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GENMETASTEM SIGNED

GENOMIC AND METABOLIC REGULATION OF METASTATIC CANCER STEM CELLS

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 GENMETASTEM project word cloud

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

biology    cell    self    host    causes    metastatic    metastasize    therapies    mesenchymal    regulate    vivo    models    animal    contractile    hypothesize    correlates    drug    regulating    functionally    regulates    understand    cytoskeletal    combines    interdisciplinary    closely    elongated    breast    glutamine    actomyosin    initiation    triggered    organs    rock    biochemistry    data    renew    regulated    acquire    tumour    mode    types    genes    emt    rho    shows    transition    markers    metastasis    invasion    carcinoma    nevertheless    amoeboid    stem    cells    ultimate    preliminary    movement    acquisition    signalling    melanoma    successfully    epithelial    unexplored    differentiate    cues    contractility    mediated    suggesting    unravelling    cancer    spread    participate    regulation    maintained    traits    resistance    distant    cscs    metabolism    deaths    stemness    migration    renewal    imaging    molecular    mat    prognostic    link    cellular    clues    interestingly    relapse    metabolic    techniques    linked    lab   

Project "GENMETASTEM" data sheet

The following table provides information about the project.

Coordinator
KING'S COLLEGE LONDON 

Organization address
address: STRAND
city: LONDON
postcode: WC2R 2LS
website: www.kcl.ac.uk

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 United Kingdom [UK]
 Project website http://www.kcl.ac.uk
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2018-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON UK (LONDON) coordinator 183˙454.00

Map

 Project objective

The major causes of cancer deaths are relapse and resistance to current therapies associated with the presence of cancer stem cells (CSCs) and metastatic growth in distant organs. CSCs have the ability to self-renew and differentiate in non-CSCs. In breast cancer, acquisition of stemness properties has been closely related to epithelial-mesenchymal transition (EMT), a key process in cancer invasion and metastasis triggered via Rho-ROCK mediated actomyosin contractility. Interestingly, in melanoma, transition from elongated-mesenchymal to amoeboid mode of movement (MAT) driven by Rho-ROCK signalling has been associated with increased stemness. Furthermore, preliminary data from host lab shows that actomyosin cytoskeletal regulates glutamine metabolism in both melanoma and breast cancer cells. Metabolic cues participate in stem cell self-renewal regulation, suggesting that, in very contractile cells, the regulation of EMT, metastatic spread and tumour initiation might be functionally linked to stemness via metabolic clues. Nevertheless, how very contractile cells regulate genes involved in all these processes remains unexplored. As increasing contractility via EMT in carcinoma cells or via MAT in melanoma cells correlates with increasing stemness, we hypothesize a molecular link between the pathways regulating both migration and stemness abilities, which will be maintained across tumour types (from carcinoma to melanoma). The main goal of this proposal is to understand how tumour cells can acquire stem cell traits to successfully metastasize and how this can be regulated by the actomyosin cytoskeletal by using an interdisciplinary approach that combines state-of-the-art techniques in molecular and cellular biology, biochemistry, in vivo imaging and animal models. This will allow to identify key important genes regulating both stemness traits and metastatic spread with the ultimate goal of unravelling novel drug targets and prognostic markers of distant relapse.

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The information about "GENMETASTEM" are provided by the European Opendata Portal: CORDIS opendata.

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