Genomic Amplification of an Endogenous Retrovirus in Zebrafish T-Cell Malignancies

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dc.contributor.authorFrazer, J. Kimble
dc.contributor.authorBatchelor, Lance A.
dc.contributor.authorBradley, Diana F.
dc.contributor.authorBrown, Kim H.
dc.contributor.authorDobrinski, Kimberly P.
dc.contributor.authorLee, Charles
dc.contributor.authorTrede, Nikolaus S.
dc.date.accessioned2019-11-15T18:09:36Z
dc.date.available2019-11-15T18:09:36Z
dc.date.issued2012-04-17
dc.descriptionCopyright © 2012 J. Kimble Frazer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
dc.description.abstractGenomic instability plays a crucial role in oncogenesis. Somatically acquired mutations can disable some genes and inappropriately activate others. In addition, chromosomal rearrangements can amplify, delete, or even fuse genes, altering their functions and contributing to malignant phenotypes. Using array comparative genomic hybridization (aCGH), a technique to detect numeric variations between different DNA samples, we examined genomes from zebrafish (Danio rerio) T-cell leukemias of three cancerprone lines. In all malignancies tested, we identified recurring amplifications of a zebrafish endogenous retrovirus. This retrovirus, ZFERV, was first identified due to high expression of proviral transcripts in thymic tissue from larval and adult fish.We confirmed ZFERV amplifications by quantitative PCR analyses of DNA from wild-type fish tissue and normal and malignant D. rerio T cells. We also quantified ZFERV RNA expression and found that normal and neoplastic T cells both produce retrovirally encoded transcripts, but most cancers show dramatically increased transcription. In aggregate, these data imply that ZFERV amplification and transcription may be related to T-cell leukemogenesis. Based on these data and ZFERV’s phylogenetic relation to viruses of the murine-leukemia-related virus class of gammaretroviridae, we posit that ZFERV may be oncogenic via an insertional mutagenesis mechanism.en_US
dc.identifier.citationJ.Kimble Frazer, Lance A. Batchelor, Diana F. Bradley, et al., “GenomicAmplification of an Endogenous Retrovirus in Zebrafish T-Cell Malignancies,” Advances in Hematology, vol. 2012, Article ID 627920, 12 pages, 2012. https://doi.org/10.1155/2012/627920.en_US
dc.identifier.doihttp://dx.doi.org/10.1155/2012/627920
dc.identifier.issn1687-9112
dc.identifier.other10.1155/2012/627920
dc.identifier.urihttp://hdl.handle.net/20.500.11868/863
dc.language.isoen_USen_US
dc.publisherAdvances in Hematology, Hindawi Publishing Corporationen_US
dc.subjectCarcinogenesisen_US
dc.subjectOncogenesisen_US
dc.subjectComparative genomic hybridizationen_US
dc.subjectDanio rerioen_US
dc.titleGenomic Amplification of an Endogenous Retrovirus in Zebrafish T-Cell Malignanciesen_US
dc.typeArticleen_US

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2012 CNHS Faculty Publications