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Human Papillomavirus (HPV) and HPV 16–Variant Distribution in Vulvar Squamous Cell Carcinoma in Sweden
  1. Gabriella Lillsunde Larsson, MSc*,,
  2. Gisela Helenius, PhD*,,
  3. Sören Andersson, MD, PhD*,,
  4. Fredrik Elgh, MD, PhD,
  5. Bengt Sorbe, MD, PhD§ and
  6. Mats G. Karlsson, MD, PhD*,
  1. *Department of Laboratory Medicine, Örebro University Hospital, and
  2. School of Health and Medical Sciences, Örebro University, Örebro, Sweden;
  3. Department of Clinical Microbiology/Virology, Umeå University Hospital, Umeå, Sweden; and
  4. §Department of Oncology, Örebro University Hospital, Örebro, Sweden.
  1. Address correspondence and reprint requests to Gabriella Lillsunde Larsson, MSc, Department of Laboratory Medicine, Örebro University Hospital, S-701 85 Örebro, Sweden. E-mail: gabriella.lillsunde-larsson{at}orebroll.se.

Abstract

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.

  • Vulvar carcinoma
  • Human papillomavirus
  • HPV 16 variants

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Footnotes

  • This study was supported by Nyckelfonden at Örebro County Council, by Örebro City Council Research Committee, and by Lions Cancerforskningsfond at the University Hospitals in Örebro and Uppsala.

  • The authors declare no conflicts of interest.

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