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• W1971291818 abstract "A unique feature of the tumor cells (Hodgkin/Reed-Sternberg (HRS)) of classical Hodgkin lymphoma (cHL) is the loss of their B-cell phenotype despite their B-cell origin. Several lines of evidence suggest that epigenomic events, especially promoter DNA methylation, are involved in this silencing of many B-cell-associated genes. Here, we show that DNA demethylation alone or in conjunction with histone acetylation is not able to reconstitute the B-cell-gene expression program in cultured HRS cells. Instead, combined DNA demethylation and histone acetylation of B-cell lines induce an almost complete extinction of their B-cell-expression program and a tremendous upregulation of numerous Hodgkin-characteristic genes, including key players such as Id2 known to be involved in the suppression of the B-cell phenotype. Since the upregulation of Hodgkin-characteristic genes and the extinction of the B-cell-expression program occurred simultaneously, epigenetic changes may also be responsible for the malignant transformation of cHL. The epigenetic upregulation of Hodgkin-characteristic genes thus plays--in addition to promoter DNA hypermethylation of B-cell-associated genes--a pivotal role for the reprogramming of HRS cells and explains why DNA demethylation alone is unable to reconstitute the B-cell-expression program in HRS cells." @default.
• W1971291818 created "2016-06-24" @default.
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• W1971291818 date "2008-02-07" @default.
• W1971291818 modified "2023-10-15" @default.
• W1971291818 title "Histone acetylation and DNA demethylation of B cells result in a Hodgkin-like phenotype" @default.
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• W1971291818 doi "https://doi.org/10.1038/leu.2008.12" @default.
• W1971291818 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18256685" @default.
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