GRHL1IN SKIN CANCER

Role of the Grhl1 gene in skin cancer

 Coordinatore INSTYTUT BIOLOGII DOSWIADCZALNEJ IM. M. NENCKIEGO POLSKIEJ AKADEMII NAUK 

 Organization address address: UL. LUDWIKA PASTEURA 3
city: WARSZAWA
postcode: 02 093

contact info
Titolo: Ms.
Nome: Marta
Cognome: Rucinska
Email: send email
Telefono: +48 22 5892 330
Fax: +48 22 8225 342

 Nazionalità Coordinatore Poland [PL]
 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-2009-RG
 Funding Scheme MC-IRG
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-05-01   -   2014-04-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTYTUT BIOLOGII DOSWIADCZALNEJ IM. M. NENCKIEGO POLSKIEJ AKADEMII NAUK

 Organization address address: UL. LUDWIKA PASTEURA 3
city: WARSZAWA
postcode: 02 093

contact info
Titolo: Ms.
Nome: Marta
Cognome: Rucinska
Email: send email
Telefono: +48 22 5892 330
Fax: +48 22 8225 342

PL (WARSZAWA) coordinator 100˙000.00

Mappa


 Word cloud

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tumor    null    mice    skin    chemically    induced    expression    grhl    cancer    tumorigenesis    deficient    gene    putative    uv   

 Obiettivo del progetto (Objective)

'Many functions of the Grainyhead-like (Grhl) transcription factors have already been studied in various animal models. So far these studies have been primarily concerned with the roles of such factors in development and wound healing. Now we have new preliminary data indicating that the Grhl factors are potential novel tumor suppressors. We have already established that the Grhl1-deficient mice have increased susceptibility to chemically induced cutaneous tumor development. We have also generated a list of putative targets of GRHL1 regulation, which are known to be involved in cancer. The proposal outlined here aims to further investigate the role of the Grhl1 gene in skin cancer. We plan to characterize the process of tumorigenesis in the Grhl1-null mice in response to chemical carcinogens and UV radiation. We will analyze the proliferation, differentiation and apoptosis in the induced skin of Grhl1-deficient mice and in the Grhl1-null keratinocytes. We will examine the expression of candidate GRHL1 target genes in these contexts and the binding of GRHL1 to its putative target sites. We will profile changes in gene expression during chemically- and UV-induced tumorigenesis in the Grhl1-deficient mice using microarray technology. Our ultimate aim is to unravel the molecular mechanisms underlying the Grhl1 function in skin cancer. The results of this work may thus have medical significance.'

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