Genome-wide retroviral insertional tagging of genes involved in cancer in Cdkn2a-deficient mice

We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a −/− mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with...

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Veröffentlicht in:	Nature genetics Jg. 32; H. 1; S. 160 - 165
Hauptverfasser:	Lund, Anders H., Turner, Geoffrey, Trubetskoy, Alla, Verhoeven, Els, Wientjens, Ellen, Hulsman, Danielle, Russell, Robert, DePinho, Ronald A., Lenz, Jack, van Lohuizen, Maarten
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	New York Nature Publishing Group US 01.09.2002 Nature Publishing Group
Schlagworte:	Agriculture Animal Genetics and Genomics Animals Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Cancer Research Cell Transformation, Neoplastic Cells, Cultured Chromosome Mapping Classical genetics, quantitative genetics, hybrids Collaboration Complications and side effects Cyclin-Dependent Kinase Inhibitor p16 - deficiency Cyclin-Dependent Kinase Inhibitor p16 - genetics Diagnosis Fundamental and applied biological sciences. Psychology Gene expression Gene Function Gene loci Gene mutations Genetic aspects Genetics Genetics of eukaryotes. Biological and molecular evolution Genome Genomes Genomics Health aspects Human Genetics Humans Infections Kinases letter Leukemia Lymphoma Lymphoma - genetics Mice Molecular Sequence Data Moloney murine leukemia virus Moloney murine leukemia virus - genetics Mutagenesis Mutagenesis, Insertional Neoplasms - genetics Proviruses - genetics Retrovirus Risk factors Sarcoma Spleen Tumorigenesis Tumors Vertebrata Netherlands United States > US Vertebrata Mammalia Gene Mouse Rodentia Tagging Malignant tumor Genome
ISSN:	1061-4036, 1546-1718
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Abstract	We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a −/− mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with loss of the Cdkn2a -encoded tumor suppressors p16INK4a and p19ARF. Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors. We isolated 747 unique sequences flanking retroviral integration sites and mapped them against the mouse genome sequence databases from Celera and Ensembl. In addition to 17 insertions targeting gene loci known to be cancer-related, we identified a total of 37 new common insertion sites (CISs), of which 8 encode components of signaling pathways that are involved in cancer. The effectiveness of large-scale insertional mutagenesis in a sensitized genetic background is demonstrated by the preference for activation of MAP kinase signaling, collaborating with Cdkn2a loss in generating the lymphoid and myeloid tumors. Collectively, our results show that large-scale retroviral insertional mutagenesis in genetically predisposed mice is useful both as a system for identifying genes underlying cancer and as a genetic framework for the assignment of such genes to specific oncogenic pathways.
AbstractList	We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a −/− mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with loss of the Cdkn2a -encoded tumor suppressors p16INK4a and p19ARF. Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors. We isolated 747 unique sequences flanking retroviral integration sites and mapped them against the mouse genome sequence databases from Celera and Ensembl. In addition to 17 insertions targeting gene loci known to be cancer-related, we identified a total of 37 new common insertion sites (CISs), of which 8 encode components of signaling pathways that are involved in cancer. The effectiveness of large-scale insertional mutagenesis in a sensitized genetic background is demonstrated by the preference for activation of MAP kinase signaling, collaborating with Cdkn2a loss in generating the lymphoid and myeloid tumors. Collectively, our results show that large-scale retroviral insertional mutagenesis in genetically predisposed mice is useful both as a system for identifying genes underlying cancer and as a genetic framework for the assignment of such genes to specific oncogenic pathways. We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a(-/-) mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with loss of the Cdkn2a-encoded tumor suppressors p16INK4a and p19ARF. Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors. We isolated 747 unique sequences flanking retroviral integration sites and mapped them against the mouse genome sequence databases from Celera and Ensembl. In addition to 17 insertions targeting gene loci known to be cancer-related, we identified a total of 37 new common insertion sites (CISs), of which 8 encode components of signaling pathways that are involved in cancer. The effectiveness of large-scale insertional mutagenesis in a sensitized genetic background is demonstrated by the preference for activation of MAP kinase signaling, collaborating with Cdkn2a loss in generating the lymphoid and myeloid tumors. Collectively, our results show that large-scale retroviral insertional mutagenesis in genetically predisposed mice is useful both as a system for identifying genes underlying cancer and as a genetic framework for the assignment of such genes to specific oncogenic pathways.We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a(-/-) mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with loss of the Cdkn2a-encoded tumor suppressors p16INK4a and p19ARF. Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors. We isolated 747 unique sequences flanking retroviral integration sites and mapped them against the mouse genome sequence databases from Celera and Ensembl. In addition to 17 insertions targeting gene loci known to be cancer-related, we identified a total of 37 new common insertion sites (CISs), of which 8 encode components of signaling pathways that are involved in cancer. The effectiveness of large-scale insertional mutagenesis in a sensitized genetic background is demonstrated by the preference for activation of MAP kinase signaling, collaborating with Cdkn2a loss in generating the lymphoid and myeloid tumors. Collectively, our results show that large-scale retroviral insertional mutagenesis in genetically predisposed mice is useful both as a system for identifying genes underlying cancer and as a genetic framework for the assignment of such genes to specific oncogenic pathways. We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a super(-/-) mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with loss of the Cdkn2a-encoded tumor suppressors p16INK4a and p19ARF. Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors. We isolated 747 unique sequences flanking retroviral integration sites and mapped them against the mouse genome sequence databases from Celera and Ensembl. In addition to 17 insertions targeting gene loci known to be cancer-related, we identified a total of 37 new common insertion sites (CISs), of which 8 encode components of signaling pathways that are involved in cancer. The effectiveness of large-scale insertional mutagenesis in a sensitized genetic background is demonstrated by the preference for activation of MAP kinase signaling, collaborating with Cdkn2a loss in generating the lymphoid and myeloid tumors. Collectively, our results show that large-scale retroviral insertional mutagenesis in genetically predisposed mice is useful both as a system for identifying genes underlying cancer and as a genetic framework for the assignment of such genes to specific oncogenic pathways. We have used large-scale insertional mutagenesis to identify functional landmarks relevant to cancer in the recently completed mouse genome sequence. We infected Cdkn2a(-/-) mice with Moloney murine leukemia virus (MoMuLV) to screen for loci that can participate in tumorigenesis in collaboration with loss of the Cdkn2a-encoded tumor suppressors p16INK4a and p19ARF. Insertional mutagenesis by the latent retrovirus was synergistic with loss of Cdkn2a expression, as indicated by a marked acceleration in the development of both myeloid and lymphoid tumors. We isolated 747 unique sequences flanking retroviral integration sites and mapped them against the mouse genome sequence databases from Celera and Ensembl. In addition to 17 insertions targeting gene loci known to be cancer-related, we identified a total of 37 new common insertion sites (CISs), of which 8 encode components of signaling pathways that are involved in cancer. The effectiveness of large-scale insertional mutagenesis in a sensitized genetic background is demonstrated by the preference for activation of MAP kinase signaling, collaborating with Cdkn2a loss in generating the lymphoid and myeloid tumors. Collectively, our results show that large-scale retroviral insertional mutagenesis in genetically predisposed mice is useful both as a system for identifying genes underlying cancer and as a genetic framework for the assignment of such genes to specific oncogenic pathways.
Audience	Academic
Author	Lund, Anders H. van Lohuizen, Maarten DePinho, Ronald A. Turner, Geoffrey Trubetskoy, Alla Verhoeven, Els Wientjens, Ellen Hulsman, Danielle Lenz, Jack Russell, Robert
Author_xml	– sequence: 1 givenname: Anders H. surname: Lund fullname: Lund, Anders H. organization: Division of Molecular Genetics, The Netherlands Cancer Institute – sequence: 2 givenname: Geoffrey surname: Turner fullname: Turner, Geoffrey organization: Department of Molecular Genetics, Albert Einstein College of Medicine – sequence: 3 givenname: Alla surname: Trubetskoy fullname: Trubetskoy, Alla organization: Department of Molecular Genetics, Albert Einstein College of Medicine – sequence: 4 givenname: Els surname: Verhoeven fullname: Verhoeven, Els organization: Division of Molecular Genetics, The Netherlands Cancer Institute – sequence: 5 givenname: Ellen surname: Wientjens fullname: Wientjens, Ellen organization: Division of Molecular Genetics, The Netherlands Cancer Institute – sequence: 6 givenname: Danielle surname: Hulsman fullname: Hulsman, Danielle organization: Division of Molecular Genetics, The Netherlands Cancer Institute – sequence: 7 givenname: Robert surname: Russell fullname: Russell, Robert organization: Department of Pathology, Albert Einstein College of Medicine – sequence: 8 givenname: Ronald A. surname: DePinho fullname: DePinho, Ronald A. organization: Department of Adult Oncology, Genetics and Medicine, Dana-Farber Cancer Institute, Harvard Medical School – sequence: 9 givenname: Jack surname: Lenz fullname: Lenz, Jack email: lenz@aecom.yu.edu organization: Department of Molecular Genetics, Albert Einstein College of Medicine – sequence: 10 givenname: Maarten surname: van Lohuizen fullname: van Lohuizen, Maarten email: m.v.lohuizen@nki.nl organization: Division of Molecular Genetics, The Netherlands Cancer Institute
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ContentType	Journal Article
Copyright	Springer Nature America, Inc. 2002 2003 INIST-CNRS COPYRIGHT 2002 Nature Publishing Group Copyright Nature Publishing Group Sep 2002
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Keywords	Vertebrata Mammalia Gene Mouse Rodentia Tagging Malignant tumor Genome
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SubjectTerms	Agriculture Animal Genetics and Genomics Animals Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Cancer Research Cell Transformation, Neoplastic Cells, Cultured Chromosome Mapping Classical genetics, quantitative genetics, hybrids Collaboration Complications and side effects Cyclin-Dependent Kinase Inhibitor p16 - deficiency Cyclin-Dependent Kinase Inhibitor p16 - genetics Diagnosis Fundamental and applied biological sciences. Psychology Gene expression Gene Function Gene loci Gene mutations Genetic aspects Genetics Genetics of eukaryotes. Biological and molecular evolution Genome Genomes Genomics Health aspects Human Genetics Humans Infections Kinases letter Leukemia Lymphoma Lymphoma - genetics Mice Molecular Sequence Data Moloney murine leukemia virus Moloney murine leukemia virus - genetics Mutagenesis Mutagenesis, Insertional Neoplasms - genetics Proviruses - genetics Retrovirus Risk factors Sarcoma Spleen Tumorigenesis Tumors Vertebrata
Title	Genome-wide retroviral insertional tagging of genes involved in cancer in Cdkn2a-deficient mice
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