| ORIGINAL ARTICLE |
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| Year : 2021 | Volume
: 12
| Issue : 2 | Page : 61-65 |
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Immunohistochemical study of the role of human papillomavirus, epstein–barr virus, and P16INK4a expression in head-and-neck squamous cell carcinomas
Babatunde Moses Duduyemi1, Evans Aboagye2
1 Department of Pathology, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana; Department of Anatomic Pathology and Forensic Medicine, Afe Babalola University, Ado Ekiti, Nigeria
2 Department of Pathology, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana
Correspondence Address:
Dr. Babatunde Moses Duduyemi
Department of Anatomic Pathology and Forensic Medicine, Afe Babalola University, Ado Ekiti
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/atp.atp_7_21
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Background: Studies over the years have established that human papillomavirus (HPV) and Epstein–Barr virus (EBV) are major etiological agents in subsets of head-and-neck squamous cell carcinomas (HNSCCs). This study further explores the concurrence of HPV and EBV together with P16INK4a expression in HNSCCs, providing additional insights into their unique role in establishing a virus-induced carcinogenesis. Materials and Methods: A retrospective cross-sectional study utilizing immunohistochemistry was employed to establish the presence of HPV, EBV, and P16INK4a expression in HNSCC archived tissue samples. Results: A total of 121 selected HNSCC cases were included in the study, with male preponderance (n = 86) and majority of the cases occurring in patients ≤54 (n = 62). The most common site of occurrence was the oral cavity (n = 29), followed by larynx (n = 27) and nasal cavity and paranasal sinuses (n = 24), respectively. The study recorded 18 (14.9%) HPV-positive tumors, 7 (5.8%) EBV-positive tumors, and 2 (1.7%) tumors coinfected with HPV and EBV. P16INK4a expression was recorded in 42.1% (n = 51) of the tumors. Although P16INK4a expression correlated weakly with both HPV (r = 0.116) and EBV (r = 0.205) positivity, it showed a statistically significant expression with EBV positivity (P = 0.024). Conclusion: The observed pattern of HPV association with P16INK4a overexpression was consistent with earlier reported studies, and as such, the study reinforces the assertion that P16INK4a can be used as a surrogate marker for HPV-positive tumors. However, additional studies are required to validate its suitability in tumor sites other than oropharyngeal squamous cell carcinoma. |
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