The novel ETS factor TEL2 cooperates with Myc in B lymphomagenesis

被引：36

作者：

Cardone, M

Kandilci, A

Carella, C

Nilsson, JA

Brennan, JA

Sirma, S

Ozbek, U

Boyd, K

Cleveland, JL

Grosveld, GC

机构：

[1] St Jude Childrens Res Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA

[2] St Jude Childrens Res Hosp, Dept Biochem, Memphis, TN 38105 USA

[3] St Jude Childrens Res Hosp, Anim Resource Ctr, Memphis, TN 38105 USA

[4] Istanbul Univ, Dept Genet, Inst Expt Med, Istanbul, Turkey

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2005年 / 25卷 / 06期

关键词：

D O I：

10.1128/MCB.25.6.2395-2405.2005

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The human ETS family gene TEL2/ETV7 is highly homologous to TELI/ETV6, a frequent target of chromosome translocations in human leukemia and specific solid tumors. Here we report that TEL2 augments the proliferation and survival of normal mouse B cells and dramatically accelerates lymphoma development in Emu-Myc transgenic mice. Nonetheless, inactivation of the p53 pathway was a hallmark of all TEL2/Emu-Myc lymphomas, indicating that TEL2 expression alone is insufficient to bypass this apoptotic checkpoint. Although TEL2 is infrequently up-regulated in human sporadic Burkitt's lymphoma, analysis of pediatric B-cell acute lymphocytic leukemia (B-ALL) samples showed increased coexpression of TEL2 and WC and/or MYCN in over one-third of B-ALL patients. Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies.

引用

页码：2395 / 2405

页数：11

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