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Titlebook: DNA Methylation and Cancer Therapy; Moshe Szyf Book 2005 Springer-Verlag US 2005 DNA.Expression.Microarray.Purine.enzymes.gene expression.

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https://doi.org/10.1007/978-3-642-24996-9ibition of the poly(ADP-ribosyl)ation process in the cell may be responsible for the anomalous hypermethylation of oncosuppressor gene promoters during tumorigenesis and to suggest the possibility that an active poly(ADP-ribosyl)ation process is also involved in maintaining the unmethylated state of
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Oliver Marchart,Wolfgang Heuer,Thomas Meyers in understanding the relation between chromatin and DNA methylation have provided some insights into the mechanisms that tie these processes to each other. It is clear that DNA methy-lation has to be understood within its chromatin context and aberrations in DNA methylation must be understood in r
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Epigenetic Mechanisms of Gene Regulation, tail modifications and chromatin remodeling, directly determine which regions of the genome are to be methylated. By studying these mechanisms in detail we should be able gain insights into how DNA methylation patterns become disrupted in tumor cells and how these defects may be corrected.
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DNA Hypo- vs. Hypermethylation in Cancer,ypermethylation. Because of this finding and the very frequent targeting of DNA sequences for this hypomethylation in diverse cancers, genomic hypomethylation is likely to contribute to carcinogenesis and not to be just a byproduct of oncogenic transformation. Therefore, caution should be used in de
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The Loss of Methyl Groups in DNA of Tumor Cells and Tissues,ucleases and reverse phase high pressure liquid chromatography analysis. The development of gene-specific hybridization techniques together with the availability of an ever-increasing number of methylation-sensitive restriction enzymes allowed the methylation status of numerous genes to be investiga
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