Merkel Cell Polyomavirus: Infection, Genome, Transcripts and Its Role in Development of Merkel Cell Carcinoma.

Simple Summary: By studying the cancer-inducing ability of polyomaviruses, several milestones in cancer research crucially contributing to our current understanding of, e.g., the tumor suppressor proteins p53 and RB1 have been achieved. However, only with the discovery of Merkel cell polyomavirus (M...

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Publicado en:Cancers Vol. 15; no. 2; pp. 444 - 465
Autores principales: Houben, Roland, Celikdemir, Büke, Kervarrec, Thibault, Schrama, David
Formato: pictorial review tables/charts Journal Article
Publicado: MDPI Jan2023
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Jan2023
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      pub: MDPI
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        10.3390/cancers15020444
        161438816
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        atl: Merkel Cell Polyomavirus: Infection, Genome, Transcripts and Its Role in Development of Merkel Cell Carcinoma.
      aug:
        au:
          Houben, Roland
          Celikdemir, Büke
          Kervarrec, Thibault
          Schrama, David
        affil: Department of Dermatology, Venereology und Allergology, University Hospital Würzburg, Josef-Schneider-Straße 2, 97080 Würzburg, Germany
      sug:
        subj:
          Carcinoma, Merkel Cell
          Polyomavirus Infections Familial and Genetic
          Genome, Human
          Gene Expression
          RNA, Messenger
          Antigens, Viral, Tumor
          Viral Proteins
          RNA, Viral
          Carcinoma, Neuroendocrine
          Oncogenes
          Models, Biological
          Tumor Virus Infections
          Skin Neoplasms
          Hamsters
          Polyomaviridae
          Carrier Proteins
      ab: Simple Summary: By studying the cancer-inducing ability of polyomaviruses, several milestones in cancer research crucially contributing to our current understanding of, e.g., the tumor suppressor proteins p53 and RB1 have been achieved. However, only with the discovery of Merkel cell polyomavirus (MCPyV) and its linkage to the highly aggressive Merkel cell carcinoma (MCC) in 2008 has a human polyomavirus-induced cancer been identified. Since then, intensive research has uncovered many details of the interaction of the virus with its human host, as well as many molecular mechanisms by which the MCPyV-encoded oncoproteins the so-called T antigens mediate oncogenic transformation. Surprisingly, many differences to the previously known polyomaviruses have been observed. In this review, we summarize the current knowledge on MCPyV and MCC and discuss some of the open questions. The best characterized polyomavirus family member, i.e., simian virus 40 (SV40), can cause different tumors in hamsters and can transform murine and human cells in vitro. Hence, the SV40 contamination of millions of polio vaccine doses administered from 1955–1963 raised fears that this may cause increased tumor incidence in the vaccinated population. This is, however, not the case. Indeed, up to now, the only polyomavirus family member known to be the most important cause of a specific human tumor entity is Merkel cell polyomavirus (MCPyV) in Merkel cell carcinoma (MCC). MCC is a highly deadly form of skin cancer for which the cellular origin is still uncertain, and which appears as two clinically very similar but molecularly highly different variants. While approximately 80% of cases are found to be associated with MCPyV the remaining MCCs carry a high mutational load. Here, we present an overview of the multitude of molecular functions described for the MCPyV encoded oncoproteins and non-coding RNAs, present the available MCC mouse models and discuss the increasing evidence that both, virus-negative and -positive MCC constitute epithelial tumors.
      pubtype: Academic Journal
      doctype:
        pictorial
        review
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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