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Year : 2020  |  Volume : 39  |  Issue : 2  |  Page : 364-370

Study the association among human papilloma virus subtypes 16 and 18, codon 72 P53 gene polymorphism, and oral squamous cell carcinoma in Upper Egypt: a case–control study

1 Department of General Surgery, Maxillofacial Unit, Assiut University Hospital, Assiut, Egypt
2 Department of Anatomy, College of Medicine, Jouf University, Al-Jawf; Department of Histology and Cell Biology, Faculty of Medicine, Assiut University, Assiut, Kingdom of Saudi Arabia
3 Department of Pathology, Faculty of Medicine, Assiut University, Assiut, Egypt

Correspondence Address:
MBBCh, MSc, Assistant Lecturer Hamdan S Abbas
Department of General Surgery, Maxillofacial Unit, Assiut University Hospital, Faculty of Medicine, Assiut University, El-Gamaa Street, Assiut 71515
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ejs.ejs_215_19

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Objectives To investigate the possible association among oral squamous cell carcinoma (OSCC), human papilloma virus (HPV) subtypes 16 and 18, and P53 codon 72 genotypes in Upper Egypt population. Patients and methods The present case–control study included patients presented to Maxillofacial Unit, General Surgery Department, Faculty of Medicine at Assiut University Hospital, Egypt. The biopsies were collected from patients with OSCC, patients with leukoplakia, and healthy oral mucosa as a control group. The P53c72 genotypes and gene expression for HPV subtypes 16 and 18 were determined using the real-time PCR method. Results The study was done on 69 patients: 45 cases (28 OSCC cases and 17 leukoplakia cases) and 24 patients as a control group. There was no statistically significant association between both OSCC and leukoplakia and P53 codon 72 gene polymorphism. The distribution of P53 genotypes in patients with OSCC was 21.4% were wild, 39.3% were mutant, and 39.3% were heterogeneous, whereas in leukoplakia, 23.6% were wild, 17.6% were mutant, and 58.8% were heterogeneous when compared with controls, where 45.8% were wild,12.5% were mutant, and 41.7% were heterogeneous. Conclusion No statistically significant correlation between HPV 16 and 18 genotypes and OSCC in the present study could be noted. Moreover, there is no association between codon 72 of P53 gene polymorphism and OSCC, so other environmental factors should be studied to detect the causal factors of oral carcinoma in our society.

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