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Human Papillomavirus (HPV) and HPV 16-Variant Distribution in Vulvar Squamous Cell Carcinoma in Sweden
Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden.
Örebro universitet, Institutionen för läkarutbildning. Örebro University Hospital, Örebro, Sweden.ORCID-id: 0000-0003-2317-5738
Örebro University Hospital, Örebro, Sweden.
Umeå University Hospital, Umeå, Sweden.
Vise andre og tillknytning
2012 (engelsk)Inngår i: International Journal of Gynecological Cancer, ISSN 1048-891X, E-ISSN 1525-1438, Vol. 22, nr 8, s. 1413-1419Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective: To investigate the human papillomavirus (HPV) and HPV type 16-variant distribution in a series of vulvar squamous cell carcinomas (VSCC) and to evaluate the impact of HPV and HPV 16-variant on prognosis.

Methods: A series of 133 patients who had a diagnosis of VSCC (1983-2008) was selected for the study. Detection of 11 high-risk HPV types (16, 18, 31, 33, 39, 45, 51, 52, 56, 58, and 59) and 2 low-risk HPV types (6 and 11) was performed with real-time polymerase chain reaction. Samples positive for HPV 16 were further analyzed for variant determination of 7 positions in the E6 gene with polymerase chain reaction and pyrosequencing.

Results: Forty (30.8%) of 130 tumors were found to be HPV positive. Human papillomavirus type 16 was found in 31 cases, HPV 18 was found in 2 cases, HPV 33 was found in 5 cases, and HPV 56 and HPV 59 were found in one case each. All but one tumor harboring HPV 16 were of European linage, and the 3 most common variants were E-p (n = 13), E-G350 (n = 7), and E-G131 (n = 5). HPV positivity was associated with the basaloid tumor type and occurred in significantly younger patients. Overall and recurrence-free survival rates were better in HPV-positive cases, but after correction for age and tumor size, HPV status was no longer an independent and significant prognostic factor. The survival rates of the various HPV 16 variants were not significantly different, but there was a trend of worse outcome for the E-G131-variant group.

Conclusions: Human papillomavirus positivity of 30.8% is similar to other reports on VSCC. To our knowledge, this first variant determination of HPV 16 in vulvar carcinoma in a Swedish cohort indicated that the variant E-G131 may have an increased oncogenic potential in patients with VSCC.

sted, utgiver, år, opplag, sider
2012. Vol. 22, nr 8, s. 1413-1419
Emneord [en]
Vulvar carcinoma, Human papillomavirus, HPV 16 variants
HSV kategori
Identifikatorer
URN: urn:nbn:se:oru:diva-43018DOI: 10.1097/IGC.0b013e31826a0471ISI: 000309543700023PubMedID: 23013732Scopus ID: 2-s2.0-84867268780OAI: oai:DiVA.org:oru-43018DiVA, id: diva2:791378
Tilgjengelig fra: 2015-02-27 Laget: 2015-02-27 Sist oppdatert: 2018-05-14bibliografisk kontrollert
Inngår i avhandling
1. Characterization of HPV-induced vaginal and vulvar carcinoma
Åpne denne publikasjonen i ny fane eller vindu >>Characterization of HPV-induced vaginal and vulvar carcinoma
2014 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
sted, utgiver, år, opplag, sider
Örebro: Örebro university, 2014. s. 83
Serie
Örebro Studies in Medicine, ISSN 1652-4063 ; 112
Emneord
vaginal carcinoma, vulvar carcinoma, HPV, integration, methylation, genotyping
HSV kategori
Forskningsprogram
Medicin
Identifikatorer
urn:nbn:se:oru:diva-38173 (URN)978-91-7529-052-2 (ISBN)
Disputas
2014-12-19, Universitetssjukhuset, Wilandersalen, Södra Grev Rosengatan, Örebro, 09:00 (svensk)
Opponent
Veileder
Tilgjengelig fra: 2014-10-27 Laget: 2014-10-27 Sist oppdatert: 2017-10-17bibliografisk kontrollert

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