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Spi-1 oncogene activation in Rauscher and Friend murine virus-induced acute erythroleukemias.

Abstract
The Friend viruses, like the Rauscher virus, cause murine acute erythroleukemias which evolve in a similar multistep process. In previous studies it has been described that the late malignant proerythroblastic transformation induced by the polycythemia-inducing strain of Friend spleen focus-forming virus (SFFVP) is correlated with Spi-1 oncogene activation by insertional mutagenesis. In this paper we report that Spi-1 genomic rearrangements were also observed in 90% of tumors induced by the anemia-inducing strain of Friend spleen focus-forming virus (SFFVA) and in all Rauscher-induced tumors analyzed. SFFVA and Rauscher proviral insertions occurred in the viral integration cluster previously characterized in SFFVP-induced tumors. The Spi-1 1.4-Kb messenger RNA was found highly expressed in all SFFVA and Rauscher-induced malignant cells as compared to normal tissues. The nucleotide sequence of Spi-1 cDNA isolated from a library constructed from SFFVA-induced tumor cells revealed no difference between the Spi-1 gene transcripts expressed in both SFFVP and SFFVA-induced leukemic cells. These results indicate that Spi-1 gene activation is a general feature in the malignant proerythroblastic transformation which occurs in mice infected with Friend and Rauscher viruses.
AuthorsF Moreau-Gachelin, D Ray, N J de Both, M J van der Feltz, P Tambourin, A Tavitian
JournalLeukemia (Leukemia) Vol. 4 Issue 1 Pg. 20-3 (Jan 1990) ISSN: 0887-6924 [Print] England
PMID2153262 (Publication Type: Journal Article)
Topics
  • Acute Disease
  • Animals
  • Friend murine leukemia virus (genetics)
  • Gene Expression Regulation, Neoplastic
  • Gene Rearrangement
  • Genes, Viral
  • Leukemia Virus, Murine (genetics)
  • Leukemia, Erythroblastic, Acute (genetics)
  • Leukemia, Experimental (genetics)
  • Mice
  • Mice, Inbred DBA
  • Oncogenes
  • Rauscher Virus (genetics)
  • Spleen Focus-Forming Viruses (genetics)
  • Transcription, Genetic
  • Transcriptional Activation
  • Tumor Cells, Cultured

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