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DLL4-LVN

Targeting the (pre)metastatic lympho-vascular niche: molecular mechanisms and therapeutic implications in melanoma

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 DLL4-LVN project word cloud

Explore the words cloud of the DLL4-LVN project. It provides you a very rough idea of what is the project "DLL4-LVN" about.

blunt    spain    dynamic    niche    me    complete    metastatic    abolishment    nodes    lab    interference    deaths    responsible    phenomenon    lymphovascular    prognosis    bec    lymphangiogenesis    undergo    signaling    normalizing    wiring    immune    express    lesions    revealed    endothelial    ligand    soengas    homing    student    90    embo    cq    lecs    compartment    patient    thin    pending    questions    mechanisms    chloroquine    lec    lymphatic    versus    lymph    belgium    sln    showing    urged    mm    dll4    mediators    kul    mechanistic    sentinel    data    angiogenesis    therapeutic    recruitment    agostinis    inactivated    regulates    genetic    cells    tumor    driving    angiogenic    blood    cancer    notch    apparently    lysosomotropic    strategy    agent    crosstalk    levels    cnio    arrival    phd    actively    pharmacologically    vasculature    establishment    unexpected    preliminary    fellowship    outgrowth    metastasis    trapped    activated    outcome    melanoma    correlate    route    tolerance    endosomal    gt    unclear    cell   

Project "DLL4-LVN" data sheet

The following table provides information about the project.

Coordinator
FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III 

Organization address
address: CALLE MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029
website: www.cnio.es

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 Spain [ES]
 Total cost 158˙121 €
 EC max contribution 158˙121 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-01-01   to  2018-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III ES (MADRID) coordinator 158˙121.00

Map

 Project objective

Tumor metastasis is responsible for >90% of cancer deaths. A tumor type where the mechanisms driving this process are especially unclear is melanoma, the only cancer where apparently thin lesions (2 mm depth) have a high potential for metastatic dissemination. As a PhD student in P. Agostinis lab (KUL, Belgium) I identified a new strategy using the lysosomotropic agent chloroquine (CQ) to blunt melanoma metastasis, by normalizing the angiogenic vasculature via increased blood endothelial cell (BEC) NOTCH signaling. The complete abolishment of metastasis by CQ urged me to study whether another route of metastasis; the lymphatic system and the sentinel lymph nodes (SLN); was also affected. The importance of this route of metastasis is supported by recent evidence showing that even before the arrival of the tumor cells, the lymph endothelial cells (LEC) and immune cells in the SLN undergo dynamic changes that actively facilitate tumor cell recruitment, metastatic outgrowth and immune tolerance. This phenomenon is referred to as the ‘lymphovascular (pre)metastatic niche’. Pending questions are how the cancer cells, LEC and immune cells crosstalk and how to target them pharmacologically. My preliminary data, obtained during a short term EMBO Fellowship in the lab of M. Soengas (CNIO, Spain) show that CQ affects lymphangiogenesis even more than angiogenesis. These effects are due to an unexpected different wiring of the NOTCH pathway in BEC versus LEC. Activated LECs express high levels of the NOTCH ligand DLL4, which is trapped and inactivated in the endosomal compartment by CQ. Genetic interference in LEC revealed that DLL4 not only regulates lymphangiogenesis, but also the production of mediators of cancer cell homing and immune tolerance. In this project I will address the mechanistic role of DLL4 in the establishment of the lymphovascular niche, correlate DLL4 levels with melanoma patient prognosis and target DLL4 pharmacologically to improve therapeutic outcome.

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The information about "DLL4-LVN" are provided by the European Opendata Portal: CORDIS opendata.

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