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.
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1 February 1999
Article|
February 01 1999
Growth Inhibition and Apoptosis Due to Restoration of E2A Activity in T Cell Acute Lymphoblastic Leukemia Cells
Steven T. Park,
Steven T. Park
From the *Department of Cell Biology and the ‡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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Garry P. Nolan,
Garry P. Nolan
From the *Department of Cell Biology and the ‡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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Xiao-Hong Sun
Xiao-Hong Sun
From the *Department of Cell Biology and the ‡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
Search for other works by this author on:
Steven T. Park
From the *Department of Cell Biology and the ‡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
Garry P. Nolan
From the *Department of Cell Biology and the ‡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
Xiao-Hong Sun
From the *Department of Cell Biology and the ‡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
Address correspondence to Xiao-Hong Sun, Department of Cell Biology and Kaplan Cancer Center, New York University Medical Center, 550 First Ave., New York, NY 10016. Phone: 212-263-6916; Fax: 212-263-8139; E-mail: [email protected]
Received:
July 17 1998
Revision Received:
October 18 1998
Online ISSN: 1540-9538
Print ISSN: 0022-1007
1999
J Exp Med (1999) 189 (3): 501–508.
Article history
Received:
July 17 1998
Revision Received:
October 18 1998
Citation
Steven T. Park, Garry P. Nolan, Xiao-Hong Sun; Growth Inhibition and Apoptosis Due to Restoration of E2A Activity in T Cell Acute Lymphoblastic Leukemia Cells . J Exp Med 1 February 1999; 189 (3): 501–508. doi: https://doi.org/10.1084/jem.189.3.501
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