LEUKEMIABARRIER

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

Coordinatore	LUNDS UNIVERSITET    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
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

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	LUNDS UNIVERSITET  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
2	LUNDS UNIVERSITET  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

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 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.'