Abstract
This study investigated the presence of human papillomavirus (HPV) DNA and viral types in 33 cases of oral squamous cells carcinoma (OSCC) and compared the immunohistochemical expression of the cell-cycle markers p21 and pRb between cases of the disease with and without HPV. DNA was extracted from paraffin-embedded tissue and amplified by PCR for the detection of HPV DNA. Viral typing was performed by dot blot hybridization. Immunohistochemistry was performed by the streptavidin-biotin technique. HPV DNA was detected in 11 (33.33%) of the 33 cases. The prevalent viral type was HPV 18 (81.81%). A significant association was observed between the presence of HPV and immunohistochemical expression of pRb, but not between p21 expression and the presence of the virus. The low frequency of detection of HPV DNA in OSCC suggests a possible participation of the virus in the development and progression of only a subgroup of these tumors.
Highlights
Various studies have investigated the role of human papillomavirus (HPV) in oral squamous cells carcinoma (OSCC) but the results are highly controversial
Lanes 1-7, samples from patients; lane 8, HeLa cell DNA infected with HPV 18; lane 9, negative control (H2O); lane 10, molecular marker (100 pb) association between the presence of HPV and immunohistochemical expression of pRb (p=0.044)
HPV DNA was detected in a low percentage of OSCC cases (33.33%), suggesting that HPV plays a key role in the development and progression of only a small subgroup of these carcinomas
Summary
Various studies have investigated the role of human papillomavirus (HPV) in oral squamous cells carcinoma (OSCC) but the results are highly controversial. Most reports have shown that HPV 16 is the most prevalent type in both oral and genital tumors[1]. Abnormalities in several components of the cell-cycle regulatory machinery have been observed in oral cancers as well as in other types of cancer. Protein p21 is a universal inhibitor of cyclin-dependent kinases (CDKs) that mediates cell cycle arrest in the G1 and G2/M phase to prevent DNA replication in cells in which this molecule is damaged. Protein pRb plays an important role in cell-cycle regulation. When cells are stimulated by growth factors, this protein is inactivated by phosphorylation and cells progress from the G1 to the S phase. The hyperphosphorylated form of pRb releases E2F transcription factors which, in turn, activate the transcription of various target genes[17]
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