ArticleJournal of virology1995
Retroviral integration at the Evi-2 locus in BXH-2 myeloid leukemia cell lines disrupts Nf1 expression without changes in steady-state Ras-GTP levels.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 64 citations in OpenAlex.
- Assessment of Ecotropic Viral Integration Site 2B (EVI2B) Gene in Juvenile Myelomonocytic Leukemia and Neurofibromatosis Type 1 NF1 Tumors.Biochemical genetics · 2024Article
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- Somatic mutations in murine models of leukemia and lymphoma: Disease specificity and clinical relevance.Genes, chromosomes & cancer · 2017Article
- Up-regulation of ribosomal genes is associated with a poor response to azacitidine in myelodysplasia and related neoplasms.International journal of hematology · 2016Article
- Synthesis and antileukemic activities of C1-C10-modified parthenolide analogues.Bioorganic & medicinal chemistry · 2015Article
- Using RNA-seq and targeted nucleases to identify mechanisms of drug resistance in acute myeloid leukemia.Scientific reports · 2014Article
- Cellular intrinsic mechanism affecting the outcome of AML treated with Ara-C in a syngeneic mouse model.PloS one · 2014Article
- Review
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- Genetically engineered mouse models in cancer research.Advances in cancer research · 2010Review
- High-throughput insertional mutagenesis screens in mice to identify oncogenic networks.Nature reviews. Cancer · 2009Review
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- The GAP-related domain of neurofibromin attenuates proliferation and downregulates N- and K-Ras activation in Nf1-negative AML cells.Leukemia research · 2007Article
- A microarray study of altered gene expression after cytarabine resistance in acute myeloid leukemia.Leukemia · 2007Article
- Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations.Leukemia · 2006Article
- Nfl gene inactivation in acute myeloid leukemia cells confers cytarabine resistance through MAPK and mTOR pathways.Leukemia · 2006Article
- Review
- Article
- A Moloney murine leukemia virus-based retrovirus with 4070A long terminal repeat sequences induces a high incidence of myeloid as well as lymphoid neoplasms.Journal of virology · 2003Article
- Retroviral integration at the Epi1 locus cooperates with Nf1 gene loss in the progression to acute myeloid leukemia.Journal of virology · 2001Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Approximately 15% of BXH-2 myeloid leukemias harbor proviral integrations at the Evi-2 common viral integration site. Evi-2 is located within a large intron of the Nf1 tumor suppressor gene, raising the possibility that proviral integration at Evi-2 predisposes mice to myeloid tumor development by disrupting Nf1 expression. This hypothesis is supported by data suggesting that mutations in the human NF1 gene are causally associated with the development of juvenile chronic myelogenous leukemia (K. M. Shannon, P. O'Connell, G. A. Martin, D. Paderanga, K. Olson, P. Dinndorf, and F. McCormick, N. Engl. J. Med. 330:597-601, 1994) and mouse studies showing that aged mice, heterozygous for a germ line Nf1 mutation, develop myeloid leukemia with loss of the wild-type Nf1 allele (T. Jacks, T. S. Shih, E. M. Schmitt, R. T. Bronson, A. Bernards, and R. A. Weinberg, Nat. Genet. 7:353-361, 1994). To determine if viral integration at Evi-2 disrupts Nf1 expression, we derived a series of BXH-2 myeloid leukemia cell lines with or without viral integrations at Evi-2. In all cell lines examined, viral integration at Evi-2 resulted in the production of only truncated Nf1 transcripts and no stable, full-length neurofibromin. Although neurofibromin is a GTPase-activating protein (GAP) for p21ras proteins, its loss in the BXH-2 leukemic cell lines was not correlated with an increased steady-state level of p21ras bound to GTP. These data suggest that neurofibromin is not the sole mediator of Ras-GAP activity in myeloid cells and may have a GAP-independent function in myeloid cells.
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