"The Leukemia-Initiating Cell: Genetic Determinants, Escape Mechanisms and Ontogenic Influence"


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 Nazionalità Coordinatore Sweden [SE]
 Totale costo 1˙999˙714 €
 EC contributo 1˙999˙714 €
 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-2013-CoG
 Funding Scheme ERC-CG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-07-01   -   2019-06-30


# participant  country  role  EC contrib. [€] 

 Organization address address: Paradisgatan 5c
city: LUND
postcode: 22100

contact info
Titolo: Dr.
Nome: David
Cognome: Bryder
Email: send email
Telefono: +46 46 222 3951
Fax: +46 46 222 4218

SE (LUND) hostInstitution 1˙999˙714.00

 Organization address address: Paradisgatan 5c
city: LUND
postcode: 22100

contact info
Titolo: Mrs.
Nome: Minna
Cognome: Jebril
Email: send email
Telefono: +46 46 222 7788

SE (LUND) hostInstitution 1˙999˙714.00


 Word cloud

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

cells    cell    aging    progenitor    mechanisms    molecular    underlie    leukemia    aml    progression    myeloid    immune    hematopoietic    incidence    identity    explore    age   

 Obiettivo del progetto (Objective)

'Acute myeloid leukemia (AML) is the most common malignant myeloid disorder in adults and strongly associated in incidence to advanced age. AML arises from immature hematopoietic progenitor cells via a sequential multistep process, but the nature of these steps remains to a large extent unknown. Therefore, while significant efforts have previously been invested in characterizing the molecular properties of late-stage AML, as diagnosed in patients, less information is available on the events that underlie leukemia initiation and progression. This includes the identity of potential mechanisms that restrict or eradicate developing leukemic cells; hurdles evaded at some point in time for AML to occur. We have developed an inducible transgenic mouse model of AML that, when combined with high-resolution cell fractionation of primitive hematopoietic progenitor cells, offers a unique opportunity to track development of AML from the very first stages of cancer development. Using this, I propose to: 1) Identify and functionally validate molecular determinants that underlie why only some hematopoietic progenitor cells progress into AML, 2) To explore the extent and identity of immune surveillance/editing that accompany progression into AML, and 3) By building on my previous work on hematopoietic aging, to explore AML progression in the context of aging. I anticipate the LEUKEMIABARRIER project to generate novel basic knowledge, not excluding with clinical relevance, with the potential to open up several new fields for further studies. This includes identification of novel cell-intrinsic regulators and immune responses, their underlying mechanisms, and their relationship to the increased incidence of AML with age.'

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