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Vulnerability of esophageal cancer to their addiction to kinase activities: evaluation and prediction of eSCC tumors responsiveness to kinase inhibitors.

Descrizione del progetto

Inibitori della chinasi come terapia contro il cancro esofageo

Il carcinoma esofageo a cellule squamose (ESCC) si presenta con varie alterazioni genetiche che influenzano l’attività degli enzimi chinasi coinvolti nelle vie di segnalazione, nel ciclo cellulare o nella proliferazione cellulare. Tuttavia, l’eterogeneità associata al malfunzionamento delle chinasi impedisce lo sviluppo di una terapia antichinasica uniforme per l’ESCC. Per sostenere la progettazione di interventi terapeutici innovativi, gli scienziati del progetto Kinaddict, finanziato dall’UE, impiegheranno approcci omici per studiare in che modo l’ESCC risponde agli inibitori delle chinasi. La comprensione dei meccanismi molecolari di queste risposte porterà allo sviluppo di biomarcatori indicativi dell’esito del trattamento e a terapie combinatorie.

Obiettivo

In decades, the 5-year survival rate of several cancers has barely been improved and the esophageal squamous cell carcinoma (eSCC) is not different with a rate around 25%. In order to increase the survival, chemoradiotherapy prior surgery has become the reference for eSCC despite still a high mortality. eSCC tumors harbor a variety of genetic alterations directly or indirectly affecting the activity of kinases involved in signaling pathways, the cell cycle or the proliferation. Evidence on how eSCC tumors are addicted to such oncogenic alterations remains missing to evaluate alternative treatment modalities. The heterogeneity of eSCC tumors presenting deregulations of diverse constellations of kinases has rendered difficult the development of a unique therapeutic strategy similar to prior successes targeting EGFR or BCR-ABL. However, as the CDK4 activity lies downstream from most of the oncogenic deregulations of signalling pathways, it has been proposed to represent the therapeutic target of choice, confirmed by the first approval by the FDA/EMA of 3 CDK4/6 inhibitors to treat ER+ breast cancer. Despite this, not all tumors respond to CDK4 inhibition and long-term treatment triggers escape mechanisms. In this context, the main aim of the present proposal consists to preclinically evaluate if and how eSCC respond to inhibitors targeting kinases with an altered activity using a multi-omics approach. In this cancer, we will (1) identify the kinases with a deregulated activity associated to different genetic landscapes and determine the addiction of eSCC to their activity, (2) characterize the sensitivity of eSCC tumors to CDK4 inhibition and decipher their molecular response for effective combined targeted therapy, and (3) experimentally define the treatment modalities of eSCC in mouse models. The results will provide a strong basis to extend the study with clinicians to human tumors to determine biomarkers of responsiveness to efficient alternative therapy.

Campo scientifico (EuroSciVoc)

CORDIS classifica i progetti con EuroSciVoc, una tassonomia multilingue dei campi scientifici, attraverso un processo semi-automatico basato su tecniche NLP. Cfr.: https://op.europa.eu/en/web/eu-vocabularies/euroscivoc.

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Meccanismo di finanziamento

MSCA-IF-EF-RI -

Coordinatore

UNIVERSITE LIBRE DE BRUXELLES
Contributo netto dell'UE
€ 178 320,00
Indirizzo
AVENUE FRANKLIN ROOSEVELT 50
1050 Bruxelles / Brussel
Belgio

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Regione
Région de Bruxelles-Capitale/Brussels Hoofdstedelijk Gewest Région de Bruxelles-Capitale/ Brussels Hoofdstedelijk Gewest Arr. de Bruxelles-Capitale/Arr. Brussel-Hoofdstad
Tipo di attività
Istituti di istruzione secondaria o superiore
Collegamenti
Costo totale
€ 178 320,00