GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE8nnn/GSE8388/primaryOK2000000GenomicsHomo sapiensExpression profiling by arrayhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE8388GEOGSE0falseEpigenetic upregulation of B-cell inappropriate genes induces extinction of B-cell program in classical Hodgkin lymphomaA unique feature of the tumour 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 cells induce a nearly complete extinction of their B-cell expression program and a tremendous up-regulation of numerous cHL characteristic genes including key players such as Id2 known to be involved in the suppression of the B-cell phenotype. Since the up-regulation of cHL 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 up-regulation of cHL characteristic genes thus play - in addition to promoter DNA-hypermethylation of B-cell associated genes – a pivotal role for the reprogramming of HRS cells and explain why DNA-demethylation alone is unable to reconstitute the B-cell expression program in HRS cells. Keywords: Epigenetic modification2007/11/01GSE8388GSM207639GSM207635GSM207636GSM207637GSM207638GSM207587GSM207642GSM207588GSM207577GSM207643GSM207644GSM207578GSM207645GSM207568GSM207634GSM207579GSM207583GSM207584GSM207585GSM207640GSM207641GSM207586GSM207581GSM207582968388Homo sapiens[18256685]