Linked Life Data

2131044

Source:http://linkedlifedata.com/resource/pubmed/id/2131044

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-12-17
pubmed:abstractText
Mutations in functional domains of steroid and thyroid hormone receptors cause these molecules to become constitutive (hormone independent) transactivators of gene transcription. Mutations in, for example, the estrogen receptor (ER) may contribute to the loss of estrogen control of some breast carcinomas. The crucial factor in determining estrogen requirement for the growth of tumors may not be the presence or absence of estrogen-regulated ER, but whether the ERs present require estrogen to be able to cause transcription activation of growth regulatory genes. This also has implications for the therapy of breast cancer because it may be necessary to design effective anticancer agents to suppress the malignant effects of ER mutants.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0959-4973
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:geneSymbol
PR, TR
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
127-32
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Nuclear hormone receptor variants: their role in malignancy and progression to hormone resistance in cancer.
pubmed:affiliation
Division of Tumor Biology, The Netherlands Cancer Institute, Amsterdam.
pubmed:publicationType
Journal Article, Review