Immunohistochemical study of genetic alterations in intraductal and invasive ductal tumors of the pancreas

Hepatogastroenterology. May-Jun 2001;48(39):879-83.

Abstract

Background/aims: 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.

Methodology: 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.

MeSH terms

  • Adenocarcinoma / genetics*
  • Adenocarcinoma / pathology
  • Chromosome Aberrations*
  • DNA-Binding Proteins / genetics*
  • Gene Expression Regulation, Neoplastic / physiology
  • Humans
  • Neoplasm Invasiveness
  • Pancreas / pathology
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / pathology
  • Prognosis
  • Proto-Oncogene Proteins p21(ras) / genetics*
  • Receptor, ErbB-2 / genetics*
  • Repressor Proteins / genetics*
  • Transcription Factors / genetics*
  • Tumor Suppressor Protein p53 / genetics*
  • Tumor Suppressor Proteins / genetics*

Substances

  • BCLAF1 protein, human
  • DNA-Binding Proteins
  • Repressor Proteins
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • Receptor, ErbB-2
  • HRAS protein, human
  • Proto-Oncogene Proteins p21(ras)