INFLAIDCAN

The role of activation-induced cytidine deaminase in inflammation-induced carcinogenesis

Coordinatore	FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III    more  Organization address address: CALLE MELCHOR FERNANDEZ ALMAGRO 3 city: MADRID postcode: 28029 contact info Titolo: Ms. Nome: Dolores Cognome: Liebanes Email: send email Telefono: +3491 2246900 Fax: +3491 2246980
Nazionalità Coordinatore	Spain [ES]
Totale costo	161˙899 €
EC contributo	161˙899 €
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-IEF-2008
Funding Scheme	MC-IEF
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-03-01   -   2011-08-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III  Organization address address: CALLE MELCHOR FERNANDEZ ALMAGRO 3 city: MADRID postcode: 28029 contact info Titolo: Ms. Nome: Dolores Cognome: Liebanes Email: send email Telefono: +3491 2246900 Fax: +3491 2246980	ES (MADRID)	coordinator	161˙899.60

Mappa

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 Obiettivo del progetto (Objective)

'Activation-induced cytidine deaminase (AID) is a DNA-modifying enzyme essential for somatic hypermutation and class switch recombination in B cells. However, deregulation of AID can induce mutations and chromosomal translocations in B cells thus promoting neoplastic transformation and cancer development. AID expression is controlled by several transcription factors like those of the Rel/NF-kappa B family. The NF-kappa B pathway can be activated by a variety of different stimuli and constitutive activation of NF-kappa B is implicated in various malignancies. Indeed, the well established link between chronic inflammation and cancer has been correlated to constitutive NF-kappa B activation by inflammatory cytokines. Although the expression of AID was originally thought to be restricted to B cells, it has been shown recently that stimulation with inflammatory cytokines also induces AID expression in different epithelial cells. Furthermore, expression of AID has been found in hepatocarcinomas, gastric cancer and bile duct carcinomas suggesting a link between inflammation, NF-kappaB activation, AID expression and cancer development. However, it remains unclear if in the observed cases AID expression is just a by-product of NF-kappa B activity or if AID actively contributes to cancer development and/or progression in vivo. In the proposed research project, I am aiming to address the role of AID in the development and progression of carcinomas in vivo. For this purpose, I am going to compare the tumour incidence and aggressiveness between wt and AID-/- mice in a model for colitis-induced carcinogenesis. In addition, I am planning to generate a reporter system in which the expression of the oncogenic KRasV12 mutant depends on the reversion of a STOP codon by AID. This will decrease the amount of mutations required for tumour development and will allow for the efficient tracking and quantification of AID activity in different tissues in vitro and in vivo.'

Introduzione (Teaser)

Cancer development usually implies the sequential accumulation of various pre-transformation events in DNA. Understanding how various DNA-modifying enzymes function could help us understand their role in promoting chromosome translocations and mutations.