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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1989-3-17
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pubmed:abstractText |
We have characterized the expression of transforming growth factor alpha (TGF alpha) and its receptor, the epidermal growth factor receptor (EGF-R), in normal and malignantly transformed human mammary epithelial cells. Human mammary epithelial cells were derived from a reduction mammoplasty (184), immortalized by benzo-a-pyrene (184A 1N4), and further transformed by the oncogenes simian virus 40 T (SV40 T), v-Ha-ras, and v-mos alone or in combination using retroviral vectors. 184 and 184A 1N4 cells require EGF for anchorage-dependent clonal growth. In mass culture, they secrete TGF alpha at high concentrations and exhibit an attenuated requirement for exogenous EGF/TGF alpha. SV40 T transformed cells have 4-fold increased EGF-R, have acquired the ability to clone in soft agar with EGF/TGF alpha supplementation, but are not tumorigenic. Cells transformed by v-mos or v-Ha-ras are weakly tumorigenic and capable of both anchorage dependent and independent growth in the absence of EGF/TGF alpha. Cells transformed by both SV40 T and v-Ha-ras are highly tumorigenic, are refractory to EGF/TGF alpha, and clone with high efficiency in soft agar. The expression of v-Ha-ras is associated with a loss of the high (but not low) affinity binding component of the EGF-R. Malignant transformation and loss of TGF alpha/EGF responsiveness did not correlate with an increase in TGF alpha production. Thus, TGF alpha production does not appear to be a tumor specific marker for human mammary epithelial cells. Differential growth responses to EGF/TGF alpha, rather than enhanced production of TGF alpha, may determine the transition from normal to malignant human breast epithelium.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0888-8809
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
3
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
203-14
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:2783757-Animals,
pubmed-meshheading:2783757-Blotting, Southern,
pubmed-meshheading:2783757-Breast Neoplasms,
pubmed-meshheading:2783757-Cell Line, Transformed,
pubmed-meshheading:2783757-Cell Transformation, Neoplastic,
pubmed-meshheading:2783757-Epidermal Growth Factor,
pubmed-meshheading:2783757-Epithelium,
pubmed-meshheading:2783757-Gene Expression Regulation,
pubmed-meshheading:2783757-Humans,
pubmed-meshheading:2783757-Mammary Glands, Animal,
pubmed-meshheading:2783757-Nucleic Acid Hybridization,
pubmed-meshheading:2783757-Oncogenes,
pubmed-meshheading:2783757-RNA, Messenger,
pubmed-meshheading:2783757-Receptor, Epidermal Growth Factor,
pubmed-meshheading:2783757-Transforming Growth Factors
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pubmed:year |
1989
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pubmed:articleTitle |
Transforming growth factor alpha production and epidermal growth factor receptor expression in normal and oncogene transformed human mammary epithelial cells.
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pubmed:affiliation |
Medical Breast Cancer Section, National Cancer Institute, Bethesda, Maryland 20892.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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