OBECAN

Role of obesity in the development of hepatocellular carcinoma

 Coordinatore FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III 

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 Nazionalità Coordinatore Spain [ES]
 Totale costo 1˙498˙043 €
 EC contributo 1˙498˙043 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2010-StG_20091118
 Funding Scheme ERC-SG
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-12-01   -   2016-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III

 Organization address address: C/ MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029

contact info
Titolo: Dr.
Nome: Guadalupe
Cognome: Sabio Buzo
Email: send email
Telefono: +34 91 453 1200
Fax: +34 914531245

ES (MADRID) hostInstitution 1˙498˙043.00
2    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III

 Organization address address: C/ MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029

contact info
Titolo: Ms.
Nome: Luzma
Cognome: Garcia Piqueres
Email: send email
Telefono: 34914531200
Fax: 34914531245

ES (MADRID) hostInstitution 1˙498˙043.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

mechanisms    microrna    inflammation    promotes    lipid    hcc    ffa    obesity    hyperinsulinemia    liver    oxidation    beta    cirrhosis    risk   

 Obiettivo del progetto (Objective)

'Obesity is associated with increased risk for epithelial tumors such as hepatocellular carcinoma (HCC). It is not known, however, whether obesity increases the risk for HCC simply because it promotes cirrhosis, a general risk factor for HCC, or through other mechanisms that operate independently of cirrhosis. Among these, obesity is associated with a chronic inflammatory state, with the release of cytokines such as IL-6 and TNFalpha, well-known HCC mediators. Obesity is normally linked to diabetes and in consequence, to hyperinsulinemia. This increase in circulating insulin levels is suggested to be a factor that contributes to cancer. Moreover, the increase in free fatty acids (FFA) in blood among obese patients promotes a compensatory response from liver that activates the transcription of genes required for beta-oxidation, leading to a reduction in non-physiological stores of lipids in the liver. This increase in beta-oxidation could result in oxidative stress, inflammation and the production of lipid peroxidation bioproducts, which are known mutagens. The precise mechanisms whereby FFA and cytosolic triglycerides exert their effects, resulting in the diabetic phenotype, remain poorly understood. Emerging evidence nonetheless links microRNA (miRNA) with lipid metabolism, suggesting that these small RNAs mediate this increase in beta-oxidation.

Our goal is to study how the components of the obesity state (inflammation, steatosis hyperinsulinemia and microRNA control of gene regulation) affect HCC development. We will use several mouse models in which one or more of these factors are reduced following induction of metabolic disease. We will also determine whether specific miRNAs that are down- or upregulated in the liver of mice on a high fat diet are implicated in HCC development.'

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