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ENDOCAM SIGNED

TARGETING ENDOTHELIAL CELL AND CANCER AMOEBOID MOVEMENT TO OVERCOME RESISTANCE TO ANTI-VEGF AND ANTI-PROTEASE THERAPIES

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 ENDOCAM project word cloud

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

containing    molecules    serine    onset    receptors    progression    candidates    vessel    ascribed    cell    cysteine    differences    synthetic    tumors    skip    regulation    protease    therapy    mechanisms    patients    humans    disease    opportunistic    preliminary    movements    outcomes    disregarded    adaptations    overcoming    strategy    cortical    impairing    angiogenesis    mpi    attack    strategies    physiological    existence    unlike    liposomes    multiple    environment    followed    experiments    mpis    expectations    anti    endothelial    vegf    indifference    motility    hypothesized    cargo    inhibitors    mimicking    mesenchymal    vegfa    actin    proteases    therapeutic    body    cancer    metallo    mature    glide    progenitor    epcs    progress    degrade    migration    cytoskeleton    resistance    ecm    amoeboid    vascular    mixture    shared    invasion    perspective    cells    treatment    physiologic    blood    ecs    ephrin    showed    time    connection    clinical    movement    stimulation    barriers    give    metalloproteinase   

Project "ENDOCAM" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI FIRENZE 

Organization address
address: Piazza San Marco 4
city: Florence
postcode: 50121
website: http://www.unifi.it

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 Italy [IT]
 Project website http://www.unifi.it
 Total cost 244˙269 €
 EC max contribution 244˙269 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-GF
 Starting year 2017
 Duration (year-month-day) from 2017-12-01   to  2020-11-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI FIRENZE IT (Florence) coordinator 244˙269.00
2    THE REGENTS OF THE UNIVERSITY OF CALIFORNIA US (OAKLAND CA) partner 0.00

Map

 Project objective

Unlike mesenchymal migration, the amoeboid motility doesn’t require proteases and is an opportunistic movement of cancer cells which allows cells to glide through, rather than degrade, ECM barriers, using movements based on adaptations of the cell body. Preliminary experiments we conducted using a mixture of physiologic inhibitors of serine-proteases, metallo-proteases and cysteine-proteases, thus mimicking a physiological environment, showed no differences in vessel formation for both Endothelial Progenitor Cells (EPCs) and mature Endothelial Cells (ECs) under mesenchymal or amoeboid conditions. Thus, we hypothesized the existence of an “amoeboid angiogenesis”. We also hypothesized that the failure of cancer treatment using synthetic metalloproteinase inhibitors (MPIs) could be ascribed to the ability of cancer and ECs to skip the attack of the MPI therapy by allowing cancer invasion and blood vessel formation using the “amoeboid” strategy. Even the VEGFA targeting partially disregarded the expectations because of the resistance onset followed by the progression of the disease. Our preliminary experiments showed also an “indifference” of ECs and EPCs to VEGF stimulation under amoeboid conditions. Therefore, the aim of this project is to identify the multiple mechanisms shared by cancer cells and ECs/EPCs in the regulation of amoeboid movement, to identify common therapeutic strategies impairing vascular growth and cancer cell invasion at the same time, overcoming resistance to anti-VEGF and anti-protease therapy. The molecules identified (ephrin, protease receptors, etc.) will be used as candidates for targeted therapy through the delivery of cargo liposomes containing inhibitors of the connection of such molecules with the cortical actin cytoskeleton, in pre-clinical experiments with the perspective of a possible application to humans. We expect that this approach will give a progress in the treatment of tumors thus improving outcomes for cancer patients.

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