Genomic insights into cancer-associated aberrant CpG island hypermethylation
Carcinogenesis is thought to occur through a combination of mutational and epimutational events that disrupt key pathways regulating cellular growth and division. The DNA methylomes of cancer cells can exhibit two striking differences from normal cells; a global reduction of DNA methylation levels a...
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pubmed-36628882013-05-24 Genomic insights into cancer-associated aberrant CpG island hypermethylation Sproul, Duncan Meehan, Richard R. Papers Carcinogenesis is thought to occur through a combination of mutational and epimutational events that disrupt key pathways regulating cellular growth and division. The DNA methylomes of cancer cells can exhibit two striking differences from normal cells; a global reduction of DNA methylation levels and the aberrant hypermethylation of some sequences, particularly CpG islands (CGIs). This aberrant hypermethylation is often invoked as a mechanism causing the transcriptional inactivation of tumour suppressor genes that directly drives the carcinogenic process. Here, we review our current understanding of this phenomenon, focusing on how global analysis of cancer methylomes indicates that most affected CGI genes are already silenced prior to aberrant hypermethylation during cancer development. We also discuss how genome-scale analyses of both normal and cancer cells have refined our understanding of the elusive mechanism(s) that may underpin aberrant CGI hypermethylation. Oxford University Press 2013-05 2013-01-21 /pmc/articles/PMC3662888/ /pubmed/23341493 http://dx.doi.org/10.1093/bfgp/els063 Text en © The Author 2013. Published by Oxford University Press. http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Sproul, Duncan Meehan, Richard R. |
spellingShingle |
Sproul, Duncan Meehan, Richard R. Genomic insights into cancer-associated aberrant CpG island hypermethylation |
author_facet |
Sproul, Duncan Meehan, Richard R. |
author_sort |
Sproul, Duncan |
title |
Genomic insights into cancer-associated aberrant CpG island hypermethylation |
title_short |
Genomic insights into cancer-associated aberrant CpG island hypermethylation |
title_full |
Genomic insights into cancer-associated aberrant CpG island hypermethylation |
title_fullStr |
Genomic insights into cancer-associated aberrant CpG island hypermethylation |
title_full_unstemmed |
Genomic insights into cancer-associated aberrant CpG island hypermethylation |
title_sort |
genomic insights into cancer-associated aberrant cpg island hypermethylation |
description |
Carcinogenesis is thought to occur through a combination of mutational and epimutational events that disrupt key pathways regulating cellular growth and division. The DNA methylomes of cancer cells can exhibit two striking differences from normal cells; a global reduction of DNA methylation levels and the aberrant hypermethylation of some sequences, particularly CpG islands (CGIs). This aberrant hypermethylation is often invoked as a mechanism causing the transcriptional inactivation of tumour suppressor genes that directly drives the carcinogenic process. Here, we review our current understanding of this phenomenon, focusing on how global analysis of cancer methylomes indicates that most affected CGI genes are already silenced prior to aberrant hypermethylation during cancer development. We also discuss how genome-scale analyses of both normal and cancer cells have refined our understanding of the elusive mechanism(s) that may underpin aberrant CGI hypermethylation. |
publisher |
Oxford University Press |
publishDate |
2013 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662888/ |
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1611980701811343360 |