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.
| Original language | English |
|---|---|
| Pages (from-to) | 503-510 |
| Number of pages | 8 |
| Journal | Oncogene |
| Volume | 17 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 30 Jul 1998 |
| Externally published | Yes |
Keywords
- Chromosomal translocation
- G-CSF receptor
- Leukemia
- cDNA subtraction
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