Insights into the Molecular Pathogenesis of Activated B-Cell-like Diffuse Large B-Cell Lymphoma and Its Therapeutic Implications

被引:21
|
作者
Lenz, Georg [1 ,2 ]
机构
[1] Univ Hosp Munster, Dept Med A, Translat Oncol, Albert Schweitzer Campus 1, D-48149 Munster, Germany
[2] Cluster Excellence EXC 1003, Cells Mot, D-48149 Munster, Germany
来源
CANCERS | 2015年 / 7卷 / 02期
基金
瑞士国家科学基金会;
关键词
ABC DLBCL; NF-kappa B pathway; B-cell receptor signaling; molecular targets; NF-KAPPA-B; GENE-EXPRESSION; MALT1; PROTEASE; ABC-DLBCL; HODGKIN LYMPHOMA; IN-VITRO; SURVIVAL; INHIBITION; SUBGROUPS; INACTIVATION;
D O I
10.3390/cancers7020812
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:811 / 822
页数:12
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