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The tyrosine-kinase inhibitor sunitinib targets vascular endothelial (VE)-cadherin: a marker of response to antitumoural treatment in metastatic renal cell carcinoma

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Polena, Helena | Creuzet, Julie | Dufies, Maeva | Sidibé, Adama | Khalil-Mgharbel, Abir | Salomon, Aude | Deroux, Alban | Quesada, Jean-Louis | Roelants, Caroline | Filhol, Odile | Cochet, Claude | Blanc, Ellen | Ferlay-Segura, Céline | Borchiellini, Delphine | Ferrero, Jean-Marc | Escudier, Bernard | Négrier, Sylvie | Pages, Gilles | Vilgrain, Isabelle

Edité par CCSD ; Cancer Research UK -

International audience. Vascular endothelial (VE)-cadherin is an endothelial cell-specific protein responsible for endothelium integrity. Its adhesive properties are regulated by post-translational processing, such as tyrosine phosphorylation at site Y685 in its cytoplasmic domain, and cleavage of its extracellular domain (sVE). In hormone-refractory metastatic breast cancer, we recently demonstrated that sVE levels correlate to poor survival. In the present study, we determine whether kidney cancer therapies had an effect on VE-cadherin structural modifications and their clinical interest to monitor patient outcome.

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