第三代表皮生长因子受体-酪氨酸激酶抑制剂研究进展  

Third-generation epidermal growth factor receptor-tyrosine kinase inhibitors： a clinical update

作　　者：王沁雪 曾晓宁[1] 刘亚南[1] 赵欣[1] 黄茂[1] 

机构地区：[1]南京医科大学第一附属医院江苏省人民医院呼吸科,210029

出　　处：《国际呼吸杂志》2016年第1期51-55,共5页International Journal of Respiration

摘　　要：肺癌是中国最常见且病死率最高的恶性肿瘤之一。近年来随着分子靶向药物的发展，尤其是表皮生长因子受体（epidermal growth factor receptor，EGFR）-酪氨酸激酶抑制剂（tyrosine kinase inhibitors，TKIs）的研发及应用，部分存在基因敏感型突变的非小细胞肺癌患者已获得了良好效果。现已进入临床应用的第一代可逆性TKIs如吉非替尼、厄洛替尼、埃克替尼用药后易继发T790M突变而导致耐药，第二代不可逆性泛ErbB家族抑制剂阿法替尼等仍未能克服此缺陷。现同时针对EGFR基因敏感型突变及T790M耐药突变的第三代不可逆性TKIS——AZD9291、c01686、HM61713已进入临床研究并取得部分可喜结果，或可成为获得性耐药肺癌患者治疗的理想选择。Lung cancer is one of the most common malignant tumors with higher mortality in China. Patients with epidermal growth factor receptor （EGFR） mutant non-small cell lung cancer have achieved favorable therapeutic effect since the development of molecular targeted therapy, especially the application of EGFR-tyrosine kinase inhibitors （TKIs）. However, patients receiving the first-generation EGFR-TKIs such as gefitinib, ertotinib and icotinib would yield progression of the disease due to acquired resistance mostly caused by T790M mutation. Since the second-generation TKIs, which serve as irreversible pan-ErbB receptors inhibitors such as afatinib, play a limited role in these patients, the third- generation TKIs targeted both EGFR and T790M mutation, including AZD9291, CO1686 and HM61713 have achieved the predictive results from clinical trials, may provide optimal options for patients with acquired resistance.

关 键 词：非小细胞肺癌 分子靶向治疗 表皮生长因子受体-酪氨酸激酶抑制剂 

分 类 号：R734.2[医药卫生—肿瘤] R969.4[医药卫生—临床医学]