Burkitt Lymphoma: Much More than MYC

被引：12

作者：

Dominguez-Sola, David ^{[1
]}

Dalla-Favera, Riccardo ^{[1
]}

机构：

[1] Columbia Univ, Inst Canc Genet, New York, NY 10032 USA

来源：

CANCER CELL | 2012年 / 22卷 / 02期

关键词：

CELLS; GENE; E2A;

D O I：

10.1016/j.ccr.2012.07.018

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.

引用

页码：141 / 142

页数：2

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