Evidence map›Paper›PMID 12910255›Full record

ReviewOncogene2003

Human neurotropic polyomavirus, JCV, and its role in carcinogenesis.

Kamel Khalili, Luis Del Valle, Jessica Otte, Michael Weaver, Jennifer Gordon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Progressive multifocal leukoencephalopathy in patients with chronic kidney disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Viruses in colorectal cancer.Molecular oncology · 2022
    Review
  9. Article
  10. Article
  11. The Role of the JC Virus in Central Nervous System Tumorigenesis.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Kamel KhaliliCenter for Neurovirology and Cancer Biology, College of Science and Technology, Temple University, 1900 North 12th Street, Philadelphia, PA 19122, USA. kamel.khalili@temple.edu
Luis Del Valle
Jessica Otte
Michael Weaver
Jennifer Gordon
Temple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of recent studies have reported the detection of the ubiquitous human polyomavirus, JC virus (JCV), in samples derived from several types of neural as well as non-neural human tumors. The human neurotropic JCV was first identified as the etiologic agent of the fatal demyelinating disease, progressive multifocal leukoencephalopathy, which usually occurs in individuals with defects in cell-mediated immunity, including AIDS. However, upon mounting evidence of the oncogenic potential of the viral regulatory protein, T-antigen, and JCV's oncogenecity in a broad range of animal models, studies were initiated to determine its potential involvement in human carcinogenesis. Initially, the most frequently observed tumors in rodent models, including medulloblastoma, astrocytoma, glioblastoma, and other neural-origin tumors were analysed. These studies were followed by analysis of non-neural tumors such as colorectal carcinomas. In a subset of each tumor type examined, JC viral genomic DNA sequences could be detected by PCR and confirmed by Southern blot hybridization or direct sequencing. In a smaller subset of the tumors, the expression of T-antigen was observed by immunohistochemical analysis. Owing to the established functions of T-antigen including its ability to interact with tumor suppressor proteins such as Rb and p53, and its ability to influence chromosomal stability, potential mechanisms of JCV T-antigen-mediated cellular dysregulation are discussed. Further, as increasing evidence suggests that T-antigen is not required for maintenance of a transformed phenotype, a hit-and-run model for T-antigen-induced transformation is proposed.

Indexed as

AnimalsAnimals, Genetically ModifiedAntigens, ViralBlotting, SouthernBrain NeoplasmsHumansImmunohistochemistryJC VirusLeukoencephalopathy, Progressive MultifocalMiceModels, BiologicalNeoplasmsPhenotypePolymerase Chain ReactionRetinoblastoma ProteinSequence Analysis, DNAAntigens, ViralRetinoblastoma ProteinTumor Suppressor Protein p53

Identifiers

PMID12910255
OpenAlexW1982194643

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.