Microsatellite instability in hyperplastic and adenomatous polyps of the stomach

Cancer. 1999 Nov 1;86(9):1649-56.


Background: Few studies have focused on the presence and significance of microsatellite instability (MSI) in gastric polyps, and the results on record are conflicting. The aim of the current study was to address this issue, taking into consideration the 2 main types of gastric polyps, the coexistence of foci of malignant transformation, and the expression of p53 and ERBB-2.

Methods: Six hyperplastic polyps, 10 adenomatous polyps, and 4 adenomatous polyps displaying foci of malignant transformation (intestinal-type carcinoma) were studied for MSI. The authors analyzed a mononucleotide repeat microsatellite (BAT-26) and 5 dinucleotide repeats in microdissected formalin fixed, paraffin embedded tissue sections that were representative of the lesions. Expression of p53 and ERBB-2 were evaluated by immunohistochemistry.

Results: BAT-26 positivity was detected in 1 of 6 hyperplastic polyps (16.7%) and in 2 of 10 adenomas (20%) without malignant transformation. In the 4 adenomatous polyps with carcinomatous foci, BAT-26 positivity was detected in 2 cases (50%) in both (adenomatous and carcinomatous) components of the lesions. p53 immunoreactivity was observed in 6 adenomatous polyps, 2 of them with malignant transformation. Overexpression of the ERBB-2 protein was detected in 1 adenomatous polyp with malignant transformation.

Conclusions: Replication error (RER+) phenotype occurs in both hyperplastic and adenomatous polyps of the stomach. The highest frequency is observed in adenomatous polyps with carcinomatous foci, suggesting that MSI may play a role in the process of malignant transformation in this setting. No significant association was observed between RER+ phenotype and overexpression of p53 or ERBB-2 proteins.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenomatous Polyps / genetics*
  • Adenomatous Polyps / pathology
  • Carcinoma / genetics
  • Carcinoma / pathology
  • Chromosome Aberrations*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Hyperplasia / genetics
  • Hyperplasia / pathology
  • Immunohistochemistry
  • Microsatellite Repeats*
  • Phenotype
  • Receptor, ErbB-2 / metabolism
  • Sequence Analysis, DNA
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / pathology
  • Tumor Suppressor Protein p53 / metabolism


  • Tumor Suppressor Protein p53
  • Receptor, ErbB-2