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Assessing The Role of Human Papillomavirus (Types 6 And 11) In Tumorigenesis and Its Relationship to P53 Tumor Suppressor Gene Protein Expression in A Series of Benign and Malignant Laryngeal Tumors.

Sep 2026 · Natural Resources for Human Health · Vol 6, pp. 1100-1114 · 0 citations · 65 references

Abstract

Background: Laryngeal benign and malignant neoplasia have a complex etiology. The two most significant ones are drinking and smoking. Laryngeal cancer has been linked to mucosal high-risk oncogenic Human Papillomavirus (hrHPV) types. Additionally, it has been shown that low-risk HPV (lrHPV) varieties are frequently found in head and neck malignancies. The etiology and carcinogenesis of various HPV types have been the subject of numerous investigations.Objectives: To evaluate a potential role of lrHPV6/11 in the pathogenesis and/or tumorigenesis of the tissues of laryngeal benign and malignant tumors by examining the co-expression of low-risk HPV 6/11 gene products and tumor suppressor gene protein (p53) expressions.Methods: Using chromogenic in situ hybridization for screening and immunohistochemistry for evaluating p53 overexpression, a retrospective study was carried out on 100 and 57 tissue block specimens with various laryngeal tumors to identify and genotype for screening and lrHPV6/11 by molecular technique. Results: The polyps group had a higher percentage of positive signal HPV6/11/p53 intensities (4:44.4%) than the malignant (5:33.3%), nodules (2:28.6%), and seemingly healthy (1:9.1%) groups. In the malignant and polyp groups, the high positive signal percentage of HPV6/11/P53 score was moderate (++) at 2:100% and 1:33%, respectively. There were notable differences in the positive signal percentage of HPV6/11/P53 low score between the nodules group (1:100%) and the polyps group (1:33.3%).Conclusion: The co-expression of lrHPV6/11DNA and p53 cannot trigger tumorigenesis, but it facilitate the aggregation of somatic mutagenesis subordinate to elevated DNA-damage and inhibition of cellular pathway for DNA damage response mechanism (cDDR) , therefore , co-infection of lrHPV type 6 as well as HPV11 with elevated level of p53 in benign and malignant laryngeal tumors could reflect a possible role in pathogenesis and tumorigenesis of potentially precancerous lesions

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