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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1994-7-5
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pubmed:abstractText |
Tamoxifen has been an effective antiestrogen in suppressing breast cancer growth which is estrogen-responsive or dependent. Early studies have provided circumstantial evidence that transforming growth factor-beta (TGF-beta) may be an autocrine mediator of tamoxifen action. Therefore, it is both fundamentally important and clinically relevant to investigate the relationship between tamoxifen and TGF-beta. In this study, we demonstrated that CAMA-1 cells, which are sensitive to tamoxifen inhibition, did not respond to TGF-beta growth inhibition. The type I and II TGF-beta receptors were undetectable by the radio-ligand affinity labeling technique. Despite the presence of a normal TGF-beta type II receptor gene, the mRNA transcript of the gene was undetectable by the extremely sensitive Intron-differential RNA/PCR method. The possibility that the lack of TGF-beta receptors might be intimately linked to the absence of normal retinoblastoma (Rb) gene products, as suggested by previous studies of retinoblastoma cells, was further investigated. The lack of TGF-beta receptor expression was found due to reasons other than the absence, deletion or abnormality of the Rb gene because a normal Rb gene and its hyper- and hypo-phosphorylated protein products were detected in CAMA-1 cells. In conclusion, our results suggest that the TGF-beta system is not obligatory for antiestrogen growth inhibition of CAMA-1 cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Estrogens,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth...,
http://linkedlifedata.com/resource/pubmed/chemical/Retinoblastoma Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Tamoxifen,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0730-2312
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:geneSymbol |
Rb,
c-myc
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
332-42
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8200913-Base Sequence,
pubmed-meshheading:8200913-Breast Neoplasms,
pubmed-meshheading:8200913-Cell Division,
pubmed-meshheading:8200913-Estrogens,
pubmed-meshheading:8200913-Female,
pubmed-meshheading:8200913-Genes, Retinoblastoma,
pubmed-meshheading:8200913-Genes, myc,
pubmed-meshheading:8200913-Humans,
pubmed-meshheading:8200913-Molecular Sequence Data,
pubmed-meshheading:8200913-Neoplasm Proteins,
pubmed-meshheading:8200913-Neoplasms, Hormone-Dependent,
pubmed-meshheading:8200913-Ovarian Neoplasms,
pubmed-meshheading:8200913-Receptors, Transforming Growth Factor beta,
pubmed-meshheading:8200913-Retinoblastoma,
pubmed-meshheading:8200913-Retinoblastoma Protein,
pubmed-meshheading:8200913-Tamoxifen,
pubmed-meshheading:8200913-Transforming Growth Factor beta,
pubmed-meshheading:8200913-Tumor Cells, Cultured
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pubmed:year |
1994
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pubmed:articleTitle |
Absence of transforming growth factor-beta responsiveness in the tamoxifen growth-inhibited human breast cancer cell line CAMA-1.
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pubmed:affiliation |
Department of Obstetrics and Gynecology, University of Minnesota, Minneapolis 55455.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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