TALC-EMT

The role of Tumour suppressor of lung cancer 1 (TSLC1) signalling in lung repair and cancer-associated epithelial-mesenchymal transitions (EMTs)

 Coordinatore UNIVERSITY COLLEGE LONDON 

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 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 1˙489˙715 €
 EC contributo 1˙489˙715 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2010-StG_20091118
 Funding Scheme ERC-SG
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-10-01   -   2015-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Dr.
Nome: Adam
Cognome: Giangreco
Email: send email
Telefono: 442077000000
Fax: 442077000000

UK (LONDON) hostInstitution 1˙489˙715.00
2    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Greta
Cognome: Borg-Carbott
Email: send email
Telefono: 442031000000
Fax: 442078000000

UK (LONDON) hostInstitution 1˙489˙715.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

metastases    lungs    repair    outcomes    emts    signalling    lung    regulates    disease    pathway    functions    cancer    cell    tslc    largely   

 Obiettivo del progetto (Objective)

'Chronic lung diseases including COPD and cancer account for more than 10% of deaths in European countries and lung cancer remains the most common and most lethal cancer type worldwide. Lung cancer mortality rates have also remained constant for over 40 years, largely due to late stage diagnosis and frequent metastases. Despite these trends the signalling pathways regulating lung cancers remain largely unexplored. Although loss of Tumour Suppressor of Lung Cancer 1 (TSLC1) is implicated in lung cancer metastases its normal lung functions remain entirely unknown. Recently, I determined that the TSLC1 signalling pathway regulates cell proliferation, motility, skin repair, and cancer severity by inhibiting stem cell EMTs. This proposal will determine how TSLC1 regulates lung EMTs to influence repair and disease outcomes. I will correlate TSLC1 expression with EMTs in repairing and diseased lungs, investigate how lung TSLC1 signalling influences repair and disease outcomes using transgenic and knockout mice, and identify mechanisms through which TSLC1 modulates lung phenotypes using in vitro overexpression and knockdown studies. This research will elucidate TSLC1 signalling pathway functions in lungs and should suggest new therapeutic opportunities for human lung disease.'

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