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Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes
The development of cancer is driven by genomic instability and mutations. In general, cancer develops via multiple steps. Each step involves the clonal evolution of cells with abrogated defense systems, such as cells with mutations in cancer-suppressor genes. However, it remains unclear how cellular...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6895985/ https://www.ncbi.nlm.nih.gov/pubmed/31653100 http://dx.doi.org/10.3390/cancers11111643 |
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author | Yoshioka, Ken-ichi Matsuno, Yusuke Hyodo, Mai Fujimori, Haruka |
author_facet | Yoshioka, Ken-ichi Matsuno, Yusuke Hyodo, Mai Fujimori, Haruka |
author_sort | Yoshioka, Ken-ichi |
collection | PubMed |
description | The development of cancer is driven by genomic instability and mutations. In general, cancer develops via multiple steps. Each step involves the clonal evolution of cells with abrogated defense systems, such as cells with mutations in cancer-suppressor genes. However, it remains unclear how cellular defense systems are abrogated and the associated clonal evolution is triggered and propagated. In this manuscript, we review current knowledge regarding mutagenesis associated with genomic destabilization and its relationship with the clonal evolution of cells over the course of cancer development, focusing especially on mechanistic aspects. |
format | Online Article Text |
id | pubmed-6895985 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-68959852019-12-24 Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes Yoshioka, Ken-ichi Matsuno, Yusuke Hyodo, Mai Fujimori, Haruka Cancers (Basel) Review The development of cancer is driven by genomic instability and mutations. In general, cancer develops via multiple steps. Each step involves the clonal evolution of cells with abrogated defense systems, such as cells with mutations in cancer-suppressor genes. However, it remains unclear how cellular defense systems are abrogated and the associated clonal evolution is triggered and propagated. In this manuscript, we review current knowledge regarding mutagenesis associated with genomic destabilization and its relationship with the clonal evolution of cells over the course of cancer development, focusing especially on mechanistic aspects. MDPI 2019-10-24 /pmc/articles/PMC6895985/ /pubmed/31653100 http://dx.doi.org/10.3390/cancers11111643 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Yoshioka, Ken-ichi Matsuno, Yusuke Hyodo, Mai Fujimori, Haruka Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes |
title | Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes |
title_full | Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes |
title_fullStr | Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes |
title_full_unstemmed | Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes |
title_short | Genomic-Destabilization-Associated Mutagenesis and Clonal Evolution of Cells with Mutations in Tumor-Suppressor Genes |
title_sort | genomic-destabilization-associated mutagenesis and clonal evolution of cells with mutations in tumor-suppressor genes |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6895985/ https://www.ncbi.nlm.nih.gov/pubmed/31653100 http://dx.doi.org/10.3390/cancers11111643 |
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