor progression and prolong patients survival,and are the first-line drugs for advanced CCA patients with FGFR2 fusion.However,almost all the patients treated with infigratinib eventually develop resistance,which require the combination with other drugs.Futibatinib may serve as a later-line drug for advanced CCA patients with V564F mutation after infigratinib resistance.For the infigratinib-resistant CCA patients harboring aberrant activation of the mitogen-activated protein kinase(MAPK)pathway,combination of the MAPK inhibitor or the heat shock protein 90 inhibitor may be considered as a novel therapeutic option.
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