The DOI matches its Crossref record; 72 of the 72 references it cites were found in a registry or an index.
Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer
Abstract
Gene function in cancer can be disrupted either through genetic alterations, which directly mutate or delete genes, or epigenetic alterations, which alter the heritable state of gene expression. The latter events are mediated by formation of transcriptionally repressive chromatin states around gene transcription start sites and an associated gain of methylation in normally unmethylated CpG islands in these regions. The genes affected include over half of the tumor suppressor genes that cause familial cancers when mutated in the germline; the selective advantage for genetic and epigenetic dysfunction in these genes is very similar. The aberrant methylation can begin very early in tumor progression and mediate most of the important pathway abnormalities in cancer including loss of cell cycle control, altered function of transcription factors, altered receptor function, disruption of normal cell-cell and cell-substratum interaction, inactivation of signal transduction pathways, loss of apoptotic signals and genetic instability. The active role of the aberrant methylation in transcriptional silencing of genes is becoming increasingly understood and involves a synergy between the methylation and histone deacetylase (HDAC) activity. This synergy can be mediated directly by HDAC interaction with DNA methylating enzymes and by recruitment through complexes involving methyl-cytosine binding proteins. In the translational arena, the promoter hypermethylation changes hold great promise as DNA tumor markers and their potentially reversible state creates a target for cancer therapeutic strategies involving gene reactivation.
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Cites
Okano, M., Bell, D. W., Haber, D. A., & Li, E. (1999) · Cell · doi:10.1016/s0092-8674(00)81656-6 · Cited by 6,143
Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands.
Herman, J. G., Graff, J. R., Myöhänen, S., Nelkin, B. D., & Baylin, S. B. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.18.9821 · Cited by 5,646
Self-citationNan, X., Ng, H.-H., Johnson, C. A., Laherty, C. D., Turner, B. M., Eisenman, R. N., & Bird, A. (1998) · Nature · doi:10.1038/30764 · Cited by 3,440
Cadherin Cell Adhesion Receptors as a Morphogenetic Regulator
Takeichi, M. (1991) · Science · doi:10.1126/science.2006419 · Cited by 3,284
Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription
Jones, P. L., Veenstra, G. J. C., Wade, P. A., Vermaak, D., Kass, S. U., Landsberger, N., Strouboulis, J., & Wolffe, A. P. (1998) · Nature Genetics · doi:10.1038/561 · Cited by 2,730
CpG island methylator phenotype in colorectal cancer
Toyota, M., Ahuja, N., Ohe-Toyota, M., Herman, J. G., Baylin, S. B., & Issa, J.-P. J. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.15.8681 · Cited by 2,523
Self-citationCancer-epigenetics comes of age
Jones, P. A., & Laird, P. W. (1999) · Nature Genetics · doi:10.1038/5947 · Cited by 2,344
Inactivation of the DNA-Repair Gene MGMT and the Clinical Response of Gliomas to Alkylating Agents
Esteller, M., Garcia-Foncillas, J., Andion, E., Goodman, S. N., Hidalgo, O. F., Vanaclocha, V., Baylin, S. B., & Herman, J. G. (2000) · New England Journal of Medicine · doi:10.1056/nejm200011093431901 · Cited by 2,224
Self-citationIncidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma
Herman, J. G., Umar, A., Polyak, K., Graff, J. R., Ahuja, N., Issa, J.-P. J., Markowitz, S., Willson, J. K. V., Hamilton, S. R., Kinzler, K. W., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.12.6870 · Cited by 1,887
Self-citationCameron, E. E., Bachman, K. E., Myöhänen, S., Herman, J. G., & Baylin, S. B. (1999) · Nature Genetics · doi:10.1038/5047 · Cited by 1,857
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Cited by
Gene Silencing in Cancer in Association with Promoter Hypermethylation
Herman, J. G., & Baylin, S. B. (2003) · New England Journal of Medicine · doi:10.1056/nejmra023075 · Cited by 3,422
Self-citationMulti-omics approaches to disease
Hasin, Y., Seldin, M., & Lusis, A. (2017) · Genome Biology · doi:10.1186/s13059-017-1215-1 · Cited by 2,953
Christman, J. K. (2002) · Oncogene · doi:10.1038/sj.onc.1205699 · Cited by 1,525
CpG island hypermethylation and tumor suppressor genes: a booming present, a brighter future
Esteller, M. (2002) · Oncogene · doi:10.1038/sj.onc.1205600 · Cited by 1,233
Cancer as an epigenetic disease: DNA methylation and chromatin alterations in human tumours
Esteller, M., & Herman, J. G. (2002) · The Journal of Pathology · doi:10.1002/path.1024 · Cited by 743
Metadata
- Authors
- Baylin, S. B.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-04-01
- Volume
- 10
- Issue
- 7
- Pages
- 687-692
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2137915568
- Cited by
- 929
- References
- 72
- FWCI
- 21.17
- Type
- journal article
- Language
- en
- Open access
- closed
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