HALLMARKS-TO-THERAPY

"Intersecting hallmarks of cancer: mechanisms of and interplay between invasion and angiogenesis, guiding new strategies for cancer therapy"

Coordinatore	ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Switzerland [CH]
Totale costo	2˙500˙000 €
EC contributo	2˙500˙000 €
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-2012-ADG_20120314
Funding Scheme	ERC-AG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-09-01   -   2018-08-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE  Organization address address: BATIMENT CE 3316 STATION 1 city: LAUSANNE postcode: 1015 contact info Titolo: Dr. Nome: Caroline Cognome: Vandevyver Email: send email Telefono: +41 21 693 35 73 Fax: +41 21 693 55 83	CH (LAUSANNE)	hostInstitution	2˙500˙000.00
2	ECOLE POLYTECHNIQUE FEDERALE DE LAUSANNE  Organization address address: BATIMENT CE 3316 STATION 1 city: LAUSANNE postcode: 1015 contact info Titolo: Prof. Nome: Douglas Cognome: Hanahan Email: send email Telefono: +41 21 693 0657 Fax: +41 21 693 0660	CH (LAUSANNE)	hostInstitution	2˙500˙000.00

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 Obiettivo del progetto (Objective)

'Acquisition of the hallmark capability for invasion and in turn metastasis is for most human cancers the defining event in progression to life threatening disease. Its determinants are remarkably complex. Genetically engineered mice can model human cancers, with tumors arising in specific organs, reflecting onco-genomic and histopathological features of particular tumor types. This project will use four mouse models to characterize newly implicated determinants of invasive tumor growth. We have observed that genetic polymorphisms can govern predisposition to invasive cancer. Additionally, therapeutic targeting of another hallmark capability – tumor angiogenesis – has revealed adaptive resistance, whereby late-stage tumors, faced with the inability to grow en masse supported by angiogenesis, switch instead to grow diffusively, by invading adjacent tissue; this phenomenon may underlay the limited benefit seen with anti-angiogenic therapies in the clinic. There are three interconnected goals: (1) Polymorphic regulation of tumor invasion. We will investigate the mechanisms and functional importance of candidate genes resident within a genetic modifier locus on mouse Chr 17 that can alternatively suppress or facilitate invasive tumor growth dependent on constitutional genetic background. (2) Adaptive induction of invasion. We will elucidate the determinants of the invasive growth capability that is induced in response to potent inhibition of angiogenesis. (3) Testing mechanism-based therapeutic co-targeting of the capabilities for invasion and angiogenesis. We will use functional genetic, genomic profiling, and pharmacological approaches to assess these two new modes of regulating invasive growth, and then apply the knowledge in preclinical trials aiming to lay the groundwork for future clinical trials in which these intersecting hallmark capabilities are coordinately disrupted, with promise for more enduring therapeutic responses and benefit to cancer patients.'