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T-NHL SUPRESSORS SIGNED

Tumor suppressor pathways counteracting oncogenic immune receptor signaling in T-Cell Lymphoma

Total Cost €

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EC-Contrib. €

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Partnership

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 T-NHL SUPRESSORS project word cloud

Explore the words cloud of the T-NHL SUPRESSORS project. It provides you a very rough idea of what is the project "T-NHL SUPRESSORS" about.

understudied    antigen    pathogenesis    sub    gain    host    hodgkin    therapies    explore    limited    immune    fundamental    largely    functions    sensing    aggressive    drive    mutations    experimental    overarching    dissect    30    conventional    additionally    programs    proliferation    survival    tcr    dependent    human    effector    events    malignant    mechanisms    manner    negative    variants    constitutive    mediated    hypothesis    molecules    expansion    significantly    suppressor    vivo    pathomechanisms    presumably    cells    oncogenically    inhibit    lymphomagenesis    activation    undefined    signaling    oncogenic    comprehensively       counteract    enforced    defense    physiological    lymphoma    inactivated    lymphomas    model    haploinsufficient    pd    thereby    nhl    mature    cell    receptor    hallmark    independent    entities    tumor    continuous    nhls    identification    malignancies    multiple    enforce    resistant    cancers    molecular    clone    regulatory    regulators    inhibitory    function    insights   

Project "T-NHL SUPRESSORS" data sheet

The following table provides information about the project.

Coordinator
KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN 

Organization address
address: ISMANINGER STRASSE 22
city: MUENCHEN
postcode: 81675
website: http://www.med.tu.muenchen.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
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 Coordinator Country Germany [DE]
 Total cost 2˙492˙937 €
 EC max contribution 2˙492˙937 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-ADG
 Funding Scheme ERC-ADG
 Starting year 2019
 Duration (year-month-day) from 2019-12-01   to  2024-11-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KLINIKUM RECHTS DER ISAR DER TECHNISCHEN UNIVERSITAT MUNCHEN DE (MUENCHEN) coordinator 2˙492˙937.00

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 Project objective

T cell non-Hodgkin lymphomas (T-NHLs) are highly aggressive malignancies that are largely resistant to conventional therapies. T-NHLs remain significantly understudied, and their molecular pathogenesis is still not well defined. Comprehensive analysis of mature T-cell lymphomas has identified multiple gain-of-function mutations in T-cell receptor (TCR) signaling molecules as an overarching hallmark of T-NHL sub-entities. Under physiological conditions, these molecules control the expansion, survival and effector function of antigen sensing T cells for host defense. Presumably, the oncogenic TCR signaling variants in lymphoma enforce these TCR programs in a constitutive manner and thereby drive continuous proliferation and expansion of the malignant clone. However, experimental in vivo evidence for this hypothesis is still limited, and the negative regulatory tumor suppressor mechanisms that can counteract oncogenic T cell signaling remain largely undefined. We recently identified the inhibitory immune receptor PD-1 as a key haploinsufficient tumor suppressor in T-cell lymphoma that is inactivated in up to 30% of human cases. The overall goal of this proposal is to comprehensively model and dissect T-cell lymphomagenesis driven by oncogenically enforced T-cell receptor pathways and to identify the PD-1 dependent and independent tumor suppressor mechanisms that inhibit these events. We will additionally explore the functions of new negative regulators within the PD-1 pathway or related pathways in antigen-mediated T cell activation. We expect that our results will provide fundamental new insights into the molecular pathomechanisms of highly aggressive T cell cancers and additionally lead to the identification of new negative regulators of antigen-mediated T cell activation.

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