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Molecular and Cellular Biology, March 2005, p. 2395-2405, Vol. 25, No. 6
0270-7306/05/$08.00+0 doi:10.1128/MCB.25.6.2395-2405.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Departments of Genetics and Tumor Cell Biology,1 Biochemistry,2 Animal Resource Center, St. Jude Children's Research Hospital, Memphis, Tennessee,4 Department of Genetics, Institute for Experimental Medicine, Istanbul University, Istanbul, Turkey3
Received 22 September 2004/ Returned for modification 24 November 2004/ Accepted 13 December 2004
The human ETS family gene TEL2/ETV7 is highly homologous to TEL1/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 Eµ-Myc transgenic mice. Nonetheless, inactivation of the p53 pathway was a hallmark of all TEL2/Eµ-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 MYC 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.
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