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• W2158207797 endingPage "R59" @default.
• W2158207797 startingPage "R50" @default.
• W2158207797 abstract "Epigenetic gene inactivation in transformed cells involves many 'belts of silencing'. One of the best-known lesions of the malignant cell is the transcriptional repression of tumor-suppressor genes by promoter CpG island hypermethylation. We are in the process of completing the molecular dissection of the entire epigenetic machinery involved in methylation-associated silencing, such as DNA methyltransferases, methyl-CpG binding domain proteins, histone deacetylases, histone methyltransferases, histone demethylases and Polycomb proteins. The first indications are also starting to emerge about how the combination of cellular selection and targeted pathways leads to abnormal DNA methylation. One thing is certain already, promoter CpG island hypermethylation of tumor-suppressor genes is a common hallmark of all human cancers. It affects all cellular pathways with a tumor-type specific profile, and in addition to classical tumor-suppressor and DNA repair genes, it includes genes involved in premature aging and microRNAs with growth inhibitory functions. The importance of hypermethylation events is already in evidence at the bedside of cancer patients in the form of cancer detection markers and chemotherapy predictors, and in the approval of epigenetic drugs for the treatment of hematological malignancies. In the very near future, the synergy of candidate gene approaches and large-scale epigenomic technologies, such as methyl-DIP, will yield the complete DNA hypermethylome of cancer cells." @default.
• W2158207797 created "2016-06-24" @default.
• W2158207797 creator A5010137759 @default.
• W2158207797 date "2007-04-15" @default.
• W2158207797 modified "2023-10-02" @default.
• W2158207797 title "Epigenetic gene silencing in cancer: the DNA hypermethylome" @default.
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• W2158207797 doi "https://doi.org/10.1093/hmg/ddm018" @default.

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