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.

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

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.)

CREDit (2020)

Chronological REference Datasets and Sites (CREDit) towards improved accuracy and precision in luminescence-based chronologies

Read More  

DEF2DEV (2019)

Identification of the mode of action of plant defensins during root development and plant defense responses.

Read More  

NarrowbandSSL (2019)

Development of Narrow Band Blue and Red Emitting Macromolecules for Solution-Processed Solid State Lighting Devices

Read More