C/EBPβ suppression by interruption of CUGBP1 resulting from a complex rearrangement of MLL

被引：14

作者：

Choi, William T.

Folsom, Matthew R.

Azim, Mohammed F.

Meyer, Claus

Kowarz, Eric

Marschalek, Rolf

Timchenko, Nikolai A.

Naeem, Rizwan C.

Lee, Dean A.

机构：

[1] Univ Texas, MD Anderson Canc Ctr, Div Pediat, Cell Therapy Sect Pediat Res Unit 853, Houston, TX 77030 USA

[2] Baylor Coll Med, Dept Pediat Hematol, Oncol Sect, Houston, TX 77030 USA

[3] Texas Childrens Hosp, Texas Childrens Canc Ctr, Cytogenet Core Lab, Houston, TX 77030 USA

[4] Univ Frankfurt, Diagnost Ctr Acute Leukemia, Inst Pharmaceut Biol, ZAFES, D-60438 Frankfurt, Germany

[5] Baylor Coll Med, Huffington Ctr Aging, Dept Pathol, Houston, TX 77030 USA

来源：

CANCER GENETICS AND CYTOGENETICS | 2007年 / 177卷 / 02期

关键词：

D O I：

10.1016/j.cancergencyto.2007.07.002

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Translocations involving the mixed-lineage leukemia gene (MLL) confer a poor prognosis in acute leukemias. In t(1;11)(q21;q23) MLL is fused reciprocally with AF1q. Here we describe a t(1: 11)(q21 q23) with a secondary event involving insertion of the telomeric portion of MLL into the p arm of chromosome 11 (11 p 11). We show that this latter event interrupts the CUG triplet repeat binding protein-1 (CUGBP1)gene, a translational enhancer of CIEBP ss. We then showed that these cells have reduced expression of CUGBP1 and C/EBP beta when compared to other AML blasts. This is the first report to describe insertional disruption of the CUGBP1 gene and to suggest a role for the CUGBP1-C/EBP beta pathway in leukemogenesis. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：108 / 114

页数：7

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