title: Immunohistochemical analysis of transforming growth factor beta in gallbladder cancer.
abstract: 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.
authors.affiliation: Department of Surgery, Tokyo Medical University, Tokyo, Japan.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Kitamura
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Kasuya
authors.forename: Akihiko
authors.initials: A
authors.lastname: Tsuchida
authors.forename: Akihiro
authors.initials: A
authors.lastname: Mimuro
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Aoki
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Aoki
authors.forename: Yasuhisa
authors.initials: Y
authors.lastname: Koyanagi
mesh_terms: D000368:Aged; D015703:Antigens, CD; D018952:Antigens, CD34 / Q000378:metabolism; D000071063:Endoglin; D005260:Female; D005706:Gallbladder Neoplasms / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / Q000378:metabolism; D016246:Lymphocytes, Tumor-Infiltrating / Q000473:pathology; D008297:Male; D008833:Microcirculation / Q000473:pathology; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000473:pathology; D011379:Prognosis; D011956:Receptors, Cell Surface; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D018952:Antigens, CD34; C064206:ENG protein, human; D000071063:Endoglin; D019394:Ki-67 Antigen; D011956:Receptors, Cell Surface; D016212:Transforming Growth Factor beta; D019010:Vascular Cell Adhesion Molecule-1