Lenz Georg
Translational Oncology, Department of Medicine A, Albert-Schweitzer Campus 1, University Hospital Münster, 48149 Münster, Germany.
Cluster of Excellence EXC 1003, Cells in Motion, 48149 Münster, Germany .
Cancers (Basel). 2015 May 22;7(2):811-22. doi: 10.3390/cancers7020812.
Within the last couple of years, the understanding of the molecular mechanisms that drive the pathogenesis of diffuse large B-cell lymphoma (DLBCL) has significantly improved. Large-scale gene expression profiling studies have led to the discovery of several molecularly defined subtypes that are characterized by specific oncogene addictions and significant differences in their outcome. Next generation sequencing efforts combined with RNA interference screens frequently identify crucial oncogenes that lead to constitutive activation of various signaling pathways that drive lymphomagenesis. This review summarizes our current understanding of the molecular pathogenesis of the activated B-cell-like (ABC) DLBCL subtype that is characterized by poor prognosis. A special emphasis is put on findings that might impact therapeutic strategies of affected patients.
在过去几年里,对驱动弥漫性大B细胞淋巴瘤(DLBCL)发病机制的分子机制的理解有了显著提高。大规模基因表达谱研究已导致发现几种分子定义的亚型,其特征是特定的致癌基因成瘾及其预后存在显著差异。下一代测序工作与RNA干扰筛选相结合,经常能识别出关键的致癌基因,这些基因会导致驱动淋巴瘤发生的各种信号通路的组成性激活。本综述总结了我们目前对预后较差的活化B细胞样(ABC)DLBCL亚型分子发病机制的理解。特别强调了可能影响受影响患者治疗策略的研究结果。