目的　研究乳腺癌组织中多药耐药基因（ Ｍ Ｐ Ｒ１） 的表达及临床意义；探讨３ 种耐药逆转剂维拉帕来（ Ｖ Ｐ Ｌ） 、三苯氧胺（ Ｔ Ａ Ｍ） 、潘生丁（ Ｄ Ｐ） 对耐阿霉素人乳腺癌细胞系 Ｍ Ｃ Ｆ７ａｄｒ 的逆转作用。方法　采用逆转录—多聚酶链式反应技术（ Ｒ Ｔ － Ｐ Ｃ Ｒ）检测２６ 例乳腺癌病人 Ｍ Ｄ Ｒ１ 的表达情况；采用 Ｍ Ｔ Ｔ 比色法测定每孔细胞的吸光度 Ａ 值， 并计算细胞抑制率（ Ｉ Ｒ ％ ） 、半数细胞抑制浓度（ Ｉ Ｃ５０） 。结 果 　 乳 腺 癌 Ｍ Ｄ Ｒ１ 基 因 阳 性 表 达 率 为 ４６２ ％ （１２／２６） ；其中在未经任何治疗的１８ 例原发乳癌中 Ｍ Ｄ Ｒ１阳性率为２７８ ％ （５／１８） ；耐药基因表达与乳腺癌的组织学类型无相关性，但在有转移和有化疗史的乳癌中， 其阳性率要明显高于 无转 移和 无 化疗 史 者（ ７２７ ％ 、８７５ ％ 、２６７ ％ 、２７７ ％ ） 。 Ｍ Ｔ Ｔ 法证实，在无细胞毒性的剂量范围内， 分别合用 Ｖ Ｐ Ｌ、 Ｔ Ａ Ｍ和 Ｄ Ｐ 前后， Ｍ Ｃ Ｆ７ａｄｒ 细胞对阿霉素的敏感性有明显差异， Ｉ Ｃ５０ 降至原来的９ ％ ～５０ ％ 。结论　乳腺癌有一定的原发耐药性， 化疗能够促进 Ｍ Ｄ Ｒ１ 的表达， Objective To investigate the expression and clinical significance of multidrug resistance gene (MRP1) in breast cancer tissues; to investigate the three drug resistance reversal agents verapamil (V P L), tamoxifen (TA M), and dipyridamole (D P ) Reversal of the adriamycin-resistant human breast cancer cell line MCF7adr. Methods Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of M D R1 in 26 breast cancer patients. The absorbance A value of cells in each well was measured by M T T colorimetric method and the cells were counted. Inhibition rate (IR%), half-cell inhibitory concentration (IC50). Results The positive rate of M D R1 gene expression in breast cancer was 46. 2% (12/26). The positive rate of M D R1 in 18 cases of primary breast cancer without any treatment was 27.8% (5/18). There was no correlation between the expression of drug resistance genes and the histological type of breast cancer, but the positive rate was significantly higher in those with metastases and breast cancer with a history of chemotherapy (72.7%, 87.5%). %, 267 %, 277 %). The M T T method confirmed that the sensitivity of M C F7adr cells to doxorubicin was significantly different before and after the combined use of V P L, T A M, and D P in the dose range without cytotoxicity, and I C50 was reduced to the original value. 9 % to 50 %. Conclusion Breast cancer has a certain degree of primary drug resistance, chemotherapy can promote the expression of M D R1,