title: Immunohistochemical study of genetic alterations in intraductal and invasive ductal tumors of the pancreas.
abstract: OBJECTIVE
  Multiple genetic alterations are involved in the development of pancreatic neoplasm. Here we investigated the incidence of p53, ras, bcl-2 and c-erbB-2 gene alterations in intraductal papillary-mucinous tumors and invasive ductal adenocarcinoma of the pancreas by immunohistochemical method to identify and analyze their relationship in terms of these genetic alterations.
  
  
  METHODS
  Fifty-four pancreatic lesions, including 18 benign (hyperplasia (3) and intraductal papillary adenoma (15)), and 16 malignant (carcinoma in situ (2) and intraductal papillary adenocarcinoma (14)) cases of intraductal papillary-mucinous tumor; and 20 cases of invasive ductal adenocarcinoma, were immunostained by avidin-biotin peroxidase conjugate method.
  
  
  RESULTS
  p53 and rasp21 expressions were significantly greater in malignant intraductal (P < 0.01, P < 0.05) and invasive ductal (P < 0.01, P < 0.01) tumors than in benign intraductal papillary-mucinous tumors; while bcl-2 and c-erbB-2 expressions were significantly greater in invasive ductal adenocarcinoma than both benign (P < 0.01, P < 0.05) and malignant (P < 0.05, P < 0.05) intraductal papillary-mucinous tumors.
  
  
  CONCLUSIONS
  Different groups of genetic alterations are involved in different phases of pancreatic tumorigenesis. p53 and ras gene alterations occur at an early stage during the development of intraductal papillary-mucinous tumor, while additional alterations of bcl-2 and c-erbB-2 occur during the development of invasive ductal adenocarcinoma of the pancreas.
authors.affiliation: Second Department of Surgery, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, Sapporo 060-8638, Japan. kamal@med.hokudai.ac.jp
authors.forename: H K
authors.initials: HK
authors.lastname: Islam
authors.forename: Y
authors.initials: Y
authors.lastname: Fujioka
authors.forename: T
authors.initials: T
authors.lastname: Tomidokoro
authors.forename: H
authors.initials: H
authors.lastname: Sugiura
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
authors.forename: S
authors.initials: S
authors.lastname: Kondo
authors.forename: H
authors.initials: H
authors.lastname: Katoh
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D002869:Chromosome Aberrations; D004268:DNA-Binding Proteins / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D006801:Humans; D009361:Neoplasm Invasiveness; D010179:Pancreas / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000235:genetics* / Q000473:pathology; D011379:Prognosis; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics*; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000235:genetics*; D012097:Repressor Proteins / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D025521:Tumor Suppressor Proteins / Q000235:genetics*
chemical_list: D004268:DNA-Binding Proteins; D016283:Proto-Oncogene Proteins p21(ras); D018719:Erb-b2 Receptor Tyrosine Kinases; D012097:Repressor Proteins; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; C119386:BCLAF1 protein, human; C501009:HRAS protein, human