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- Publisher Website: 10.1073/pnas.95.3.1126
- Scopus: eid_2-s2.0-0032477876
- PMID: 9448296
- WOS: WOS:000071878500059
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Article: Tissues of MSH2-deficient mice demonstrate hypermutability on exposure to a DNA methylating agent
Title | Tissues of MSH2-deficient mice demonstrate hypermutability on exposure to a DNA methylating agent |
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Authors | |
Issue Date | 1998 |
Citation | Proceedings of the National Academy of Sciences of the United States of America, 1998, v. 95, n. 3, p. 1126-1130 How to Cite? |
Abstract | The mutational response of mismatch repair-deficient animals to the alkylating agent N-methyl-N-nitrosourea was evaluated by using a transgenic lacI reporter system. Although the mutations detected in MSH2 heterozygotes were similar to those of controls, MSH2(-/-) animals demonstrated striking increases in mutation frequency in response to this agent. G:C to A:T transitions at GpG sites, as opposed to CpG sites, dominated the mutational spectrum of both MSH2(+/+) and MSH2(-/-) N-methyl-N-nitrosourea -treated animals. Extrapolating to humans with hereditary non-polyposis colorectal cancer, the results suggest that MSH2 heterozygotes are unlikely to be at increased risk of mutation, even when exposed to potent DNA methylating agents. In contrast, mismatch repair-deficient cells spontaneously arising within individuals with hereditary non-polyposis colorectal cancer would likely exhibit hypermutability in response to such mutagens, an outcome predicted to accelerate the pace of tumorigenesis. |
Persistent Identifier | http://hdl.handle.net/10722/291458 |
ISSN | 2023 Impact Factor: 9.4 2023 SCImago Journal Rankings: 3.737 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Andrew, Susan E. | - |
dc.contributor.author | Mckinnon, Margaret | - |
dc.contributor.author | Cheng, Benjamin S. | - |
dc.contributor.author | Francis, Agnes | - |
dc.contributor.author | Penney, Janice | - |
dc.contributor.author | Reitmair, Armin H. | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Jirik, Frank R. | - |
dc.date.accessioned | 2020-11-17T14:54:24Z | - |
dc.date.available | 2020-11-17T14:54:24Z | - |
dc.date.issued | 1998 | - |
dc.identifier.citation | Proceedings of the National Academy of Sciences of the United States of America, 1998, v. 95, n. 3, p. 1126-1130 | - |
dc.identifier.issn | 0027-8424 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291458 | - |
dc.description.abstract | The mutational response of mismatch repair-deficient animals to the alkylating agent N-methyl-N-nitrosourea was evaluated by using a transgenic lacI reporter system. Although the mutations detected in MSH2 heterozygotes were similar to those of controls, MSH2(-/-) animals demonstrated striking increases in mutation frequency in response to this agent. G:C to A:T transitions at GpG sites, as opposed to CpG sites, dominated the mutational spectrum of both MSH2(+/+) and MSH2(-/-) N-methyl-N-nitrosourea -treated animals. Extrapolating to humans with hereditary non-polyposis colorectal cancer, the results suggest that MSH2 heterozygotes are unlikely to be at increased risk of mutation, even when exposed to potent DNA methylating agents. In contrast, mismatch repair-deficient cells spontaneously arising within individuals with hereditary non-polyposis colorectal cancer would likely exhibit hypermutability in response to such mutagens, an outcome predicted to accelerate the pace of tumorigenesis. | - |
dc.language | eng | - |
dc.relation.ispartof | Proceedings of the National Academy of Sciences of the United States of America | - |
dc.title | Tissues of MSH2-deficient mice demonstrate hypermutability on exposure to a DNA methylating agent | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1073/pnas.95.3.1126 | - |
dc.identifier.pmid | 9448296 | - |
dc.identifier.pmcid | PMC18694 | - |
dc.identifier.scopus | eid_2-s2.0-0032477876 | - |
dc.identifier.volume | 95 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 1126 | - |
dc.identifier.epage | 1130 | - |
dc.identifier.isi | WOS:000071878500059 | - |
dc.identifier.issnl | 0027-8424 | - |