Merkel cell polyomavirus (MCPyV) is associated with Merkel cell carcinoma (MCC). In tumor cells the MCPyV large T antigen (LT-Ag) is frequently found truncated and this is considered a major tumor-specific signature. The role of MCPyV in other, non-MCC tumours, is little known. Viral DNA and/or tumour-specific mutations have been sometimes detected in different tumours, but such data are not unequivocal and the involvement of the virus in the tumorigenesis is not clear. In a previous study, we demonstrated a significantly higher prevalence of MCPyV DNA in formalin fixed paraffin embedded (FFPE) porocarcinoma tissues compared to the normal skin. In the present study, we investigated the presence of truncating mutations in MCPyV LT-Ag coding region in porocarcinoma specimens. Using several overlapped PCR primer pairs, the complete LT-Ag sequence from two biopsies were obtained. No truncating mutations were detected. The lack of truncating mutations in LT-Ag sequence does not seem to support the role of MCPyV in porocarcinoma oncogenesis. However, an oncogenetic mechanism, different from that proposed for MCC and not associated with the LT-Ag mutations/deletions, cannot be excluded. Further studies of more sequences coding for LT-Ag would be needed to verify this hypothesis.

中文翻译：

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从毛孔癌获得的默克尔细胞多瘤病毒 (MCPyV) DNA 的大 T 抗原 (LT-Ag) 序列中未检测到截短突变

默克尔细胞多瘤病毒 (MCPyV) 与默克尔细胞癌 (MCC) 相关。在肿瘤细胞中，MCPyV 大 T 抗原 (LT-Ag) 经常被发现被截短，这被认为是主要的肿瘤特异性特征。 MCPyV 在其他非 MCC 肿瘤中的作用鲜为人知。有时在不同的肿瘤中检测到病毒DNA和/或肿瘤特异性突变，但这些数据并不明确，并且病毒在肿瘤发生中的参与尚不清楚。在之前的一项研究中，我们证明与正常皮肤相比，福尔马林固定石蜡包埋 (FFPE) 毛孔癌组织中 MCPyV DNA 的患病率显着更高。在本研究中，我们研究了毛孔癌标本中 MCPyV LT-Ag 编码区是否存在截短突变。使用几个重叠的 PCR 引物对，从两次活检中获得了完整的 LT-Ag 序列。没有检测到截短突变。 LT-Ag 序列中缺乏截短突变似乎并不支持 MCPyV 在毛孔癌发生中的作用。然而，不能排除与 MCC 提出的致癌机制不同且与 LT-Ag 突变/缺失无关的致癌机制。需要对更多 LT-Ag 编码序列进行进一步研究来验证这一假设。