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.

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

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.)

LiverMacRegenCircuit (2020)

Elucidating the role of macrophages in liver regeneration and tissue unit formation

Read More  

MY MITOCOMPLEX (2021)

Functional relevance of mitochondrial supercomplex assembly in myeloid cells

Read More  

SymCO (2020)

Asymptotic Symmetries: from Concepts to Observations

Read More