{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lin YC"],"funding":["NIEHS NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["1461-8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4076807"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["35(7)"],"pubmed_abstract":["Aflatoxin B1 (AFB1) is a known carcinogen associated with early-onset hepatocellular carcinoma (HCC) and is thought to contribute to over half a million new HCCs per year. Although some of the fundamental risk factors are established, the molecular basis of AFB1-induced mutagenesis in primate cells has not been rigorously investigated. To gain insights into genome instability that is produced as a result of replicating DNAs containing AFB1 adducts, site-specific mutagenesis assays were used to establish the mutagenic potential of the persistent ring-opened AFB1 adduct, AFB1-formamidopyrimidine (AFB1-FAPY). This lesion was highly mutagenic, yielding replication error frequencies of 97%, with the predominant base substitution being a G to T transversion. This transversion is consistent with previous mutational data derived from aflatoxin-associated HCCs. In vitro translesion synthesis assays demonstrated that polymerase (pol) ζ was the most likely candidate polymerase that is responsible for the G to T mutations induced by this adduct."],"journal":["Carcinogenesis"],"pubmed_title":["Molecular basis of aflatoxin-induced mutagenesis-role of the aflatoxin B1-formamidopyrimidine adduct."],"pmcid":["PMC4076807"],"funding_grant_id":["R01 GM032431","P01 CA160032","P30 ES000267","P30 CA068485","GM 032431","T32 ES007028","R01 CA055678","T32 GM071338","P30 ES00267"],"pubmed_authors":["Lin YC","Stone MP","Makarova AV","Lloyd RS","Li L","Burgers PM"],"additional_accession":[]},"is_claimable":false,"name":"Molecular basis of aflatoxin-induced mutagenesis-role of the aflatoxin B1-formamidopyrimidine adduct.","description":"Aflatoxin B1 (AFB1) is a known carcinogen associated with early-onset hepatocellular carcinoma (HCC) and is thought to contribute to over half a million new HCCs per year. Although some of the fundamental risk factors are established, the molecular basis of AFB1-induced mutagenesis in primate cells has not been rigorously investigated. To gain insights into genome instability that is produced as a result of replicating DNAs containing AFB1 adducts, site-specific mutagenesis assays were used to establish the mutagenic potential of the persistent ring-opened AFB1 adduct, AFB1-formamidopyrimidine (AFB1-FAPY). This lesion was highly mutagenic, yielding replication error frequencies of 97%, with the predominant base substitution being a G to T transversion. This transversion is consistent with previous mutational data derived from aflatoxin-associated HCCs. In vitro translesion synthesis assays demonstrated that polymerase (pol) ζ was the most likely candidate polymerase that is responsible for the G to T mutations induced by this adduct.","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jul","modification":"2025-04-04T10:09:02.259Z","creation":"2019-03-27T01:31:07Z"},"accession":"S-EPMC4076807","cross_references":{"pubmed":["24398669"],"doi":["10.1093/carcin/bgu003"]}}