TitleBreaking bad in the germinal center: how deregulation of BCL6 contributes to lymphomagenesis.
Publication TypeJournal Article
Year of Publication2014
AuthorsHatzi, Katerina, and Melnick Ari
JournalTrends Mol Med
Date Published2014 Jun
KeywordsCell Survival, DNA-Binding Proteins, Enhancer Elements, Genetic, Epigenesis, Genetic, Gene Expression Regulation, Gene Expression Regulation, Neoplastic, Humans, Immune System, Lymphoma, B-Cell, Molecular Targeted Therapy, Promoter Regions, Genetic, Proto-Oncogene Proteins c-bcl-6

<p>The B cell lymphoma 6 (BCL6) transcriptional repressor is a master regulator of the germinal center (GC) B cell program, required for their unique proliferative and stress tolerant phenotype. Most B cell lymphomas arise from GC B cells and are dependent on the continued or deregulated expression of BCL6 to maintain their survival. The actions of BCL6 in B cells involve formation of distinct chromatin modifying complexes that silence specific promoter and enhancer networks, respectively. The same biochemical mechanisms are maintained in malignant lymphoma cells. Targeted inhibition of these BCL6 functions has emerged as the basis for rational design of lymphoma therapies and combinatorial regimens. In this review, we summarize recent advances on BCL6 mechanisms of action and the deregulation of its target gene networks in lymphoma.</p>

Alternate JournalTrends Mol Med
PubMed ID24698494
PubMed Central IDPMC4041810
Grant ListR01 CA104348 / CA / NCI NIH HHS / United States
R01 CA143032 / CA / NCI NIH HHS / United States