CMLMULTIHIT

Establishment of a novel CML model using Multi-Hit technology

 Coordinatore LUDWIG BOLTZMANN GESELLSCHAFT GMBH 

 Organization address address: NUSSDORFER STRASSE 64 6 STOCK
city: WIEN
postcode: 1090

contact info
Titolo: Dr.
Nome: Dagmar
Cognome: Stoiber-Sakaguchi
Email: send email
Telefono: -68365
Fax: -13876

 Nazionalità Coordinatore Non specificata
 Totale costo 170˙981 €
 EC contributo 170˙981 €
 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-IIF
 Funding Scheme MC-IIF
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-05-17   -   2012-05-16

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    LUDWIG BOLTZMANN GESELLSCHAFT GMBH

 Organization address address: NUSSDORFER STRASSE 64 6 STOCK
city: WIEN
postcode: 1090

contact info
Titolo: Dr.
Nome: Dagmar
Cognome: Stoiber-Sakaguchi
Email: send email
Telefono: -68365
Fax: -13876

AT (WIEN) coordinator 170˙981.20

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

crisis    occurs    cml    therapy    bcr    cp    chronic    tyrosine    kinase    expression    patients    resistance    imatinib    indispensable    ap    molecule    transition    abl    blast    accelerated    cytogenetic    bc   

 Obiettivo del progetto (Objective)

'The chronic phase of chronic myeloid leukaemia (CML) is characterized by the expression of the chimeric BCR-ABL gene, extended survival, and profligate growth of maturing granulocyte stemline. It provided the rationale for producing first imatinib and then a series of small molecules designed to inhibit the tyrosine kinase activity of the BCR-ABL oncoprotein, all of which can induce complete cytogenetic remissions in the majority of patients with CML in the chronic phase (CP). Selective inhibition of the BCR-ABL tyrosine kinase by imatinib is a promising new therapeutic strategy in patients with CML. Despite significant haematologic and cytogenetic responses, resistance occurs, particularly in patients with advanced disease, accelerated phase and blast crisis. The mechanism by which the transition from chronic to accelerated phase (AP) or blast crisis (BC) occurs remains poorly understood. The AP and BC phase of CML are usually manifested by additionally acquired oncogene aberrations, resistance to therapy, advancing anaplasia, progressive organomegaly, and increased blast count. Abnormal expression of some proto-oncogenes may accompany or even precede AP or BC of CML. Therefore, it is a critical issue to identify the molecule(s) which is (are) involved in the transition from CP to BC. To better understand such a complex clinical course of human CML, the generation of animal models that closely resemble the situation in people is indispensable. Our objective is to reveal the in vivo pathogenesis of CML with advanced phase using a novel mouse model. Moreover, an indispensable molecule for CML transition can be expected to be found in our study, which might be exploited for both prognostic indicators as well as new targets for therapy.'

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