CHICAGO—In general, the prognosis is good for patients with oropharyngeal cancer. In particular, tumor human papillomavirus (HPV) status is a strong and independent prognostic factor for survival among these patients. HPV status is also associated with progression-free status, suggesting that HPV-positive and HPV-negative oropharyngeal squamous cell carcinomas are distinct diagnoses, with different causes and risk factor profiles.
Explore this issue:July 2016
Research has also shown that HPV-16 is strongly coupled with the neoplastic process and that its presence is compellingly associated with oropharyngeal cancer. In an analysis published in 2005, Shahnaz Begum, MBBS, PhD, assistant professor of pathology at The Johns Hopkins University in Baltimore, and colleagues found that viral integration does not occur through the tonsillar epithelium as a field integration. Instead, p16 expression is intrinsic to the crypt epithelium and is sharply demarcated from the surface epithelium (Clin Cancer Res. 2005;11:5694-5699). P16 expression also localizes to HPV-positive cancers. The findings led Dr. Begum and colleagues to suggest that evidence of HPV-16 integration may be a meaningful finding for risk assessment, early cancer detection, and disease surveillance. In contrast, high p16 expression may not be particularly meaningful.
Additionally, research published in 2010 by Kie Kian Ang, MD, PhD [deceased], formerly a radiation oncologist at the University of Texas MD Anderson Cancer Center in Houston, and colleagues revealed a strong agreement between tumor HPV status and expression of p16, an established biomarker for the function of the HPV E7 oncoprotein (Head Neck. 2010;32:829-836). “Our data clearly indicate that HPV status and status with respect to tobacco smoking are major independent prognostic factors for patients with oropharyngeal squamous cell carcinoma, probably because they determine the molecular profile of the cancer and thus the response to therapy,” wrote the authors in their paper. “Although HPV-positive oropharyngeal squamous cell carcinoma is genetically distinct from the HPV-negative cancer with respect to patterns of loss of heterozygosity, chromosomal abnormalities, and gene-expression profiles and is inversely correlated with biomarkers for a poor prognosis in squamous-cell carcinoma of the head and neck (mutations or expression of epidermal growth factor receptor), no specific mechanism has been shown to explain the higher rates of response to radiation therapy and chemotherapy among patients with HPV-positive cancer. Epidemiologic data indicate that tobacco smoking is not a strong cofactor for the development of HPV-positive oropharyngeal squamous-cell carcinoma.”