Table of Contents Author Guidelines Submit a Manuscript
Journal of Skin Cancer
Volume 2016, Article ID 1368103, 9 pages
http://dx.doi.org/10.1155/2016/1368103
Research Article

Cutaneous Human Papillomavirus Infection and Development of Subsequent Squamous Cell Carcinoma of the Skin

1Department of Cancer Epidemiology, Moffitt Cancer Center, Tampa, Florida, USA
2University of South Florida, Morsani College of Medicine, Tampa, Florida, USA
3Department of Dermatology, University of South Florida, College of Medicine, Tampa, FL, USA
4Department of Cutaneous Surgery, University of South Florida, College of Medicine, Tampa, FL, USA
5Cutaneous Oncology Program, Moffitt Cancer Center, Tampa, Florida, USA
6Departments of Pathology and Cell Biology, University of South Florida, College of Medicine, Tampa, FL, USA
7Infections and Cancer Biology Group, International Agency for Research on Cancer-World Health Organization, Lyon 69372, France

Received 25 August 2016; Revised 5 October 2016; Accepted 16 October 2016

Academic Editor: Günther Hofbauer

Copyright © 2016 Shalaka S. Hampras et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The role of cutaneous human papillomavirus (HPV) infection in the development of subsequent cutaneous squamous cell carcinoma (SCC) is unknown. Pathologically confirmed cases of SCC () enrolled in a previously conducted case-control study were included in a retrospective cohort study to examine the association of cutaneous HPV at the time of SCC diagnosis with the risk of subsequent SCC development. Data on HPV seropositivity, HPV DNA in eyebrow hairs (EB) and SCC tumors were available from the parent study. Incidence of subsequent SCC was estimated using person-years of follow up. Cox Proportional Hazards ratios were estimated to evaluate the associations of both, HPV seropositivity and HPV DNA positivity with subsequent SCC. The five year cumulative incidence of subsequent SCC was 72%. Seropositivity to cutaneous HPV was not associated with the risk of subsequent SCC (HR = 0.83, 95% CI = 0.41–1.67). Any beta HPV infection in EB was associated with reduced risk (HR = 0.30, 95% CI = 0.11–0.78) of subsequent SCC among cases who were positive for beta HPV DNA in tumor tissue. Infection with beta HPV type 2 (HR = 0.32, 95% CI = 0.12–0.86) in EB was associated with reduced risk of subsequent SCC among HPV DNA positive SCCs. In conclusion, beta HPV infection was inversely associated with the risk of subsequent SCC.