Abstract
ObjectivesTo study the correlation between the putative cancer stem cell (CSC) markers aldehyde dehydrogenase 1 (ALDH1), cluster of differentiation 44 (CD44), sex-determining region Y-box 2 (SOX2), and octamer-binding protein 4 (OCT4) and human papilloma virus (HPV) infection using p16, the surrogate marker of HPV in oral epithelial dysplasia (OED) and normal mucosa.MethodsFive sections each from 40 histopathologically diagnosed cases of different grades of OED and 10 cases of normal oral mucosa without dysplasia were immunohistochemically stained with p16, ALDH1, CD44, SOX2, and OCT4, respectively.ResultsExpression of ALDH1 and SOX2 was significantly increased in OED cases, whereas CD44 and OCT4 expression was increased in normal mucosa. P16-positive OED cases showed upregulation of ALDH1 and OCT4 expression as compared to p16-negative cases, while CD44 and SOX2 expression was downregulated in p16-positive OED cases; however, the results were not statistically significant.ConclusionThe present study indicated a suggestive link between p16 and cancer stem cell marker expression in HPV-associated OED, and that p16 has a significant role in CSC progression in OED. This is the first study to evaluate the expression of putative CSC markers in HPV-associated OED. However, low study numbers are a potential limiting factor in this study.
Highlights
Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer death worldwide, with 95% of cases being oral squamous cell carcinoma (OSCC).[1]
Expression of aldehyde dehydrogenase 1 (ALDH1) and sex-determining region Y-box 2 (SOX2) was significantly increased in oral epithelial dysplasia (OED) cases, whereas cluster of differentiation 44 (CD44) and octamer-binding protein 4 (OCT4) expression was increased in normal mucosa
P16-positive OED cases showed upregulation of ALDH1 and OCT4 expression as compared to p16-negative cases, while CD44 and SOX2 expression was downregulated in p16-positive OED cases; the results were not statistically significant
Summary
Head and neck squamous cell carcinoma (HNSCC) is one of the leading causes of cancer death worldwide, with 95% of cases being oral squamous cell carcinoma (OSCC).[1] Oral squamous cell carcinoma is often preceded by potentially malignant disorders of the oral mucosa with an unpredictable course of progression.[2] The presence of epithelial dysplasia in potentially malignant oral disorders is generally regarded as one of the most significant predictors of malignant transformation.[3] Various studies reported a malignant transformation rate in the range 10.5%– 12.1% amongst patients with histologically confirmed oral epithelial dysplasia (OED) undergoing longterm follow-up.[4]. Even though tobacco and alcohol use are the primary risk factors for HNSCC, 25% to 35% of cases have been shown to be associated with human papillomavirus (HPV).[5,6] Patients with HPV-positive oropharyngeal tumors have distinct clinical features and a more favorable prognosis compared to those with HPV-negative tumors.[6] The reported prevalence of HPV in OSCC varies from 4% to 95%.7. Progression characteristics are not fully elucidated, this HPV-associated oral dysplasia could potentially progress into HPV-associated OSCC.[8,9]
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