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Detection of Helicobacter pylori and its virulence markers associated with analysis of the expression of IL-17 family genes and its receptors: a possible trigger for Gastric Cancer


The persistent infection of gastric mucosa by the Helicobacter pylori (H. pylori) causes a chronic inflammation and creates a favorable microenvironment to the onset of atrophic gastritis with a possible progression to gastric cancer. The stimulus to the immune and inflammatory response leads to epithelial changes which stimulate the apoptosis, and the imbalance between the inflammatory process and cell death and proliferation the main factor related to the progression of atrophic gastritis to gastric cancer. The deregulation in gene and protein expression of molecules which take part in these controlled events may contribute to the progression of gastric diseases, as well as genetic characteristics of the bacteria. Thus, from gastric biopsies samples of patients who are dyspeptics and have gastric cancer, the aims of this project are: (I) To evaluate the expression of Interleukin 17 Family (IL 1-7) and their respective receptors. (II) To detect polymorphisms of clinical interest in the genes of IL 1-7 and their receptors. (III) To diagnosis the presence of the H. pylori and its main pathogenicity markers, the genes genes cagA, cagE, cagG, cagM, cagT, dupA, oipA and vacA. (IV). To correlate the expression of these genes with the presence of polymorphisms, of the and gastric cancer. (V) To identify the genes (ILs17 e IL17Rs) which are differently expressed and, by using bioinformatics, to identify the microRNAs which have these genes as targets. In summary, the techniques which will be used are PCR, quantitative PCR in real time (q-PCR), and new generation sequencing in 300 samples of gastric biopsies divided in five groups (Control, Gastritis and Cancer;). The development of this approach may open new perspectives to the characterization and interaction of factors which are involved in peptic and gene regulation diseases with its virulence markers, the expression of inflammatory molecules and gastric cancer. Altogether, the results aim a better understanding of the physio pathological mechanisms of these diseases and biomarkers and risk groups for the progression of gastric cancer may arise. (AU)

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