Evidence map›Paper›PMID 25342630›Full record

ReviewNature reviews. Cancer2014

Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?

Simran S Sabharwal, Paul T Schumacker

Abstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 801 papers.

0numbers the graph read from it
0cells of the map it votes in
801citing 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

801 citing papers in PubMed.

  1. Review
  2. Bibliometric analysis and visualization of inflammation in the field of diabetic retinopathy research (2006-2025).Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
    Article
  3. Sex and Gender Perspective in Obesity and Gastric Cancer.The world journal of men's health · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. A Catalytic Osmium Redox Couple Collapses Cancer Redox Balance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  19. Article
  20. Article

741 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

2 authors.

Simran S SabharwalDepartment of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.
Paul T SchumackerDepartment of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA.

Funding

Respiratory and Metabolic Adaptation to HypoxiaR01HL035440 · NHLBI · UNIVERSITY OF CHICAGO · PI SCHUMACKER, PAUL T · 1986 to 2018
$5.0M
Metabolic Regulation of Pulmonary Vascular RemodelingR01HL122062 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHUMACKER, PAUL T · 2014 to 2017
$2.0M
NHLBI NIH HHS HL122062NHLBI NIH HHS HL35440NHLBI NIH HHS R01 HL035440NHLBI NIH HHS R01 HL122062
6 · The paper itself

Abstract

Mitochondria cooperate with their host cells by contributing to bioenergetics, metabolism, biosynthesis, and cell death or survival functions. Reactive oxygen species (ROS) generated by mitochondria participate in stress signalling in normal cells but also contribute to the initiation of nuclear or mitochondrial DNA mutations that promote neoplastic transformation. In cancer cells, mitochondrial ROS amplify the tumorigenic phenotype and accelerate the accumulation of additional mutations that lead to metastatic behaviour. As mitochondria carry out important functions in normal cells, disabling their function is not a feasible therapy for cancer. However, ROS signalling contributes to proliferation and survival in many cancers, so the targeted disruption of mitochondria-to-cell redox communication represents a promising avenue for future therapy.

Indexed as

AnimalsCell Transformation, NeoplasticDNA, MitochondrialHumansMitochondriaMutationNeoplasmsOxidation-ReductionReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID25342630
PMCPMC4657553

What OpenQuestion holds

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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.