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P53-tumor suppressor gene overexpression in human papilloma virus-infected patients with oral squamous cell carcinoma | ||
| Journal of baghdad college of dentistry | ||
| Article 1, Volume 23, Issue 0, 2011, Pages 70-76 | ||
| Authors | ||
| Saad Hasan Mohammed Ali; Athraa Yahya Al-Hijazi; Basim M.Khashman | ||
| Abstract | ||
| Background: Via molecular DNA hybridization, more than 120 different genotypes of human papilloma virus have been confirmed. Many studies have described an association of high risk-HPV genotypes and overexpression of mutated P53 gene with a variety of oral benign tumors as well as malignant squamous cell carcinomas. This study aimed to: 1) Determine the prevalence of HPV DNA in archival tissue specimens with a range from apparently healthy tissue to invasive oral S.C.C by using one of the recent versions of insitu hybridaization. 2) Define the genotypes of the obtained HPV and to find out rational significance and relation of such genotypes to the severity of underlying lesions. 3) Study the correlation of over expressed products of mutant p53 genes with HPV-negative and HPV-related oral cancers. Materials and methods: A total number of 72 tissue specimens were collected from 41 patients with oral squamous cell (OSCC) and 31 individuals with apparently-healthy oral tissues (AHOT). The molecular detection methods for HPV detection and genotyping were performed by in situ hybridization using cocktailed- and specified high- risk HPV DNA probes, respectively. Immunohistochemical method was used to demonstrate the prevalence of P53 overexpression in those oral cancers. Results: Among oral OSCC group, 16 archived tissue blocks were found to contain HPV DNA related to the cocktailed HPV genotypes. This result constituted 39% of the total oral SCC screened for HPV DNA. HPV-18 positive oral SCC tissue blocks constituted (68.75%) whereas HPV genotypes 16& 31/33 constituted (43.75%) & (12.5%), respectively. Mixed infection of HPV genotypes was found in 31.3%. Interestingly, HPV DNA detection was documented in 3.2% of those appeared as healthy tissues on histopathological examinations. Among oral SCC group, 22(53.7%) showed over expression of P53 tumor suppression gene. Interestingly, the co-occurrence of mutated P53 overexpression and high oncogenic risk HPV genotypes was documented in 75% of Iraqi patients with OSCC. Conclusions: The significant prevalence of high oncogenic HPV genotypes detection in those patients with OSCC indicates a herald marks for the spread of such important sexually transmitted infection among Iraqi general population. Both of mutated p53 genes as well as high-oncogenic risk HPV genotypes could play an important role in oral carcinogenesis. | ||
| Keywords | ||
| oral squamous cell carcinoma; Human Papilloma Virus; In Situ Hybridization | ||
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