ArticleProceedings of the National Academy of Sciences of the United States of America2008
T antigen mutations are a human tumor-specific signature for Merkel cell polyomavirus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 357 papers.
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357 citing papers in PubMed, 725 citations in OpenAlex.
- Prospective Study of Human Polyomaviruses and Risk of Cutaneous Squamous Cell Carcinoma in the United States.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016Trial
- Beyond oncogenesis: the unexplored benefits of viruses in cancer immunity.Nature reviews. Cancer · 2026Review
- An immunocompetent model of MCPyV-driven Merkel cell carcinoma reveals tumor evolution under immune selection.bioRxiv : the preprint server for biology · 2026Article
- Sequence-Anchored Shared Tumor-Specific Epitopes for Pre-Manufactured HLA-Matched mRNA Cancer Vaccine Libraries: A Pan-Cancer Framework.Biomolecules · 2026Article
- mRNA vaccine design targeting Merkel cell polyomavirus for immunotherapy of Merkel cell carcinoma.Scientific reports · 2026Article
- Review
- RB1 inactivation in cutaneous carcinomas.Histopathology · 2026Review
- Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses.Journal of virology · 2026Review
- Synthetic consensus DNA vaccines against Merkel cell polyomavirus large and small T antigens induce robust polyfunctional T cell responses.Frontiers in immunology · 2026Article
- Pharmacologic reversion of Merkel cell carcinoma via CBP/p300 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A short intrinsically disordered domain of MCPyV ALTO regulates TBK1 signaling during MCPyV infection.Journal of virology · 2025Article
- E2F1-3 activate Merkel cell polyomavirus early transcription and replication.bioRxiv : the preprint server for biology · 2025Article
- Targeting an essential viral oncoprotein with an IL-7-enhanced mRNA vaccine induces durable immunity to Merkel cell carcinoma.Cell reports · 2025Article
- A Polyomavirus-Positive Merkel Cell Carcinoma Mouse Model Supports a Unified Origin for Somatic and Germ Cell Cancers.Cancers · 2025Article
- Genome integration of human DNA oncoviruses.Journal of virology · 2025Review
- Merkel Cell Carcinoma: Current Treatment Landscape and Emerging Therapeutic Targets.Current oncology reports · 2025Review
- Review
- Kit-mediated autophagy suppression driven by a viral oncoprotein emerges as a crucial survival mechanism in Merkel cell carcinoma.Autophagy · 2025Article
- Article
- Review
297 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Merkel cell polyomavirus (MCV) is a virus discovered in our laboratory at the University of Pittsburgh that is monoclonally integrated into the genome of approximately 80% of human Merkel cell carcinomas (MCCs). Transcript mapping was performed to show that MCV expresses transcripts in MCCs similar to large T (LT), small T (ST), and 17kT transcripts of SV40. Nine MCC tumor-derived LT genomic sequences have been examined, and all were found to harbor mutations prematurely truncating the MCV LT helicase. In contrast, four presumed episomal viruses from nontumor sources did not possess this T antigen signature mutation. Using coimmunoprecipitation and origin replication assays, we show that tumor-derived virus mutations do not affect retinoblastoma tumor suppressor protein (Rb) binding by LT but do eliminate viral DNA replication capacity. Identification of an MCC cell line (MKL-1) having monoclonal MCV integration and the signature LT mutation allowed us to functionally test both tumor-derived and wild type (WT) T antigens. Only WT LT expression activates replication of integrated MCV DNA in MKL-1 cells. Our findings suggest that MCV-positive MCC tumor cells undergo selection for LT mutations to prevent autoactivation of integrated virus replication that would be detrimental to cell survival. Because these mutations render the virus replication-incompetent, MCV is not a "passenger virus" that secondarily infects MCC tumors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.