Endothelin B receptor, a new target in cancer immune therapy.

Détails

Ressource 1Télécharger: 19567593AM .pdf (1022.74 [Ko])
Etat: Public
Version: Author's accepted manuscript
ID Serval
serval:BIB_B040F90D1DBC
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Endothelin B receptor, a new target in cancer immune therapy.
Périodique
Clinical Cancer Research
Auteur⸱e⸱s
Kandalaft L.E., Facciabene A., Buckanovich R.J., Coukos G.
ISSN
1078-0432 (Print)
ISSN-L
1078-0432
Statut éditorial
Publié
Date de publication
2009
Volume
15
Numéro
14
Pages
4521-4528
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; ReviewPublication Status: ppublish
Résumé
The endothelins and their G protein-coupled receptors A and B have been implicated in numerous diseases and have recently emerged as pivotal players in a variety of malignancies. Tumors overexpress the endothelin 1 (ET-1) ligand and the endothelin-A-receptor (ET(A)R). Their interaction induces tumor growth and metastasis by promoting tumor cell survival and proliferation, angiogenesis, and tissue remodeling. On the basis of results from xenograft models, drug development efforts have focused on antagonizing the autocrine-paracrine effects mediated by ET-1/ET(A)R. In this review, we discuss a novel role of the endothelin-B-receptor (ET(B)R) in tumorigenesis and the effect of its blockade during cancer immune therapy. We highlight key characteristics of the B receptor such as its specific overexpression in the tumor compartment; and specifically, in the tumor endothelium, where its activation by ET-1 suppresses T-cell adhesion and homing to tumors. We also review our recent findings on the effects of ET(B)R-specific blockade in increasing T-cell homing to tumors and enhancing the efficacy of otherwise ineffective immunotherapy.
Mots-clé
Animals, Endothelium, Vascular/drug effects, Endothelium, Vascular/metabolism, Humans, Immunotherapy/methods, Intercellular Adhesion Molecule-1/metabolism, Models, Biological, Neoplasms/immunology, Neoplasms/metabolism, Oligopeptides/pharmacology, Piperidines/pharmacology, Receptor, Endothelin B/antagonists & inhibitors, Receptor, Endothelin B/metabolism, T-Lymphocytes/drug effects, T-Lymphocytes/immunology
Pubmed
Web of science
Open Access
Oui
Création de la notice
14/10/2014 11:42
Dernière modification de la notice
20/08/2019 15:19
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