Helicobacter pylori ( H.pylori )infection is an important aetiological risk factor of gastric cancer, and has been classified as group I or definite carcinogen by the World Health Organization. The molecular mechanism of H.pylori leading to gastric cancer is still unclear. It has been increasingly recognized that cell proliferation and appoptosis,telomerase activition, genetic instability and abnormal DNA methylation are involved in the development of H.pylori related gastric cancer and its precursors. To better understand the pathogenesis of gastric cancer, a revie of the role of H.pylori infections in the induction of molecular events in gastric epithelial cells is presented in this paper.

In recent years, gastrointestinal pace-maker or electrical stimulation has been proposed as a therapeutic option. The interstitial cells of Cajal (ICC) are the pacemaker cells in the gastrointestinal tract.They have special properties that make them unique in their ability to generate and propagate slow waves in gastrointestinal muscles which determine the frequency, the direction and velocity of the propagation of peristaltic activity, in concert with the enteric nervous system for GI motility. Gastrointestinal pacing has been used in the treatment of gastroparesis syndrome, morbid obesity, irritable bowel syndrome, functional dyspepsia and gastroesophageal reflux disease. To better understand the gastrointestinal pacing, a review of its effects and mechanism is presented in this series of papers.

Gastric cancer is a result of interaction of multiple factors. In previous studies it was found that genetic instability, abnormality of DNA methylation, telomere loss, mismatch of repair gene and k-ras mutation, loss of heterozygosity (LOH) of some of cancer-inhibitory genes such as APC, MCC and DCC, disbalance between cell proliferation and apoptosis, etc. were associated with the development of gastric cancer. It was also discovered that tretinoin, sodium selenite, sodium butyrate and epigallocatechin-3-gallate (EGCG) may be effective in preventing gastric carcinoma and gene therapy may partially reverse the malignant phenotype of gastric cancer cells.

0 05). Conclusion mtMSI may be involved in the carcinogenesis of some hepatocellular carcinomas, but mtMSI is not associated with nMSI.

Objective The study was to explore the relationship between Helicobacter pylori ( H.pylori ) infection and aberrant mucin expression in gastric mucosa. Methods H.pylori infection was diagnosed by Warthin Starry staining method, and different kinds of mucin were detected using the immunohistochemical method. Results Positive staining of MUC2 mucin was found in 14 out of 21 patients with mucosa positive for H.pylori ( 66 7%), whereas only 6 cases showed MUC2 mucin expression in 18 H.pylori negative patients (33 3%) ( P 0 05). Conclusion H.pylori infection may alter the expression of some mucin genes in pericancerous gastric mucosa and destroy the gastric mucosa barrier

0 05). The individuals with 677CT and 677CT+TT genotypes had a 0 21 fold [95% confidence interval(CI), 0 43 0 99] and 0 26 fold (95%CI,0 07 0 98) reduced risk of developing gastric cardia cancer compared with those with 677CC genotype. The individuals with 677TT genotype had a 3 63 fold (95%CI,1 04 12 72) increased risk of developing gastric corpus cancer. MTHFR 677CT polymorphism was not correlated with H.pylori infection in gastric cancer. Conclusion The polymorphism of MTHFR 677CT is associated with increased risk of gastric corpus cancer and reduced risk of gastric cardia cancer, but not with H.pylori infection

Objective To investigate the effects of expressions of NF ?B and survivin on the anti tumor activity of TRAIL in gastric carcinoma cells. Methods Gastric carcinoma cells were cultured in RPMI 1640. The apoptotic rates of gastric carcinoma cells SGC 7901, MKN28, AGS, and MKN45 after treatment with TRAIL were analyzed by flow cytometry. The expressions of NF ?B and survivin in the 4 gastric carcinoma cells were determined by Western blotting. Results At 24 h after gastric carcinoma cells exposed to TRAIL at the dose of 300 ng/mL, the apoptosis percent ages were 36 05% for MKN28, 20 27% for MKN45, 16 50% for AGS, and 11 80% for SGC 7901. Western blotting showed that expressions of NF ?B and survivin were lower in MKN28 than those in MKN45, AGS and SGC 7901. Conclusion The anti tumor sensitivity of TRAIL to gastric carcinoma cells is related to the expressions of NF ?B and survivin.

The relationship between the intestinal metaplasia subtypes and the development of gastric carcinoma (GC) was. investigated with mucohistochemical staining on 576 biopsy specimens taken from patientswith intestinal metaplasia (IM) and 85 specimens taken from gastrointestinal mucosa of normal adults and fetus,IM was classified into 3 types, complete (type Ⅰ) and 2 classes of incomplete (types Ⅱ & Ⅲ) depending on the absence or presence of sulphomucin within the mucin secreting columnar cells. Type III IM was significantly more common in patients with GC and in those with dysplasia than in patients with benign gastric pa,tholgy(P

The expression of gastric carcinoma related antigen was observed in 110 gastrectomy specimens with gastric carcinoma and 343 biopsy specimens with intestinal metaplasia by ABC immunohistochemical staining with MG 7 , a monoclonal antibody against human gastric carcinoma. Intestinal metaplasia was classified into types I, II and III by histochemical mucin stainings. Among the 110 cases of gastric carcinomas, 92 (83.6%) showed the positive reaction for MG 7 related antigen. In different types of intestinal metaplasia, type III (46.7%) exhibited a significantly higher positive rate for MG 7 related antigen than type II (25.6%) and type I (18.6%) (P

Quantitative DNA measurements were done in mitotic figures in cells from early gastric carcinoma of intestinal type(n = 8), slight (n=10), moderate (n=10) and severe dysplasia (n = 8), and simple intestinal metaplasia (n=10). The mean DNA values were found to increase gradually from intestinal metaplasia to early gastric carcinoma, with the sequence of from slight, moderate to severe dysplasia, and the differences between each two adjacent groups being statistically signi ficant (P