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    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
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

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 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.'