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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。
Tamoxifen (TAM) is the most effective and long-term first-line endocrine therapy for estrogen receptor (ER) -positive breast cancer, which can effectively reduce the mortality and relapse of patients with ER-positive breast cancer rate. However, clinical data show that about 50% of ER-positive breast cancer patients show intrinsic resistance to endocrine therapy, whereas 30% to 40% of those responding to TAM therapy develop acquired resistance. In this review, we investigated the effects of ERα36, G protein-coupled estrogen receptor (GPER), anterior gradient 2 (AGR2) and amplii ed in breast cancer 1 AIB1) These proteins, which are related to ERα and its signaling pathway, focus on the mechanism of TAM resistance in ER-positive breast cancer so as to provide new ideas for the treatment of ER-positive breast cancer.