Abstract
Our objective was to assess the presence of three polyomaviruses, namely SV40, JCPyV, and BKPyV, and human papillomaviruses (HPV) in adenoid cystic carcinomas (ACC) of the minor salivary glands (MiSG) in the head and neck region. The study comprised 68 MiSG ACC patients operated during 1974–2012 at the Helsinki University Hospital (Helsinki, Finland). Medical records and 68 histological samples were reviewed. Polyomaviruses were detected with quantitative PCR and the DNA-positive samples were further analyzed for the presence of viral tumor T antigen (T-ag) with immunohistochemistry. HPV genotyping was performed with a Multiplex HPV Genotyping Kit. Only JCPyV DNA was found in ACC samples, being present in 7 (10.3%) out of the 68 samples. The viral load of JCPyV was low varying between 1 to 226 copies/μg DNA. The JCPyV-positive samples originated from trachea (two samples), paranasal sinuses (one), and oral cavity (two). Additionally, JCPyV positivity was found in one lung metastasis of a tracheal tumor and one local disease failure of an oral cavity tumor. Three JCPyV DNA-positive samples showed weak nuclear staining for large T-ag. In conclusion, only JCPyV but not SV40, BKPyV, or HPV was found in ACC from the upper and lower airways. JCPyV copy numbers were low which might support its role as a “hit and run agent” in ACC carcinogenesis.
Highlights
Adenoid cystic carcinoma (ACC) is a rare malignancy of glandular structures, which most commonly (70%) appears in salivary glands [1]
All 68 samples remained negative for BK polyomavirus (BKPyV), Simian vacuolating virus 40 (SV40), and human papilloma virus (HPV) but seven of 68 (10.3%) samples showed JC polyomavirus (JCPyV) DNA positivity
Our present results show that JCPyV may be found in minor salivary glands (MiSG) ACC samples by quantitative polymerase chain reaction (qPCR)
Summary
Adenoid cystic carcinoma (ACC) is a rare malignancy of glandular structures, which most commonly (70%) appears in salivary glands [1]. Minor glands (MiSGs) are involved more often than major glands (MaSGs) [1, 2]. Etiopathogenesis for ACC as well as for many other salivary gland tumors is still unknown. In ACC, genetic studies have found MYB/NFIB translocations and this fusion oncogene is overexpressed [3]. Studies have provided evidence for Notch-pathway alterations in 11 to 29% of patients [4]. As the pathogenesis of ACC remains unknown, even viral background should be considered. Distinguished viral etiological factors among head and neck cancers are Epstein-Barr virus (EBV) in nasopharyngeal carcinoma and human papilloma virus (HPV) 16 in oropharyngeal squamous cell carcinoma [5, 6]
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