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J. Exp. Med.,
Volume 189, Number 3, February 1, 1999 501-508
By
From the * Department of Cell Biology and the Two models have been proposed for the molecular mechanism by which the Tal1 oncogene
causes T cell acute lymphoblastic leukemia (T-ALL). The activation model suggests that Tal1
as heterodimers with the E2A transcription factor activates the expression of oncogenes. The
inhibition model postulates that Tal1 interferes with the tumor-suppressing function of E2A. In
the Jurkat T cell line, originally derived from a patient with T-ALL, Tal1 is complexed with
E2A proteins and the transcriptional activity of E2A is very low. When E2A activity was restored by expressing an E2A-Tal1 fusion protein, E-T/2, the Jurkat cells underwent growth
arrest and subsequently apoptosis, thus supporting the inhibition model and suggesting that
E2A loss may contribute to leukemic progression.
Department of Cell Biology and Kaplan Cancer
Center, New York University Medical Center, New York 10016; and the § Department of Molecular
Pharmacology and Department of Microbiology and Immunology, Stanford University School of
Medicine, Stanford, California 94305
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