pylori as a class I human carcinogen, it now is well accepted that gastric infection https://www.selleckchem.com/products/BIBW2992.html by H. pylori is a risk factor for development of gastric cancer [8]. Although the precise pathogenetic role of H. pylori in gastric carcinogenesis remains unclear, it has been clarified that this organism contributes to modifications in epithelial cell proliferation, which may be the initiating event in a cascade culminating in the development of gastric cancer [9], but

it is not known whether the increased risk is due to the presence of mutant p53 generated by chronic gastritis or to a direct action of the bacteria on the p53 oncogene [10, 11]. The p53 gene mutation is associated with approximately 70% of tumors of different orignis [12, 13]. p53 gene serves as a “”gatekeeper of the cell”", for its role in preventing the accumulation of genetic alterations through the regulation of critical checkpoints between the end of G1 and the beginning of S to redirect cells with a mutation in the genome toward apoptosis or programmed cell death. This key oncogene thus prevents the perpetuation of a defective genome AZD5363 cost and the development of a cancer [14]. Several recent studies have been published on the presence of p53 in patients with H. pylori infection, stomach cancer, or both. However, the conclusions are contradictory, and it has

been difficult to develop a single coherent Bafilomycin A1 datasheet hypothesis that can account for all findings communicated to date [15]. Palli et al [16] found p53 mutants in 33 of Sitaxentan 105 cases of gastric cancer and Domek et al [17] worked with the hypothesis that tumorigenesis involves

deregulation of cell proliferation and apoptosis. These researchers investigated cell proliferation and apoptosis in the gastric epithelium of children infected with H. pylori, and found that the apoptotic index was significantly higher in patients with H. pylori gastritis than in patients with secondary gastritis or healthy control subjects. They also reported that apoptosis decreased when the bacterial infection was eradicated. Wu et al, reported the existence of different pathways of gastric carcinogenesis in different histological subtypes of gastric cancer and its progression, in which H. pylori infection can play an important role [18]. Hibi et al, concluded that persistent H. pylori infection caused gastritis, with degeneration and regeneration of the epithelium that increased cell proliferation and the accumulation of p53 [19]. This in turn increased instability of the gene, as reflected by the development of carcinoma, using immunohistochemical methods to investigate p53 expression, and concluded that expression is associated with histopathological phenotypes, and that genetic alterations may not be affected by H. pylori infection [20]. Chang et al, noted the possibility that H.