English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

It has been suggested that  BK ‐polyomavirus is linked to oncogenesis via high expression levels of large T‐antigen in some urothelial neoplasms arising following kidney transplantation. However, a causal association between  BK ‐polyomavirus, large T‐antigen expression and oncogenesis has never been demonstrated in humans. Here we describe an investigation using high‐throughput sequencing of tumour  DNA  obtained from an urothelial carcinoma arising in a renal allograft. We show that a novel  BK ‐polyomavirus strain, named  CH ‐1, is integrated into exon 26 of the myosin‐binding protein  C1  gene (  MYBPC1  ) on chromosome 12 in tumour cells but not in normal renal cells. Integration of the  BK ‐polyomavirus results in a number of discrete alterations in viral gene expression, including: (a) disruption of  VP1  protein expression and robust expression of large T‐antigen; (b) preclusion of viral replication; and (c) deletions in the non‐coding control region ( NCCR ), with presumed alterations in promoter feedback loops. Viral integration disrupts one   MYBPC1   gene copy and likely alters its expression. Circular episomal  BK ‐polyomavirus gene sequences are not found, and the renal allograft shows no productive polyomavirus infection or polyomavirus nephropathy. These findings support the hypothesis that integration of polyomaviruses is essential to tumourigenesis. It is likely that dysregulation of large T‐antigen, with persistent over‐expression in non‐lytic cells, promotes cell growth, genetic instability and neoplastic transformation. © 2015 Authors. Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

The oncogenic potential of BK ‐polyomavirus is linked to viral integration into the human genome