Evidence map›Paper›PMID 38531982›Full record

ReviewNature cancer2024

The pleiotropic functions of reactive oxygen species in cancer.

Katherine Wu, Ahmed Ezat El Zowalaty, Volkan I Sayin, Thales Papagiannakopoulos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
34.8field-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

76 citing papers in PubMed, 149 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. A Catalytic Osmium Redox Couple Collapses Cancer Redox Balance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. A BBB-permeable βScience advances · 2026
    Article
  18. Review
  19. Article
  20. Article

16 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

4 authors at 3 institutions in 3 countries.

Katherine WuDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-0472-0166
Ahmed Ezat El ZowalatyInstitute of Clinical Sciences, Department of Surgery, Sahlgrenska Center for Cancer Research, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0001-6177-6142
Volkan I SayinInstitute of Clinical Sciences, Department of Surgery, Sahlgrenska Center for Cancer Research, University of Gothenburg, Gothenburg, Sweden. volkan.sayin@gu.se.ORCID http://orcid.org/0000-0002-5225-8260
Thales PapagiannakopoulosDepartment of Pathology, New York University Grossman School of Medicine, New York, NY, USA. thales.papagiannakopoulos@nyulangone.org.ORCID http://orcid.org/0000-0002-2251-1624
New York University · USSahlgrenska University Hospital · SEZagazig University · EG

Funding

Medical Scientist Research Service AwardT32GM136573 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SULMAN, ERIK · 2020 to 2024
$6.8M
Identifying metabolic dependencies in genetic subtypes of KRAS-driven lung cancerR37CA222504 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PAPAGIANNAKOPOULOS, THALES · 2018 to 2024
$3.3M
Uncovering Genotype Specific Vulnerabilities in KRAS Mutant Lung Cancer?R01CA227649 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PAPAGIANNAKOPOULOS, THALES · 2018 to 2022
$1.9M
Dissecting the role of redox homeostasis and ferroptosis in lung cancerF30CA275258 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WU, KATHERINE · 2023 to 2025
$161k
American Cancer Society (American Cancer Society, Inc.) RSG-17-200-01-TBECancerfonden (Swedish Cancer Society) 20-1278NCI NIH HHS F30 CA275258U.S. Department of Health & Human Services | National Institutes of Health (NIH) F30CA275258U.S. Department of Health & Human Services | National Institutes of Health (NIH) T32GM136573U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA227649U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R37CA222504Vetenskapsrådet (Swedish Research Council) S18-034
6 · The paper itself

Abstract

Cellular redox homeostasis is an essential, dynamic process that ensures the balance between reducing and oxidizing reactions within cells and thus has implications across all areas of biology. Changes in levels of reactive oxygen species can disrupt redox homeostasis, leading to oxidative or reductive stress that contributes to the pathogenesis of many malignancies, including cancer. From transformation and tumor initiation to metastatic dissemination, increasing reactive oxygen species in cancer cells can paradoxically promote or suppress the tumorigenic process, depending on the extent of redox stress, its spatiotemporal characteristics and the tumor microenvironment. Here we review how redox regulation influences tumorigenesis, highlighting therapeutic opportunities enabled by redox-related alterations in cancer cells.

Indexed as

NeoplasmsOxidative StressCarcinogenesisHumansOxidation-ReductionReactive Oxygen SpeciesTumor MicroenvironmentReactive Oxygen Species

Identifiers

PMID38531982
OpenAlexW4394738629

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.