Evidence map›Paper›PMID 28939825›Full record

ArticleNature communications2017

Mitochondrial mutations drive prostate cancer aggression.

Julia F Hopkins, Veronica Y Sabelnykova, Joachim Weischenfeldt, Ronald Simon, Jennifer A Aguiar, Rached Alkallas, Lawrence E Heisler, Junyan Zhang, John D Watson, Melvin L K Chua and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 124 citations in OpenAlex.

  1. Trial
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  9. Exploring the oncogenic impact of heteroplasmicMitochondrial communications · 2025
    Article
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  11. Article
  12. Article
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  15. Aging-Related Mitochondrial Dysfunction Is Associated With Fibrosis in Benign Prostatic Hyperplasia.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

21 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

21 authors at 5 institutions in 2 countries.

Julia F HopkinsInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3. Julia.Hopkins@oicr.on.ca.
Veronica Y SabelnykovaInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3.
Joachim WeischenfeldtGenome Biology Unit, European Molecular Biology Laboratory, Heidelberg, 69120, Germany.
Ronald SimonInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany.
Jennifer A AguiarInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3.
Rached AlkallasInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3.
Lawrence E HeislerInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3.
Junyan ZhangPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada, M5G 1L7.
John D WatsonInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3.
Melvin L K ChuaPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada, M5G 1L7.ORCID http://orcid.org/0000-0002-1648-1473
Michael FraserPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada, M5G 1L7.
Francesco FaveroBiotech Research & Innovation Centre (BRIC) and Finsen Laboratory, Copenhagen, 2200, Denmark.
Chris LawerenzDivision of Theoretical Bioinformatics, German Cancer Research Center, Heidelberg, 69120, Germany.
Christoph PlassDivision of Epigenomics and Cancer Risk Factors, German Cancer Research Center, Heidelberg, 69120, Germany.
Guido SauterInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany.
John D McPhersonGenome Technologies Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3.ORCID http://orcid.org/0000-0001-8049-9347
Theodorus van der KwastDepartment of Pathology and Laboratory Medicine, Toronto General Hospital/University Health Network, Toronto, ON, Canada, M5G 2C4.
Jan KorbelGenome Biology Unit, European Molecular Biology Laboratory, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-2798-3794
Thorsten SchlommMartini-Clinic, Prostate Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, 20246, Germany.
Robert G BristowPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada, M5G 1L7. Rob.Bristow@rmp.uhn.on.ca.
Paul C BoutrosInformatics and Biocomputing Program, Ontario Institute for Cancer Research, Toronto, ON, Canada, M5G 0A3. Paul.Boutros@oicr.on.ca.ORCID http://orcid.org/0000-0003-0553-7520
Ontario Institute for Cancer Research · CAUniversity Health Network · CAUniversität Hamburg · DEEuropean Molecular Biology Laboratory · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear mutations are well known to drive tumor incidence, aggression and response to therapy. By contrast, the frequency and roles of mutations in the maternally inherited mitochondrial genome are poorly understood. Here we sequence the mitochondrial genomes of 384 localized prostate cancer patients, and identify a median of one mitochondrial single-nucleotide variant (mtSNV) per patient. Some of these mtSNVs occur in recurrent mutational hotspots and associate with aggressive disease. Younger patients have fewer mtSNVs than those who diagnosed at an older age. We demonstrate strong links between mitochondrial and nuclear mutational profiles, with co-occurrence between specific mutations. For example, certain control region mtSNVs co-occur with gain of the MYC oncogene, and these mutations are jointly associated with patient survival. These data demonstrate frequent mitochondrial mutation in prostate cancer, and suggest interplay between nuclear and mitochondrial mutational profiles in prostate cancer.In prostate cancer, the role of mutations in the maternally-inherited mitochondrial genome are not well known. Here, the authors demonstrate frequent, age-dependent mitochondrial mutation in prostate cancer. Strong links between mitochondrial and nuclear mutational profiles are associated with clinical aggressivity.

Indexed as

Point MutationAdenocarcinomaAdultAgedAged, 80 and overAge FactorsDNA, MitochondrialGenes, mycGenetic Association StudiesGenome, MitochondrialHumansMaleMiddle AgedNeoplasm InvasivenessProstatic NeoplasmsSurvival AnalysisDNA, Mitochondrial

Identifiers

PMID28939825
PMCPMC5610241
OpenAlexW2756387833

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.