Reprogramming of the tumour B-cell phenotype in Hodgkin lymphoma.
Hodgkin and Reed-Sternberg (HRS) cells, the tumour cells in classical Hodgkin lymphoma, derive from mature B cells but have largely lost their B-cell phenotype. This extensive reprogramming is unique among B-cell lymphomas. A recent study by Dörken and colleagues provides an interesting insight into the mechanisms for this reprogramming by demonstrating that the key B-cell-determining transcription factor E2A is inhibited in HRS cells by the deregulated expression of its inhibitors activated B-cell factor (ABF)-1 and inhibitor of differentiation and DNA binding (Id)2.
Küppers
Ralf
R
Institute for Cell Biology (Tumor Research), University of Duisburg-Essen, Medical School, 45122 Essen, Germany. ralf.kuppers@uni-essen.de
Bräuninger
Andreas
A
D002454:Cell Differentiation; D006689:Hodgkin Disease / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D015448:Leukemia, B-Cell / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D010641:Phenotype; D016539:Reed-Sternberg Cells / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
D014157:Transcription Factors