论文部分内容阅读
肿瘤细胞对抗癌药物多药耐药性的产生及化疗中出现的骨髓抑制是目前临床治疗恶性肿瘤面临的主要问题。多药耐药基因(mdr1)编码产生的相对分子量为170 kD的跨膜蛋白(P-gp),可将多种化疗药物排出细胞外,从而避免药物对细胞的损害。正常骨髓造血于祖细胞mdr1基因表达水平极低,故化疗中易产生骨髓抑制。本研究旨在探讨将已转染mdr1基因的小鼠骨髓细胞回输入同种小鼠体内后,受体鼠对化疗药物骨髓毒性的耐受性有无增强,从基因水平寻找一种解决化疗中骨髓抑制的措施。
The emergence of multi-drug resistance of tumor cells to anticancer drugs and myelosuppression in chemotherapy are the main problems in clinical treatment of malignant tumors. Multidrug resistance gene (mdr1) encoding a transmembrane protein (P-gp) with a relative molecular weight of 170 kD, can be a variety of chemotherapeutic drugs excreted from the cell, so as to avoid drug damage to cells. Normal bone marrow hematopoietic progenitor cells mdr1 gene expression is very low, so chemotherapy is prone to bone marrow suppression. This study aimed to investigate whether the mdr1 gene transfected mice bone marrow cells back into the same kind of mice, the recipient mice on chemotherapy drug bone marrow toxicity whether or not enhanced, looking for a solution from the gene level in chemotherapy Myelosuppression measures.