Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2011-1-26
pubmed:abstractText
The most critical step for initiation and progression of estrogen receptor-? (ER?)-positive breast cancers is thought to be upregulation of ER? expression. There are several factors involved in this mechanism, i.e., increased promoter activity of the ER? gene (ESR1) at the transcriptional level, ESR1 gene amplification, and diminished degradation of ER? protein through ubiquitination and proteasomal pathways. Mediating these factors, ER? protein levels seem to be controlled, although the details of the mechanism remain to be clarified. In addition, for upregulation of estrogen signaling, functional changes in its action in cancer cells originating from normal epithelial cells, i.e., estrogen stimulation, which then leads to proliferation of ER?-positive cancer cells, has been recognized, but this action has not been observed in normal epithelial cells. These alterations are therefore likely to contribute to the pathogenesis of ER?-positive breast cancers.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1860-1499
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
193-6
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Mechanisms of estrogen receptor-? upregulation in breast cancers.
pubmed:affiliation
Department of Surgery, Division of Breast and Endocrine Surgery, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan. ymiyoshi@hyo-med.ac.jp
pubmed:publicationType
Journal Article, Review