| Grant number: | 15/11613-9 |
| Support Opportunities: | Scholarships in Brazil - Master |
| Start date: | March 01, 2016 |
| End date: | February 28, 2017 |
| Field of knowledge: | Biological Sciences - Genetics - Human and Medical Genetics |
| Principal Investigator: | Lucas Trevizani Rasmussen |
| Grantee: | Luanna Munhoz Zabaglia |
| Host Institution: | Pró-Reitoria de Pesquisa e Pós-Graduação. Universidade do Sagrado Coração (USC). Bauru , SP, Brazil |
Abstract MicroRNAs appear to play an important role in controlling the expression of genes associated with inflammation, such as IL -2 and TNF -alpha , proliferation and cell death, and the imbalance of this control a possible cause of the development of gastritis and gastric cancer. The Helicobacter pylori is a gram-negative bacterium that colonizes the gastric mucosa is responsible for various gastroduodenal diseases such as gastritis, ulcers and gastric cancers, and appears to induce the production of TNF- alpha, which acts as a potent inhibitor of gastric secretion contributing to the development of peptic diseases , and is the most powerful mediator of the inflammatory response against gram-negative bacteria. Combined with the virulence factors of H. pylori, genetic host factors may also contribute to the development of gastric diseases, especially gastric cancer. Thus, from 150 samples of gastric biopsies of dyspeptic patients with gastric cancer, the present project objectives are: (I) analyses the gene expression of microRNAs 146a, 155, e 181c; (II) analyses the gene expression of mRNA: TNF-± e IL-2; (III) Correlate the gene expression of microRNAs and mRNA studded; (IV) Correlate the gene expression of microRNAs and mRNA with presence of H. pylori and cagA gene; (V) characterizing the polymorphism rs2069762 (IL-2: +114T>G), rs2069762 (IL-2: -330T>G) e rs1800629 (TNF-±: -308 G>A) from IL-2 e TNF-alpha respectively. The development of this approach may open new perspectives for the characterization of factors involved in peptic disease, gene regulation, as well as clarification on the interaction among genes involved in gastric diseases, seeking a better understanding of the pathophysiological mechanisms of these diseases. Together these data may suggest biomarkers and groups at risk for progression to gastric cancer. | |
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