Evidence map›Paper›PMID 26560882›Full record

ArticleNeurosurgical review2016

JC polyomavirus in the aetiology and pathophysiology of glial tumours.

Tihomir Eftimov, Yavor Enchev, Iliya Tsekov, Plamen Simeonov, Zlatko Kalvatchev, Elitsa Encheva

Abstract read
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In one paragraph

Article in Neurosurgical review, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Environmental Hazards and Glial Brain Tumors: Association or Causation?International journal of molecular sciences · 2025
    Review
  2. Article
  3. Occupational livestock or animal dust exposure and offspring cancer risk in Denmark, 1968-2016.International archives of occupational and environmental health · 2020
    Article
  4. Review
  5. Relationship Among Viremia/Viral Infection, Alloimmunity, and Nutritional Parameters in the First Year After Pediatric Kidney Transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017
    Observational
  6. Review
  7. Article
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

6 authors at 3 institutions in 1 country.

Tihomir EftimovClinic of Neurosurgery, Military Medical Academy, Sofia, Bulgaria.
Yavor EnchevDepartment of Neurosurgery, University Hospital "St. Marina", Medical University of Varna, 1 "Hristo Smirnenski" Boulevard, 9010, Varna, Bulgaria. dr.y.enchev@gmail.com.
Iliya TsekovCenter for Diagnosis and Analysis of Viruses and Viral Diseases, Military Medical Academy, Sofia, Bulgaria.
Plamen SimeonovClinic of Neurosurgery, Military Medical Academy, Sofia, Bulgaria.
Zlatko KalvatchevCenter for Diagnosis and Analysis of Viruses and Viral Diseases, Military Medical Academy, Sofia, Bulgaria.
Elitsa EnchevaDepartment of Imaging Diagnostics and Radiotherapy, University Hospital "St. Marina", Medical University of Varna, Varna, Bulgaria.
Military Medical Academy · BGMedical University of Varna · BGUniversity Hospital St. Marina · BG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glial brain tumours with their poor prognosis, limited treatment modalities and unclear detailed pathophysiology represent a significant health concern. The purpose of the current study was to investigate and describe the possible role of the human polyomavirus JC as an underlying cancerogenic or co-cancerogenic factor in the complex processes of glial tumour induction and development. Samples from 101 patients with glial tumours were obtained during neurosurgical tumour resection. Small tissue pieces were taken from several areas of the histologically verified solid tumour core. Biopsies were used for DNA extraction and subsequent amplification reactions of sequences from the JC viral genome. Real-time polymerase chain reaction was used for detection and quantification of its non-coding control region (NCCR) and gene encoding the regulatory protein Large T antigen (LT). An average of 37.6% of all patients was found to be LT positive, whereas only 6.9% tested positive for NCCR. The analysis of the results demonstrated significant variance between the determined LT prevalence and the rate for NCCR, with a low starting copy number in all positive samples and threshold cycles in the range of 36 to 42 representing viral load in the range from 10 to 1000 copies/μl. The results most probably indicate incomplete JC viral replication. Under such conditions, mutations in the host cell genome may be accumulated due to interference of the virus with the host cell machinery, and eventually malignant transformation may occur.

Indexed as

JC VirusAntigens, Viral, TumorBiopsyBrain NeoplasmsDNA, NeoplasmGene DosageGlioblastomaHumansMutationPolyomavirus InfectionsRNA, Long NoncodingTumor Virus InfectionsViral LoadAntigens, Viral, TumorDNA, NeoplasmRNA, Long NoncodingCancerogenesisGlial tumoursGlioblastoma multiformeJC polyomavirus

Identifiers

PMID26560882
OpenAlexW2191115291

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.