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RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma

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Human Papillomavirus and Rising Oropharyngeal Cancer Incidence in the United States

Anil K Chaturvedi¹, Eric A Engels¹, Ruth M Pfeiffer¹

¹Anil K. Chaturvedi, Eric A. Engels, Ruth M. Pfeiffer, Nicolas Wentzensen, William F. Anderson, and Philip S. Rosenberg, National Cancer Institute; Sean Altekruse, Surveillance, Epidemiology, and End Results Program, National Cancer Institute, Rockville, MD; Brenda Y. Hernandez and Marc T. Goodman, Cancer Research Center of Hawaii, Honolulu, HI; Weihong Xiao, Esther Kim, Bo Jiang, and Maura L. Gillison, The Ohio State University, Columbus, OH; Maria Sibug-Saber, Wendy Cozen, and Lihua Liu, University of Southern California at Los Angeles, Los Angeles; Richard C. Jordan, University of California and Radiation Therapy Oncology Group Biospecimen Resource, San Francisco, CA; and Charles F. Lynch, University of Iowa, Iowa City, IA.

Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology

|June 7, 2023

Abstract

Purpose:

Recent increases in incidence and survival of oropharyngeal cancers in the United States have been attributed to human papillomavirus (HPV) infection, but empirical evidence is lacking.

Patients And Methods:

HPV status was determined for all 271 oropharyngeal cancers (1984-2004) collected by the three population-based cancer registries in the Surveillance, Epidemiology, and End Results (SEER) Residual Tissue Repositories Program by using polymerase chain reaction and genotyping (Inno-LiPA), HPV16 viral load, and HPV16 mRNA expression. Trends in HPV prevalence across four calendar periods were estimated by using logistic regression. Observed HPV prevalence was reweighted to all oropharyngeal cancers within the cancer registries to account for nonrandom selection and to calculate incidence trends. Survival of HPV-positive and HPV-negative patients was compared by using Kaplan-Meier and multivariable Cox regression analyses.

Results:

HPV prevalence in oropharyngeal cancers significantly increased over calendar time regardless of HPV detection assay (P trend < .05). For example, HPV prevalence by Inno-LiPA increased from 16.3% during 1984 to 1989 to 71.7% during 2000 to 2004. Median survival was significantly longer for HPV-positive than for HPV-negative patients (131 v 20 months; log-rank P < .001; adjusted hazard ratio, 0.31; 95% CI, 0.21 to 0.46). Survival significantly increased across calendar periods for HPV-positive (P = .003) but not for HPV-negative patients (P = .18). Population-level incidence of HPV-positive oropharyngeal cancers increased by 225% (95% CI, 208% to 242%) from 1988 to 2004 (from 0.8 per 100,000 to 2.6 per 100,000), and incidence for HPV-negative cancers declined by 50% (95% CI, 47% to 53%; from 2.0 per 100,000 to 1.0 per 100,000). If recent incidence trends continue, the annual number of HPV-positive oropharyngeal cancers is expected to surpass the annual number of cervical cancers by the year 2020.

Conclusion:

Increases in the population-level incidence and survival of oropharyngeal cancers in the United States since 1984 are caused by HPV infection.

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