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BACKGROUND:Patients with oropharyngeal squamous cell carcinoma (OPSCC) treated with intensity-modulated radiotherapy (IMRT) were stratified by p16 status, neck dissection, and chemotherapy to correlate these factors with outcomes. METHODS: A total of 112 patients with OPSCC treated with IMRT from 2002 to 2008 were retrospectively analyzed. All patients received RT to 66-70 Gray. Forty-five of the tumors were p16 positive (p16þ), 27 were p16 negative (p16À), and 41 had unknown p16 status. Sixty-two patients had postradiation neck dissections. Nine patients with p16À tumors and 28 patients with p16þ tumors received chemotherapy. The distribution of T, N, and stage grouping among the p16þ and p16À patients was not significantly different, and 87.5% patients had stage III/IV disease. RESULTS: The median follow-up was 26.3 months. For patients with p16þ tumors, p16À tumors, and the overall cohort, the actuarial 3-year locoregional progression-free survival rate was 97.8%,73.5%, and 90.5% respectively (P ¼ .006) and the disease-free survival rate was 88.2%, 61.4%, and 81.7%, respectively (P ¼ .004). Patients with p16þ tumors had an 89.5% and 87.5% pathologic complete response (CR) on neck dissection with and without chemotherapy, respectively. In contrast, patients with p16À tumors had a 66.7% and 25.0% pathologic CR on neck dissection with and without chemotherapy, respectively. CONCLUSIONS: In this series, p16 status was found to be a significant predictive biomarker and patients with p16þ tumors had much better outcomes than patients with p16À tumors. Further investigation is warranted to determine whether less intense therapy is appropriate for selected patients with p16þ OPSCC, whereas more aggressive strategies are needed to improve outcomes in patients with p16À disease.

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In conjunction with other clinical parameters, p16 status can help predict the need for post-RT ND in patients with OP-SCCA. Although close observation may be warranted in selected patients with p16+ tumors, patients with p16- tumors are at much higher risk for residual neck disease, even when initial nodal disease is less advanced.

BACKGROUND:Patients with human papillomavirus (HPV)-positive oropharyngeal carcinoma (OC) have better prognosis than patients with HPV-negative OC. The objective of the current study was to assess how different practices across the United States treat patients with OC with respect to screening for HPV DNA or p16. METHODS: Five hundred forty-two randomly selected radiation oncologists were sent an 11-question survey by email regarding the use of HPV/p16 screening in OC. The questionnaire addressed demographics of the practice, intensity-modulated radiotherapy (IMRT) use, screening practices for HPV DNA or p16, which year this began, the use of HPV or p16 data to direct patient care, and future plans for its use if it had not already been instituted. RESULTS: One hundred ninety-two responses (39.6%) were received. Thirty-five percent of respondents (67 of 188) reported screening for HPV DNA routinely, whereas 4.8% of respondents (9 of 188) reported screening for p16. Of the physicians who did not use screening techniques, 37.2% (44 of 118 respondents) reported future plans to institute these screening techniques, 20% (9 of 45 respondents) stated plans to institute these techniques in the next 6 months, 55.5% (25 of 45 respondents) stated plans to institute these techniques within 6 months to 1 year, and 22.2% (10 of 45 respondents) stated plans to institute these techniques within 1 to 2 years. Academic physicians were more likely to use screening techniques (62.7%; P < .001) compared with private practitioners (31.4%). Only 12.4% of respondents reported using HPV or p16 data to direct care. CONCLUSIONS: Approximately 40.4% of radiation oncology practices that responded to a survey in the United States screened for HPV DNA or p16 in OC, whereas only 12.4% used it to further direct care. This number appears to be growing rapidly. Clinical trials to further elucidate how HPV or p16 status should direct care in OC are warranted. Cancer 2010;116:514-9.