LYMPHOMA

Modeling lymphoma pathogenesis in mice - from basic mechanisms to pre-clinical models

 Coordinatore MAX-DELBRUCK-CENTRUM FUR MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT 

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 Nazionalità Coordinatore Germany [DE]
 Totale costo 2˙487˙787 €
 EC contributo 2˙487˙787 €
 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-2010-AdG_20100317
 Funding Scheme ERC-AG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-07-01   -   2016-06-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    MAX-DELBRUCK-CENTRUM FUR MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT

 Organization address address: ROBERT ROSSLE STRASSE 10
city: BERLIN
postcode: 13125

contact info
Titolo: Dr.
Nome: Ioannis
Cognome: Legouras
Email: send email
Telefono: 493094000000
Fax: 493094000000

DE (BERLIN) hostInstitution 2˙487˙787.00
2    MAX-DELBRUCK-CENTRUM FUR MOLEKULARE MEDIZIN IN DER HELMHOLTZ-GEMEINSCHAFT

 Organization address address: ROBERT ROSSLE STRASSE 10
city: BERLIN
postcode: 13125

contact info
Titolo: Prof.
Nome: Peter Klaus Georg
Cognome: Rajewsky
Email: send email
Telefono: 16175497389
Fax: 16172783129

DE (BERLIN) hostInstitution 2˙487˙787.00

Mappa


 Word cloud

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

human    disease    malignancies    infected    mouse    virus    genetic    hodgkin    lymphomagenesis    infection    special    cell    humans    combinations    lymphomas    cells    ebv    mutations    iquest    surveillance    immune   

 Obiettivo del progetto (Objective)

'Human B cell lymphomas including multiple myeloma and Hodgkin¿s disease are frequent malignancies and a major clinical problem. Their high incidence is due to special features of normal B cell development that promote chromosomal translocations and other genetic alterations. Another contributing factor is Epstein-Barr-Virus (EBV), a B cell-transforming virus endemic in humans. EBV-infected cells are usually eliminated by the immune system, but in immunosuppressed (post-transplant or AIDS) patients, EBV infection spreads and drives lymphomagenesis. We have generated a novel genetic tool that allows us to introduce combinations of loss- and gain-of-function mutations specifically into B cells in the mouse, to analyze the cooperation of oncogenic factors thought to contribute to B lymphomagenesis in humans. The unique feature of this method is that only a small fraction of cells is mutated (mimicking the sporadic nature of somatic cancerogenesis) and that cells having acquired either single or combined mutations can be observed side-by-side. Using a large set of mutant alleles, we will test whether the interplay of certain combinations of survival, proliferation and differentiation signals determines the development of different classes of human B cell malignancies. A special focus is on Hodgkin¿s disease, where EBV infection and genetic reprogramming play a critical role. We will also investigate the mechanism of immune surveillance of EBV-infected B cells and EBV-driven B cell lymphomas. Ultimately we hope to elucidate key pathways of lymphoma pathogenesis, identify novel contributing mutations, and generate preclinical mouse models to assess therapeutic strategies and mechanisms of tumor immune surveillance.'

Altri progetti dello stesso programma (FP7-IDEAS-ERC)

NANOSTRUCTURE (2011)

"Solving the nanostructure problem: Understanding, exploiting and designing functional disordered materials"

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ANTINEUTRINONOVA (2012)

Probing Fundamental Physics with Antineutrinos at the NOvA Experiment

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FEP (2012)

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