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The deletion TLR2 -196 to -174 and its implications for Helicobacter pylori infection in gastric carcinogenesis and evaluation of gene expression

Grant number: 13/25077-6
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): July 01, 2014
Effective date (End): December 31, 2015
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Juliana Garcia de Oliveira Cucolo
Grantee:Giovana Meleiro Bovolini
Host Institution: Centro de Ciências da Saúde. Universidade do Sagrado Coração (USC). Bauru , SP, Brazil


Currently, cancer has been a major cause of death worldwide and gastric cancer is the fourth most common malignant tumor. This problem of global health is a disease in which genetic and environmental factors are involved. A major indicator of risk for gastric cancer is infection by the bacterium Helicobacter pylori, which colonizes the stomach and affects approximately 50 % of the world population. Gastric infection by this organism has been strongly linked to the etiology of carcinogenesis of the stomach, since the active host inflammatory response, which may cause gastrointestinal ulcers, lymphomas, and chronic inflammation. Thus, it has been evaluated the association of genetic polymorphisms of factors involved in the inflammatory process, which can modulate the pattern of the host immune response. This is the case known as Toll-like (TLR) receptors that recognize molecular patterns associated with the microorganisms, including TLR2 (receptor for bacterial lipoproteins ) is involved in response to infection by H. pylori. Given the scarcity of studies of polymorphisms of these genes in dyspeptic patients and its possible involvement in the pathogenesis of H. pylori and gastric carcinogenesis proposed to evaluate the TLR2 -196 to -174 deletion in patients with chronic gastritis, gastric cancer, and a group control subjects, histopathological examination was normal. In order to trace a genetic profile of this polymorphism in association with increased risk for gastric lesions and H. pylori infection, so as to assess the levels of expression in the gastric mucosa by PCR in real-time and the possible association of this deletion in the promoter region at the level of protein expression of the receptors. Studies of molecular epidemiology and susceptibility to diseases are being intensified, so have been relevant to the understanding of individual variability and cancer predisposition.(AU)

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