Abstract
ObjectivesThe purpose of this study is to determine the prevalence and clinical impact of human papillomavirus (HPV) related laryngeal squamous cell carcinoma (LSCC).MethodsA total of 106 LSCC patients who underwent primary surgical resection with or without adjuvant radiotherapy/chemoradiotherapy were enrolled retrospectively. Tumors collected from paraffin-embedded samples were used for HPV detection by polymerase chain reaction and in situ hybridization technique. Clinicopathological parameters were recorded for analysis.ResultsThe prevalence of HPV in patients with LSCC was 13.2% in our series and 12 out of 14 (85.7%) HPV-positive tumors were HPV-16. The patients with HPV-positive tumors were older (p = 0.042), less local/regional recurrence (p = 0.037) and non-smoker (p = 0.068). There was no significant difference in the 5-year overall survival (OS) (p = 0.8056) between HPV-positive and -negative tumors. The patients with HPV-positive tumors had a better 5-year disease-specific survival (DSS) (100% vs. 84.8%, p = 0.1485), although the difference did not reach statistical significance. However, the local/regional control rate was significantly better in HPV-positive tumors than in HPV-negative tumors (100% vs. 75%, p = 0.0494).ConclusionsA low prevalence of HPV infection in our series suggests that HPV is not a major cause of LSCC. However, a 100% local/regional control rate and DSS were observed in HPV-positive tumors. This finding suggests a different tumor behavior between HPV-positive and HPV-negative LSCC. Further research with a larger sample size is necessary to confirm our observations.
Highlights
The high-oncogenic risk types of human papillomavirus (HPV) can induce tumorigenesis via the E6 and E7 viral oncoproteins
Additional Information and Declarations can be found on page 9
Previous reports have not observed a survival advantage in HPV-positive laryngeal squamous cell carcinoma (LSCC), we found that patients with HPVpositive LSCC had 100% 5-disease-specific survival (DSS) and 100% local/regional control rates if they underwent primary surgery
Summary
The high-oncogenic risk types of human papillomavirus (HPV) can induce tumorigenesis via the E6 and E7 viral oncoproteins. These oncoproteins can functionally inactivate the tumor suppressor proteins p53 and pRb, resulting in a loss of cell cycle regulation and immortalization of keratinocytes (Havre et al, 1995; Munger & Howley, 2002). HPV and head and neck squamous cell carcinoma (HNSCC) was identified, with an overall prevalence of 25% of tumors harboring HPV There is mounting evidence of a strong association between HPV and oropharyngeal squamous cell carcinoma (OPSCC), as documented in Europe and the United States (Ang et al, 2010).
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