Polyomavirus JCPyV infrequently detectable in adenoid cystic carcinoma of the oral cavity and the airways

dc.contributor.authorHanna Hämetoja
dc.contributor.authorJaana Hagström
dc.contributor.authorCaj Haglund
dc.contributor.authorLeif Bäck
dc.contributor.authorAntti Mäkitie
dc.contributor.authorStina Syrjänen
dc.contributor.organizationfi=hammaslääketieteen laitos|en=Institute of Dentistry|
dc.contributor.organizationfi=tyks, vsshp|en=tyks, varha|
dc.contributor.organization-code1.2.246.10.2458963.20.64787032594
dc.contributor.organization-code2607500
dc.converis.publication-id41794406
dc.converis.urlhttps://research.utu.fi/converis/portal/Publication/41794406
dc.date.accessioned2022-10-28T13:28:27Z
dc.date.available2022-10-28T13:28:27Z
dc.description.abstract<p>Our objective was to assess the presence of three polyomaviruses, namely SV40, JCPyV, and BKPyV, and human papillomaviruses (HPV) in adenoid cystic carcinomas (ACC) of the minor salivary glands (MiSG) in the head and neck region. The study comprised 68 MiSG ACC patients operated during 1974–2012 at the Helsinki University Hospital (Helsinki, Finland). Medical records and 68 histological samples were reviewed. Polyomaviruses were detected with quantitative PCR and the DNA-positive samples were further analyzed for the presence of viral tumor T antigen (T-ag) with immunohistochemistry. HPV genotyping was performed with a Multiplex HPV Genotyping Kit. Only JCPyV DNA was found in ACC samples, being present in 7 (10.3%) out of the 68 samples. The viral load of JCPyV was low varying between 1 to 226 copies/μg DNA. The JCPyV-positive samples originated from trachea (two samples), paranasal sinuses (one), and oral cavity (two). Additionally, JCPyV positivity was found in one lung metastasis of a tracheal tumor and one local disease failure of an oral cavity tumor. Three JCPyV DNA-positive samples showed weak nuclear staining for large T-ag. In conclusion, only JCPyV but not SV40, BKPyV, or HPV was found in ACC from the upper and lower airways. JCPyV copy numbers were low which might support its role as a “hit and run agent” in ACC carcinogenesis.</p>
dc.format.pagerange609
dc.format.pagerange616
dc.identifier.eissn1432-2307
dc.identifier.jour-issn0945-6317
dc.identifier.olddbid182333
dc.identifier.oldhandle10024/165427
dc.identifier.urihttps://www.utupub.fi/handle/11111/39531
dc.identifier.urnURN:NBN:fi-fe2021042827214
dc.language.isoen
dc.okm.affiliatedauthorLaine, Hanna
dc.okm.affiliatedauthorSyrjänen, Stina
dc.okm.affiliatedauthorDataimport, tyks, vsshp
dc.okm.discipline1182 Biochemistry, cell and molecular biologyen_GB
dc.okm.discipline3111 Biomedicineen_GB
dc.okm.discipline319 Forensic science and other medical sciencesen_GB
dc.okm.discipline1182 Biokemia, solu- ja molekyylibiologiafi_FI
dc.okm.discipline3111 Biolääketieteetfi_FI
dc.okm.discipline319 Oikeuslääketiede ja muut lääketieteetfi_FI
dc.okm.internationalcopublicationinternational co-publication
dc.okm.internationalityInternational publication
dc.okm.typeA1 ScientificArticle
dc.publisherSpringer
dc.publisher.countryGermanyen_GB
dc.publisher.countrySaksafi_FI
dc.publisher.country-codeDE
dc.relation.doi10.1007/s00428-019-02617-6
dc.relation.ispartofjournalVirchows Archiv
dc.relation.issue5
dc.relation.volume475
dc.source.identifierhttps://www.utupub.fi/handle/10024/165427
dc.titlePolyomavirus JCPyV infrequently detectable in adenoid cystic carcinoma of the oral cavity and the airways
dc.year.issued2019

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