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This study found that the development of Merkel cell carcinoma from hair follicles in mice can be driven by in vivo reprogramming with ATOH1 and relies on p53 loss for progression.

This study suggests that Merkel cell polyomavirus T antigen-positive cells resembling Merkel cell carcinoma may originate from epithelial cells in human hair follicles, potentially informing future transgenic mouse models for this cancer.

This review summarizes current evidence on how beta-human papillomavirus and Merkel cell polyomavirus may contribute to the development of nonmelanoma and Merkel cell skin carcinomas, respectively, but it reports no new clinical findings.

This review discusses the molecular mechanisms by which oncogenic viruses contribute to cancer development through manipulation of host cellular functions and highlights the need for further research into virus-associated cancers, reporting no new results.

This study found that T cell-deficient mice developed distinct papilloma phenotypes after MmuPV1 infection, and hyperimmune sera transfer could prevent this infection.