Detection of H.pylori DNA in gastric epithelial cells by in situ hybridization

AIM: To investigate the presence of H. pylori DNA withingastric epithelial cells in patients with H. pylori infection andits possible carcinogenic mechanism.METHODS: Total 112 patients, with pathologically confirmedchronic superficial gastritis, chronic atrophic gastritis,intestinal metaplasia, atypical hyperplasia or gastrio cancerwere studied .Among them, 28 were H. pylori negative and84 H. pylori positive. H. pylori DNA in gastric epithelialcells was detected by GenPoint catalyzed signalamplification system for in situ hybridization.RESULTS: In the H. pylori positive group, zero out of 24chronic superficial gastritis (0. 0 %), four out of 25precancerous changes (16.0 %) and thirteen out of 35gastric cancers (37. 1 %) showed H. pylori DNA in thenucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells wereprogressively inoreased in chronic superficial gastritis,precancerous changes and gastric cancer groups (χ2 = 12.56, P = 0. 002); One out of 24 ohronic superficial gastritis(4.2 %), eleven out of 25 precancerous ohangas (44.0 %)and thirteen out of 35 gastric cancers (37. 1 %) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (χ2 =10.86, P = 0.004). In the H. pylorinegative group, only onepatient with gastric cancer was found H. pylori DNA in thenucleus of gastric epithelial cells; Only two patients, onepatient with precancerous changes and another with gastriccancer, showed H. pylori DNA in the cytoplasm of gastricepithelial calls. Furthermore, H. pylori DNA must have been inthe ayteplasm as long as it existed in the nucleus of gastricepithelial cells.CONCLUSION: H. pyloriDNA exists both in the nucleus andthe cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronicsuperficial gastritis, precancerous changes to gastric canceris associated with higher positive rates of H. pylori DNApresence in the nucleus of gastric epithelial cells.

AIM: To investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and its possible carcinogenic mechanism. METHODS: Total 112 patients, with pathologically confirmed chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, atypical hyperplasia or gastric cancer were studied. Among them, 28 were H.pylori negative and 84 H.pylori positive. H.pylori DNA in gastric epithelial cells was detected by GenPoint catalyzed signal amplification system for in situ hybridization. RESULTS: In the H.pylori positive group, zero out of 24 chronic superficial gastritis (0.0%), four out of 25 precancerous changes (16.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the nucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups (chi(2)=12.56, P=0.002); One out of 24 chronic superficial gastritis (4.2%), eleven out of 25 precancerous changes (44.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (chi(2)=10.86, P=0.004). In the H.pylori negative group, only one patient with gastric cancer was found H.pylori DNA in the nucleus of gastric epithelial cells; Only two patients, one patient with precancerous changes and another with gastric cancer, showed H.pylori DNA in the cytoplasm of gastric epithelial cells. Furthermore, H.pylori DNA must have been in the cytoplasm as long as it existed in the nucleus of gastric epithelial cells. CONCLUSION: H.pylori DNA exists both in the nucleus and the cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronic superficial gastritis, precancerous changes to gastric cancer is associated with higher positive rates of H.pylori DNA presence in the nucleus of gastric epithelial cells.