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IDEAL SIGNED

Inhibitor of DUX4-IGH to Erase Acute lymphoblastic Leukaemia

Total Cost €

EC-Contrib. €

Partnership

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IDEAL project word cloud

Explore the words cloud of the IDEAL project. It provides you a very rough idea of what is the project "IDEAL" about.

genetic activation though drives caused bone expression cancer share death rearrangements patients lowering scientist blocking assays predict dux4 animal delay professional acquire cellular validation lab strategies morbidity ideal renewal therapeutic binding dbd independent toxicity clonogenic transformation locus leukemia acute significantly disease binds proteomics domain paediatric fusion employ giving ectopic overlapping lymphoblastic cell proteins leadership settings regulator models healthcare clinical 7 inhibitor induces dna outcome self transcription inhibition see efficacy xenografts proliferation treatment personal antileukemic block drive murine genes expand latency absence transplantation expertise leukaemia patient marrow igh

Project "IDEAL" data sheet

The following table provides information about the project.

Coordinator	OSPEDALE SAN RAFFAELE SRL Organization address address: VIA OLGETTINA 60 city: MILANO postcode: 20132 website: www.hsr.it contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	Italy [IT]
Total cost	171˙473 €
EC max contribution	171˙473 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2018
Funding Scheme	MSCA-IF-EF-SE
Starting year	2020
Duration (year-month-day)	from 2020-02-01 to 2022-01-31

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	OSPEDALE SAN RAFFAELE SRL OSPEDALE SAN RAFFAELE SRL Organization address address: VIA OLGETTINA 60 city: MILANO postcode: 20132 website: www.hsr.it contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	IT (MILANO)	coordinator	171˙473.00

Map

Project objective

The second most important cause of death and morbidity in Europe is cancer and B-cell acute lymphoblastic leukaemia (B-ALL) is the most common paediatric cancer and cause of cancer-related death before 20 years. In up to 7% of cases, the disease is caused by rearrangements of the genetic regulator DUX4 to the IGH locus, giving rise to the DUX4-IGH fusion. While ectopic expression of DUX4 induces cell death, DUX4-IGH drives transformation. Even though the two proteins share the same DNA binding domain (dbd), DUX4 and DUX4-IGH drive the transcription of non-overlapping target genes. Through proteomics, my lab identified a specific DUX4-IGH inhibitor, which directly binds to DUX4-IGH dbd blocking the activation of target genes. Based on this evidence, the goal of IDEAL is to test the antileukemic activity of the inhibitor in pre-clinical settings. Using cellular models, I will test the ability of the inhibitor to block transformation driven by DUX4-IGH. I expect to see a significant inhibition of DUX4-IGH driven transformation in the presence of its inhibitor, associated with reduced proliferation, clonogenic and self-renewal potential. To test the efficacy of DUX4-IGH inhibition in leukemia development, I will employ animal models (murine bone marrow transplantation assays and patient derived xenografts of DUX4-IGH B-ALL) and assess disease latency in the presence or absence of the inhibitor. I predict that the inhibitor will block or significantly delay DUX4-IGH B-ALL. Pre-clinical validation of the DUX4-IGH inhibitor will help defining effective therapeutic strategies for DUX4-IGH B-ALL patients, improving clinical outcome and lowering treatment toxicity, thus overall promoting Europe's healthcare. Through IDEAL I will expand my expertise in leukaemia research and I will acquire project management and leadership abilities that will foster my personal and professional development as an independent scientist.

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The information about "IDEAL" are provided by the European Opendata Portal: CORDIS opendata.