ArticleOncogene2002
Large-scale identification of novel potential disease loci in mouse leukemia applying an improved strategy for cloning common virus integration sites.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 42 citations in OpenAlex.
- Pro-oncogenic potential of NM23-H2 in hepatocellular carcinoma.Experimental & molecular medicine · 2012Article
- Regulation of endoderm formation and left-right asymmetry by miR-92 during early zebrafish development.Development (Cambridge, England) · 2011Article
- Impairment of alternative splice sites defining a novel gammaretroviral exon within gag modifies the oncogenic properties of Akv murine leukemia virus.Retrovirology · 2007Article
- MicroRNAs and genomic instability.Seminars in cancer biology · 2007Review
- Detecting statistically significant common insertion sites in retroviral insertional mutagenesis screens.PLoS computational biology · 2006Article
- Persistent transactivation by meis1 replaces hox function in myeloid leukemogenesis models: evidence for co-occupancy of meis1-pbx and hox-pbx complexes on promoters of leukemia-associated genes.Molecular and cellular biology · 2006Article
- Review
- Radiation leukemia virus common integration at the Kis2 locus: simultaneous overexpression of a novel noncoding RNA and of the proximal Phf6 gene.Journal of virology · 2005Article
- A new common integration site, Int7, for the mouse mammary tumor virus in mouse mammary tumors identifies a gene whose product has furin-like and thrombospondin-like sequences.Journal of virology · 2005Article
- The common viral insertion site Evi12 is located in the 5'-noncoding region of Gnn, a novel gene with enhanced expression in two subclasses of human acute myeloid leukemia.Journal of virology · 2005Article
- High incidence of proviral integrations in the Hoxa locus in a new model of E2a-PBX1-induced B-cell leukemia.Genes & development · 2005Article
- Analysis of wild-type and mutant SL3-3 murine leukemia virus insertions in the c-myc promoter during lymphomagenesis reveals target site hot spots, virus-dependent patterns, and frequent error-prone gap repair.Journal of virology · 2005Article
- Substitution of feline leukemia virus long terminal repeat sequences into murine leukemia virus alters the pattern of insertional activation and identifies new common insertion sites.Journal of virology · 2005Article
- Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Large-scale identification of disease genes involved in acute myeloid leukemia.Journal of virology · 2004Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The identification of common virus integration sites (cVIS) in retrovirally induced tumors in mice provides a powerful strategy to isolate novel transforming genes. Applying virus LTR-specific inverse-PCR and RT-PCR combined with automated sequencing on CasBr-M Murine Leukemia Virus (MuLV) induced myeloid leukemias, 126 virus integration sites were cloned. Using locus- and LTR-specific primers, a nested-PCR/Southern-blotting procedure was developed on genomic DNA from a large panel of MuLV-induced leukemias, to analyse whether a particular virus insertion represented a cVIS. In fact 39 out of 41 integrations analysed this way appeared to represent a common virus integration. We recognized six previously cloned cVISs, i.e. Evi1, Hoxa7, c-Myb, Cb2/Evi11, Evi12, and His1 and 33 novel common insertions, designated Cas-Br Virus Integration Site (Casvis). Among this group we found integrations in or near genes encoding nuclear proteins, e.g. Dnmt-2, Nm23-M2, Ctbp1 or Erg, within receptor genes, e.g. Cb2 or mrc1, novel putative signaling or transporter genes, the ringfinger-protein gene Mid1 and a panel of genes encoding novel proteins with unknown function. The finding that 39 out of 41 integrations analysed represented a cVIS, suggests that the majority of the other virus insertions that were not yet analysed by the PCR/Southern-blotting method are located in a cVIS as well and may therefore also harbor novel disease genes.
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