Susceptibility to Astrocytoma in Mice Mutant for Nf1 and Trp53 Is Linked to Chromosome 11 and Subject to Epigenetic Effects
Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 101; no. 35; pp. 13008 - 13013 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
31.08.2004
National Acad Sciences |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 |
| DOI | 10.1073/pnas.0401236101 |
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| Abstract | Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F1progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6, 129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. |
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| AbstractList | Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F1progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6, 129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F sub(1) progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F1 progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions.Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F1 progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F1 progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53. Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F 1 progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53 . Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common during tumor progression. We have shown previously that mice mutant for Trp53 and Nf1 develop astrocytoma, progressing to glioblastoma, on a C57BL/6J strain background. In contrast, here we present data that mice mutant for Trp53 and Nf1 on a 129S4/SvJae background are highly resistant to developing astrocytoma. Through analysis of F 1 progeny, we demonstrate that susceptibility to astrocytoma is linked to chromosome 11, and that the modifier gene(s) responsible for differences in susceptibility is closely linked to Nf1 and Trp53 . Furthermore, this modifier of astrocytoma susceptibility is itself epigenetically modified. These data demonstrate that epigenetic effects can have a strong effect on whether cancer develops in the context of mutant ras signaling and mutant p53, and that this mouse model of astrocytoma can be used to identify modifier phenotypes with complex inheritance patterns that would be unidentifiable in humans. Because analysis of gene function in the mouse is often performed on a mixed C57BL/6,129 strain background, these data also provide a powerful example of the potential of these strains to mask interesting gene functions. |
| Author | Loisel, Dagan A. Tuskan, Robert G. Jacks, Tyler Christy, Emily Tsang, Shirley Reilly, Karlyne M. Smith, C. Dahlem Vogelstein, Bert Ledger, Jeremy Bronson, Roderick T. Munroe, David J. |
| AuthorAffiliation | Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD 21702; ‡ Department of Biology and Center for Cancer Research and § Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02169; ¶ Department of Pathology, Harvard Medical School, Boston, MA 02115; and Laboratories of ∥ Animal Sciences Program and Molecular Technology, Science Applications International Corporation, Frederick, MD 21702 |
| AuthorAffiliation_xml | – name: Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD 21702; ‡ Department of Biology and Center for Cancer Research and § Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02169; ¶ Department of Pathology, Harvard Medical School, Boston, MA 02115; and Laboratories of ∥ Animal Sciences Program and Molecular Technology, Science Applications International Corporation, Frederick, MD 21702 |
| Author_xml | – sequence: 1 givenname: Karlyne M. surname: Reilly fullname: Reilly, Karlyne M. – sequence: 2 givenname: Robert G. surname: Tuskan fullname: Tuskan, Robert G. – sequence: 3 givenname: Emily surname: Christy fullname: Christy, Emily – sequence: 4 givenname: Dagan A. surname: Loisel fullname: Loisel, Dagan A. – sequence: 5 givenname: Jeremy surname: Ledger fullname: Ledger, Jeremy – sequence: 6 givenname: Roderick T. surname: Bronson fullname: Bronson, Roderick T. – sequence: 7 givenname: C. Dahlem surname: Smith fullname: Smith, C. Dahlem – sequence: 8 givenname: Shirley surname: Tsang fullname: Tsang, Shirley – sequence: 9 givenname: David J. surname: Munroe fullname: Munroe, David J. – sequence: 10 givenname: Tyler surname: Jacks fullname: Jacks, Tyler – sequence: 11 givenname: Bert surname: Vogelstein fullname: Vogelstein, Bert |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15319471$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by Bert Vogelstein, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, and approved July 9, 2004 This paper was submitted directly (Track II) to the PNAS office. To whom correspondence should be addressed. E-mail: kreilly@ncifcrf.gov. Abbreviations: NF1, neurofibromatosis type 1; SSLP, simple sequence length polymorphism; NPcis, Nf1;Trp53cis; B6, C57BL/6J; 129, 129S4/SvJae; A, A/J; DB, DBA/2J; CB, CBA/J; 129S1, 129S1/SvImJ; 129X1, 129X1/SvJ; SNP, single nucleotide polymorphism; chr, chromosome; WHO, World Health Organization; NCBI, National Center for Biotechnology Information; dbSNP, Single Nucleotide Polymorphism Database. Data deposition: The SNP data reported in this paper have been deposited in the NCBI Single Nucleotide Polymorphism Database (dbSNP) (dbSNP ID nos. 28476647-28476655; see also Table 4, which is published as supporting information on the PNAS web site). |
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| Snippet | Astrocytoma is the most common malignant brain tumor in humans. Loss of the p53 signaling pathway and up-regulation of the ras signaling pathway are common... |
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| SubjectTerms | Alleles Animals Apoptosis Regulatory Proteins Astrocytoma Astrocytoma - genetics Astrocytoma - pathology Biological Sciences Carrier Proteins - genetics Crosses, Genetic Cytoplasmic inheritance Female Genetic inheritance Genetic Linkage Genetic mutation Genetic Predisposition to Disease Heat-Shock Proteins - genetics Inbred strains Inbreeding Male Medical genetics Mice Models, Genetic Neurofibromin 1 - genetics Tumors |
| Title | Susceptibility to Astrocytoma in Mice Mutant for Nf1 and Trp53 Is Linked to Chromosome 11 and Subject to Epigenetic Effects |
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