학술논문
Detection of wildtype Merkel cell polyomavirus genomic sequence and VP1 transcription in a subset of Merkel cell carcinoma.
Document Type
Article
Author
Kervarrec, Thibault; Appenzeller, Silke; Tallet, Anne; Jullie, Marie‐Laure; Sohier, Pierre; Guillonneau, Francois; Rütten, Arno; Berthon, Patricia; Le Corre, Yannick; Hainaut‐Wierzbicka, Ewa; Blom, Astrid; Beneton, Nathalie; Bens, Guido; Nardin, Charline; Aubin, Francois; Dinulescu, Monica; Visée, Sebastien; Herfs, Michael; Touzé, Antoine; Guyétant, Serge
Source
Subject
*MERKEL cell carcinoma
*MERKEL cells
*NUCLEIC acid hybridization
*POLYOMAVIRUSES
*ONCOGENES
*GENE expression
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Language
ISSN
0309-0167
Abstract
Aims: Merkel cell carcinoma (MCC) is frequently caused by the Merkel cell polyomavirus (MCPyV). Characteristic for these virus‐positive (VP) MCC is MCPyV integration into the host genome and truncation of the viral oncogene Large T antigen (LT), with full‐length LT expression considered as incompatible with MCC growth. Genetic analysis of a VP‐MCC/trichoblastoma combined tumour demonstrated that virus‐driven MCC can arise from an epithelial cell. Here we describe two further cases of VP‐MCC combined with an adnexal tumour, i.e. one trichoblastoma and one poroma. Methods and results: Whole‐genome sequencing of MCC/trichoblastoma again provided evidence of a trichoblastoma‐derived MCC. Although an MCC‐typical LT‐truncating mutation was detected, we could not determine an integration site and we additionally detected a wildtype sequence encoding full‐length LT. Similarly, Sanger sequencing of the combined MCC/poroma revealed coding sequences for both truncated and full‐length LT. Moreover, in situ RNA hybridization demonstrated expression of a late region mRNA encoding the viral capsid protein VP1 in both combined as well as in a few cases of pure MCC. Conclusion: The data presented here suggest the presence of wildtype MCPyV genomes and VP1 transcription in a subset of MCC. [ABSTRACT FROM AUTHOR]