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Open AccessArticle

Oral HPV16 Prevalence in Oral Potentially Malignant Disorders and Oral Cavity Cancers

1
Saliva & Liquid Biopsy Translational Research Team, The School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology and the Translational Research Institute, Queensland, Brisbane, QLD 4059, Australia
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Janssen Diagnostics, a division of Janssen Pharmaceutical NV, 2340 Beerse, Belgium
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School of Dentistry, The University of Queensland, Herston, QLD 4006, Australia
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Logan Hospital Integrated Specialist ENT Service, Metro South Health Service District, Queensland Health, Meadowbrook, QLD 4131, Australia
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Department of Maxillo-Facial Surgery, Royal Brisbane and Women’s Hospital, The University of Queensland, Butterfield St, Herston, QLD 4029, Australia
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Royal Brisbane and Women’s Hospital, Central Integrated Regional Cancer Service, The University of Queensland School of Medicine, Queenslands Health, Brisbane, QLD 4029, Australia
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Faculty of Medicine, The University of Queensland, Translational Research Institute, Brisbane, QLD 4102, Australia
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Janssen Vaccines & Prevention BV, 2333CN Leiden, The Netherlands
*
Author to whom correspondence should be addressed.
Biomolecules 2020, 10(2), 223; https://doi.org/10.3390/biom10020223 (registering DOI)
Received: 17 December 2019 / Revised: 28 January 2020 / Accepted: 30 January 2020 / Published: 3 February 2020
The role of human papillomavirus type 16 (HPV16) in oral potentially malignant disorders (OPMD) and oral cavity carcinoma (OC) is still under debate. We investigated HPV16 prevalence in unstimulated saliva, oral rinse samples, oral swabs and tumour biopsies collected from OPMD (n = 83) and OC (n = 106) patients. HPV16 genotype, viral load, physical status (episomal vs. integrated) and tumour p16INK4a expression were determined. Oral HPV16 prevalence was higher in OC than in OPMD, but this difference was not statistically significant (7.5% (8/106) versus 3.6% (3/83), odds ratio (OR): 2.18, 95% confidence interval (CI): 0.56, 8.48, p = 0.26). There was a significant association (p < 0.05) between oral HPV16 infection and heavy tobacco consumption. Real-time PCR results indicated that no integration events occurred in either OPMD or OC cases based on the HPV16 E2/E6 ratio. HPV16 positive OPMD and OC patients had similar HPV16 E2 and E6 viral loads. The inter-rater agreement between tumour p16INK4a expression and oral HPV16 infection was considered as fair (k = 0.361) for OC. Our data suggest that the involvement of HPV16 in oral carcinogenesis is limited. View Full-Text
Keywords: human papillomavirus; oral potentially malignant disorder; oral cavity cancer; saliva; viral load and HPV integration human papillomavirus; oral potentially malignant disorder; oral cavity cancer; saliva; viral load and HPV integration
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Tang, K.D.; Menezes, L.; Baeten, K.; Walsh, L.J.; Whitfield, B.C.S.; Batstone, M.D.; Kenny, L.; Frazer, I.H.; Scheper, G.C.; Punyadeera, C. Oral HPV16 Prevalence in Oral Potentially Malignant Disorders and Oral Cavity Cancers. Biomolecules 2020, 10, 223.

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