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Merkel cell carcinoma (MCC) is tightly linked to infection by Merkel cell polyomavirus (MCPyV) in most cases. Mutated MCPyV T-antigen, which is expressed by the virus, inactivates the RB1 tumor suppressor protein, which leads to accelerated proliferation. Still unclear is whether differences between MCPyV+ and MCPyV- MCC manifest in differing genomic profiles.
Harms and colleagues addressed this question through genomic investigation of eight MCPyV+ and seven MCPyV- tumors. They found that MCPyV- MCC has a relatively high mutational load of over 10 mutations per megabase (Mb), with UVB-signature C→T transitions representing more than 85% of mutations. In addition to finding previously identified inactivating mutations in TP53, RB1, and PIK3C…