LUNELY

"ALK as a common target for the pathogenesis and therapy in lymphoma, lung carcinoma and neuroblastoma"

 Coordinatore UNIVERSITA DEGLI STUDI DI TORINO 

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 Nazionalità Coordinatore Italy [IT]
 Totale costo 1˙010˙000 €
 EC contributo 1˙010˙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-2009-StG
 Funding Scheme ERC-SG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-11-01   -   2014-04-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI TORINO

 Organization address address: Via Giuseppe Verdi 8
city: TORINO
postcode: 10124

contact info
Titolo: Ms.
Nome: Antonietta
Cognome: Davello
Email: send email
Telefono: 390117000000
Fax: 390112000000

IT (TORINO) hostInstitution 1˙010˙000.00
2    UNIVERSITA DEGLI STUDI DI TORINO

 Organization address address: Via Giuseppe Verdi 8
city: TORINO
postcode: 10124

contact info
Titolo: Prof.
Nome: Roberto
Cognome: Chiarle
Email: send email
Telefono: +39 011 6336860
Fax: +39 011 6336887

IT (TORINO) hostInstitution 1˙010˙000.00

Mappa


 Word cloud

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small    alk    mouse    mutations    pathogenetic    cancer    vitro    anaplastic    lung    nature    cancers    neuroblastoma    gene    models    therapies    solid    et    carcinoma    translocations    al    lymphoma    validate    alcl    lymphomas    positive    tumours    validation    therapy   

 Obiettivo del progetto (Objective)

'The Anaplastic Lymphoma Kinase (ALK) has been discovered as the result of chromosomal translocations in Anaplastic Large Cell Lymphomas (ALCL) (Chiarle et al Nat Rev Cancer. 2008, 8:11). In ALCL, the role of the ALK oncogenic translocations has been established in vitro and in transgenic mouse models. Recent findings have shown ALK translocations, mutations or amplifications in other types of solid cancers, such as lung carcinoma (Soda et al. Nature. 2007, 448:561) and neuroblastoma (Mossè et al. Nature 2008, 455: 930). However, the role of ALK gene mutations in these solid tumours remains largely undetermined. This lack of knowledge is even worse given the fact that a therapy that targets ALK in these tumours could be feasible. Aim 1. Targeting of ALK in ALCL lymphomas. ALCL ALK positive lymphomas will be tested for small molecule inhibitors of the activity of ALK. In addition, a combination of gene silencing, such as small interfering RNA (siRNA), and vaccination against ALK will be validated as selective ALK therapies. Aim 2. Characterization of the role of ALK in lung cancer through the generation of mouse models. We propose to characterize the pathogenetic role of ALK in lung cancer by in vitro studies and by generating mouse models for ALK positive lung cancers. These mouse models will be fundamental to validate the innovative therapies against ALK positive lung carcinoma. Aim 3. Validation of ALK as an oncogene and a therapeutic target in neuroblastoma. We plan to develop mouse models of neuroblastoma to investigate the pathogenetic role of ALK in the onset and maintenance of neuroblastoma in vivo. These mouse model of neuroblastoma will be used for the validation of ALK specific therapies. Overall, the proposed project will define the role of ALK in lymphoma, neuroblastoma and lungcancer and validate its potential use as a a target for therapy in those tumours. The impact of these novel therapies will be of great value in these deadly tumours.'

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