乳腺癌多西他赛耐药的分子机制  

Molecular Mechanisms of Docetaxel Resistance in Breast Cancer

作　　者：吴新刚[1] 黄谦[1] 向安萍[1] 

机构地区：[1]岳阳职业技术学院医学基础部,湖南岳阳414000

出　　处：《肿瘤防治研究》2014年第4期413-415,共3页Cancer Research on Prevention and Treatment

基　　金：湖南省教育厅基金资助项目(11C1284)

摘　　要：多西他赛(DTX)已广泛应用于乳腺癌的辅助化疗、新辅助化疗和转移性乳腺癌的治疗。然而,由于天然耐药的存在和获得性耐药的产生,严重制约了DTX的临床应用。已知的乳腺癌多西他赛的耐药机制主要包括:药物作用靶点的改变、解毒酶的激活、细胞凋亡相关基因的异常表达、DNA甲基化状态、ATP结合盒(ABC)转运蛋白的过表达、微小RNA的表达异常等。Docetaxel has been used widely for the treatment of breast cancer in neoadjuvant, adjuvant and metastatic settings. However, its therapeutic usefulness is limited by innate or acquired resistance. The known mechanisms of docetaxel resistance in breast cancer include the alteration of drug target, the activation of detoxifying enzymes, the aberrant expression of apoptosis-related genes, the DNA methylation status, the overexpression of the ATP-binding cassette transporters, and the abnormal microRNA expression.

关 键 词：多西他赛 乳腺肿瘤 多药耐药 

分 类 号：R737.9[医药卫生—肿瘤]