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dc.contributor.authorNagar, S.
dc.contributor.authorRemmel, R. P.
dc.date.accessioned2009-04-15T12:13:31Z
dc.date.available2009-04-15T12:13:31Z
dc.date.issued2006-03-13
dc.identifier.citationOncogene 2006, 25 (11):1659-1672en
dc.identifier.issn0950-9232
dc.identifier.pmid16550166
dc.identifier.doi10.1038/sj.onc.1209375
dc.identifier.urihttp://hdl.handle.net/10146/64997
dc.descriptionKEYWORD CLASSIFICATION: Carcinogens;Cell Transformation,Neoplastic;Chemoprevention;genetics;Genotype;Glucuronosyltransferase;Humans;metabolism;mechanisms of carcinogenesis;Pharmacogenetics;Phenotype;Polymorphism,Genetic;Risk Factors;toxicity.en
dc.description.abstractThe uridine diphosphoglucuronosyltransferases (UGTs) belong to a superfamily of enzymes that catalyse the glucuronidation of numerous endobiotics and xenobiotics. Several human hepatic and extrahepatic UGT isozymes have been characterized with respect to their substrate specificity, tissue expression and gene structure. Genetic polymorphisms have been identified for almost all the UGT family members. A wide variety of anticancer drugs, dietary chemopreventives and carcinogens are known to be conjugated by members of both UGT1A and UGT2B subfamilies. This review examines in detail each UGT isozyme known to be associated with cancer and carcinogenesis. The cancer-related substrates for several UGTs are summarized, and the functionally relevant genetic polymorphisms of UGTs are reviewed. A number of genotype-phenotype association studies have been carried out to characterize the role of UGT pharmacogenetics in several types of cancer, and these examples are discussed here. In summary, this review focuses on the role of the human UGT genetic polymorphisms in carcinogenesis, chemoprevention and cancer risk.
dc.language.isoenen
dc.relation.urlhttp://www.nature.com/onc/journal/v25/n11/abs/1209375a.htmlen
dc.subjectDrug metabolismen
dc.subjectUridine diphosphoglucuronosyltransferaseen
dc.subjectGenetic polymorphismsen
dc.subject.meshCarcinogens
dc.subject.meshCell Transformation, Neoplastic
dc.subject.meshChemoprevention
dc.subject.meshGenotype
dc.subject.meshGlucuronosyltransferase
dc.subject.meshHumans
dc.subject.meshPharmacogenetics
dc.subject.meshPhenotype
dc.subject.meshPolymorphism, Genetic
dc.subject.meshRisk Factors
dc.titleUridine diphosphoglucuronosyltransferase pharmacogenetics and cancer.en
dc.typeArticleen
dc.identifier.journalOncogeneen
html.description.abstractThe uridine diphosphoglucuronosyltransferases (UGTs) belong to a superfamily of enzymes that catalyse the glucuronidation of numerous endobiotics and xenobiotics. Several human hepatic and extrahepatic UGT isozymes have been characterized with respect to their substrate specificity, tissue expression and gene structure. Genetic polymorphisms have been identified for almost all the UGT family members. A wide variety of anticancer drugs, dietary chemopreventives and carcinogens are known to be conjugated by members of both UGT1A and UGT2B subfamilies. This review examines in detail each UGT isozyme known to be associated with cancer and carcinogenesis. The cancer-related substrates for several UGTs are summarized, and the functionally relevant genetic polymorphisms of UGTs are reviewed. A number of genotype-phenotype association studies have been carried out to characterize the role of UGT pharmacogenetics in several types of cancer, and these examples are discussed here. In summary, this review focuses on the role of the human UGT genetic polymorphisms in carcinogenesis, chemoprevention and cancer risk.


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