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dc.contributor.authorMinglei Guoen_US
dc.contributor.authorLei Gongen_US
dc.contributor.authorLin Heen_US
dc.contributor.authorLois Lehman-McKeemanen_US
dc.contributor.authorYu-Jui Wanen_US
dc.date.accessioned2009-05-05T16:16:15Z
dc.date.available2009-05-05T16:16:15Z
dc.date.issued2008-05-01en_US
dc.identifier.citationMinglei Guo;Lei Gong;Lin He;Lois Lehman-McKeeman;Yu-Jui Wan: Hepatocyte RXRalpha deficiency in matured and aged mice: impact on the expression of cancer-related hepatic genes in a gender-specific manner. BMC Genomics 2008, 9(1):403.en_US
dc.identifier.urihttp://hdl.handle.net/2271/620en_US
dc.description.abstractBACKGROUND:The occurrence of liver cancer is higher in males than in females, and the incidence increases during aging. Signaling pathways regulated by retinoid × receptor a (RXRa) are involved in hepatocellular carcinogenesis. The phenotype of hepatocyte RXRa deficient mice is different between genders. To explore the impact of hepatocyte RXRa deficiency on gender-dependent hepatic gene expression, we compared the expression profiles of cancer-related genes in 6 and 24 month old male and female mice.RESULTS:In 6 month old mice, male mutant mice showed more cancer-related genes with alteration in mRNA levels than females did (195 vs. 60). In aged mice (24 month), female mutant mice showed greater deviation in mRNA expression levels of cancer-related genes than their male counterparts (149 vs. 82). The genes were classified into five categories according to their role in carcinogenesis: apoptosis, metastasis, cell growth, stress, and immune respnse. In each category, dependent upon age and gender, the genes as well as the number of genes with altered mRNA levels due to RXRa deficiency varies.CONCLUSION:The change in hepatic cancer-related gene expression profiles due to RXRa deficiency was gender- and age-dependent. The alteration of mRNA levels of cancer-related genes implied that aberrant RXRa signaling could potentially increase the risk of liver cancer and that retinoid signaling might contribute to gender- and age-associated liver cancer incidence.en_US
dc.languageenen_US
dc.language.isoen_USen_US
dc.publisherBioMedCentralen_US
dc.relation.isversionofhttp://www.biomedcentral.com/1471-2164/9/403en_US
dc.relation.hasversionhttp://www.biomedcentral.com/content/pdf/1471-2164-9-403.pdfen_US
dc.rightsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0en_US
dc.subject.meshBacterial Proteins/geneticsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshDNA Transposable Elements/geneticsen_US
dc.subject.meshEvolution, Molecularen_US
dc.subject.meshGene Duplicationen_US
dc.subject.meshGene Rearrangementen_US
dc.subject.meshGene Transfer, Horizontalen_US
dc.subject.meshGenome, Bacterial/ geneticsen_US
dc.subject.meshGenomicsen_US
dc.subject.meshMicrosatellite Repeatsen_US
dc.subject.meshOryza sativa/ microbiologyen_US
dc.subject.meshReproducibility of Resultsen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshXanthomonas/ geneticsen_US
dc.titleHepatocyte RXRalpha deficiency in matured and aged mice: impact on the expression of cancer-related hepatic genes in a gender-specific manneren_US
dc.typeArticleen_US
dc.identifier.doi10.1186/1471-2164-9-403en_US
dc.identifier.pmid18452608en_US
dc.rights.accessrightsopenAccessen_US
dc.date.captured2009-04-27en_US


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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.