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CpG island methylator phenotype in colorectal cancer
Open accessAbstract
Aberrant methylation of promoter region CpG islands is associated with transcriptional inactivation of tumor-suppressor genes in neoplasia. To understand global patterns of CpG island methylation in colorectal cancer, we have used a recently developed technique called methylated CpG island amplification to examine 30 newly cloned differentially methylated DNA sequences. Of these 30 clones, 19 (63%) were progressively methylated in an age-dependent manner in normal colon, 7 (23%) were methylated in a cancer-specific manner, and 4 (13%) were methylated only in cell lines. Thus, a majority of CpG islands methylated in colon cancer are also methylated in a subset of normal colonic cells during the process of aging. In contrast, methylation of the cancer-specific clones was found exclusively in a subset of colorectal cancers, which appear to display a CpG island methylator phenotype (CIMP). CIMP+ tumors also have a high incidence of p16 and THBS1 methylation, and they include the majority of sporadic colorectal cancers with microsatellite instability related to hMLH1 methylation. We thus define a pathway in colorectal cancer that appears to be responsible for the majority of sporadic tumors with mismatch repair deficiency.
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“Keywords Acute myeloid leukemia, azacitidine, decitabine, DNA methylation, epigenetics, hypomethylating agents, myelodysplastic syndrome, transcriptional regulation History Received 12 October 2014 Revised 26 November 2014 Accepted 1 December 2014 Published online 8 January 2015”
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Metadata
- Authors
- Toyota, M., Ahuja, N., Ohe-Toyota, M., Herman, J. G., Baylin, S. B., & Issa, J.-P. J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-07-20
- Volume
- 96
- Issue
- 15
- Pages
- 8681-8686
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2128146359
- Cited by
- 2,523
- References
- 3
- FWCI
- 21.75
- Type
- journal article
- Language
- en
- Open access
- green
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