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AID/APOBEC deaminases and cancer

Mutations are the basis for evolution and the development of genetic diseases. Especially in cancer, somatic mutations in oncogenes and tumor suppressor genes alongside the occurrence of passenger mutations have been observed by recent deep-sequencing approaches. While mutations have long been consi...

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Autores principales: Rebhandl, Stefan, Huemer, Michael, Greil, Richard, Geisberger, Roland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4468319/
https://www.ncbi.nlm.nih.gov/pubmed/26097867
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author Rebhandl, Stefan
Huemer, Michael
Greil, Richard
Geisberger, Roland
author_facet Rebhandl, Stefan
Huemer, Michael
Greil, Richard
Geisberger, Roland
author_sort Rebhandl, Stefan
collection PubMed
description Mutations are the basis for evolution and the development of genetic diseases. Especially in cancer, somatic mutations in oncogenes and tumor suppressor genes alongside the occurrence of passenger mutations have been observed by recent deep-sequencing approaches. While mutations have long been considered random events induced by DNA-replication errors or by DNA damaging agents, genome sequencing led to the discovery of non-random mutation signatures in many human cancer. Common non-random mutations comprise DNA strand-biased mutation showers and mutations restricted to certain DNA motifs, which recently have become attributed to the activity of the AID/APOBEC family of DNA deaminases. Hence, APOBEC enzymes, which have evolved as key players in natural and adaptive immunity, have been proposed to contribute to cancer development and clonal evolution of cancer by inducing collateral genomic damage due to their DNA deaminating activity. This review focuses on how mutagenic events through AID/APOBEC deaminases may contribute to cancer development.
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spelling pubmed-44683192015-06-19 AID/APOBEC deaminases and cancer Rebhandl, Stefan Huemer, Michael Greil, Richard Geisberger, Roland Oncoscience Review Mutations are the basis for evolution and the development of genetic diseases. Especially in cancer, somatic mutations in oncogenes and tumor suppressor genes alongside the occurrence of passenger mutations have been observed by recent deep-sequencing approaches. While mutations have long been considered random events induced by DNA-replication errors or by DNA damaging agents, genome sequencing led to the discovery of non-random mutation signatures in many human cancer. Common non-random mutations comprise DNA strand-biased mutation showers and mutations restricted to certain DNA motifs, which recently have become attributed to the activity of the AID/APOBEC family of DNA deaminases. Hence, APOBEC enzymes, which have evolved as key players in natural and adaptive immunity, have been proposed to contribute to cancer development and clonal evolution of cancer by inducing collateral genomic damage due to their DNA deaminating activity. This review focuses on how mutagenic events through AID/APOBEC deaminases may contribute to cancer development. Impact Journals LLC 2015-04-28 /pmc/articles/PMC4468319/ /pubmed/26097867 Text en Copyright: © 2015 Rebhandl et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Review
Rebhandl, Stefan
Huemer, Michael
Greil, Richard
Geisberger, Roland
AID/APOBEC deaminases and cancer
title AID/APOBEC deaminases and cancer
title_full AID/APOBEC deaminases and cancer
title_fullStr AID/APOBEC deaminases and cancer
title_full_unstemmed AID/APOBEC deaminases and cancer
title_short AID/APOBEC deaminases and cancer
title_sort aid/apobec deaminases and cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4468319/
https://www.ncbi.nlm.nih.gov/pubmed/26097867
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