Histone acetylation and DNA demethylation of B cells result in a Hodgkin-like phenotype

摘要: A unique feature of the tumor cells (Hodgkin/Reed-Sternberg (HRS)) classical Hodgkin lymphoma (cHL) is loss their B-cell phenotype despite origin. Several lines evidence suggest that epigenomic events, especially promoter DNA methylation, are involved in this silencing many B-cell-associated genes. Here, we show demethylation alone or conjunction with histone acetylation not able to reconstitute B-cell-gene expression program cultured HRS cells. Instead, combined and induce an almost complete extinction B-cell-expression a tremendous upregulation numerous Hodgkin-characteristic genes, including key players such as Id2 known be suppression phenotype. Since genes occurred simultaneously, epigenetic changes may also responsible for malignant transformation cHL. The thus plays--in addition hypermethylation genes--a pivotal role reprogramming explains why unable