Source:http://linkedlifedata.com/resource/pubmed/id/12579267
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2003-2-11
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pubmed:abstractText |
TGF-beta is highly expressed in various cancer cells, yet its mechanism suppressing the cell cycle fails and cell proliferation accelerates, resulting in carcinogenesis. However, there are only a very few reports on animal experiments or clinical specimens with regard to the TGF-beta in gallbladder cancer. We performed immunohistochemical analysis of TGF-beta expression with regard to cell proliferation, angiogenesis, and tumor cell infiltration in clinical specimens of gallbladder cancer. TGF-beta immunoreactivity was significantly higher in advanced cancer than in early cancer. With regard to Ki-67 labeling index, there was no significant difference between early cancer and advanced one. There was no statistically significant difference of the density of pre-existing blood vessels (CD34) between TGF-beta-positive group and negative one. The density of angiogenic vessels (CD105) was significantly greater in the TGF-beta-positive group than in the negative one. Tumor-associated macrophage infiltration was significantly higher in the TGF-beta-positive group than in the negative one. No statistically significant differences in cumulative survival rate were noted between patients in the TGF-beta-positive and TGF-beta-negative groups. In conclusion, our study revealed that in patients with gallbladder cancer, expression of TGF-beta increases according to cancer progression and strongly influences angiogenesis and macrophage infiltration, which contributes to tumor proliferation, but acts weakly on cancer cells by itself.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD34,
http://linkedlifedata.com/resource/pubmed/chemical/ENG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ki-67 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:issn |
1021-335X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
327-32
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12579267-Aged,
pubmed-meshheading:12579267-Antigens, CD,
pubmed-meshheading:12579267-Antigens, CD34,
pubmed-meshheading:12579267-Female,
pubmed-meshheading:12579267-Gallbladder Neoplasms,
pubmed-meshheading:12579267-Humans,
pubmed-meshheading:12579267-Immunoenzyme Techniques,
pubmed-meshheading:12579267-Ki-67 Antigen,
pubmed-meshheading:12579267-Lymphocytes, Tumor-Infiltrating,
pubmed-meshheading:12579267-Male,
pubmed-meshheading:12579267-Microcirculation,
pubmed-meshheading:12579267-Middle Aged,
pubmed-meshheading:12579267-Neovascularization, Pathologic,
pubmed-meshheading:12579267-Prognosis,
pubmed-meshheading:12579267-Receptors, Cell Surface,
pubmed-meshheading:12579267-Transforming Growth Factor beta,
pubmed-meshheading:12579267-Vascular Cell Adhesion Molecule-1
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pubmed:articleTitle |
Immunohistochemical analysis of transforming growth factor beta in gallbladder cancer.
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pubmed:affiliation |
Department of Surgery, Tokyo Medical University, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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