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Sub-category:
Head & Neck Cancer
Category:
Head and Neck Cancer
Meeting:
2011 ASCO Annual Meeting
Session Type and Session Title:
Poster Discussion Session, Head and Neck Cancer
Abstract No:
5529
Citation:
J Clin Oncol 29: 2011 (suppl; abstr 5529)
Author(s):
A. Chaturvedi, E. Engels, R. Pfeiffer, B. Y. Hernandez, W. Xiao, E. Kim, B. Jiang, M. Goodman, M. Sibug-Saber, W. Cozen, L. Liu, C. Lynch, N. Wentzensen, R. Jordan, S. Altekruse, W. F. Anderson, P. Rosenberg, M. L. Gillison; National Cancer Institute, Rockville, MD; Cancer Research Center of Hawaii, Honolulu, HI; The Ohio State University, Columbus, OH; University of Southern California, Los Angeles, CA; University of Iowa, Iowa City, IA; University of California, San Francisco, San Francisco, CA; Department of Health and Human Services/National Institutes of Health/National Cancer Institute/Division of Cancer Epidemiology and Genetics, Bethesda, MD
Abstracts that were granted an exception in accordance with ASCO's Conflict of Interest Policy are designated with a caret symbol (^) here and in the printed Proceedings.
Abstract Disclosures
Abstract:
Background: Recent increases in incidence and survival of oropharyngeal cancers in the United States (U.S.) have been attributed to human papillomavirus (HPV) infection, but empirical evidence is lacking. Methods: HPV status was determined for 271 oropharyngeal cancer cases (1984-2004) collected by population-based cancer registries of the National Cancer Institute’s Surveillance, Epidemiology, and End Results program in Hawaii, Iowa, and Los Angeles. Tumor HPV status was determined by PCR and genotyping (Inno-LiPA), HPV16 viral load, HPV16 mRNA expression, and HPV16 in situ hybridization. Trends in HPV prevalence across four calendar periods were estimated using logistic regression. Survival of HPV-positive and HPV-negative cases was compared by Kaplan-Meier and multivariate Cox regression analyses. Results: HPV prevalence in oropharyngeal cancers significantly increased over calendar time regardless of HPV detection assay (p-trend<0.05). For example, HPV prevalence by Inno-LiPA increased more than 4-fold from 16.3% during 1984-1989 to 72.7% during 2000-2004. Median survival was significantly greater for HPV-positive vs. HPV-negative cases (131 vs. 20 months; log-rank p<0.001; adjusted hazard ratio=0.31; 95%CI=0.21-0.46). Survival significantly increased across calendar periods for HPV-positive (p=0.003) but not for HPV-negative cases (p=0.18). The difference in survival between HPV-positive and HPV-negative cases was greater for cases treated by radiation (HR= 0.23; 95%CI=0.09-0.59) than those not treated by radiation (HR=0.80; 95%CI=0.40-1.60; p-interaction=0.002). Population-level incidence of HPV-positive oropharyngeal cancers increased by 225% during 1988-2004 (0.8/100,000 to 2.6/100,000), while incidence for HPV-negative cancers declined by 50% (2.0/100,000 to 1.0/100,000). Should recent incidence trends continue, the annual number of HPV-positive oropharyngeal cancers among men is expected to surpass that of cervical cancers among women by the year 2020 in the U.S. Conclusions: Increases in the population-level incidence and survival of oropharyngeal cancers in the U.S. since 1984 are caused by HPV infection.
 Associated Presentation(s):
Other Abstracts in this Sub-Category:
Abstracts by A. Chaturvedi:
Presentations by A. Chaturvedi:
Educational Book Manuscripts by A. Chaturvedi:
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