title: Carcinogenic Potential of Biliary Epithelium of Congenital Choledochal Cyst Model in Rats: A Special Reference to HDAC Expression.
abstract: OBJECTIVE
  Pancreaticobiliary maljunction (PBM) is well known to have carcinogenic potential. The goal of this study was to clarify the carcinogenic potential of the epithelium of choledochal cyst particularly by paying attention of HDAC1 and COX-2 expressions.
  
  
  METHODS
  Six-week male Lewis rats were divided into two groups; 1) single dose of dibutyltin dichloride (8 mg/kg) was administered intravenously (DBTC group), 2) saline administration was done with the same manner (control group). Morphological changes of biliary tract and expressions of carcinogenesis-related genes, Ki67, HDAC1 and cyclooxygenase-2 (COX-2) were examined immunohistochemically after administration.
  
  
  RESULTS
  In the DBTC group, the bile duct had been gradually dilated on day 3 after administration and the biliary epithelium of dilated bile duct was papillary proliferated on day 7. Ki67 and COX-2 expressions gradually increased and reached the highest value of 6.0% and 3.6% on day 14, respectively. HDAC1 expression increased at the early postoperative period prior to other oncogene, and reached the highest level of 15% on day 7.
  
  
  CONCLUSIONS
  These findings suggested that HDAC1 played an important role in carcinogenesis of PBM through the regulation of COX-2.
authors.forename: Hisako
authors.initials: H
authors.lastname: Kuyama
authors.forename: Yuji
authors.initials: Y
authors.lastname: Morine
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Shimada
authors.forename: Yu
authors.initials: Y
authors.lastname: Saito
authors.forename: Tohru
authors.initials: T
authors.lastname: Utsunomiya
authors.forename: Hiroki
authors.initials: H
authors.lastname: Ishibashi
authors.forename: Satoru
authors.initials: S
authors.lastname: Imura
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Ikemoto
authors.forename: Hiroki
authors.initials: H
authors.lastname: Mori
authors.forename: Jun
authors.initials: J
authors.lastname: Hanaoka
mesh_terms: D000818:Animals; D001650:Bile Duct Neoplasms / Q000139:chemically induced / Q000201:enzymology* / Q000473:pathology; D001652:Bile Ducts / Q000201:enzymology* / Q000473:pathology; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D015529:Choledochal Cyst / Q000139:chemically induced / Q000201:enzymology* / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004108:Dilatation, Pathologic; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000201:enzymology* / Q000473:pathology; D056284:Histone Deacetylase 1 / Q000378:metabolism*; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D009947:Organotin Compounds; D011917:Rats, Inbred Lew; D015398:Signal Transduction; D013997:Time Factors
chemical_list: D019394:Ki-67 Antigen; D009947:Organotin Compounds; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; C515890:Hdac1 protein, rat; D056284:Histone Deacetylase 1; C020735:dibutyldichlorotin