Korean J Helicobacter Up Gastrointest Res.  2011 Jun;11(1):45-51. 10.7704/kjhugr.2011.11.1.45.

Effect of Helicobacter pylori Infection on p16, p53, CEA, EGFR Expression in Gastric Neoplasia

Affiliations
  • 1Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea. hyskim@yonsei.ac.kr
  • 2Department of Pathology, Yonsei University Wonju College of Medicine, Wonju, Korea.
  • 3Department of Internal Medicine, Hallym University College of Medicine, Chuncheon, Korea.

Abstract

BACKGROUND/AIMS
Gastric cancer is one of the most widespread cancers and the second leading cause of cancer-related death worldwide. Although Helicobacter pylori (H. pylori) has been classified as a type I carcinogen for gastric cancer, the exact pathway has remained indistinct. In this study, we investigated the effects of H. pylori on oncogenic proteins (epidermal growth factor receptor [EGFR], CEA), tumor suppressor (p53) and cell-cycle regulator (p16) expression, using immunohistochemical stains, in gastric neoplasias.
MATERIALS AND METHODS
From April 2007 until July 2009, 166 patients with consecutive gastric neoplasias resected were retrospectively enrolled; 35 gastric dysplasias, 70 early gastric cancers and 60 advanced gastric cancers. We examined the relationship of clinicopathologic features of gastric neoplasias such as age, sex, p16, p53, EGFR, tissue CEA, TNM stage, Lauren classification, location, histologic type of neoplasia to H. pylori infection status.
RESULTS
H. pylori infection detected in the samples of gastric dysplasia, early gastric cancer (EGC) and advanced gastric cancer (AGC) were 15 (41.7%), 38 (54.3%) and 33 (55.0%) samples. p53, CEA and EGFR stains expression were associated with cancer stage (P<0.05). There was no relation between the immunohistochemical stains (p16, p53, CEA, EGFR) and H. pylori infection.
CONCLUSIONS
This study failed to show any relation of immunohistochemical markers of p16, p53, EGFR, CEA expressions to H. pylori infection in gastric dysplasia as well as gastric cancer. Further study is necessary to investigate the effect of H. pylori infection on p16, p53, CEA, EGFR expressions in precancerous lesions such as atrophic gastritis and intestinal metaplasia.

Keyword

Gastric neoplasms; Cyclin-dependent kinase inhibitor p16; Helicobacter

MeSH Terms

Coloring Agents
Cyclin-Dependent Kinase Inhibitor p16
Gastritis, Atrophic
Helicobacter
Helicobacter pylori
Humans
Metaplasia
Proteins
Retrospective Studies
Stomach Neoplasms
Coloring Agents
Cyclin-Dependent Kinase Inhibitor p16
Proteins
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