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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.

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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
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surname: 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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