肿瘤细胞对MTX产生耐药机制的研究进展  

Progress on the mechanism of tumor MTX resistance

作　　者：韩冬[1] 孟祥宁[1] 傅松滨[1] 

机构地区：[1]哈尔滨医科大学医学遗传学研究室,150081

出　　处：《国际遗传学杂志》2010年第6期349-354,共6页International Journal of Genetics

基　　金：国家自然科学基金面上项目（30771198、30971583、30801350）

摘　　要：氨甲蝶呤（methotrexate,MTX）广泛用于多种肿瘤的化疗,如乳腺癌、结肠癌及白血病等,然而逐渐产生的耐药限制了MTX的治疗效果.肿瘤细胞对MTX的耐药机制涉及MTX的摄入减少,MTX胞外溢出增多,MTX多聚谷氨酸化水平不足,主要靶基因二氢叶酸还原酶基因（dihydrofolate reductase,DHFR）的过表达、突变及肿瘤相关基因的异常表达等多个方面.全面了解肿瘤细胞MTX耐药的分子机制将有助于指导临床用药及为新药的研发提供理论依据.本文综述了肿瘤细胞对MTX产生耐药机制的研究进展.Methotrexate（MTX） is widely used to treat several types of tumors, including breast cancer,colon cancer, and leukemia. However, the usefulness of MTX is limited by the development of drug resistance.Resistance to MTX may be acquired through different ways, including reduction in the influx of MTX, increased MTX effiux from the cells, inefficient polyglutamate of MTX, increased expression and mutation of the target gene DHFR, abnormal expression of tumor related genes and so on. Therefore, a better understanding of the molecular mechanism of MTX resistance is important for the clinical use as well as the development of new drugs. This paper will have a brief review of the progression on the mechanism of MTX resistance.

关 键 词：氨甲蝶呤 化疗 恶性肿瘤 耐药性 

分 类 号：R714.22[医药卫生—妇产科学]