More Pravin, Kheur Supriya, Patekar Deepali, Kheur Mohit, Gupta Archana A, Raj A Thirumal, Patil Shankargouda
Department of Oral Pathology and Microbiology, M. A. Rangoonwala College of Dental Sciences, Pune, India.
Department of Oral Pathology and Microbiology, Dr. D. Y. Patil Dental College and Hospital, Dr. D. Y. Patil Vidyapeeth, Pune, India.
Transl Cancer Res. 2020 Apr;9(4):3119-3125. doi: 10.21037/tcr.2020.03.81.
Published studies assessing the association of human papillomavirus (HPV) and oral cancer, often include cases with additional confounders such as alcohol, tobacco, thus, precluding the assessment of HPV as a independent risk factor. Further apart from eliciting the mere presence of HPV, it is vital that the nature of the association is delineated for eliciting a causal inference. Thus, the present study assessed the presence and nature of the association of HPV in oral cancer cases with and without known risk factors.
The study compares the prevalence of HPV in oral cancer cases with known risk factors (group 1, n=15) to oral cancer (group 2, n=15) and oral epithelial dysplasia (group 3, n=15) cases with no known risk factors using PCR. Cases which are positive for HPV were subjected to p16 and p53 immunostaining to determine potential causal inference.
HPV 16 was detected in only 1 case of group I, 3 cases of group II, and was absent in group III. HPV 18 was negative in all the 3 groups. All the HPV positive cases were negative for p16 and positive for p53 immunostaining.
Only a minor proportion of oral cancer cases without risk factors were positive for HPV 16. Even among these HPV 16 positive cases, the immunostaining profile (p53 positive and p16 negative) excludes the involvement of E6 and E7 mediated carcinogenesis. Thus even the weak HPV association noted in the present study cases may not be of causal nature.
已发表的评估人乳头瘤病毒（HPV）与口腔癌关联的研究，通常纳入了酒精、烟草等其他混杂因素的病例，因此无法将HPV作为独立风险因素进行评估。除了确定HPV的单纯存在之外，明确这种关联的性质对于得出因果推断至关重要。因此，本研究评估了有无已知风险因素的口腔癌病例中HPV关联的存在情况及性质。
本研究采用聚合酶链反应（PCR），比较了有已知风险因素的口腔癌病例（第1组，n = 15）与无已知风险因素的口腔癌病例（第2组，n = 15）及口腔上皮发育异常病例（第3组，n = 15）中HPV的患病率。HPV检测呈阳性的病例进行p16和p53免疫染色，以确定潜在的因果推断。
第1组仅1例检测到HPV 16，第2组有3例，第3组未检测到。3组中HPV 18均为阴性。所有HPV阳性病例p16免疫染色均为阴性，p53免疫染色均为阳性。
无风险因素的口腔癌病例中只有一小部分HPV 16呈阳性。即使在这些HPV 16阳性病例中，免疫染色特征（p53阳性和p16阴性）排除了E6和E7介导的致癌作用。因此，即使在本研究病例中观察到的HPV弱关联可能也不是因果性质的。
