Opendata, web and dolomites

DLL4-LVN

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

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 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.

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

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.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "DLL4-LVN" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.3.2.)

ACES (2019)

Antarctic Cyclones: Expression in Sea Ice

Read More  

POSPORI (2019)

Polymer Optical Sensors for Prolonged Overseeing the Robustness of civil Infrastructures

Read More  

PRISME (2019)

PRogram for ISolation Manufacturing in Europe (PRISME)

Read More