Human papillomavirus genotype prevalence in invasive penile cancers from a registry-based United States population - Abstract

Background: Human papillomavirus (HPV) is estimated to play an etiologic role in 40-50% of penile cancers worldwide.

Estimates of HPV prevalence in U.S. penile cancer cases are limited.

Methods: HPV DNA was evaluated in tumor tissue from 79 invasive penile cancer patients diagnosed in 1998-2005 within the catchment areas of seven U.S. cancer registries. HPV was genotyped using PCR-based Linear Array and INNO-LiPA assays and compared by demographic, clinical, and pathologic characteristics and survival. Histological classification was also obtained by independent pathology review.

Results: HPV DNA was present in 50 of 79 (63%) of invasive penile cancer cases. Sixteen viral genotypes were detected. HPV 16, found in 46% (36/79) of all cases (72% of HPV-positive cases) was the most prevalent genotype followed equally by HPV 18, 33, and 45, each of which comprised 5% of all cases. Multiple genotypes were detected in 18% of viral positive cases. HPV prevalence did not significantly vary by age, race/ethnicity, population size of geographic region, cancer stage, histology, grade, penile subsite, or prior cancer history. Penile cases diagnosed in more recent years were more likely to be HPV-positive. Overall survival did not significantly vary by HPV status.

Conclusion: The relatively high prevalence of HPV in our study population provides limited evidence of a more prominent and, possibly, increasing role of infection in penile carcinogenesis in the U.S. compared to other parts of the world.

Written by:
Hernandez BY, Goodman MT, Unger ER, Steinau M, Powers A, Lynch CF, Cozen W, Saber MS, Peters ES, Wilkinson EJ, Copeland G, Hopenhayn C, Huang Y, Watson M, Altekruse SF, Lyu C, Saraiya M.   Are you the author?
University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA; Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA; Department of Epidemiology, College of Public Health, The University of Iowa, Iowa City, IA, USA; Departments of Preventive Medicine and Pathology, USC Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA; Department of Epidemiology, School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA, USA; Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, USA; Michigan Department of Community Health, Lansing, MI, USA; Department of Epidemiology, College of Public Health, University of Kentucky, Lexington, KY, USA; Florida Department of Health, Tallahassee, FL, USA; Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention, and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA, USA; Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA; Battelle Memorial Institute, Durham, NC, USA.

Reference: Front Oncol. 2014 Feb 5;4:9.
doi: 10.3389/fonc.2014.00009


PubMed Abstract
PMID: 24551592

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