Abstract
e17004 Background: HPV-associated head and neck squamous cell carcinoma (HNSCC) seems to increase during the last decades and has been commonly described to associate with younger patients. However the true prevalence of HPV in this specific population remains unclear. Methods: We collected archival 56 paraffin-embedded tumor tissue samples from HNSCC patients diagnosed and treated at King Chulalongkorn Memorial Hospital between 2000 and 2010. The major inclusion criterion was the age at diagnosis less than 45 year-old. HPV status was determined by HPV polymerase chain reaction (PCR) with degenerated primer covered over 37 HPV serotypes including high-risk HPV6, 11, 16, 18, 31 and 33. Additional immunohistochemical stain (IHC) of p16 was performed. The clinicopathological correlations with HPV status were analyzed. Results: Fourteen (25%) of the 56 HNSCC samples exhibited HPV DNA by PCR. Among cancer sites, 7 of 23 (30%) oral cavity, 3 of 11 (27%) oropharynx, and 4 of 22 (18%) hypopharynx and larynx primary organs displayed HPV DNA in tumor tissues. There was no major difference in the demographic data, tumor characteristics and treatment modalities between HPV DNA-negative and HPV DNA-positive samples. HPV DNA-positive tumors tended to have a better 2-year overall survival when compared with HPV DNA-negative tumors (66 and 40 percent, respectively) (p=0.10). After adjusted for independent prognostic variables of cigarette smoking, alcohol consumption, site of primary tumor and nodal status, only HPV DNA status was a predictor for a better survival (HR 0.16; 95%CI, 0.01-0.66). Additional IHC for p16 expression revealed 8 of 48 (16%) of p16 overexpression with twenty-two percent concordant rate with HPV PCR. Conclusions: Though HPV genome was moderately found in our young HNSCC patients, HPV DNA was not associated with a significant better survival in the primary analysis. Nevertheless, multivariate analysis adjusting for prognostic variables demonstrated a significant better prognosis in HPV DNA-positive tumors in this subset of HNSCC. Low concordant rate between HPV DNA and p16 overexpression in these young populations may caution the use of p16 overexpression as a surrogate marker of HPV.
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