It is abundantly clear that mutations, whether inherited throughthe germ line or, more commonly, arising in somatic tissueslater in life,1 can cause cancer. These mutations abnormallyenhance the function of some genes, the oncogenes, or causeother genes, the tumor-suppressor genes, to lose function.1Students of the neoplastic process, however, have argued fordecades about whether the initiation and progression of cancerare due only to mutations or, as well, to epigenetic changesthat are not caused by alterations in the primary nucleotidesequence of DNA. Recent investigations have proved not onlythat both views are correct, but . . . [Full Text of this Article]
What is DNA Methylation?
The Molecular Role of DNA Methylation
Maintenance of Genes in a Transcriptionally Silent State
CpG Islands
DNA Methylation in Cancer
Losses of DNA Methylation in Cancer
Gains in DNA Methylation in Gene Promoters
Biologic Effects of Promoter Hypermethylation
Proteins That Mediate DNA Methylation
DNMTS
Methyl Cytosine–Binding Proteins, Nucleosomes, and Histone Acetylation
Gene Silencing and Chromatin
Nucleosomes
Histone Acetylation
The Histone Code
Clinical Implications of Gene Silencing in Cancer
Reversal of Gene Silencing to Prevent or Treat Cancer
Inhibitors of Histone Deacetylases
Inhibition of DNMTs
Hypermethylation of CpG Islands as a Molecular Marker for Cancer
Early Detection of Cancer
Confounding Issues
Hypermethylation and Prognosis in Cancer
Source Information
From the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins (J.G.H.) and the Departments of Oncology (J.G.H.) and Medicine (S.B.B.), Johns Hopkins Medical Institutions, Baltimore.
Address reprint requests to Dr. Herman at hermanji@jhmi.edu or to Dr. Baylin at sbaylin@jhmi.edu.
Related Letters:
Gene Silencing
Kirk J., Herman J. G., Baylin S. B.
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N Engl J Med 2004;
350:947-948, Feb 26, 2004.
Correspondence
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