ROSCAN

The role of ROS/RNS during inflammation-associated and sporadic carcinogenesis

Coordinatore	CHEMOTHERAPEUTISCHES FORSCHUNGSINSTITUT GEORG-SPEYER-HAUS STIFTUNG    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	1˙500˙000 €
EC contributo	1˙500˙000 €
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-2011-StG_20101109
Funding Scheme	ERC-SG
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-10-01   -   2016-09-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN  Organization address address: ISMANINGER STRASSE 22 city: MUENCHEN postcode: 81675 contact info Titolo: Ms. Nome: Inge Cognome: Linder Email: send email Telefono: 498941000000 Fax: +49 89 41404926	DE (MUENCHEN)	beneficiary	461˙327.78
2	CHEMOTHERAPEUTISCHES FORSCHUNGSINSTITUT GEORG-SPEYER-HAUS STIFTUNG  Organization address address: PAUL EHRLICH STRASSE 42-44 city: FRANKFURT postcode: 60596 contact info Titolo: Mr. Nome: Robert Cognome: Dornberger Email: send email Telefono: +49 6963395333 Fax: +49 6963395353	DE (FRANKFURT)	hostInstitution	1˙038˙672.25
3	CHEMOTHERAPEUTISCHES FORSCHUNGSINSTITUT GEORG-SPEYER-HAUS STIFTUNG  Organization address address: PAUL EHRLICH STRASSE 42-44 city: FRANKFURT postcode: 60596 contact info Titolo: Prof. Nome: Florian Cognome: Greten Email: send email Telefono: +49 89 41406789 Fax: +49 00 00000000	DE (FRANKFURT)	hostInstitution	1˙038˙672.25

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 Obiettivo del progetto (Objective)

'A link between inflammation and cancer has been suspected over a long period of time and in recent years genetic evidence supporting such notion could be obtained. Several signaling pathways, such as NF-κB and STAT3, could be identified by our group as well as other groups to play important roles during tumor promotion and progression. Chronic inflammation leads to the formation of reactive oxygen and nitrogen species, which are known to cause DNA damage and inactivation of DNA repair mechanisms, thereby presumably inducing tumor-initiating mutations. On the other hand, oxidative stress has been documented to trigger apoptosis and cellular senescence. However, in vivo evidence demonstrating the consequences of increased oxidative stress on tumor development in a distinct genetic model is lacking. Selenoproteins of the glutathione peroxidase and thioredoxin reductase family are important anti-oxidant scavenger systems. Using cell type specific inactivation (epithelial cells an myeloid cells) of several of these family members in various well established and relevant models of inflammation-associated and sporadic colon tumorigenesis we will directly examine the role of these anti-oxidant systems. These models will allow us to genetically determine the outcome of increased lipid peroxidation and accumulation of reactive oxygen species in each cell type and to address whether cancer development is supported or inhibited under such conditions and will help to identify which phase of tumor development is affected. Furthermore, we expect to obtain results that will determine whether increased levels of ROS/RNS found during chronic inflammation are capable of initiating tumorigenesis. Our proposed experiments are supposed to provide fundamental insight into the molecular changes in the tumor microenvironment, which will ultimately help to identify novel strategies to prevent and treat colorectal cancer.'