KRAS突变肺腺癌的研究进展  

Research progress of KRAS mutation in lung adenocarcinoma

作　　者：金晨星 赵翌[1] Jin Chenxing;Zhao Yi(Department of Oncology,First Affiliated Hospital of Dalian Medical University,Dalian 116011,China)

机构地区：[1]大连医科大学附属第一医院肿瘤科,116011

出　　处：《国际肿瘤学杂志》2020年第3期180-184,共5页Journal of International Oncology

摘　　要：鼠类肉瘤病毒癌基因(KRAS)是肺癌的驱动基因,其突变常发生于经表皮生长因子受体-酪氨酸激酶抑制剂(EGFR-TKI)治疗后耐药的肺腺癌中,因患者预后较差且尚未有针对性靶向药物而引起关注。近年研究发现KRAS突变可通过影响信号传导和转录激活因子3(STAT3)、G蛋白偶联受体(GPCR)、程序性死亡受体-配体1(PD-L1)的表达、哺乳动物雷帕霉素靶蛋白(mTOR)信号通路的活化及多种基因的共突变促进肿瘤进展,影响治疗和预后。新型小分子KRAS G12C抑制剂AMG 510的Ⅰ期临床试验结果为治疗提供了希望。总结KRAS突变肺腺癌的发病机制、预后相关因素、靶向治疗及免疫治疗等,有助于提高对KRAS突变的认识,为后续研究提供思路与依据。As the driver gene of lung cancer,Kirsten rat sarcoma viral oncogene(KRAS)mutation often occurs in lung adenocarcinoma resistant to treatment with epidermal growth factor receptor-tyrosine kinase inhibitors(EGFR-TKIs),which has attracted attention due to its poor prognosis and lack of targeted drugs.Recent studies have found that KRAS mutation can promote tumor progression and affect treatment and prognosis by affecting the expressions of signal transducer and activator of transcription 3(STAT3),G-protein-coupled receptor(GPCR)and programmed death receptor-ligand 1(PD-L1),mammalian target of rapamycin(mTOR)signaling pathway activation and co-mutation of multiple genes.A phaseⅠclinical trial shows that AMG 510,a novel small molecule KRAS G12C inhibitor,is hopeful in treatment.Summarizing the pathogenesis,prognostic factors,targeted therapy and immunotherapy of KRAS mutation in lung adenocarcinoma is helpful to improve the understanding of KRAS mutation and can provide ideas and basis for subsequent studies.

关 键 词：癌 非小细胞肺 治疗应用 KRAS基因 

分 类 号：R734[医药卫生—肿瘤]