TP53 dysfunction in diffuse large B-cell lymphoma

被引:43
作者
Lu, Ting-Xun [1 ,2 ]
Young, Ken H. [3 ]
Xu, Wei [1 ]
Li, Jian-Yong [1 ,4 ]
机构
[1] Nanjing Med Univ, Jiangsu Prov Hosp, Affiliated Hosp 1, Dept Hematol, Nanjing 210029, Jiangsu, Peoples R China
[2] Jiangnan Univ, Dept Oncol, Affiliated Hosp, Wuxi 214062, Jiangsu, Peoples R China
[3] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77072 USA
[4] Nanjing Med Univ, Collaborat Innovat Ctr Canc Personalized Med, Nanjing 210029, Jiangsu, Peoples R China
关键词
TP53; miRNA; Copy number alterations; MDM2; Mutation; MESSENGER-RNA TRANSLATION; TUMOR-SUPPRESSOR P53; GENE-MUTATIONS; POOR SURVIVAL; RISK STRATIFICATION; NEGATIVE REGULATION; RITUXIMAB-CHOP; EXPRESSION; PROTEIN; PATHWAY;
D O I
10.1016/j.critrevonc.2015.08.006
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The aberrations of TP53 gene and dysregulation of the TP53 pathway are important in the pathogenesis of many human cancers, including malignant lymphomas, especially for diffuse large B cell lymphoma (DLBCL). By regulating many downstream target genes or molecules, TP53 governs major defenses against tumor growth and promotes cellular DNA repair, apoptosis, autophagy, cell cycle arrest, signaling, transcription, immune or inflammatory responses and metabolism. Dysfunction of TP53, including microRNA regulations, copy number alterations of TP53 pathway and TP53 itself, dysregulation of TP53 regulators, and somatic mutations by abnormal TP53 function modes, play an important role in lymphoma generation, progression and invasion. The role of TP53 in DLBCL has been widely explored recently. In this review, we summarized recent advances on different mechanisms of TP53 in DLBCL and new therapeutic approaches to overcome TP53 inactivation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:47 / 55
页数:9
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