Abstract
IntroductionsThe incidence of human papillomavirus (HPV)-related oropharyngeal squamous cell carcinoma (OPSCCs) is rising in developed nations. Studies have shown that these virally mediated tumours are epidemiologically, clinically, and biologically different than other head and neck squamous cell carcinomas and traditional concepts of field cancerization may not apply to HPV-related oropharyngeal cancer.ObjectiveThe purpose of this study was to evaluate the rate of second primary tumors and the diagnostic yield of field cancerization work up in the upper aerodigestive tract in patients with HPV-related and HPV-unrelated oropharyngeal squamous cell carcinoma.DesignRetrospective review.SettingTertiary cancer care centers in Alberta.MethodsRetrospective review of 406 patients diagnosed with OPSCC in Alberta between 2005 and 2009. HPV-status of tumours was determined by tissue microarray using immunohistochemistry staining for p16.Main outcome measuresPrimary outcome: incidence of upper aerodigestive tract second primary tumours in p16-positive versus p16-negative OPSCC. Secondary outcomes: diagnostic yield of traditional field cancerization work-up in p16-positive versus negative patients.ResultsThe overall rate of SPTs was 7.4% (30/406). The incidence rate of SPTs was significantly lower in p16-positive patients (0.7 per 100 patient-yrs vs. 8.5 in p16-negative, p < 0.0001). Field cancerization work-up for synchronous lesions in the upper aerodigestive tract, including panendoscopy and whole-body PET-CT, had decreased diagnostic yield in p16-positive patients (2.8% vs. 10.2% in HPV-negative patients, p=0.02).ConclusionsPatients with HPV-related OPSCC, who are non-smokers have decreased risk of developing second primary tumours in the upper aerodigestive tract and have low yield on field cancerization work-up. This study provides further evidence that virally mediated OPSCC are distinct and may benefit from alternate diagnostic pathways.
Highlights
The incidence of human papillomavirus (HPV)-related oropharyngeal squamous cell carcinoma (OPSCCs) is rising in developed nations [1,2,3,4]
The incidence rate of SPTs was significantly lower in p16-positive patients (0.7 per 100 patient-yrs vs. 8.5 in p16-negative, p < 0.0001)
This study provides further evidence that virally mediated OPSCC are distinct and may benefit from alternate diagnostic pathways
Summary
The incidence of human papillomavirus (HPV)-related oropharyngeal squamous cell carcinoma (OPSCCs) is rising in developed nations [1,2,3,4]. The concept of ‘field cancerization’ has been described in head and neck squamous cell carcinoma (HNSCC) with traditional risk factors such as alcohol and tobacco. It proposes that HNSCCs have a high propensity for local recurrences and second primary tumours due to a large pre-neoplastic field of mucosal epithelium exposed to carcinogens. Molecular studies have shown that this epithelium contains cells that have alterations of the PI3K-PTEN-AKT pathway [10]. This pathway results in perturbed p53 and retinoblastoma (RB) pathways, both of which are broadly implicated in carcinogenesis [11]. This includes routine panendoscopy and PET-CT scanning in many centers for detection of second primary tumours in this musocal field [12,13]
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