Abstract |
Approximately 25-30% of childhood pre-B cell acute lymphoblastic leukemias ( pre-B ALL) is characterized by the presence of a (1;19)(q23;p13.3) translocation. The presence of this translocation is generally accompanied by a poor prognosis. The chimeric gene resulting from this chromosomal rearrangement encodes a hybrid transcription factor, E2A-Pbx1. In an attempt to delineate the genetic cascade initiated by E2A-Pbx1, we sought to identify genes that are deregulated by this transcription factor in t(1;19) pre-B ALL. We show here that the gene encoding the granulocyte colony-stimulating factor receptor (G-CSFr) is specifically upregulated in pre-B cells expressing E2A-Pbx1. G-CSFr is also expressed in cell lines established from t(1;19) pre-B cell leukemia and on primary t(1;19) tumor cells, but not on control cells. These data indicate that G-CSFr gene is a target for deregulation by E2A-Pbx1.
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Authors | W B de Lau, J Hurenkamp, P Berendes, I P Touw, H C Clevers, M A van Dijk |
Journal | Oncogene
(Oncogene)
Vol. 17
Issue 4
Pg. 503-10
(Jul 30 1998)
ISSN: 0950-9232 [Print] England |
PMID | 9696044
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Homeodomain Proteins
- Oncogene Proteins, Fusion
- Receptors, Granulocyte Colony-Stimulating Factor
- E2A-Pbx1 fusion protein
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Topics |
- B-Lymphocytes
- Burkitt Lymphoma
(genetics, metabolism)
- Chromosomes, Human, Pair 1
- Chromosomes, Human, Pair 19
- Gene Expression Regulation
- Hematopoietic Stem Cells
- Homeodomain Proteins
(genetics, metabolism)
- Humans
- Oncogene Proteins, Fusion
(genetics, metabolism)
- Receptors, Granulocyte Colony-Stimulating Factor
(genetics, physiology)
- Translocation, Genetic
- Tumor Cells, Cultured
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