Evidence map›Paper›PMID 35614494›Full record

ReviewCancer cell international2022

Revisiting characteristics of oncogenic extrachromosomal DNA as mobile enhancers on neuroblastoma and glioma cancers.

Mohsen Karami Fath, Nastaran Karimfar, Andarz Fazlollahpour Naghibi, Shahriyar Shafa, Melika Ghasemi Shiran, Mehran Ataei, Hossein Dehghanzadeh, Mohsen Nabi Afjadi, Tahereh Ghadiri, Zahra Payandeh and 1 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Detecting Extrachromosomal DNA from Routine Histopathology.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
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

11 authors.

Mohsen Karami FathDepartment of Cellular and Molecular Biology, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran.
Nastaran KarimfarFaculty of Veterinary Medicine, Islamic Azad University, Tabriz Branch, Tabriz, Iran.
Andarz Fazlollahpour NaghibiFaculty of Medicine, Islamic Azad University, Sari Branch, Sari, Iran.
Shahriyar ShafaSchool of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Melika Ghasemi ShiranDepartment of Biology, Faculty of Sciences, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Mehran AtaeiDepartment of Biology, Faculty of Sciences, Shahid Chamran University, Ahvaz, Iran.
Hossein DehghanzadehKhoy University of Medical Sciences, Khoy, Iran.
Mohsen Nabi AfjadiDepartment of Biochemistry, Faculty of Biological Science, Tarbiat Modares University, Tehran, Iran. mohsennabi66@gmail.com.
Tahereh GhadiriDepartment of Neuroscience and Cognition, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. ghadiri21980@yahoo.com.
Zahra PayandehDepartment Medical Biochemistry and Biophysics, Division Medical Inflammation Research, Karolinska Institute, Stockholm, Sweden. zahra.payandeh@ki.se.
Vahideh TarhrizMolecular Medicine Research Center, Biomedicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran. t.tarhriz@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer can be induced by a variety of possible causes, including tumor suppressor gene failure and proto-oncogene hyperactivation. Tumor-associated extrachromosomal circular DNA has been proposed to endanger human health and speed up the progression of cancer. The amplification of ecDNA has raised the oncogene copy number in numerous malignancies according to whole-genome sequencing on distinct cancer types. The unusual structure and function of ecDNA, and its potential role in understanding current cancer genome maps, make it a hotspot to study tumor pathogenesis and evolution. The discovery of the basic mechanisms of ecDNA in the emergence and growth of malignancies could lead researchers to develop new cancer therapies. Despite recent progress, different aspects of ecDNA require more investigation. We focused on the features, and analyzed the bio-genesis, and origin of ecDNA in this review, as well as its functions in neuroblastoma and glioma cancers.

Indexed as

AmplificationCancerDrug resistanceExtrachromosomal circular DNAOncogene

Identifiers

PMID35614494
PMCPMC9131661

What OpenQuestion holds

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Registered trials

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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.