Large-scale identification of novel potential disease loci in mouse leukemia applying an improved strategy for cloning common virus integration sites

Joosten, Marieke; Vankan-Berkhoudt, Yolanda; Tas, Maarten; Lunghi, Monja; Jenniskens, Y.M. Bastiaansen; Parganas, Evan; Valk, Peter J.M.; Löwenberg, Bob; Akker, Eric van den; Delwel, Ruud

doi:10.1038/sj.onc.1205813

Cited by 38 publications

(24 citation statements)

References 35 publications

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“…11 and located 176 kb downstream of Nf1 (neurofibromatosis 1) is mmu-miR-193 which can be found in a cluster with four other miRNAs. Retroviral integration into Nf1 principally results in myeloid tumors [75,76,79,80]. The mmu-miRNA-142 is also found further distal on chr.…”

Section: Mouse Mirnas and Genomic Locationmentioning

confidence: 88%

MicroRNAs and genomic instability

Hüppi

Volfovsky

Mackiewicz

et al. 2007

Seminars in Cancer Biology

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A new species of non-coding RNA, microRNAs (miRNAs) has been identified that may regulate the expression of as many as one third to one half of all protein encoding genes. MicroRNAs are found throughout mammalian genomes, but an association between the location of these miRNAs and regions of genomic instability (or fragile sites) in humans has been suggested [1]. In this review we discuss the possible role of altered miRNA expression on human cancer and conduct an analysis correlating the physical location of murine miRNAs with sites of genetic alteration in mouse models of cancer.

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Section: Mouse Mirnas and Genomic Locationmentioning

confidence: 88%

MicroRNAs and genomic instability

Hüppi

Volfovsky

Mackiewicz

et al. 2007

Seminars in Cancer Biology

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“…An additional advantage of RIM is that the proviral sequence serves as a tag to identify flanking genes. The power of RIM is best exemplified by recent reports identifying Ͼ2,000 tags associated with hematologic malignancies in the mouse (11)(12)(13). Interestingly, in mice carrying oncogenes associated with lymphomagenesis, including CD2-myc (14), E2A-PBX1 (15), Pim1 and Pim2 (16), Cdkn1b (encoding p27 Kip1 ) (17), and Cdkn2a (18), RIM studies have allowed the identification of genes that synergize with defined genetic alterations in cancer development.…”

mentioning

confidence: 97%

Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia

Castilla

Perrat

Martínez

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

117

110

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Acute myeloid leukemia subtype M4 with eosinophilia is associated with a chromosome 16 inversion that creates a fusion gene CBFB-MYH11. We have previously shown that CBFB-MYH11 is necessary but not sufficient for leukemogenesis. Here, we report the identification of genes that specifically cooperate with CBFB-MYH11 in leukemogenesis. Neonatal injection of Cbfb-MYH11 knock-in chimeric mice with retrovirus 4070A led to the development of acute myeloid leukemia in 2-5 months. Each leukemia sample contained one or a few viral insertions, suggesting that alteration of one gene could be sufficient to synergize with Cbfb-MYH11. The chromosomal position of 67 independent retroviral insertion sites (RISs) was determined, and 90% of the RISs mapped within 10 kb of a flanking gene. In total, 54 candidate genes were identified; six of them were common insertion sites (CISs). CIS genes included members of a zinc finger transcription factors family, Plag1 and Plagl2, with eight and two independent insertions, respectively. CIS genes also included Runx2, Myb, H2-T24, and D6Mm5e. Comparison of the remaining 48 genes with single insertion sites with known leukemia-associated RISs indicated that 18 coincide with known RISs. To our knowledge, this retroviral genetic screen is the first to identify genes that cooperate with a fusion gene important for human myeloid leukemia.

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“…Improvements in techniques for insert cloning and sequencing has enabled studies which clone hundreds of insertion sites (Li et al, 1999;Hansen et al, 2000;Hwang et al, 2002;Joosten et al, 2002;Johansson et al, 2004;Suzuki et al, 2002;Mikkers et al, 2002a, b). Mapping larger numbers of insertions is best handled by applications that have been optimized for finding high-quality matches for large numbers of sequences relatively rapidly such as BLAT (Kent, 2002) or SSAHA (Ning et al, 2001).…”

Section: Mapping and Analysismentioning

confidence: 99%

Retroviral insertional mutagenesis: past, present and future

et al. 2005

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Retroviral insertion mutagenesis screens in mice are powerful tools for efficient identification of oncogenic mutations in an in vivo setting. Many oncogenes identified in these screens have also been shown to play a causal role in the development of human cancers. Sequencing and annotation of the mouse genome, along with recent improvements in insertion site cloning has greatly facilitated identification of oncogenic events in retrovirus-induced tumours. In this review, we discuss the features of retroviral insertion mutagenesis screens, covering the mechanisms by which retroviral insertions mutate cellular genes, the practical aspects of insertion site cloning, the identification and analysis of common insertion sites, and finally we address the potential for use of somatic insertional mutagens in the study of nonhaematopoietic and nonmammary tumour types.

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Large-scale identification of novel potential disease loci in mouse leukemia applying an improved strategy for cloning common virus integration sites

Cited by 38 publications

References 35 publications

MicroRNAs and genomic instability

MicroRNAs and genomic instability

Identification of genes that synergize with Cbfb-MYH11 in the pathogenesis of acute myeloid leukemia

Retroviral insertional mutagenesis: past, present and future

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