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MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC

MYC is one of the best‐studied oncogenes in terms of mouse models of malignancy. MYC overexpression has been targeted to several tissues using transgenic constructs, and more recently as mouse models have evolved, conditional systems have been developed to allow the regulation of MYC expression or a...

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Detalles Bibliográficos
Autores principales: Morton, Jennifer P., Sansom, Owen J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528411/
https://www.ncbi.nlm.nih.gov/pubmed/23523308
http://dx.doi.org/10.1016/j.molonc.2013.02.015
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author Morton, Jennifer P.
Sansom, Owen J.
author_facet Morton, Jennifer P.
Sansom, Owen J.
author_sort Morton, Jennifer P.
collection PubMed
description MYC is one of the best‐studied oncogenes in terms of mouse models of malignancy. MYC overexpression has been targeted to several tissues using transgenic constructs, and more recently as mouse models have evolved, conditional systems have been developed to allow the regulation of MYC expression or activity in vivo. The ability to target MYC expression to specific tissues and cell lineages, as well as the ability to regulate that expression, has made genetically engineered mouse models (GEMM) a valuable resource for studying the importance of MYC in the process of tumourigenesis. Here we review how these models have been used to address the role of MYC in tumour initiation and maintenance, how subtle changes in levels of MYC can influence tumourigenesis, and finally the ongoing efforts to target endogenous MYC genetically and with novel therapies.
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spelling pubmed-55284112017-08-15 MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC Morton, Jennifer P. Sansom, Owen J. Mol Oncol Special Papers MYC is one of the best‐studied oncogenes in terms of mouse models of malignancy. MYC overexpression has been targeted to several tissues using transgenic constructs, and more recently as mouse models have evolved, conditional systems have been developed to allow the regulation of MYC expression or activity in vivo. The ability to target MYC expression to specific tissues and cell lineages, as well as the ability to regulate that expression, has made genetically engineered mouse models (GEMM) a valuable resource for studying the importance of MYC in the process of tumourigenesis. Here we review how these models have been used to address the role of MYC in tumour initiation and maintenance, how subtle changes in levels of MYC can influence tumourigenesis, and finally the ongoing efforts to target endogenous MYC genetically and with novel therapies. John Wiley and Sons Inc. 2013-03-08 2013-04 /pmc/articles/PMC5528411/ /pubmed/23523308 http://dx.doi.org/10.1016/j.molonc.2013.02.015 Text en © 2013 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Special Papers
Morton, Jennifer P.
Sansom, Owen J.
MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC
title MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC
title_full MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC
title_fullStr MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC
title_full_unstemmed MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC
title_short MYC‐y mice: From tumour initiation to therapeutic targeting of endogenous MYC
title_sort myc‐y mice: from tumour initiation to therapeutic targeting of endogenous myc
topic Special Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528411/
https://www.ncbi.nlm.nih.gov/pubmed/23523308
http://dx.doi.org/10.1016/j.molonc.2013.02.015
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