title: Telomerase activity and Bcl-2 expression in gallbladders of pancreaticobiliary maljunction patients: a preliminary study.
abstract: BACKGROUND
  The congenital anomaly pancreaticobiliary maljunction (PBM) is considered to be a precancerous disease. PBM carcinogenesis is believed to be an accumulation of gene abnormalities, but the early events causing PBM carcinogenesis are still unclear. In the present study, telomerase activity and Bcl-2 expression in the gallbladder mucosa of PBM and non-PBM gallbladders were investigated.
  
  
  METHODS
  The operative gallbladder materials were from five control cases, two cases of non-PBM gallbladder cancer, three of PBM gallbladder cancer, and three of non-neoplastic PBMs. Multiple sampling was performed from each gallbladder. The studies performed were: (1) immunohistochemistry of p53, Ki-67, and Bcl-2; (2) survey of k-ras point mutations; and (3) measurement of telomerase activity in each sample.
  
  
  RESULTS
  In the cases of non-PBM cancer, abnormalities from the above studies were detected only in the cancerous lesions. Normal-appearing mucosa did not show Bcl-2 expression or telomerase activity. However, in the cases of PBM cancer, normal-appearing mucosa showed telomerase activity and Bcl-2 expression, but did not show p53, Ki-67, or k-ras abnormalities. In the non-neoplastic PBM, all samples showed Bcl-2 expression, and many showed telomerase activity.
  
  
  CONCLUSIONS
  Bcl-2 expression and activation of telomerase are probably early events causing carcinogenesis of the PBM gallbladder mucosa. They might be important factors causing carcinogenesis associated with chronic inflammation.
authors.affiliation: Department of Surgery-2, Yokohama City University, School of Medicine, 3-9 Fukuura, Kanazawa-ku, 236-0004, Yokohama, Japan.
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Ichikawa
authors.forename: Masako
authors.initials: M
authors.lastname: Kamiyama
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sekido
authors.forename: Takashi
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Yasuhiko
authors.initials: Y
authors.lastname: Miura
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Kamiya
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Morita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Shimada
mesh_terms: D005704:Gallbladder / Q000378:metabolism* / Q000473:pathology; D005706:Gallbladder Neoplasms / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D017354:Point Mutation; D011230:Precancerous Conditions / Q000378:metabolism* / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D016283:Proto-Oncogene Proteins p21(ras) / Q000378:metabolism; D019098:Telomerase / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D019394:Ki-67 Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D019098:Telomerase; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras)