| http://purl.uniprot.org/citations/20732909 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20732909 | http://www.w3.org/2000/01/rdf-schema#comment | "Methylating agents are widely distributed environmental carcinogens. Moreover, they are being used in cancer chemotherapy. The primary target of methylating agents is DNA, and therefore, DNA repair is the first-line barrier in defense against their toxic and carcinogenic effects. Methylating agents induce in the DNA O(6)-methylguanine (O(6)MeG) and methylations of the ring nitrogens of purines. The lesions are repaired by O(6)-methylguanine-DNA methyltransferase (Mgmt) and by enzymes of the base excision repair (BER) pathway, respectively. Whereas O(6)MeG is well established as a pre-carcinogenic lesion, little is known about the carcinogenic potency of base N-alkylation products such as N3-methyladenine and N3-methylguanine. To determine their role in cancer formation and the role of BER in cancer protection, we checked the response of mice with a targeted gene disruption of Mgmt or N-alkylpurine-DNA glycosylase (Aag) or both Mgmt and Aag, to azoxymethane (AOM)-induced colon carcinogenesis, using non-invasive mini-colonoscopy. We demonstrate that both Mgmt- and Aag-null mice show a higher colon cancer frequency than the wild-type. With a single low dose of AOM (3 mg/kg) Aag-null mice showed an even stronger tumor response than Mgmt-null mice. The data provide evidence that both BER initiated by Aag and O(6)MeG reversal by Mgmt are required for protection against alkylation-induced colon carcinogenesis. Further, the data indicate that non-repaired N-methylpurines are not only pre-toxic but also pre-carcinogenic DNA lesions."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.org/dc/terms/identifier | "doi:10.1093/carcin/bgq174"xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/author | "Samson L.D."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/author | "Kaina B."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/author | "Neurath M.F."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/author | "Nagel G."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/author | "Wirtz S."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/author | "Eshkind L."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/name | "Carcinogenesis"xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/pages | "2111-2117"xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/title | "Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis."xsd:string |
| http://purl.uniprot.org/citations/20732909 | http://purl.uniprot.org/core/volume | "31"xsd:string |
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