
@article{fraga_dna_2002,
	title = {{DNA} methylation: a profile of methods and applications},
	volume = {33},
	issn = {0736-6205},
	shorttitle = {{DNA} methylation},
	abstract = {Ever since methylcytosine was found in genomic {DNA}, this epigenetic alteration has become a center of scientific attraction, especially because of its relation to gene silencing in disease. There is currently a wide range of methods designed to yield quantitative and qualitative information on genomic {DNA} methylation. The earliest approaches were concentrated on the study of overall levels of methylcytosine, but more recent efforts havefocused on the study ofthe methylation status of specific {DNA} sequences. Particularly, optimization of the methods based on bisulfite modification of {DNA} permits the analysis of limited {CpGs} in restriction enzyme sites (e.g., combined bisulfite restriction analyses and methylation-sensitive single nucleotide primer extension) and the overall characterization based on differential methylation states (e.g., methylation-specific {PCR}, {MethyLight}, and methylation-sensitive single-stranded conformational polymorphism) and allows very specific patterns of methylation to be revealed (bisulfite {DNA} sequencing). In addition, novel methods designed to search for new methylcytosine hot spots have yielded further data without requiring prior knowledge of the {DNA} sequence. We hope this review will be a valuable tool in selecting the best techniques to address particular questions concerning the cytosine methylation status of genomic {DNA.}},
	language = {eng},
	number = {3},
	journal = {{BioTechniques}},
	author = {Fraga, Mario F and Esteller, Manel},
	month = sep,
	year = {2002},
	note = {{PMID:} 12238773},
	keywords = {5-Methylcytosine, Chromatography, High Pressure Liquid, Cytosine, {DNA}, {DNA} Methylation, Electrophoresis, Capillary, Genome, Microchemistry, Polymerase Chain Reaction, Restriction Mapping, Sequence Analysis, {DNA}, Sulfites},
	pages = {632, 634, 636--649}
},

@article{gu_genome-scale_2010,
	title = {Genome-scale {DNA} methylation mapping of clinical samples at single-nucleotide resolution},
	volume = {7},
	issn = {1548-7105},
	doi = {10.1038/nmeth.1414},
	abstract = {Bisulfite sequencing measures absolute levels of {DNA} methylation at single-nucleotide resolution, providing a robust platform for molecular diagnostics. We optimized bisulfite sequencing for genome-scale analysis of clinical samples: here we outline how restriction digestion targets bisulfite sequencing to hotspots of epigenetic regulation and describe a statistical method for assessing significance of altered {DNA} methylation patterns. Thirty nanograms of {DNA} was sufficient for genome-scale analysis and our protocol worked well on formalin-fixed, paraffin-embedded samples.},
	language = {eng},
	number = {2},
	journal = {Nature methods},
	author = {Gu, Hongcang and Bock, Christoph and Mikkelsen, Tarjei S and Jäger, Natalie and Smith, Zachary D and Tomazou, Eleni and Gnirke, Andreas and Lander, Eric S and Meissner, Alexander},
	month = feb,
	year = {2010},
	note = {{PMID:} 20062050},
	keywords = {Base Sequence, Chromosome Mapping, Colonic Neoplasms, {DNA} Methylation, {DNA}, Neoplasm, Genetic Testing, Humans, Molecular Sequence Data, Nucleotides, Reproducibility of Results, Sensitivity and Specificity},
	pages = {133--136}
},

@article{frommer_genomic_1992,
	title = {A genomic sequencing protocol that yields a positive display of 5-methylcytosine residues in individual {DNA} strands.},
	volume = {89},
	issn = {0027-8424, 1091-6490},
	url = {http://www.pnas.org/content/89/5/1827},
	doi = {10.1073/pnas.89.5.1827},
	abstract = {The modulation of {DNA-protein} interactions by methylation of protein-binding sites in {DNA} and the occurrence in genomic imprinting, X chromosome inactivation, and fragile X syndrome of different methylation patterns in {DNA} of different chromosomal origin have underlined the need to establish methylation patterns in individual strands of particular genomic sequences. We report a genomic sequencing method that provides positive identification of 5-methylcytosine residues and yields strand-specific sequences of individual molecules in genomic {DNA.} The method utilizes bisulfite-induced modification of genomic {DNA}, under conditions whereby cytosine is converted to uracil, but 5-methylcytosine remains nonreactive. The sequence under investigation is then amplified by {PCR} with two sets of strand-specific primers to yield a pair of fragments, one from each strand, in which all uracil and thymine residues have been amplified as thymine and only 5-methylcytosine residues have been amplified as cytosine. The {PCR} products can be sequenced directly to provide a strand-specific average sequence for the population of molecules or can be cloned and sequenced to provide methylation maps of single {DNA} molecules. We tested the method by defining the methylation status within single {DNA} strands of two closely spaced {CpG} dinucleotides in the promoter of the human kininogen gene. During the analysis, we encountered in sperm {DNA} an unusual methylation pattern, which suggests that the high methylation level of single-copy sequences in sperm may be locally modulated by binding of protein factors in germ-line cells.},
	language = {en},
	number = {5},
	urldate = {2013-09-24},
	journal = {Proceedings of the National Academy of Sciences},
	author = {Frommer, M. and {McDonald}, L. E. and Millar, D. S. and Collis, C. M. and Watt, F. and Grigg, G. W. and Molloy, P. L. and Paul, C. L.},
	month = mar,
	year = {1992},
	note = {{PMID:} 1542678},
	pages = {1827--1831},
	file = {Full Text PDF:C:\Users\t\AppData\Roaming\Zotero\Zotero\Profiles\kqhsfvpb.default\zotero\storage\KD7D29V2\Frommer et al. - 1992 - A genomic sequencing protocol that yields a positi.pdf:application/pdf;Snapshot:C:\Users\t\AppData\Roaming\Zotero\Zotero\Profiles\kqhsfvpb.default\zotero\storage\DRNQ6D2H\1827.html:text/html}
},

@article{egger_epigenetics_2004,
	title = {Epigenetics in human disease and prospects for epigenetic therapy},
	volume = {429},
	issn = {1476-4687},
	doi = {10.1038/nature02625},
	abstract = {Epigenetic mechanisms, which involve {DNA} and histone modifications, result in the heritable silencing of genes without a change in their coding sequence. The study of human disease has focused on genetic mechanisms, but disruption of the balance of epigenetic networks can cause several major pathologies, including cancer, syndromes involving chromosomal instabilities, and mental retardation. The development of new diagnostic tools might reveal other diseases that are caused by epigenetic alterations. Great potential lies in the development of 'epigenetic therapies'--several inhibitors of enzymes controlling epigenetic modifications, specifically {DNA} methyltransferases and histone deacetylases, have shown promising anti-tumorigenic effects for some malignancies.},
	language = {eng},
	number = {6990},
	journal = {Nature},
	author = {Egger, Gerda and Liang, Gangning and Aparicio, Ana and Jones, Peter A},
	month = may,
	year = {2004},
	note = {{PMID:} 15164071},
	keywords = {Disease, {DNA} Methylation, Epigenesis, Genetic, Gene Silencing, Genetic Therapy, Genetics, Medical, Humans},
	pages = {457--463}
},

@article{__????
},

@article{jeggo_azacytidine-induced_1986,
	title = {Azacytidine-induced reactivation of a {DNA} repair gene in Chinese hamster ovary cells.},
	volume = {6},
	issn = {0270-7306},
	url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC367863/},
	abstract = {Six X-ray-sensitive (xrs) strains of the {CHO-K1} cell line were shown to revert at a very high frequency after treatment with 5-azacytidine. This suggested that there was a methylated xrs+ gene in these strains which was structurally intact, but not expressed. The xrs strains did not complement one another, and the locus was autosomally located. In view of the frequency of their isolation and their somewhat different phenotypes, we propose that the xrs strains are mutants derived from an active wild-type gene. However, there is in addition a methylated silent gene present in the genome. Azacytidine treatment reactivated this gene. We present a model for the functional hemizygosity of mammalian cell lines, which is based on the inactivation of genes by de novo hypermethylation. In contrast to results with xrs strains, other repair-defective lines were found not to be reverted by azacytidine.},
	number = {8},
	urldate = {2013-09-24},
	journal = {Molecular and Cellular Biology},
	author = {Jeggo, P A and Holliday, R},
	month = aug,
	year = {1986},
	note = {{PMID:} 2431295
{PMCID:} {PMC367863}},
	pages = {2944--2949},
	file = {PubMed Central Full Text PDF:C:\Users\t\AppData\Roaming\Zotero\Zotero\Profiles\kqhsfvpb.default\zotero\storage\WBMWN7RP\Jeggo und Holliday - 1986 - Azacytidine-induced reactivation of a DNA repair g.pdf:application/pdf}
}