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

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.