๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Role of estrogen receptor variants in the development of hormone resistance in breast cancer

โœ Scribed by Mels Sluyser


Publisher
Elsevier Science
Year
1992
Tongue
English
Weight
762 KB
Volume
25
Category
Article
ISSN
0009-9120

No coin nor oath required. For personal study only.

โœฆ Synopsis


Recent evidence suggests that the progression to hormone resistance in some breast tumors is due to mutations in the estrogen receptor (ER). Various types of ER variants have been found in breast cancer biopsies and breast cancer cell lines. The ER variants include dominant-positive receptors that are transcriptionally active in the absence of estrogen, and dominantnegative receptors that are themselves transcriptionally inactive but prevent the action of the normal receptor. The mechanisms by which these variants cause loss of hormonal control is becoming clear. ER variants may be prognostic factors for breast cancer. By modifying the action of ER variants, it should be possible to develop new strategies for treatment of malignant breast disease.


๐Ÿ“œ SIMILAR VOLUMES


Effects of estrogen on breast cancer dev
โœ Wei Yue; Ji-Ping Wang; Yuebai Li; Ping Fan; Guijian Liu; Nan Zhang; Mark Conaway ๐Ÿ“‚ Article ๐Ÿ“… 2010 ๐Ÿ› John Wiley and Sons ๐ŸŒ French โš– 565 KB

Development of breast cancer involves genetic factors as well as lifetime exposure to estrogen. The precise molecular mechanisms whereby estrogens influence breast tumor formation are poorly understood. While estrogen receptor alpha (ERalpha) is certainly involved, nonreceptor mediated effects of es

Steroid hormone receptors and coregulato
โœ Nanna Sarvilinna; Heli Eronen; Susanna Miettinen; Annika Vienonen; Timo Ylikomi ๐Ÿ“‚ Article ๐Ÿ“… 2005 ๐Ÿ› John Wiley and Sons ๐ŸŒ French โš– 281 KB

## Abstract Resistance to hormonal therapy is often a problem in the treatment of breast cancer patients. It has been suggested that resistance could be explained by altered nuclear hormone receptor or coregulator levels or inappropriately increased agonist activity of selective estrogen receptor m