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pubmed-article:10626250pubmed:abstractTextGenetic alterations of the BCL-6 gene in mice and man have established BCL-6 as a pivotal regulator of normal differentiation of B and T lymphocytes as well as one of the most frequently translocated oncogenes in human B cell lymphomas. As an oncogene, BCL-6 has not been easy to place into existing paradigms of cellular transformation. Rather, it is likely that the function of BCL-6 as a regulator of lymphocyte differentiation is subverted in BCL-6-induced lymphomas. The lymphomas in which BCL-6 is translocated are all suspected to arise from the germinal center B lymphocyte. Given the selective expression of BCL-6 protein in normal germinal center B lymphocytes and the requirement for BCL-6 in germinal center development, the functions of BCL-6 in normal and malignant B cells are probably intertwined. The BCL-6 protein is a potent transcriptional repressor which presumably controls lymphocyte differentiation and induces lymphomas by regulating the expression of key downstream target genes.lld:pubmed
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pubmed-article:10626250pubmed:articleTitleRegulation of lymphocyte cell fate decisions and lymphomagenesis by BCL-6.lld:pubmed
pubmed-article:10626250pubmed:affiliationMetabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. lstaudt@box-1.nih.govlld:pubmed
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