Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2010-5-14
pubmed:abstractText
Estrogens play a crucial role in regulating the growth and differentiation of breast cancers, with approximately two thirds of all breast tumors expressing the estrogen receptor alpha (ERalpha). Therefore, therapeutic strategies directed at inhibiting the action of ERalpha by using anti-estrogens such as tamoxifen, or reducing estrogens levels by using aromatase inhibitors, such as letrozole, anastrozole, or exemestane, are the standard treatments offered to women with ERalpha-positive cancer. However, not all patients respond to endocrine therapies (termed de novo resistance), and a large number of patients who do respond will eventually develop disease progression or recurrence while on therapy (acquired resistance). Recently, variant forms of the receptor have been identified owing to alternative splicing or gene mutation. This article reviews these variant receptors and their clinical relevance in resistance to endocrine therapy, by addressing their molecular cross-talk with growth factor receptors and signaling components. Understanding the complexity of receptor-mediated signaling has promise for new combined therapeutic options that focus on more efficient blockade of receptor cross-talk.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1078-0432
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2010 AACR.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2702-8
pubmed:dateRevised
2011-3-10
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Estrogen receptor mutations and changes in downstream gene expression and signaling.
pubmed:affiliation
Centro Sanitario and Department of Cellular Biology, University of Calabria, Arcavacata di Rende, Cosenza, Italy.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural