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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.

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

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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