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Influence of obesity in the non-muscle invasive bladder cancer development on high-fat diet fed mice

Grant number: 12/24800-3
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): March 01, 2013
Effective date (End): February 28, 2014
Field of knowledge:Health Sciences - Medicine - Surgery
Principal researcher:Leonardo Oliveira Reis
Grantee:Marina Zamuner Correia dos Santos
Home Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

Bladder cancer is the fourth solid tumor occurring in adults and the second most common of the genitourinary tumors. The association between obesity and the development of bladder cancer has been observed in several studies that show the existence of a relationship between increased mortality and a high Body Mass Index (BMI). It is known that obesity, diabetes mellitus and metabolic syndrome are epidemiologically linked to an increased predisposition to some cancers. Recently the role of subclinical inflammation in obesity in carcinogenesis gained prominence. It is believed that obesity acts as a tumor promoter, and its effects depend mainly on tumorigenic pro-inflammatory response caused by it. One of the main characteristics of inflammation is the infiltration of macrophages in adipose tissue, producing cytokines and other chemical mediators regulated by the target gene activation via NF-kappaB dependent IKK². Recent studies brought strong evidence that the activation of the NF-kappaB pathway is a crucial mediator in tumor promotion, because the genes transcribed in this pathway express proteins involved in the regulation of cell cycle progression / cell death. The contribution of the canonical pathway of NF-kappaB activation in inflammation and cell proliferation is well accepted and its sustained activation has been described in various malignancies. It is proposed, therefore, that this pathway is determinant in the association between inflammation, tumor promotion and progression.