Genetic alterations in gastric cancer: relation to histological subtypes, tumor stage, and Helicobacter pylori infection

Gastroenterology. 1997 May;112(5):1457-65. doi: 10.1016/s0016-5085(97)70071-4.


Background & aims: A different spectrum of genetic changes including p53, c-erbB-2, c-met, adenomatous polyposis coli (APC), and deleted in colorectal cancer (DCC) is involved in gastric cancer (GC). The aim of this study was to correlate these alterations with histological subtypes, tumor stages, and Helicobacter pylori infection.

Methods: Specimens of 163 patients with GC were immunostained for p53, c-erbB-2, and c-met, and polymerase chain reaction was performed in them to determine loss of heterozygosity (LOH) of APC and DCC.

Results: Overexpression of p53 was more frequent in early intestinal than early diffuse GC and was noted in the stage progression of diffuse but not intestinal GC. Overexpression of c-erbB-2 occurred more commonly in intestinal GC and advanced GC of both types. Overexpression of c-met was greater in diffuse GC, particularly at advanced stage. LOH of APC was more common in intestinal GC irrespective of the stage but rarely in diffuse GC. LOH of DCC occurred primarily in advanced intestinal GC and infrequently in early GC or advanced diffuse GC. Alterations of these five genes were not correlated with H. pylori infection.

Conclusions: A distinct genetic pathway exists in gastric carcinogenesis of different histological subtypes and their tumor progression, in which H. pylori infection may play an equal role or no role.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenomatous Polyposis Coli / genetics
  • Aged
  • Colorectal Neoplasms / genetics
  • Female
  • Gene Deletion
  • Gene Expression
  • Genes, erbB-2
  • Genes, p53
  • Helicobacter Infections / complications*
  • Heterozygote
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Neoplasm Staging
  • Polymerase Chain Reaction
  • Proto-Oncogene Proteins c-met
  • Receptor Protein-Tyrosine Kinases / genetics
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / microbiology
  • Stomach Neoplasms / pathology


  • Proto-Oncogene Proteins c-met
  • Receptor Protein-Tyrosine Kinases