Abstract
Objective Head and Neck Squamous Cell Carcinoma (HNSCC) represents the sixth most common malignancy worldwide and is characterized by dismal prognosis and poor patient survival. More than 75% of HNSCCs arise on a precancerous lesion. CD44 is a membrane bound glycoprotein stem-cell marker strongly expressed in normal oral mucosal epithelium. Upregulated in HNSCC, CD44 participates in key cell functions including cell division, migration and adhesion, and is recognized as a negative prognosticator for the disease. In addition, HPV(+) tumors show decreased CD44 levels when compared to HPV(-) neoplasms. We aimed to investigate the role of HPV infection in the regulation of CD44 expression in oral epithelial dysplasia (OED) and invasive HNSCC. Methods Formalin fixed, paraffin embedded specimens of HPV(+) OED (N=16), HPV(-) OED (N=15) and HNSCC (N=29) were evaluated by immunohistochemistry for CD44. Among the carcinoma specimens, five were HPV(+) and 24 HPV(-); 13 well-differentiated (WD), 5 moderately-differentiated (MD) and 6 poorly-differentiated (PD). HPV positivity was confirmed by immunohistochemistry for the surrogate marker p16. CD44 immunoreactivity was semi-quantitatively evaluated. Statistical analysis was performed using one-way ANOVA. Results HPV(+) OEDs (mean expression=1.74) showed significantly lower CD44 membranous immunoexpression than HPV(-) OEDs (mean expression=2.42, p Conclusions Lower CD44 expression in HPV(+) OEDs and HNSCCs may reflect decreased numbers of stem cells in HPV-driven lesions. The latter, can explain the limited frequency of malignant transformation in HPV(+) OEDs and better survival rates for patients with HPV(+) tumors.
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