Brenda Y Hernandez1, Charles F Lynch2, Owen T M Chan3, Marc T Goodman4, Elizabeth R Unger5, Martin Steinau5, Trevor D Thompson6, Maura Gillison7, Christopher Lyu8, Mona Saraiya6. 1. University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA. Electronic address: brenda@cc.hawaii.edu. 2. Department of Epidemiology, College of Public Health, The University of Iowa, Iowa City, IA, USA. 3. University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA. 4. Cedars-Sinai Medical Center, Los Angeles, CA, USA. 5. Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA. 6. Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA, USA. 7. The University of Texas MD Anderson Cancer Center, Houston, TX, USA. 8. Rho Federal Systems Division, Inc, Chapel Hill, NC, USA.
Abstract
OBJECTIVES: The role of HPV in oral cavity cancers was investigated using two markers of viral exposure. MATERIALS AND METHODS: HPV DNA and p16INK4a expression were evaluated in tumor tissue from a U.S. population-based sample of 122 invasive oral cavity cancer cases. RESULTS: HPV DNA was detected in 38 of 122 (31%) oral cavity tumors. Seven genotypes were detected including HPV 16, which was found in 22% of tumors. p16INK4a was expressed in 30% of tumors and was poorly correlated with HPV DNA detection (Kappa <0.1). Joint positivity for HPV 16 and/or 18 and p16INK4a was observed in only 7% of cases. When comparing cases diagnosed in 1993-1999 and in 2000-2004, positivity for HPV DNA 16/18 increased from 19% to 39% (p = 0.02) and joint HPV 16/18 - p16INK4a positivity increased from 0% to 12% (p = 0.01). For gingival tumors, HPV 16 and/or 18 positivity was 67% compared to 11-38% for other sites (p = 0.02); joint HPV 16/18 - p16INK4a positivity was 33% compared to 0-8% for other sites (p = 0.01). The association of HPV with gingival tumors and more recent diagnosis period remained after adjustment for age and stage (p < 0.05). Neither HPV DNA nor p16INK4a were associated with overall survival. CONCLUSIONS: Based on both HPV DNA and p16INK4a, HPV is etiologically linked to a limited subset of oral cavity cancers. However, the role of HPV in oral cavity cancer may vary widely by subsite and may have increased over time, similar to trends observed for oropharyngeal cancer.
OBJECTIVES: The role of HPV in oral cavity cancers was investigated using two markers of viral exposure. MATERIALS AND METHODS:HPV DNA and p16INK4a expression were evaluated in tumor tissue from a U.S. population-based sample of 122 invasive oral cavity cancer cases. RESULTS:HPV DNA was detected in 38 of 122 (31%) oral cavity tumors. Seven genotypes were detected including HPV 16, which was found in 22% of tumors. p16INK4a was expressed in 30% of tumors and was poorly correlated with HPV DNA detection (Kappa <0.1). Joint positivity for HPV 16 and/or 18 and p16INK4a was observed in only 7% of cases. When comparing cases diagnosed in 1993-1999 and in 2000-2004, positivity for HPV DNA 16/18 increased from 19% to 39% (p = 0.02) and joint HPV 16/18 - p16INK4a positivity increased from 0% to 12% (p = 0.01). For gingival tumors, HPV 16 and/or 18 positivity was 67% compared to 11-38% for other sites (p = 0.02); joint HPV 16/18 - p16INK4a positivity was 33% compared to 0-8% for other sites (p = 0.01). The association of HPV with gingival tumors and more recent diagnosis period remained after adjustment for age and stage (p < 0.05). Neither HPV DNA nor p16INK4a were associated with overall survival. CONCLUSIONS: Based on both HPV DNA and p16INK4a, HPV is etiologically linked to a limited subset of oral cavity cancers. However, the role of HPV in oral cavity cancer may vary widely by subsite and may have increased over time, similar to trends observed for oropharyngeal cancer.
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