| pubmed-article:2303779 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C0021764 | lld:lifeskim |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C0006556 | lld:lifeskim |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:2303779 | lifeskim:mentions | umls-concept:C1519697 | lld:lifeskim |
| pubmed-article:2303779 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:2303779 | pubmed:dateCreated | 1990-3-16 | lld:pubmed |
| pubmed-article:2303779 | pubmed:abstractText | We introduced an IL-6 cDNA expression vector into a murine B cell line, the growth of which definitely required the presence of exogenous IL-6. The transfected cells secreted substantial amounts of IL-6, to which they themselves responded by proliferating without further requirement of exogenous IL-6. The proliferation was a direct function of cell density and was inhibitable by antibodies to IL-6, indicating the autocrine nature of the growth. The IL-6 cDNA-transfected cells displayed greatly enhanced tumorigenicity when inoculated into syngeneic and nude mice. Our data suggest that an IL-6 autocrine self stimulation confers on B cells a selective growth advantage and results in the induction of progression of the malignant state of B cells. | lld:pubmed |
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| pubmed-article:2303779 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2303779 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2303779 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2303779 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:2303779 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:2303779 | pubmed:author | pubmed-author:TadaTT | lld:pubmed |
| pubmed-article:2303779 | pubmed:author | pubmed-author:KarasuyamaHH | lld:pubmed |
| pubmed-article:2303779 | pubmed:author | pubmed-author:TohyamaNN | lld:pubmed |
| pubmed-article:2303779 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2303779 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:2303779 | pubmed:volume | 171 | lld:pubmed |
| pubmed-article:2303779 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2303779 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2303779 | pubmed:pagination | 389-400 | lld:pubmed |
| pubmed-article:2303779 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2303779 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2303779 | pubmed:articleTitle | Growth autonomy and tumorigenicity of interleukin 6-dependent B cells transfected with interleukin 6 cDNA. | lld:pubmed |
| pubmed-article:2303779 | pubmed:affiliation | Department of Immunology, Faculty of Medicine, University of Tokyo, Japan. | lld:pubmed |
| pubmed-article:2303779 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2303779 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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