Opendata, web and dolomites

SKin SCiENCE SIGNED

Skin Keratinocyte Stem CEll proliferatioN in field CancErisation

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 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.

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

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.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "SKIN SCIENCE" 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 "SKIN SCIENCE" are provided by the European Opendata Portal: CORDIS opendata.

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

RipGEESE (2020)

Identifying the ripples of gene regulation evolution in the evolution of gene sequences to determine when animal nervous systems evolved

Read More  

NSTree (2020)

Understanding substrate delivery for cell wall biosynthesis in plants

Read More  

MetEpiC (2020)

P53-dependent Metabolic and Epigenetic Reprogramming in Carcinogenesis

Read More