ArticleJournal of virology2008
BK virus as a cofactor in the etiology of prostate cancer in its early stages.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Pooled it
- BK polyomavirus in a Portuguese healthy group: seroprevalence, viral Excretion, and implications for transmission pathways.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Article
- Article
- Article
- Polyploid Giant Cancer Cells Generated from Human Cytomegalovirus-Infected Prostate Epithelial Cells.Cancers · 2023Article
- Human BKV large T genome detection in prostate cancer and benign prostatic hyperplasia tissue samples by nested PCR: A case-control study.Molecular biology research communications · 2023Article
- Multiple pathogens and prostate cancer.Infectious agents and cancer · 2022Review
- The microbiome and prostate cancer.Prostate cancer and prostatic diseases · 2022Review
- Differential Microbial Signature Associated With Benign Prostatic Hyperplasia and Prostate Cancer.Frontiers in cellular and infection microbiology · 2022Article
- Tissue Pathogens and Cancers: A Review of Commonly Seen Manifestations in Histo- and Cytopathology.Pathogens (Basel, Switzerland) · 2021Review
- Prostate Microbiota and Prostate Cancer: A New Trend in Treatment.Frontiers in oncology · 2021Review
- Pathogenicity of BK virus on the urinary system.Central European journal of urology · 2020Review
- The case for BK polyomavirus as a cause of bladder cancer.Current opinion in virology · 2019Review
- A correlation study ofInfectious agents and cancer · 2019Article
- More than just oncogenes: mechanisms of tumorigenesis by human viruses.Current opinion in virology · 2018Review
- Role of BK human polyomavirus in cancer.Infectious agents and cancer · 2018Review
- Treatment for presumed BK polyomavirus nephropathy and risk of urinary tract cancers among kidney transplant recipients in the United States.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018Article
- Going viral? Linking the etiology of human prostate cancer to theEMBO molecular medicine · 2017Article
- BK Polyomavirus: Clinical Aspects, Immune Regulation, and Emerging Therapies.Clinical microbiology reviews · 2017Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Prostate cancer has been projected to cause almost 10% of all male cancer deaths in the United States in 2007. The incidence of mutations in the tumor suppressor genes Rb1 and p53, especially in the early stages of the disease, is low compared to those for other cancers. This has led to the hypothesis that a human virus such as BK virus (BKV), which establishes a persistent subclinical infection in the urinary tract and encodes oncoproteins that interfere with these tumor suppressor pathways, is involved. Previously, we detected BKV DNA in the epithelial cells of benign and proliferative inflammatory atrophy ducts of cancerous prostate specimens. In the present report, we demonstrate that BKV is present at a much lower frequency in noncancerous prostates. Additionally, in normal prostates, T-antigen (TAg) expression is observed only in specimens harboring proliferative inflammatory atrophy and prostatic intraepithelial neoplasia. We further demonstrate that the p53 gene from atrophic cells expressing TAg is wild type, whereas tumor cells expressing detectable nuclear p53 contain a mix of wild-type and mutant p53 genes, suggesting that TAg may inactivate p53 in the atrophic cells. Our results point toward a role for BKV in early prostate cancer progression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.