The Metabolism, Analysis, and Targeting of Steroid Hormones in Breast and Prostate Cancer

被引:73
作者
Capper, Cameron P. [1 ,2 ]
Rae, James M. [1 ,2 ]
Auchus, Richard J. [3 ,4 ]
机构
[1] Univ Michigan, Dept Internal Med, Div Hematol Oncol, Ann Arbor, MI 48019 USA
[2] Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48019 USA
[3] Univ Michigan, Sch Med, Dept Internal Med, Div Metab Diabet & Endocrinol, Room 5560A,MSRB2,1150 W Med Ctr Dr, Ann Arbor, MI 48019 USA
[4] Univ Michigan, Sch Med, Dept Pharmacol, Room 5560A,MSRB2,1150 W Med Ctr Dr, Ann Arbor, MI 48019 USA
来源
HORMONES & CANCER | 2016年 / 7卷 / 03期
基金
美国国家卫生研究院;
关键词
LIGAND-BINDING DOMAIN; NUCLEAR RECEPTOR SUPERFAMILY; TERM TISSUE-CULTURE; ANDROGEN-RECEPTOR; POSTMENOPAUSAL WOMEN; AROMATASE INHIBITORS; 3-BETA-HYDROXYSTEROID DEHYDROGENASE; ESTROGEN PRODUCTION; CYTOCHROME B(5); 17-ALPHA-HYDROXYLASE/17,20 LYASE;
D O I
10.1007/s12672-016-0259-0
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Breast and prostate cancers are malignancies in which steroid hormones drive cellular proliferation. Over the past century, this understanding has led to successful treatment strategies aimed to inhibit hormone-mediated tumor growth. Nonetheless, disease relapse and progression still pose significant clinical problems, with recurrent and metastatic tumors often exhibiting resistance to current drug therapies. The central role of androgens and estrogens in prostate and breast cancer etiology explains not only why endocrine therapies are often initially successful but also why many tumors ultimately become resistant. It is hypothesized that reducing the concentration of active hormones in the systemic circulation may be insufficient to block cancer progression, as this action selects for tumor cells that can generate active steroids from circulating precursors. This review aims to highlight the currently known differences of steroid biosynthesis in normal physiology versus hormone-dependent cancers, modern approaches to the assessment and targeting of these pathways, and priorities for future research.
引用
收藏
页码:149 / 164
页数:16
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