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Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think

Notch signaling is often considered a model hematopoietic proto-oncogene because of its role as the main trigger of T cell acute lymphoblastic leukemia (T-ALL). Although its role in T-ALL is well characterized and further supported by a high frequency of activating NOTCH1 mutations in T-ALL patients...

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Detalles Bibliográficos
Autores principales: Lobry, Camille, Oh, Philmo, Aifantis, Iannis
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182047/
https://www.ncbi.nlm.nih.gov/pubmed/21948802
http://dx.doi.org/10.1084/jem.20111855
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author Lobry, Camille
Oh, Philmo
Aifantis, Iannis
author_facet Lobry, Camille
Oh, Philmo
Aifantis, Iannis
author_sort Lobry, Camille
collection PubMed
description Notch signaling is often considered a model hematopoietic proto-oncogene because of its role as the main trigger of T cell acute lymphoblastic leukemia (T-ALL). Although its role in T-ALL is well characterized and further supported by a high frequency of activating NOTCH1 mutations in T-ALL patients, it still remains an open question whether the effects of Notch signaling are causative in other types of cancer, including solid tumors. Growing evidence supported by recent studies unexpectedly shows that Notch signaling can also have a potent tumor suppressor function in both solid tumors and hematological malignancies. We discuss the intriguing possibility that the pleiotropic functions of Notch can be tumor suppressive or oncogenic depending on the cellular context.
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spelling pubmed-31820472012-03-26 Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think Lobry, Camille Oh, Philmo Aifantis, Iannis J Exp Med Minireview Notch signaling is often considered a model hematopoietic proto-oncogene because of its role as the main trigger of T cell acute lymphoblastic leukemia (T-ALL). Although its role in T-ALL is well characterized and further supported by a high frequency of activating NOTCH1 mutations in T-ALL patients, it still remains an open question whether the effects of Notch signaling are causative in other types of cancer, including solid tumors. Growing evidence supported by recent studies unexpectedly shows that Notch signaling can also have a potent tumor suppressor function in both solid tumors and hematological malignancies. We discuss the intriguing possibility that the pleiotropic functions of Notch can be tumor suppressive or oncogenic depending on the cellular context. The Rockefeller University Press 2011-09-26 /pmc/articles/PMC3182047/ /pubmed/21948802 http://dx.doi.org/10.1084/jem.20111855 Text en © 2011 Lobry et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Minireview
Lobry, Camille
Oh, Philmo
Aifantis, Iannis
Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think
title Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think
title_full Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think
title_fullStr Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think
title_full_unstemmed Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think
title_short Oncogenic and tumor suppressor functions of Notch in cancer: it’s NOTCH what you think
title_sort oncogenic and tumor suppressor functions of notch in cancer: it’s notch what you think
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182047/
https://www.ncbi.nlm.nih.gov/pubmed/21948802
http://dx.doi.org/10.1084/jem.20111855
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