Inactivation of DNA repair—prospects for boosting cancer immune surveillance

The emergence of drug resistance depends on the ability of the genome of cancer cells to constantly mutate and evolve under selective pressures. The generation of new mutations is accelerated when genes involved in DNA repair pathways are altered. Notably, although the emergence of new mutations fos...

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Autores principales: Truini, Anna, Germano, Giovanni, Bardelli, Alberto
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Comment
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6260742/
https://www.ncbi.nlm.nih.gov/pubmed/30486892
http://dx.doi.org/10.1186/s13073-018-0603-9
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author Truini, Anna
Germano, Giovanni
Bardelli, Alberto
author_facet Truini, Anna
Germano, Giovanni
Bardelli, Alberto
author_sort Truini, Anna
collection PubMed
description The emergence of drug resistance depends on the ability of the genome of cancer cells to constantly mutate and evolve under selective pressures. The generation of new mutations is accelerated when genes involved in DNA repair pathways are altered. Notably, although the emergence of new mutations fosters drug resistance, new variants can nevertheless become novel antigens that promote immune surveillance and even restrict cancer growth.
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spelling pubmed-62607422018-11-30 Inactivation of DNA repair—prospects for boosting cancer immune surveillance Truini, Anna Germano, Giovanni Bardelli, Alberto Genome Med Comment The emergence of drug resistance depends on the ability of the genome of cancer cells to constantly mutate and evolve under selective pressures. The generation of new mutations is accelerated when genes involved in DNA repair pathways are altered. Notably, although the emergence of new mutations fosters drug resistance, new variants can nevertheless become novel antigens that promote immune surveillance and even restrict cancer growth. BioMed Central 2018-11-28 /pmc/articles/PMC6260742/ /pubmed/30486892 http://dx.doi.org/10.1186/s13073-018-0603-9 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Comment
Truini, Anna
Germano, Giovanni
Bardelli, Alberto
Inactivation of DNA repair—prospects for boosting cancer immune surveillance
title Inactivation of DNA repair—prospects for boosting cancer immune surveillance
title_full Inactivation of DNA repair—prospects for boosting cancer immune surveillance
title_fullStr Inactivation of DNA repair—prospects for boosting cancer immune surveillance
title_full_unstemmed Inactivation of DNA repair—prospects for boosting cancer immune surveillance
title_short Inactivation of DNA repair—prospects for boosting cancer immune surveillance
title_sort inactivation of dna repair—prospects for boosting cancer immune surveillance
topic Comment
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6260742/
https://www.ncbi.nlm.nih.gov/pubmed/30486892
http://dx.doi.org/10.1186/s13073-018-0603-9
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