Pathways to tamoxifen resistance

被引:218
作者
Riggins, Rebecca B.
Schrecengost, Randy S.
Guerrero, Michael S.
Bouton, Amy H.
机构
[1] Univ Virginia, Hlth System, Dept Microbiol, Charlottesville, VA 22908 USA
[2] Univ Virginia, Hlth System, Ctr Canc, Charlottesville, VA 22908 USA
[3] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA
关键词
tamoxifen; antiestrogen; aromatase inhibitor; fulvestrant; estrogen receptor;
D O I
10.1016/j.canlet.2007.03.016
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Therapies that target the synthesis of estrogen or the function of estrogen receptor(s) have been developed to treat breast cancer. While these approaches have proven to be beneficial to a large number of patients, both de novo and acquired resistance to these drugs is a significant problem. Recent advances in our understanding of the molecular mechanisms that contribute to resistance have provided a means to begin to predict patient responses to these drugs and develop rational approaches for combining therapeutic agents to circumvent or desensitize the resistant phenotype. Here, we review common mechanisms of antiestrogen resistance and discuss the implications for prediction of response and design of effective combinatorial treatments. (C) 2007 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:1 / 24
页数:24
相关论文
共 221 条
[1]   Tumor-specific low molecular weight forms of cyclin E induce genomic instability and resistance to p2l, p27, and antiestrogens in breast cancer [J].
Akli, S ;
Zheng, PJ ;
Multani, AS ;
Wingate, HF ;
Pathak, S ;
Zhang, N ;
Tucker, SL ;
Chang, S ;
Keyomarsi, K .
CANCER RESEARCH, 2004, 64 (09) :3198-3208
[2]   Low-molecular-weight cyclin E: the missing link between biology and clinical outcome [J].
Akli, S ;
Keyomarsi, K .
BREAST CANCER RESEARCH, 2004, 6 (05) :188-191
[3]   Steroid receptors and cell cycle in normal mammary epithelium [J].
Anderson, E ;
Clarke, RB .
JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA, 2004, 9 (01) :3-13
[4]   SERINE-167 IS THE MAJOR ESTRADIOL-INDUCED PHOSPHORYLATION SITE ON THE HUMAN ESTROGEN-RECEPTOR [J].
ARNOLD, SF ;
OBOURN, JD ;
JAFFE, H ;
NOTIDES, AC .
MOLECULAR ENDOCRINOLOGY, 1994, 8 (09) :1208-1214
[5]   PHOSPHORYLATION OF THE HUMAN ESTROGEN-RECEPTOR ON TYROSINE-537 IN-VIVO AND BY SRC FAMILY TYROSINE KINASES IN-VITRO [J].
ARNOLD, SF ;
OBOURN, JD ;
JAFFE, H ;
NOTIDES, AC .
MOLECULAR ENDOCRINOLOGY, 1995, 9 (01) :24-33
[6]   HER-2 amplification, HER-1 expression, and tamoxifen response in estrogen receptor-positive metastatic breast cancer: A southwest oncology group study [J].
Arpino, G ;
Green, SJ ;
Allred, DC ;
Lew, D ;
Martino, S ;
Osborne, CK ;
Elledge, RM .
CLINICAL CANCER RESEARCH, 2004, 10 (17) :5670-5676
[7]  
Ascenzi Paolo, 2006, Molecular Aspects of Medicine, V27, P299, DOI 10.1016/j.mam.2006.07.001
[8]   Estrogen receptor activation at serine 305 is sufficient to upregulate cyclin D1 in breast cancer cells [J].
Balasenthil, S ;
Barnes, CJ ;
Rayala, SK ;
Kumar, R .
FEBS LETTERS, 2004, 567 (2-3) :243-247
[9]   Progesterone receptor status significantly improves outcome prediction over estrogen receptor status alone for adjuvant endocrine therapy in two large breast cancer databases [J].
Bardou, VJ ;
Arpino, G ;
Elledge, RM ;
Osborne, CK ;
Clark, GM .
JOURNAL OF CLINICAL ONCOLOGY, 2003, 21 (10) :1973-1979
[10]  
Becker M, 2005, MOL CANCER THER, V4, P151