ArticleThe Journal of experimental medicine1993
Suppressible and nonsuppressible autocrine mast cell tumors are distinguished by insertion of an endogenous retroviral element (IAP) into the interleukin 3 gene.
Article in The Journal of experimental medicine, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Rate of recombinational deletion among human endogenous retroviruses.Journal of virology · 2007Article
- Isolation and characterization of dominant and recessive IL-3-independent hematopoietic transformants.Oncogene · 2006Article
- A GFP-based assay for rapid screening of compounds affecting ARE-dependent mRNA turnover.Nucleic acids research · 2004Article
- Global analysis of differential gene expression after transformation with the v-H-ras oncogene in a murine tumor model.Oncogene · 2001Article
- Somatic mRNA turnover mutants implicate tristetraprolin in the interleukin-3 mRNA degradation pathway.Molecular and cellular biology · 2000Article
- Article
- Cyclosporin A promotes translational silencing of autocrine interleukin-3 via ribosome-associated deadenylation.Molecular and cellular biology · 1999Article
- c-jun N-terminal kinase is involved in AUUUA-mediated interleukin-3 mRNA turnover in mast cells.The EMBO journal · 1998Article
- Rapamycin destabilizes interleukin-3 mRNA in autocrine tumor cells by a mechanism requiring an intact 3' untranslated region.Molecular and cellular biology · 1997Article
- Direct identification of differentially expressed genes by cycle sequencing and cycle labelling using the differential display PCR primers.Nucleic acids research · 1997Article
- Recurrent T cell receptor rearrangements in the cytotoxic T lymphocyte response in vivo against the p815 murine tumor.The Journal of experimental medicine · 1996Article
- AUH, a gene encoding an AU-specific RNA binding protein with intrinsic enoyl-CoA hydratase activity.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
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3 authors.
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Abstract
After v-H-ras expression, the interleukin 3 (IL-3)-dependent PB-3c mast cells progress in vivo to two different classes of IL-3 autocrine tumors. Class I tumors show a germline configuration of the IL-3 gene and represent more than 90% of tumors analyzed so far. Somatic cell fusion of class I tumor lines with the nontumorigenic parental PB-3c resulted in loss of oncogenic IL-3 expression by a posttranscriptional mechanism with concomitant tumor suppression. Class II tumors arise rarely and contain an insertion in one IL-3 allele. This alteration was linked to enhanced IL-3 gene transcription. For one tumor, the insertion was shown to be an endogenous retroviral element (intracisternal A-particle). Cell hybrids of class II tumors with PB-3c remained IL-3 independent, expressed IL-3, and formed tumors rapidly. These results suggest that the v-H-ras oncogene synergizes with a recessive and a dominant lesion in class I and II tumors, respectively, both of which lead to the autocrine production of IL-3.
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