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Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling
The cancer genome provides the blueprint for identifying oncogenic mutations driving tumor growth and these mutant proteins and pathways are the targets for precision cancer therapies. However, many oncogenes are capable of reprogramming the landscape of active portion of the genome, commonly known...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5871882/ https://www.ncbi.nlm.nih.gov/pubmed/29872691 http://dx.doi.org/10.1038/s41698-017-0005-2 |
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author | Liu, Feng Mischel, Paul S. Cavenee, Webster K. |
author_facet | Liu, Feng Mischel, Paul S. Cavenee, Webster K. |
author_sort | Liu, Feng |
collection | PubMed |
description | The cancer genome provides the blueprint for identifying oncogenic mutations driving tumor growth and these mutant proteins and pathways are the targets for precision cancer therapies. However, many oncogenes are capable of reprogramming the landscape of active portion of the genome, commonly known as the epigenome. This creates fluidity, and thereby heterogeneity, that demands consideration of this additional layer of complexity for effective therapeutic design and application. Molecular dissection of the epigenome may identify oncogene-induced, actionable vulnerabilities, broadening the spectrum of precision oncology treatments. |
format | Online Article Text |
id | pubmed-5871882 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58718822018-06-05 Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling Liu, Feng Mischel, Paul S. Cavenee, Webster K. NPJ Precis Oncol Perspective The cancer genome provides the blueprint for identifying oncogenic mutations driving tumor growth and these mutant proteins and pathways are the targets for precision cancer therapies. However, many oncogenes are capable of reprogramming the landscape of active portion of the genome, commonly known as the epigenome. This creates fluidity, and thereby heterogeneity, that demands consideration of this additional layer of complexity for effective therapeutic design and application. Molecular dissection of the epigenome may identify oncogene-induced, actionable vulnerabilities, broadening the spectrum of precision oncology treatments. Nature Publishing Group UK 2017-03-20 /pmc/articles/PMC5871882/ /pubmed/29872691 http://dx.doi.org/10.1038/s41698-017-0005-2 Text en © The Author(s) 2017 This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Perspective Liu, Feng Mischel, Paul S. Cavenee, Webster K. Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
title | Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
title_full | Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
title_fullStr | Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
title_full_unstemmed | Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
title_short | Precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
title_sort | precision cancer therapy is impacted by oncogene-dependent epigenome remodeling |
topic | Perspective |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5871882/ https://www.ncbi.nlm.nih.gov/pubmed/29872691 http://dx.doi.org/10.1038/s41698-017-0005-2 |
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