默克尔细胞多瘤病毒(MCPyV)与默克尔细胞癌(MCC)有关。在肿瘤细胞中,经常发现MCPyV大T抗原(LT-Ag)被截短,这被认为是主要的肿瘤特异性特征。MCPyV在其他方面的作用,非MCC肿瘤,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。但是这些数据并不明确,病毒在肿瘤发生中的参与也不清楚。在之前的研究中,我们证实,与正常皮肤相比,在福尔马林固定石蜡包埋(FFPE)的腺癌组织中,MCPyVDNA的患病率明显更高.在本研究中,我们调查了胃癌标本中MCPyVLT-Ag编码区截断突变的存在。使用几个重叠的PCR引物对,从两个活检获得完整的LT-Ag序列。没有检测到截短突变。LT-Ag序列中缺乏截断突变似乎不支持MCPyV在骨癌肿瘤发生中的作用。然而,一种致癌机制,与MCC的建议不同,与LT-Ag突变/缺失无关,不能排除。需要对更多编码LT-Ag的序列的进一步研究来验证这一假设。
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.