Notch1-dependent lymphomagenesis is assisted by but does not essentially require pre-TCR signaling
Author:
Affiliation:
1. From Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA; the Department of Experimental Medicine and Pathology, University “La Sapienza,” Rome, Italy; and the Institute for Research in Biomedicine, Bellinzona, Switzerland.
Abstract
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Link
http://ashpublications.org/blood/article-pdf/108/1/305/470283/zh801306000305.pdf
Reference21 articles.
1. Ellisen LW, Bird J, West DC, et al. TAN-1, the human homolog of the Drosophila notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms. Cell. 1991;66: 649-661.
2. Weng AP, Ferrando AA, Lee W, et al. Activating mutations of NOTCH1 in human T cell acute lymphoblastic leukemia. Science. 2004;306: 269-271.
3. Pear WS, Aster JC, Scott ML, et al. Exclusive development of T cell neoplasms in mice transplanted with bone marrow expressing activated Notch alleles. J Exp Med. 1996;183: 2283-2291.
4. Allman D, Karnell FG, Punt JA, et al. Separation of Notch1 promoted lineage commitment and expansion/transformation in developing T cells. J Exp Med. 2001;194: 99-106.
5. Wolfer A, Wilson A, Nemir M, MacDonald HR, Radtke F. Inactivation of Notch1 impairs VDJ-β rearrangement and allows pre-TCR-independent survival of early alpha beta lineage thymocytes. Immunity. 2002;16: 869-879.
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