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CpG island methylator phenotype in colorectal cancer.
- M. Toyota, N. Ahuja, M. Ohe-Toyota, J. Herman, S. Baylin, J. Issa
- BiologyProceedings of the National Academy of Sciences…
- 20 July 1999
A pathway in colorectal cancer appears to be responsible for the majority of sporadic tumors with mismatch repair deficiency, and is defined as CpG island methylator phenotype (CIMP); CIMP+ tumors also have a high incidence of p16 and THBS1 methylation, and they include the majority with microsatellite instability related to hMLH 1 methylation.
Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma.
The results suggest that microsatellite instability in sporadic colorectal cancer often results from epigenetic inactivation of hMLH1 in association with DNA methylation.
Decitabine improves patient outcomes in myelodysplastic syndromes
Aberrant DNA methylation, which results in leukemogenesis, is frequent in patients with myelodysplastic syndromes (MDS) and is a potential target for pharmacologic therapy. Decitabine indirectly…
A simple method for estimating global DNA methylation using bisulfite PCR of repetitive DNA elements.
- A. Yang, M. Estécio, Ketan Doshi, Y. Kondo, E. Tajara, J. Issa
- BiologyNucleic acids research
- 1 February 2004
This method is less labor intensive and requires less DNA than previous methods of assessing global DNA methylation, and can be used as a surrogate marker of genome-wide methylation changes.
Alterations in DNA methylation: a fundamental aspect of neoplasia.
CpG island methylator phenotype in cancer
- J. Issa
- Biology, MedicineNature Reviews Cancer
- 1 December 2004
DNA hypermethylation in CpG-rich promoters is now recognized as a common feature of human neoplasia, and CIMP-associated cancers seem to have a distinct epidemiology, a distinct histology, distinct precursor lesions and distinct molecular features.
Integrated genetic and epigenetic analysis identifies three different subclasses of colon cancer
- Lanlan Shen, M. Toyota, J. Issa
- BiologyProceedings of the National Academy of Sciences
- 20 November 2007
Together, the integrated genetic and epigenetic analysis reveals that colon cancers correspond to three molecularly distinct subclasses of disease.
Integrative genomic characterization of oral squamous cell carcinoma identifies frequent somatic drivers.
Although genomic alterations are dominated by loss of tumor suppressor genes, 80% of patients harbored at least one genomic alteration in a targetable gene, suggesting that novel approaches to treatment may be possible for this debilitating subset of head and neck cancers.
Inactivation of the CDKN2/p16/MTS1 gene is frequently associated with aberrant DNA methylation in all common human cancers.
In tumors, de novo methylation of the 5' CpG island is a frequent mode of inactivation of CDKN2/p16 and this alteration of p16 in colon cancer was particularly striking, since inactivation does not occur through homozygous deletion in this tumor type.
Identification of differentially methylated sequences in colorectal cancer by methylated CpG island amplification.
It is proposed that MCA is a useful technique to study methylation and to isolate CpG islands differentially methylated in cancer.