It is now known that gastric cancer is primarily a disease with an epigenetic origin. It has been shown that infection by H. pylori triggers a pathological progression in gastric mucosa that starts with chronic gastritis progresses to atrophic gastritis, intestinal metaplasia, dysplasia and eventually gastric cancer. It is believed that the inflammatory response generated by the infection significantly increases the production of reactive oxygen species known to cause oxidation of the DNA molecule. Additionally, there is evidence in the literature showing that infection with H. pylori is closely associated with a reduction in efficiency of DNA repair mechanisms, which would favor the accumulation of mutations and genomic instability, favoring the genesis of gastric cancer. In this sense, the data obtained by our research group show that the repair genes MLH1 and MGMT are associated with infection with a hypermethylation in the promoter region and repression in the expression of these genes in the same patients. Thus, in view of the importance of epigenetic changes in the regulation of repair mechanisms and the close relationship between these deficiencies with carcinogenesis, as well as the lack of studies showing the effect of infection by H. pylori in modulating the epigenetic mechanisms that control DNA repair mechanisms, we intend to evaluate in vitro the role of infection by H. pylori in modulating epigenetic mechanisms related to DNA repair systems.
News published in Agência FAPESP Newsletter about the scholarship:
SANTOS, JULIANA C.;
JR PEDRAZZOLI, JOSE;
RIBEIRO, MARCELO L.
Paradoxical role of SOX2 in gastric cancer.
AMERICAN JOURNAL OF CANCER RESEARCH,
Web of Science Citations: 16.
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