【摘要】 他莫昔芬(tamoxifen,TAM)是治疗雌激素受体(estrogen receptor,ER)阳性乳腺癌最有效且应用时间最长的一线内分泌治疗药物,能够有效降低ER阳性乳腺癌患者的死亡率和复发率。然而,临床资料显示约50%的ER阳性乳腺癌患者对内分泌治疗显示出固有耐药,而在对TAM治疗有反应的患者中,30%~40%可发展成获得性耐药。本文从ERα36、G蛋白偶联雌激素受体(G protein-coupled estrogen receptor,GPER)、前梯度蛋白2(anterior gradient 2,AGR2)和乳腺癌扩增性抗原1(amplii ed in breast cancer 1,AIB1)这些与ERα及其信号通路有关的蛋白着眼,阐释ER阳性乳腺癌TAM耐药的机制,以期为ER阳性乳腺癌的治疗提供新思路。更多还原

【Abstract】 Tamoxifen(TAM) has emerged as the most effective drug and acts as a first-line therapy in the treatment of estrogen receptor(ER)-positive breast cancer in the past four decades. Moreover, it can reduce the recurrence rate and the mortality of patients with ER-positive breast cancer. However, clinical studies have reported that approximately 50% of ER-positive breast cancer has a de novo resistance to TAM, and 30% to 40% of the remaining responsive patients will acquire resistance to TAM. This review focuses on ERα36, G protein-coupled estrogen receptor(GPER), anterior gradient 2(AGR2) and amplified in breast cancer 1(AIB1), which were correlated with ERα and ERα-related singal pathway, to explain the mechanism of TAM resistance and discuss their possible clinical roles.更多还原