Please use this identifier to cite or link to this item: https://doi.org/10.1038/ng.2847
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dc.titleTransposon mutagenesis identifies genes driving hepatocellular carcinoma in a chronic hepatitis B mouse model
dc.contributor.authorBard-Chapeau, E.A.
dc.contributor.authorNguyen, A.-T.
dc.contributor.authorRust, A.G.
dc.contributor.authorSayadi, A.
dc.contributor.authorLee, P.
dc.contributor.authorChua, B.Q.
dc.contributor.authorNew, L.-S.
dc.contributor.authorDe Jong, J.
dc.contributor.authorWard, J.M.
dc.contributor.authorChin, C.K.Y.
dc.contributor.authorChew, V.
dc.contributor.authorToh, H.C.
dc.contributor.authorAbastado, J.-P.
dc.contributor.authorBenoukraf, T.
dc.contributor.authorSoong, R.
dc.contributor.authorBard, F.A.
dc.contributor.authorDupuy, A.J.
dc.contributor.authorJohnson, R.L.
dc.contributor.authorRadda, G.K.
dc.contributor.authorChan, E.C.Y.
dc.contributor.authorWessels, L.F.A.
dc.contributor.authorAdams, D.J.
dc.contributor.authorJenkins, N.A.
dc.contributor.authorCopeland, N.G.
dc.date.accessioned2014-12-12T07:35:16Z
dc.date.available2014-12-12T07:35:16Z
dc.date.issued2014-01
dc.identifier.citationBard-Chapeau, E.A., Nguyen, A.-T., Rust, A.G., Sayadi, A., Lee, P., Chua, B.Q., New, L.-S., De Jong, J., Ward, J.M., Chin, C.K.Y., Chew, V., Toh, H.C., Abastado, J.-P., Benoukraf, T., Soong, R., Bard, F.A., Dupuy, A.J., Johnson, R.L., Radda, G.K., Chan, E.C.Y., Wessels, L.F.A., Adams, D.J., Jenkins, N.A., Copeland, N.G. (2014-01). Transposon mutagenesis identifies genes driving hepatocellular carcinoma in a chronic hepatitis B mouse model. Nature Genetics 46 (1) : 24-32. ScholarBank@NUS Repository. https://doi.org/10.1038/ng.2847
dc.identifier.issn10614036
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/116010
dc.description.abstractThe most common risk factor for developing hepatocellular carcinoma (HCC) is chronic infection with hepatitis B virus (HBV). To better understand the evolutionary forces driving HCC, we performed a near-saturating transposon mutagenesis screen in a mouse HBV model of HCC. This screen identified 21 candidate early stage drivers and a very large number (2,860) of candidate later stage drivers that were enriched for genes that are mutated, deregulated or functioning in signaling pathways important for human HCC, with a striking 1,199 genes being linked to cellular metabolic processes. Our study provides a comprehensive overview of the genetic landscape of HCC. © 2014 Nature America, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1038/ng.2847
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentPHARMACY
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1038/ng.2847
dc.description.sourcetitleNature Genetics
dc.description.volume46
dc.description.issue1
dc.description.page24-32
dc.description.codenNGENE
dc.identifier.isiut000329113500008
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