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In vivo studies and screens for new factors that promote or suppress tumor metastasis

Ziel

Metastasis is the process whereby a primary tumor (usually highly malignant in nature) spreads to distant locations in the body. Understanding step-by-step how particular confined tumors acquire invasiveness and/or spreading potential is a scientific challenge that can help us to develop new strategies for metastatic cancer prevention or treatment. In mouse models and in humans, the inactivation of the E-cadherin gene and the activation of genes of the SNAIL family are markers of the initiation of metastasis from epithelial tumors – a process that is called epithelial-mesenchimal transition, and that is similar, albeit not identical, to what occurs during normal development. In vivo, however, neither the activation of E-cadherin nor the activation of SNAIL genes is sufficient to trigger malignant transformation, indicating that additional unknown factors are required for this process to take place. Our project has as its main objective to develop and explore genetically traceable animal models that recapitulate the initial steps in malignant transformation of tumorous growth in vivo. With these animal models we intend to understand the molecular mechanisms that activate (or inactivate) genes that trigger metastasis and that convert a stationary eptithelial cell into an invasive one (ie, one with the capacity to invade and degrade the basal lamina). We hope that these models will help to open new fields of investigation to isolate new potential targets for therapeutic intervention.

Aufforderung zur Vorschlagseinreichung

FP7-PEOPLE-2007-2-1-IEF
Andere Projekte für diesen Aufruf anzeigen

Koordinator

UNIVERSIDAD MIGUEL HERNANDEZ DE ELCHE
EU-Beitrag
€ 159 166,60
Adresse
AVENIDA DE LA UNIVERSIDAD S-N
03202 Elche
Spanien

Auf der Karte ansehen

Region
Este Comunitat Valenciana Alicante/Alacant
Aktivitätstyp
Higher or Secondary Education Establishments
Kontakt Verwaltung
Rafael Gandía Balaguer (Mr.)
Links
Gesamtkosten
Keine Daten