BMC Cancer (Sep 2020)

Tobacco exposure as a major modifier of oncologic outcomes in human papillomavirus (HPV) associated oropharyngeal squamous cell carcinoma

  • Hesham Elhalawani,
  • Abdallah S. R. Mohamed,
  • Baher Elgohari,
  • Timothy A. Lin,
  • Andrew G. Sikora,
  • Stephen Y. Lai,
  • Abdelrahman Abusaif,
  • Jack Phan,
  • William H. Morrison,
  • G. Brandon Gunn,
  • David I. Rosenthal,
  • Adam S. Garden,
  • Clifton D. Fuller,
  • Vlad C. Sandulache

DOI
https://doi.org/10.1186/s12885-020-07427-7
Journal volume & issue
Vol. 20, no. 1
pp. 1 – 12

Abstract

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Abstract Background The incidence of oropharyngeal squamous cell carcinoma (OPSCC) in the US is rapidly increasing, driven largely by the epidemic of human papillomavirus (HPV)-mediated OPSCC. Although survival for patients with HPV mediated OPSCC (HPV+ OPSCC) is generally better than that of patients with non-virally mediated OPSCC, this effect is not uniform. We hypothesized that tobacco exposure remains a critical modifier of survival for HPV+ OPSCC patients. Methods We conducted a retrospective analysis of 611 OPSCC patients with concordant p16 and HPV testing treated at a single institute (2002–2013). Survival analysis was performed using Kaplan-Meier analysis and Cox regression. Recursive partitioning analysis (RPA) was used to define tobacco exposure associated with survival (p 30 PY patients didn’t differ significantly from HPV- patients (p = 0.72, p = 0.27, respectively). HPV+ > 30 PY patients had substantially lower 5-year OS when compared to their ≤30 PYs counterparts: 78.4% vs 91.6%; p = 0.03, 76% vs 88.3%; p = 0.07, and 52.3% vs 74%; p = 0.05, for stages I, II, and III (AJCC 8th Edition Manual), respectively. Conclusions Tobacco exposure can eliminate the survival benefit associated with HPV+ status in OPSCC patients. Until this effect can be clearly quantified using prospective datasets, de-escalation of treatment for HPV + OPSCC smokers should be avoided.

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