ROSCAN

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

 Coordinatore CHEMOTHERAPEUTISCHES FORSCHUNGSINSTITUT GEORG-SPEYER-HAUS STIFTUNG 

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

Mappa

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 Word cloud

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models    inflammation    genetic    cells    tumorigenesis    oxidative    oxidant    evidence    cancer    dna    species    chronic    reactive    stress    inactivation    determine    tumor    anti    family    oxygen    initiating    cell   

 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.'

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