Paradoxical clinical effect of estrogen on breast cancer risk: a "new" biology of estrogen-induced apoptosis.
Paradoxical clinical effect of estrogen on breast cancer risk: a "new" biology of estrogen-induced apoptosis.
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DOI：
10.1158/1940-6207.capr-11-0185
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发表时间：
2011-05
期刊：
影响因子：
--
通讯作者：
Ford LG
中科院分区：
文献类型：
--
作者：
Jordan VC;Ford LG
雌激素替代疗法（ERT）可降低乳腺癌的发病率，这是一项妇女健康倡议（WHI）在10，739名绝经后子宫切除术妇女中进行的双盲、安慰剂对照随机试验。虽然自相矛盾，因为雌激素被认为是刺激乳腺癌的生长，实验室数据支持在正确的环境条件下雌激素诱导的细胞凋亡的机制。长期抗雌激素治疗或雌激素剥夺导致抗激素抵抗的最终发展和演变。细胞群体出现的脆弱性，因为雌激素不再是一个生存信号，而是一个凋亡触发器。雌激素缺乏的绝经后妇女中ERT的抗肿瘤作用与实验室模型一致。
Administration of estrogen replacement therapy (ERT) decreases the incidence of breast cancer, as shown in a double-blind, placebo-controlled randomized trial of the Women’s Health Initiative (WHI) in 10,739 postmenopausal women with a prior hysterectomy. Though paradoxical because estrogen is recognized to stimulate breast cancer growth, laboratory data support a mechanism of estrogen-induced apoptosis under the correct environmental circumstances. Long-term antiestrogen treatment or estrogen deprivation causes the eventual development and evolution of antihormone resistance. Cell populations emerge with a vulnerability, as estrogen is no longer a survival signal but is an apoptotic trigger. The antitumor effect of ERT in estrogen-deprived postmenopausal women is consistent with laboratory models.