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 Blood, 1 February 2006, Vol. 107, No. 3, pp. 1124-1132.
Prepublished online as a Blood First Edition Paper on October 18, 2005; DOI 10.1182/blood-2005-03-1196.

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Submitted March 24, 2005
Accepted September 20, 2005

The ETS factor TEL2 is a hematopoietic onco-protein

Cintia Carella, Mark Potter, Jacqueline Bonten, Jerold E Rehg, Geoffrey Neale, and Gerard C Grosveld*

Department of Genetics/Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN, USA
Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA
Hartwell Center, St. Jude Children's Research Hospital, Memphis, TN, USA

* Corresponding author; email: gerard.grosveld{at}stjude.org.

TEL2/ETV7 is highly homologous to the ETS transcription factor TEL/ETV6, a frequent target of chromosome translocation in human leukemia. Although both proteins are transcriptional inhibitors binding similar DNA recognition sequences, they have opposite biological effects; TEL inhibits proliferation while TEL2 promotes it. In addition, forced expression of TEL2 but not TEL blocks vitamin D3-induced differentiation of U937 and HL60 myeloid cells. TEL2 is expressed in the hematopoietic system and its expression is upregulated in bone marrow samples of some leukemia patients, suggesting a role in oncogenesis. Recently we also showed that TEL2 cooperates with Myc in B-lymphomagenesis in mice. Here we show that forced expression of TEL2 alone in mouse bone marrow causes a myeloproliferative disease with a long latency period but with high penetrance. This suggested that secondary mutations are necessary for disease development. Treating mice transplanted with TEL2 expressing bone marrow with the chemical carcinogen N-Ethyl-N-nitrosourea (ENU) resulted in significantly accelerated disease onset. Although the mice developed a GFP+ myeloid disease with 30% of the mice showing elevated white blood counts, they all died of T cell lymphoma, which was GFP-. Together our data identify TEL2 as a bona fide oncogene but leukemic transformation is dependent on secondary mutations.


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A. Kandilci and G. C. Grosveld
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