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SKin SCiENCE SIGNED

Skin Keratinocyte Stem CEll proliferatioN in field CancErisation

Total Cost €

0

EC-Contrib. €

0

Partnership

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 SKin SCiENCE project word cloud

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

intraepithelial    p63    adult    arises    epithelia    85    expression    carcinoma    assembled    undergo    carcinomas    genetic    carcinogens    delta    continual    multiple    me    uncovered    cancerisation    overexpression    collaborations    hpv8    keratinocyte    proliferation    epidermodysplasia    give    human    original    malignant    drug    susceptible    primary    causes    malignancies    skin    arise    ovary    prostate    innovative    cancer    utilising    expansion    switch    promotes    colon    transformation    exposes    dysregulation    pancreas    differentiation    activated    breast    vulva    lungs    cell    model    oesophagus    disease    hpv8tg    cancers    immunosuppression    therapeutic    bladder    stem    international    78    potentially    discovery    mice    epithelial    strategies    rare    neck    gene    ing    isoforms    area    organisation    basis    cervix    hypothesise    hierarchical    neoplasia    renewal    scc    ta    tissue    head    responsible    np63    infection    mortality    stomach    protective    verruciformis    population    expert    environmental    signalling    fc    barrier    mouse    dependent    lived    mechanism    tissues    ksc   

Project "SKin SCiENCE" data sheet

The following table provides information about the project.

Coordinator
CARDIFF UNIVERSITY 

Organization address
address: NEWPORT ROAD 30-36
city: CARDIFF
postcode: CF24 ODE
website: www.cardiff.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]
 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-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-06-01   to  2020-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CARDIFF UNIVERSITY UK (CARDIFF) coordinator 183˙454.00

Map

 Project objective

Epithelia provide a protective barrier that exposes them to environmental carcinogens. Cancers of epithelial tissues, called carcinoma, account for 85% of all cancers and 78% of all cancer associated mortality. Epithelia undergo continual proliferation and renewal with hierarchical differentiation dependent upon long lived adult tissue stem cell. Many carcinomas arise from pre-malignant transformation, intraepithelial neoplasia referred to as field cancerisation (FC), which is an area that can give rise to multiple primary cancers. FC is a feature of malignancies involving the head and neck,oesophagus, stomach, lungs, cervix, vulva, bladder, colon, breast, ovary, pancreas, prostate and skin. By studying skin FC in a rare genetic disease, Epidermodysplasia verruciformis, and utilising a mouse model of HPV8 infection, I uncovered a novel keratinocyte stem cell (KSC) basis, driven by ΔNp63 expression, common to all causes of skin FC. I now propose to build on this original finding and utilising an innovative approach to determine the cell signalling pathway involved in expansion of this novel KSC population. I hypothesise that the common mechanism in skin FC, potentially relevant to FC in other tissues, arises from dysregulation of a signalling pathway that results in a switch from p63 TA to ΔN isoforms resulting in expansion of a KSC population that is susceptible to transformation. I propose to use multiple strategies to: 1)Identify the HPV8 gene that is responsible for ΔNp63 overexpression, 2)Determine which signalling pathway(s) is/are activated in HPV8tg mice, resulting in ΔNp63 overexpression 3)Determine the pathway(s) is/are responsible for ΔNp63 overexpression in human skin FC; and 4)Determine whether immunosuppression promotes SCC formation in HPV8tg mice. I have assembled expert international collaborations and relevant partner organisation to help me in this project, so that I can identify novel therapeutic targets for future drug discovery and development.

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

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