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No detectable truncating mutations in large T antigen (LT-Ag) sequence of Merkel cell polyomavirus (MCPyV) DNA obtained from porocarcinomas.
Arvia, Rosaria; Sollai, Mauro; Massi, Daniela; Asensio-Calavia, Patricia; Urso, Carmelo; Zakrzewska, Krystyna.
Affiliation
  • Arvia R; Department of Experimental and Clinical Medicine, University of Florence, Viale Morgagni 48, 50134, Florence, Italy. rosaria.arvia@unifi.it.
  • Sollai M; Department of Pathology, IRCC Humanitas Research Hospital, Milan, Rozzano, Italy.
  • Massi D; Division of Pathological Anatomy, Department of Health Sciences, University of Florence, Florence, Italy.
  • Asensio-Calavia P; Biotechnology of Macromolecules Research Group, Instituto de Productos Naturales y Agrobiología (IPNA-CSIC), San Cristóbal de La Laguna, Spain.
  • Urso C; Dermatopathology Study Center of Florence, Florence, Italy.
  • Zakrzewska K; Department of Experimental and Clinical Medicine, University of Florence, Viale Morgagni 48, 50134, Florence, Italy.
Infect Agent Cancer ; 19(1): 9, 2024 Mar 21.
Article in En | MEDLINE | ID: mdl-38515111
ABSTRACT
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.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Infect Agent Cancer Year: 2024 Document type: Article Affiliation country:

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Infect Agent Cancer Year: 2024 Document type: Article Affiliation country:
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