Oral Cancer: Human Papilloma Virus and Epithelial Dysplasia

A study by Dr. Francesca Angiero, et al investigated the role of human papillomavirus (HPV) DNA and p16 and p53 protein expressions regarding their role in transforming dysplasia into squamous cell carcinoma of the oral cavity in a group of patients who did not smoke or drink alcohol.
The study analyzed 56 oral biopsies from the patient group, and the specimens were divided into 3 groups. The 3 groups were as follows: group A—31 cases of hyperplastic mucosa and mild dysplasia; group B—14 cases of moderate and severe dysplasia; and group C—11 cases of invasive squamous cell carcinomas. Immunohistochemical methods were used to detect p16 and p53 protein expressions; nested polymerase chain reaction for HPV and catalyzed signal-amplified colorimetric DNA in situ hybridization methods were used to detect HPV DNA and typing of high-risk genotype.
The study found that p16 protein was absent from all specimens in group A, but was present in 92.86% of the specimens in group B and 54.55% in group C. HPV DNA was detected in 35.71% of the specimens in group A and 27.27% of group B. The HPVs detected were of both high- and low-risk genotypes. All of the group B and group C specimens with HPV DNA also overexpressed p16 protein. The study suggests that HPV could be a molecular marker in the group B and group C specimens in patients who neither smoke nor drink alcohol. HPV 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. (Source: Anticancer Research, September 1, 2010, Volume 30, Number 9, pages 3435 to 3440; for online abstract, go to ar.iiarjournals.org)