The human TEL gene is a new member of the ETS family of transcription factors which is involved in several 12p13 chromosomal abnormalities present in various human hematological malignancies. The most frequent is the t(12;21)(p13;q22), specific for childhood acute lymphoblastic leukemia, which fuses two genes, TEL and AML1, that have previously been shown to be independently involved in myeloid malignant proliferations.

TEL proteins are nuclear and display specific DNA binding activity toward classical ETS binding sites. In addition, we show that TEL mRNAs initiate translation at either of the two first in-frame ATGs (codon 1 and 43) to encode 50 kDa and 57 kDa TEL proteins. In vivo, each of these primary translational products is modified by multiple phosphorylation events.

We also show that a 65 aminoacids NH2 subdomain of TEL possesses homotypic oligomerization properties that seem essential for oncogenic potencies of several oncoprotein harbouring this motif.