METABOLISMCONNECT

Can metabolic states induced by diabetes and obesity promote cancer?

Coordinatore	VIB    more  Organization address address: Rijvisschestraat 120 city: ZWIJNAARDE - GENT postcode: 9052 contact info Titolo: Mr. Nome: Rik Cognome: Audenaert Email: send email Telefono: +32 92446611
Nazionalità Coordinatore	Belgium [BE]
Totale costo	100˙000 €
EC contributo	100˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2013-CIG
Funding Scheme	MC-CIG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-10-01   -   2017-09-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	VIB  Organization address address: Rijvisschestraat 120 city: ZWIJNAARDE - GENT postcode: 9052 contact info Titolo: Mr. Nome: Rik Cognome: Audenaert Email: send email Telefono: +32 92446611	BE (ZWIJNAARDE - GENT)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Continuous research on cancer has unraveled genetic alterations and subsequently signal transduction pathways changed in a cancer cell, thereby it emerged that many of the genetic factors commonly altered in cancer cells often target metabolic genes. An altered metabolism allows cancer cells to sustain their proliferative needs. Yet, whether altered metabolic fluxes and metabolite concentrations, which define the metabolic state of a cell, are only a consequence or can be a cause of cancer is a major question in the field. The hypothesis that certain metabolic states can precondition a cell for cancer is supported by epidemiological studies showing that patients suffering from diabetes or obesity have an increased risk to develop cancer and an increased cancer mortality rate. We propose to elucidate whether certain metabolic states promote liver cancer, which is in 30% of the cases associated with diabetes and obesity. We will measure metabolite concentrations and metabolic fluxes in tumorigenic versus non-malignant liver cells in vitro, to systematically identify metabolic states that are sufficient to drive an oncogenic transformation in the liver. Subsequently, we will map them in vivo onto metabolic states quantified in a diet and carcinogen induced mouse model, with the final goal to unravel the causal link between the increased liver cancer risk and the metabolic syndrome. Elucidating this metabolic interface will provide a mechanistic understanding of tumor initiating events in patients suffering from the metabolic syndrome. It will subsequently lead to new therapeutic strategies to prevent increased tumor events and cancer driven mortality rates in such patients.'