Evidence map›Paper›PMID 33188621›Full record

ReviewCellular oncology (Dordrecht, Netherlands)2021

The Duchenne muscular dystrophy gene and cancer.

Leanne Jones, Michael Naidoo, Lee R Machado, Karen Anthony

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Exploring Dystrophin Expression and Mutations in theInternational journal of molecular sciences · 2026
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  10. Biomedicines · 2025
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  15. Differential expression ofTranslational lung cancer research · 2024
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  18. Biomarkers for Early Detection of Cancer: Molecular Aspects.International journal of molecular sciences · 2023
    Article
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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

4 authors at 2 institutions in 2 countries.

Leanne JonesCentre for Physical Activity and Life Sciences, University of Northampton, University Drive, Northampton, NN1 5PH, UK.
Michael NaidooCentre for Physical Activity and Life Sciences, University of Northampton, University Drive, Northampton, NN1 5PH, UK.
Lee R MachadoCentre for Physical Activity and Life Sciences, University of Northampton, University Drive, Northampton, NN1 5PH, UK.
Karen AnthonyCentre for Physical Activity and Life Sciences, University of Northampton, University Drive, Northampton, NN1 5PH, UK. Karen.Anthony@northampton.ac.uk.ORCID http://orcid.org/0000-0002-3638-2405
University of Northampton · GBUniversity of Leicester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMutation of the Duchenne muscular dystrophy (DMD) gene causes Duchenne and Becker muscular dystrophy, degenerative neuromuscular disorders that primarily affect voluntary muscles. However, increasing evidence implicates DMD in the development of all major cancer types. DMD is a large gene with 79 exons that codes for the essential muscle protein dystrophin. Alternative promotor usage drives the production of several additional dystrophin protein products with roles that extend beyond skeletal muscle. The importance and function(s) of these gene products outside of muscle are not well understood.

conclusionsWe highlight a clear role for DMD in the pathogenesis of several cancers, including sarcomas, leukaemia's, lymphomas, nervous system tumours, melanomas and various carcinomas. We note that the normal balance of DMD gene products is often disrupted in cancer. The short dystrophin protein Dp71 is, for example, typically maintained in cancer whilst the full-length Dp427 gene product, a likely tumour suppressor, is frequently inactivated in cancer due to a recurrent loss of 5' exons. Therefore, the ratio of short and long gene products may be important in tumorigenesis. In this review, we summarise the tumours in which DMD is implicated and provide a hypothesis for possible mechanisms of tumorigenesis, although the question of cause or effect may remain. We hope to stimulate further study into the potential role of DMD gene products in cancer and the development of novel therapeutics that target DMD.

Indexed as

AnimalsDystrophinGenetic Predisposition to DiseaseHumansModels, BiologicalMuscular Dystrophy, DuchenneNeoplasmsDystrophinCancerDMDDp71Duchenne muscular dystrophyDystrophin

Identifiers

PMID33188621
PMCPMC7906933
OpenAlexW3094403008

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.