| First Author | Chretien S | Year | 1994 |
| Journal | Blood | Volume | 83 |
| Issue | 7 | Pages | 1813-21 |
| PubMed ID | 8142650 | Mgi Jnum | J:17433 |
| Mgi Id | MGI:65471 | Doi | 10.1182/blood.v83.7.1813.1813 |
| Citation | Chretien S, et al. (1994) Putative oncogenic role of the erythropoietin receptor in murine and human erythroleukemia cells. Blood 83(7):1813-21 |
| abstractText | To determine whether the erythropoietin receptor (Epo-R) plays a role in the course of malignant erythropoietic disorders, this gene was studied in murine and human erythroleukemia cells. An altered Epo-R gene was found in a murine Friend erythroleukemia cell line, FCL1, due to a spleen focus-forming virus (SFFV) long terminal repeat insertion within the noncoding region of the first exon, leading to Epo-R mRNA overexpression. A similar mechanism of Epo-R activation has previously been described in the T3CL-2 Friend erythroleukemia cell line. An elevated number of Epo-binding sites has been observed in two human erythroleukemia cell lines, TF-1 and UT7. In UT7 cells, homogeneously staining region of the short arm of chromosome 19 [hsr (19)] was evidenced, which contained an amplification of the Epo-R gene. This Epo-R gene amplification was confirmed by the quantification of Southern blots in which the intensity of the Epo-R signal was compared in UT7 DNA and in DNA from normal cells. The Epo-R gene was present in UT7 at a mean number of seven to eight copies per cell. Interestingly, the Epo-R gene was rearranged; the breakpoint region was located near the 3' end of the gene, 3 kb downstream from the end of the last exon. Taken together, these results suggest that, in both murine and human systems, genetic alterations of the Epo-R gene are not rare events and could be involved in the occurrence of the erythroleukemic process. |
