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.

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

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.)

MY MITOCOMPLEX (2021)

Functional relevance of mitochondrial supercomplex assembly in myeloid cells

Read More  

CYBERSECURITY (2018)

Cyber Security Behaviours

Read More  

LUNG-BIM (2019)

Induction of B cell immunity in the lung mucosa

Read More