The DOI matches its Crossref record; 164 of the 164 references it cites were found in a registry or an index.
DNA hypermethylation in disease: mechanisms and clinical relevance
Open accessAbstract
Increasing numbers of studies implicate abnormal DNA methylation in cancer and many non-malignant diseases. This is consistent with numerous findings about differentiation-associated changes in DNA methylation at promoters, enhancers, gene bodies, and sites that control higher-order chromatin structure. Abnormal increases or decreases in DNA methylation contribute to or are markers for cancer formation and tumour progression. Aberrant DNA methylation is also associated with neurological diseases, immunological diseases, atherosclerosis, and osteoporosis. In this review, I discuss DNA hypermethylation in disease and its interrelationships with normal development as well as proposed mechanisms for the origin of and pathogenic consequences of disease-associated hypermethylation. Disease-linked DNA hypermethylation can help drive oncogenesis partly by its effects on cancer stem cells and by the CpG island methylator phenotype (CIMP); atherosclerosis by disease-related cell transdifferentiation; autoimmune and neurological diseases through abnormal perturbations of cell memory; and diverse age-associated diseases by age-related accumulation of epigenetic alterations.
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Cites
DNA methylation age of human tissues and cell types
Horvath, S. (2013) · Genome Biology · doi:10.1186/gb-2013-14-10-r115 · Cited by 7,075
Integrative analysis of 111 reference human epigenomes
Roadmap Epigenomics Consortium, Kundaje, A., Meuleman, W., Ernst, J., Bilenky, M., Yen, A., Heravi-Moussavi, A., Kheradpour, P., Zhang, Z., Wang, J., et al. (2015) · Nature · doi:10.1038/nature14248 · Cited by 6,368 · cited 14×
“In cancers, the disease-linked promoter DNA hypermethylation (which usually occurs with the loss of H3K27me3) might prevent induction of transcription under otherwise inducing conditions [29,78], as seen in some bivalent promoters upon differentiation of ESC [79].”
BackgroundMethodInfluentialThe Genotype-Tissue Expression (GTEx) pilot analysis: Multitissue gene regulation in humans
The GTEx Consortium, Ardlie, K. G., Deluca, D. S., Segrè, A. V., Sullivan, T. J., Young, T. R., Gelfand, E. T., Trowbridge, C. A., Maller, J. B., Tukiainen, T., et al. (2015) · Science · doi:10.1126/science.1262110 · Cited by 5,062
Weber, M., Hellmann, I., Stadler, M. B., Ramos, L., Pääbo, S., Rebhan, M., & Schübeler, D. (2007) · Nature Genetics · doi:10.1038/ng1990 · Cited by 2,221
Machine Learning Identifies Stemness Features Associated with Oncogenic Dedifferentiation
Malta, T. M., Sokolov, A., Gentles, A. J., Burzykowski, T., Poisson, L., Weinstein, J. N., Kamińska, B., Huelsken, J., Omberg, L., Gevaert, O., et al. (2018) · Cell · doi:10.1016/j.cell.2018.03.034 · Cited by 2,180
Merlo, A., Herman, J. G., Mao, L., Lee, D. J., Gabrielson, E., Burger, P. C., Baylin, S. B., & Sidransky, D. (1995) · Nature Medicine · doi:10.1038/nm0795-686 · Cited by 1,986
Global epigenomic reconfiguration during mammalian brain development
Lister, R., Mukamel, E. A., Nery, J. R., Urich, M., Puddifoot, C. A., Johnson, N. D., Lucero, J., Huang, Y., Dwork, A. J., Schultz, M. D., et al. (2013) · Science · doi:10.1126/science.1237905 · Cited by 1,830
DNA methylation in cancer: too much, but also too little
Ehrlich, M. (2002) · Oncogene · doi:10.1038/sj.onc.1205651 · Cited by 1,538
Self-citationSchlesinger, Y., Straussman, R., Keshet, I., Farkash, S., Hecht, M., Zimmerman, J., Eden, E., Yakhini, Z., Ben-Shushan, E., Reubinoff, B. E., et al. (2007) · Nature Genetics · doi:10.1038/ng1950 · Cited by 1,226 · cited 4×
“However, most promoters that display cancer-associated hypermethylation are linked to genes that were already silenced in control tissues by repressive chromatin marks (polycomb or PcG repression, enrichment in histone H3 lysine-27 trimethylation, H3K27me3) [29,75,76].”
BackgroundInfluentialCpG island methylator phenotype in cancer
Issa, J.-P. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1507 · Cited by 1,098
Cited by
Epigenetics of Muscle- and Brain-Specific Expression of KLHL Family Genes
Ehrlich, K. C., Baribault, C., & Ehrlich, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21218394 · Cited by 35
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Metadata
- Authors
- Ehrlich, M.
- Venue
- Epigenetics
- Publisher
- Informa UK Limited
- Published
- 2019-07-08
- Volume
- 14
- Issue
- 12
- Pages
- 1141-1163
- ISSN
- 1559-2294 (ISSN-L)
- 1559-2308
- OpenAlex
- W2956473282
- Cited by
- 373
- References
- 164
- FWCI
- 11.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
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