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TOwards Personalized medicine: defining the role of the bone marrow microenvironment in multiple myeloma

 Coordinatore UNIVERSITAIR MEDISCH CENTRUM UTRECHT 

 Organization address address: HEIDELBERGLAAN 100
city: UTRECHT
postcode: 3584 CX

contact info
Titolo: Mr.
Nome: Joost
Cognome: Warsanis
Email: send email
Telefono: 31887568064
Fax: 31887553660

 Nazionalità Coordinatore Netherlands [NL]
 Totale costo 274˙889 €
 EC contributo 274˙889 €
 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-2011-IOF
 Funding Scheme MC-IOF
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-09-17   -   2015-09-16

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAIR MEDISCH CENTRUM UTRECHT

 Organization address address: HEIDELBERGLAAN 100
city: UTRECHT
postcode: 3584 CX

contact info
Titolo: Mr.
Nome: Joost
Cognome: Warsanis
Email: send email
Telefono: 31887568064
Fax: 31887553660

NL (UTRECHT) coordinator 274˙889.10

Mappa


 Word cloud

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

disease    human    pcs    healthy    mm    bme    survival    genetic    effect    expansion    cells    expand    survive    model    mgus    progression    bmscs    bm   

 Obiettivo del progetto (Objective)

'Multiple myeloma (MM), the second most common hematological malignancies, is characterized by an expansion of malignant plasma cells (PCs) in the bone marrow (BM). Despite the development of novel therapies, MM remains an incurable disease with a 5-7 year survival expectancy. MM is usually proceeded by an asymptomatic premalignant state of clonal PC expansion, i.e. MGUS. Progression of MGUS to MM is a multistep process, which is partially dependent on the acquisition of genetic alterations. However, the fact that MM cells strongly depend on the human BM environment (BME) to survive and expand indicates the crucial role of the BME in the etiology of MM. This project aims to study the BME in MM, in relation to disease progression from MGUS to MM, in order to understand the effect of the BME on the tumor cell, supplying new clues on the necessary factors for MM growth. To this end, I will compare BM stromal cells (BMSCs) from MGUS and MM patients, and those from healthy volunteers, on genomic, molecular, and functional level. Data from these studies will be implemented in a novel human MM model. Since this model is based on BMSCs, it enables to study the role of the BME derived from (1)“healthy” BMSCs, genetically manipulated and (2) MM-derived BMSCs. Both approaches allow analyzing the effect of the BME on MM outgrowth. Moreover, in the second approach the effect of MM-derived BMSCs on the proliferation and survival of MGUS-derived PCs will be analyzed to decipher the role of the BME in disease progression. These experiments will show if the BME can induce the progression of MGUS to MM or that secondary genetic aberrations in MGUS-derived PCs are needed. Taken together, this project will clearly contribute to the understanding of how MM cells use and/or manipulate the BME to survive, progress and expand, but even so important how they develop therapy resistance, information necessary to develop innovative therapeutic strategies and to improve patient’s quality of live'

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