生发中心的“恶变”：BCL6失调如何促成淋巴瘤发生。
Breaking bad in the germinal center: how deregulation of BCL6 contributes to lymphomagenesis.
作者信息
Hatzi Katerina, Melnick Ari
机构信息
Division of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.
Division of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY 10065, USA; Department of Pharmacology, Weill Cornell Medical College, New York, NY 10065, USA.
出版信息
Trends Mol Med. 2014 Jun;20(6):343-52. doi: 10.1016/j.molmed.2014.03.001. Epub 2014 Mar 31.
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.
B细胞淋巴瘤6（BCL6）转录抑制因子是生发中心（GC）B细胞程序的主要调节因子，对于其独特的增殖和应激耐受表型是必需的。大多数B细胞淋巴瘤起源于GC B细胞，并且依赖于BCL6的持续或失调表达来维持其存活。BCL6在B细胞中的作用涉及形成分别使特定启动子和增强子网络沉默的不同染色质修饰复合物。这些相同的生化机制在恶性淋巴瘤细胞中得以维持。对这些BCL6功能的靶向抑制已成为淋巴瘤治疗和联合方案合理设计的基础。在本综述中，我们总结了BCL6作用机制及其在淋巴瘤中靶基因网络失调方面的最新进展。
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