卵巢癌化疗耐药作用机制的基因研究进展

卵巢癌是妇科肿瘤中致死率最高的肿瘤,其主要原因之一是卵巢癌细胞易对化疗产生耐药而导致治疗失败。卵巢癌的发生与发展常常联系一系列基因的变化,从分子水平上了解卵巢癌细胞对化疗产生耐药机理,寻找更有效的化疗药物,是提高卵巢癌疗效的关键。本文将近年来此方面的研究进展作一概括。研究发现HER-2、XIAP和bcl-X(L)基因的高表达、Bcl-2和c-myc基因的低表达与卵巢癌患者对化疗药物产生耐药有关。一系列具抗耐药和与卵巢癌化疗药物有协同作用的基因SU5416、EpoB、Apo2L/TRAIL、PSC833、TP53、BCL-2、BAX和MEK1蛋白、MAPKs、JNK、p38和ERK的出现,为改善卵巢癌化疗效果,提高治愈率,带来了新的希望。

Gene study on the mechanism of chemoresistance in ovarian cancer

Ovarian cancer is the main cause of death in the gynecologic malignant tumors . One of the main reasons is that the cells of ovarian cancer resistance to the chemotherapy, thus impede to the successful treatment. The progression and development of ovarian cancer frequently link to a series of complex changes of genes. To understand the molecular mechanism of chemoresistance and search for more effective anticancer drugs is the key to improve the therapy of ovarian cancer. We introduce the new findings in these fields in recent years. Studies showed that the overexpression of HER-2,XIAP,bcl-X(L) and the underexpression of Bcl-2 and c-myc were associated with chemoresistance. Some anti-chemoresistance and improving the efficacy of cancer therapy, such as SU5416, EpoB, Apo2L/TRAIL, PSC833, TP53, BCL-2, BAX, MEK1 protein, MAPKs, JNK, p38 and ERK, provide the strong support and bring the new hope to improve the effect of chemotherapy.