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UNPACK PD-L1 SIGNED

Molecular mechanism and inhibition of extracellular vesicle-mediated PD-L1 release in melanoma cells

Total Cost €

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EC-Contrib. €

0

Partnership

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 UNPACK PD-L1 project word cloud

Explore the words cloud of the UNPACK PD-L1 project. It provides you a very rough idea of what is the project "UNPACK PD-L1" about.

ligand    pro    power    herein    sought    lay    uncover    therapy    groundwork    screen    restore    secrete    tumour    plasma    intend    evs    mouse    ev    stage    blockade    immunosuppression    plausible    extracellular    upregulation    tested    therapeutic    drive    meant    anti    suppression    clinically    loading    receptor    therapies    melanoma    bottlenecks    surround    membrane    responders    initiated    stratify    modality    circulating    mechanisms    subsequent    unanticipated    ideally    druggable    types    strategy    express    patients    responder    highlighting    models    mediated    immune    cancer    inhibition    broaden    vesicles    reveal    programmed    direction    secretion    outcome    vitro    cell    l1    inhibitors    pd    levels    center    block    tumor    inhibiting    tumorigenic    combining    death    systemic    candidates    little    optical    function    agents    efficacy    basic    suppress    limited    reporters    successful    cells    oncological    gaps    bioluminescent    mechanism    guide    molecular    inhibit    checkpoint    clear    remove    clinical    drug    treat    harnessing    release    small    rationale    bracket    exploited   

Project "UNPACK PD-L1" data sheet

The following table provides information about the project.

Coordinator
STICHTING VUMC 

Organization address
address: DE BOELELAAN 1117
city: AMSTERDAM
postcode: 1081 HV
website: www.vumc.nl

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 Netherlands [NL]
 Total cost 175˙572 €
 EC max contribution 175˙572 € (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-ST
 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    STICHTING VUMC NL (AMSTERDAM) coordinator 175˙572.00

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 Project objective

Harnessing the power of the immune system to treat cancer has long been a sought after goal of oncological research. Immune checkpoint inhibitors, such as anti-programmed death receptor 1 (PD-1) blockade therapies, have now taken center stage. However not all patients respond, highlighting gaps in our understanding of the mechanisms of tumour immunosuppression. Upregulation of the PD-1 ligand (PD-L1) on tumour cells initiated this therapeutic direction, yet it is becoming clear that the modality of PD-L1-mediated immune suppression is not limited to the plasma membrane. Like many tumor cells, melanoma cells secrete small extracellular vesicles (EVs) with pro-tumorigenic properties. Melanoma EVs express PD-L1 that suppress T cell function and facilitate tumour growth in pre-clinical mouse models. This systemic mechanism is clinically relevant, as circulating EV-PD-L1 levels can stratify anti-PD-1 clinical responders from non-responders. Thus inhibiting EV-PD-L1 may increase anti-PD-1 efficacy and broaden the responder bracket. One plausible strategy would be to block tumor EV secretion, yet little is known about the molecular mechanisms that drive PD-L1 loading and release. Herein, I intend to uncover the molecular mechanisms of EV PD-L1 release from melanoma cells using state-of-the-art optical and bioluminescent reporters to reveal novel druggable targets. This basic knowledge will be exploited to guide subsequent inhibition, through a drug screen for candidates that inhibit EV-PD-L1 release and restore T cell function. Ideally the outcome of this in vitro study will provide a strong rationale for combining anti-PD-1 agents with inhibitors of EV-PD-L1 secretion, to be tested in pre-clinical mouse models. If successful, melanoma EV blockade may remove the unanticipated bottlenecks that surround the efficacy of anti-PD-1 therapy. In the long term this study is meant to lay groundwork for tumor EV inhibition as a therapeutic strategy for cancer types beyond melanoma.

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The information about "UNPACK PD-L1" are provided by the European Opendata Portal: CORDIS opendata.

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