Frequency and Role of HPV in the Progression of Epithelial Dysplasia to Oral Cancer

Abstract. Background: Human papillomavirus DNA (HPV
DNA) and p16 and p53 protein expressions were investigated
for their role in transforming dysplasia into squamous cell
carcinoma of the oral cavity in a non-smoker and non-drinker
patient group. Materials and Methods: A total of 56 oral
biopsies from non-smoker and non-drinker patients were
analyzed. The specimens were grouped into three categories:
group 1 included 31 cases of hyperplastic mucosa and mild
dysplasia, group 2 included 14 cases of moderate and severe
dysplasia, while group 3 comprised 11 cases of invasive
squamous cell carcinomas. In all cases, immunohistochemical
methods were performed to detect p16 and p53 protein
expressions. The nested polymerase chain reaction for HPV
(nested HPV-PCR) and the catalyzed signal-amplified
colorimetric DNA in situ hybridization (CSAC-ISH) methods
were applied for HPV DNA detection and typing of high-risk
genotype. Results: P16 protein, absent from all specimens of
group 1, was especially noted in group 2 (92.86%) and in
group3 (54.55%). Five out of 14 of group 2 cases (35.71%)
and 3/11 (27.27%) of group 3 were HPV DNA positive. The
HPVs detected were of both high-risk and low-risk genotype.
The analysis of the relationship between HPV and p16
protein expression revealed that all the group 2 and 3 samples
with HPV DNA, overexpressed p16 protein. Conclusion: The
results suggest that HPV could be a molecular marker in
group 2 and 3 specimens in non-smoker and non-drinker
patients. The virus may play an etiological role in
carcinogenesis in the oral cavity. The association between
HPV and p16 overexpression suggests a molecular
mechanism similar to that found in cervical cancer.