Notch tumor suppressor function

Détails

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Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_3DB0E583975D
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
Institution
Titre
Notch tumor suppressor function
Périodique
Oncogene
Auteur(s)
Dotto G. P.
ISSN
1476-5594
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
27
Numéro
38
Pages
5115-5123
Langue
anglais
Résumé
Cancer development results from deregulated control of stem cell populations and alterations in their surrounding environment. Notch signaling is an important form of direct cell-cell communication involved in cell fate determination, stem cell potential and lineage commitment. The biological function of this pathway is critically context dependent. Here we review the pro-differentiation role and tumor suppressing function of this pathway, as revealed by loss-of-function in keratinocytes and skin, downstream of p53 and in cross-connection with other determinants of stem cell potential and/or tumor formation, such as p63 and Rho/CDC42 effectors. The possibility that Notch signaling elicits a duality of signals, involved in growth/differentiation control and cell survival will be discussed, in the context of novel approaches for cancer therapy
Mots-clé
adverse effects, Animals, Apoptosis, Cell Differentiation, Cell Transformation,Neoplastic, DNA Damage, Female, Genes,Tumor Suppressor, genetics, Humans, Keratinocytes, Mice, Neoplasms, Oncogene Proteins,Viral, pathology, physiology, physiopathology, radiation effects, Receptor,Notch1, Receptors,Notch, Signal Transduction, Species Specificity, Switzerland, therapy, Tumor Suppressor Protein p53, Tumor Suppressor Proteins, Tumor Virus Infections, Ultraviolet Rays, Uterine Cervical Neoplasms, virology
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/01/2009 23:12
Dernière modification de la notice
20/08/2019 14:34
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