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BCM-UPS SIGNED

Dissecting the role of the ubiquitin proteasome system in the pathogenesis and therapy of B-cell malignancies

Total Cost €

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EC-Contrib. €

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Partnership

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 BCM-UPS project word cloud

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

crls    dna    efficacy    mcl    global    therapeutic    crl    proteasome    genomic    spectrometry    ubiquitylation    ubiquitin    events    remained    integrity    myeloma    serve    cohorts    malignancies    enzymes    damage    ups    genome    substrates    strategy    appreciated    relevance    ligases    mantle    previously    multiple    deubiquitylating    maintaining    incurable    biomarkers    imids    preclinical    pathophysiology    usp24    dubs    hypothesis    orphan    genetic    cellular    entities    candidates    cullin    cell    oncogenes    mass    decipher    prognosis    distinguished    validate    mostly    crbn    mouse    instability    candidate    poor    ligase    discovered    dub    fundamental    levels    fbxo3    respectively    multistep    screens    patient    mm    deregulated    modalities    machinery    evolution    unravel    suppressors    inhibitors    foundation    treatment    reaching    pathogenesis    models    fbxo25    disease    counterparts    family    aberrant    tumour    critically    drugs    suggests    interdisciplinary    elusive    lymphoma    ring    imunomodulatory    roles    identities   

Project "BCM-UPS" 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.
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surname: n.a.
function: n.a.
email: n.a.
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 Coordinator Country Germany [DE]
 Total cost 1˙973˙255 €
 EC max contribution 1˙973˙255 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-CoG
 Funding Scheme ERC-COG
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2021-08-31

 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 1˙973˙255.00

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 Project objective

B-cell malignancies are characterized by high levels of genomic instability, which critically contribute to their pathogenesis and evolution. Recently, the fundamental role of the ubiquitin proteasome system (UPS) in maintaining genome integrity has been appreciated. Two major new therapeutic modalities in B-cell malignancies, proteasome inhibitors and imunomodulatory drugs (IMiDs), target the UPS and demonstrate particular efficacy in multiple myeloma (MM) and mantle cell lymphoma (MCL), two incurable entities with poor prognosis. This suggests the presence of aberrant ubiquitylation events, whose identities have however remained mostly elusive. Our recent studies identify fundamental roles of orphan ubiquitin ligases of the Cullin Ring ligase family (CRLs) and their counterparts, the deubiquitylating enzymes (DUBs) in the cellular DNA damage response machinery, and characterize these candidates as novel oncogenes or tumour suppressors in MM and MCL. These findings provide the foundation for our hypothesis that deregulated ubiquitylation events involving CRLs and DUBs have a far reaching impact on the pathogenesis of B-cell malignancies and can serve as new therapeutic targets and biomarkers. We therefore propose a multistep strategy in which we will (1) characterize previously orphan CRLs and DUBs, which we have distinguished as candidate oncogenes and tumour suppressors in MM (FBXO3, USP24), MCL (FBXO25), or MM and MCL (CRBN), respectively; (2) decipher the global role of CRLs and DUBs in MM and MCL using defined genetic screens; (3) identify relevant substrates of CRLs/DUBs discovered in (2) using mass spectrometry; and (4) validate CRL/DUB candidates in preclinical mouse models and defined patient cohorts as to their disease relevance. We expect that our interdisciplinary approach will unravel the overall role of the UPS in the pathophysiology, evolution and treatment of B-cell malignancies.

 Publications

year authors and title journal last update
List of publications.
2018 Catharina Wenk, Anne-Kathrin Garz, Sonja Grath, Christina Huberle, Denis Witham, Marie Weickert, Roberto Malinverni, Julia Niggemeyer, Michèle Kyncl, Judith Hecker, Charlotta Pagel, Christopher B. Mulholland, Catharina Müller-Thomas, Heinrich Leonhardt, Florian Bassermann, Robert A. J. Oostendorp, Klaus H. Metzeler, Marcus Buschbeck, Katharina S. Götze
Direct modulation of the bone marrow mesenchymal stromal cell compartment by azacitidine enhances healthy hematopoiesis
published pages: 3447-3461, ISSN: 2473-9529, DOI: 10.1182/bloodadvances.2018022053
Blood Advances 2/23 2019-06-06

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