Adeno-Associated Virus Type 2 and Hepatocellular Carcinoma

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dc.contributor.authorBerns, Kenneth I.
dc.contributor.authorByrne, Barry J.
dc.contributor.authorFlotte, Terence R.
dc.contributor.authorGao, Guang Ping
dc.contributor.authorHauswirth, William W.
dc.contributor.authorHerzog, Roland W.
dc.contributor.authorMuzyczka, Nicholas
dc.contributor.authorVandenDriessche, Thierry
dc.contributor.authorXiao, Xiao
dc.contributor.authorZolotukhin, Sergei
dc.contributor.authorSrivastava, Arun
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.contributor.departmentOffice of the Dean
dc.contributor.departmentHorae Gene Therapy Center
dc.contributor.departmentDepartment of Pediatrics, Division of Pulmonary and Allergy
dc.date2022-08-11T08:10:14.000
dc.date.accessioned2022-08-23T17:00:16Z
dc.date.available2022-08-23T17:00:16Z
dc.date.issued2015-12-01
dc.date.submitted2016-11-14
dc.description.abstractIn a recent Nature Genetics letter, entitled “Recurrent AAV2-related insertional mutagenesis in human hepatocellular carcinomas,” Nault and colleaguesdocument that of 193 patients with hepatocellular carcinoma (HCC), 11 contained an integrated genome sequence of the wild-type adeno-associated virus 2 (AAV2), and suggest that AAV2 is associated with oncogenic insertional mutagenesis in human HCC. Because AAV2 has long been known to be a nonpathogenic human parvovirus and, in fact, has been shown to possess antitumor activity, it is critical that the scientific and clinical implications of these studies be rigorously assessed to justify their conclusions. We have carefully analyzed the data presented by Nault and colleaguesand reached a conclusion that is at variance with that of the authors.
dc.identifier.citationHum Gene Ther. 2015 Dec;26(12):779-81. doi: 10.1089/hum.2015.29014.kib. <a href="http://dx.doi.org/10.1089/hum.2015.29014.kib">Link to article on publisher's site</a>
dc.identifier.contextkey9373899
dc.identifier.doi10.1089/hum.2015.29014.kib
dc.identifier.issn1043-0342 (Linking)
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/peds_pp/73
dc.identifier.pmid26690810
dc.identifier.submissionpathpeds_pp/73
dc.identifier.urihttps://hdl.handle.net/20.500.14038/43761
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26690810&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1089/hum.2015.29014.kib
dc.source.issue12
dc.source.journaltitleHuman gene therapy
dc.source.pages779-81
dc.source.volume26
dc.subjectCancer Biology
dc.subjectGenetics and Genomics
dc.subjectNeoplasms
dc.subjectTherapeutics
dc.titleAdeno-Associated Virus Type 2 and Hepatocellular Carcinoma
dc.typeJournal Article
dspace.entity.typePublication
html.description.abstract<p>In a recent <em>Nature Genetics</em> letter, entitled “Recurrent AAV2-related insertional mutagenesis in human hepatocellular carcinomas,” Nault and colleaguesdocument that of 193 patients with hepatocellular carcinoma (HCC), 11 contained an integrated genome sequence of the wild-type adeno-associated virus 2 (AAV2), and suggest that AAV2 is associated with oncogenic insertional mutagenesis in human HCC.</p> <p>Because AAV2 has long been known to be a nonpathogenic human parvovirus and, in fact, has been shown to possess antitumor activity, it is critical that the scientific and clinical implications of these studies be rigorously assessed to justify their conclusions. We have carefully analyzed the data presented by Nault and colleaguesand reached a conclusion that is at variance with that of the authors.</p>
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