Pathology and Cell Biology, Institute for Cancer Genetics, Columbia University, New York City, New York.
Immunol Rev. 2019 Mar;288(1):240-261. doi: 10.1111/imr.12745.
B cell lymphomas comprise a heterogeneous group of genetically, biologically, and clinically distinct neoplasms that, in most cases, originate from the clonal expansion of B cells in the germinal center (GC). In recent years, the advent of novel genomics technologies has revolutionized our understanding of the molecular pathogenesis of lymphoid malignancies as a multistep process that requires the progressive accumulation of multiple genetic and epigenetic alterations. A common theme that emerged from these studies is the ability of lymphoma cells to co-opt the same biological programs and signal transduction networks that operate during the normal GC reaction, and misuse them for their own survival advantage. This review summarizes recent progress in the understanding of the genetic and epigenetic mechanisms that drive the malignant transformation of GC B cells. These insights provide a conceptual framework for the identification of cellular pathways that may be explored for precision medicine approaches.
B 细胞淋巴瘤是一组具有遗传、生物学和临床特征的异质性肿瘤,它们在大多数情况下起源于生发中心(GC)中 B 细胞的克隆性扩增。近年来,新型基因组学技术的出现彻底改变了我们对淋巴样恶性肿瘤的分子发病机制的理解,这种发病机制是一个多步骤的过程,需要逐步积累多种遗传和表观遗传改变。这些研究中出现的一个共同主题是,淋巴瘤细胞能够利用正常 GC 反应中所涉及的相同生物学程序和信号转导网络,并将其滥用于自身的生存优势。本综述总结了近年来对驱动 GC B 细胞恶性转化的遗传和表观遗传机制的理解方面的进展。这些研究成果为确定可能用于精准医疗的细胞途径提供了一个概念框架。