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Human Papillomavirus and Oropharyngeal Cancer Survival To the Editor: Ang et al. (July 1 issue)1 developed a risk model for death from oropharyngeal squamous-cell carcinoma on the basis of human papillomavirus (HPV) status, pack-years of tobacco smoking, tumor stage, and nodal stage. Their results showed that the risk of death significantly increased with each additional pack-year of tobacco smoking. It would be interesting to include in the statistical Cox regression analysis the pattern of alcohol consumption. Recent studies2 have indicated that alcohol consumption has a role in the genesis of head and neck cancer in HPV-positive patients, showing consistency with the observation and hypothesis (reinforced by the study by Ang et al.) that HPV infection is not a sufficient cause of cancer and that it requires the accumulation of additional cellular changes. Gabriele Rossi, M.D. Walden University Minneapolis, MN
[email protected] No potential conflict of interest relevant to this letter was reported. 1. Ang KK, Harris J, Wheeler R, et al. Human papillomavirus
and survival of patients with oropharyngeal cancer. N Engl J Med 2010;363:24-35.
this week’s letters 1576 Human Papillomavirus and Oropharyngeal Cancer Survival 1577 An Entirely Subcutaneous Implantable Cardioverter–Defibrillator 1578 Interstitial Lung Disease and Gefitinib 1580 Dietary Therapy in Hypertension 1583 Poppers-Associated Retinal Toxicity
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2. Smith EM, Rubenstein LM, Haugen TH, Hamsikova E, Turek
LP. Tobacco and alcohol use increases the risk of both HPVassociated and HPV-independent head and neck cancers. Cancer Causes Control 2010;21:1369-78.
To the Editor: In the Discussion section of their article, Ang et al. conclude that p16 expression is a very good surrogate for tumor HPV status. We do not agree with such a view, since p16 is often overexpressed in basaloid carcinomas that are not related to HPV infection. With the use of E6/ E7 messenger RNA levels as conclusive evidence of HPV involvement, positive p16 immunostaining of squamous-cell cancer of the head and neck is 100% sensitive but only 79% specific.1 This discrepancy implies that to a certain extent p16 is not a perfect surrogate. Since the overwhelming majority of HPV-associated oropharyngeal cancers (90 to 95%) are attributable to HPV-16 and since the specificity of positive HPV-16 in situ hybridization is close to 100%,2 it is more rational to recommend the combination of p16 immunostaining and HPV-16 in situ hybridization as a detection method to eliminate avoidable errors in future clinical trials. Xiaofang Gao, M.D. Liangan Chen, Ph.D., M.D. Chinese People’s Liberation Army General Hospital Beijing, China
[email protected] No potential conflict of interest relevant to this letter was reported. 1. Smeets SJ, Hesselink AT, Speel EJ, et al. A novel algorithm
for reliable detection of human papillomavirus in paraffin embedded head and neck cancer specimen. Int J Cancer 2007;121: 2465-72. 2. Adelstein DJ, Ridge JA, Gillison ML, et al. Head and neck squamous cell cancer and the human papillomavirus: summary of a National Cancer Institute State of the Science Meeting, November 9-10, 2008, Washington, D.C. Head Neck 2009;31:1393-422.
n engl j med 363;16 nejm.org october 14, 2010
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