Journal article
Human papillomavirus DNA detection, p16 INK4a , and oral cavity cancer in a U.S. population
Oral oncology, Vol.91, pp.92-96
04/2019
DOI: 10.1016/j.oraloncology.2019.03.001
PMCID: PMC6498424
PMID: 30926069
Abstract
The role of HPV in oral cavity cancers was investigated using two markers of viral exposure.
HPV DNA and p16
expression were evaluated in tumor tissue from a U.S. population-based sample of 122 invasive oral cavity cancer cases.
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. p16
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 p16
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 - p16
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 - p16
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 p16
were associated with overall survival.
Based on both HPV DNA and p16
, 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.
Details
- Title: Subtitle
- Human papillomavirus DNA detection, p16 INK4a , and oral cavity cancer in a U.S. population
- Creators
- Brenda Y Hernandez - University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USA. Electronic address: brenda@cc.hawaii.eduCharles F Lynch - Department of Epidemiology, College of Public Health, The University of Iowa, Iowa City, IA, USAOwen T M Chan - University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI, USAMarc T Goodman - Cedars-Sinai Medical Center, Los Angeles, CA, USAElizabeth R Unger - Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USAMartin Steinau - Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USATrevor D Thompson - Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA, USAMaura Gillison - The University of Texas MD Anderson Cancer Center, Houston, TX, USAChristopher Lyu - Rho Federal Systems Division, Inc, Chapel Hill, NC, USAMona Saraiya - Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, GA, USAHPV Typing of Cancer Workgroup
- Resource Type
- Journal article
- Publication Details
- Oral oncology, Vol.91, pp.92-96
- DOI
- 10.1016/j.oraloncology.2019.03.001
- PMID
- 30926069
- PMCID
- PMC6498424
- NLM abbreviation
- Oral Oncol
- ISSN
- 1368-8375
- eISSN
- 1879-0593
- Publisher
- England
- Grant note
- CC999999 / Intramural CDC HHS P30 CA086862 / NCI NIH HHS P30 CA071789 / NCI NIH HHS
- Language
- English
- Date published
- 04/2019
- Academic Unit
- Epidemiology
- Record Identifier
- 9983995000702771
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