It is known that H. pylori infection triggers a pathological progression in the gastric mucosa which eventually culminates in the development of gastric cancer. Inevitably, the infection causes an inflammatory response in the host, which generates reactive oxygen species and nitrogen, which can cause protein alterations, damage to cell membranes and oxidation of the DNA molecule, which are known to be important steps in the development of gastric cancer . Furthermore, there is evidence in the literature and obtained by our research group, showing that H. pylori infection is closely associated with a reduction in the efficiency of DNA repair mechanisms, which would favor the accumulation of mutations and genomic instability favoring the genesis of gastric cancer. Some recent studies show the importance of the regulation of oncogenic Wnt/b-catenin and its downstream targets (mainly belonging SOX family) in various types of cancer. However, the association between genes and targets of Wnt/b-catenin in the DNA repair pathways are still poorly explored, especially in gastric carcinogenesis . Thus, we intend to evaluate the possible role of regulatory genes associated with the Wnt/b-catenin in the mechanisms of DNA repair modulated by H. pylori. (AU)
Articles published in Agência FAPESP Newsletter about the research grant:
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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