Evidence map›Paper›PMID 33922139›Full record

ReviewAntioxidants (Basel, Switzerland)2021

Oxidative Stress in Cancer Cell Metabolism.

Saniya Arfin, Niraj Kumar Jha, Saurabh Kumar Jha, Kavindra Kumar Kesari, Janne Ruokolainen, Shubhadeep Roychoudhury, Brijesh Rathi, Dhruv Kumar

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 329 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
329citing papers in PubMed, 3 pooled it
37.6field-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

329 citing papers in PubMed, 3 syntheses or guidelines pooled it, 627 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. The role of metals in cancer and the use of metal chelators as a potential treatment strategy.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  7. Article
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  11. On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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  20. Review

269 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

8 authors at 5 institutions in 2 countries.

Saniya ArfinAmity Institute of Molecular Medicine and Stem Cell Research (AIMMSCR), Amity University Uttar Pradesh, Sec 125, Noida 201303, India.
Niraj Kumar JhaDepartment of Biotechnology, School of Engineering & Technology (S.E.T.), Sharda University, Greater Noida 201310, India.ORCID 0000-0001-9486-4069
Saurabh Kumar JhaDepartment of Biotechnology, School of Engineering & Technology (S.E.T.), Sharda University, Greater Noida 201310, India.
Kavindra Kumar KesariDepartment of Applied Physics, School of Science, Aalto University, 00076 Espoo, Finland.ORCID 0000-0003-3622-9555
Janne RuokolainenDepartment of Applied Physics, School of Science, Aalto University, 00076 Espoo, Finland.
Shubhadeep RoychoudhuryDepartment of Life Science and Bioinformatics, Assam University, Silchar 788011, India.
Brijesh RathiLaboratory for Translational Chemistry and Drug Discovery, Department of Chemistry, Hansraj College, University of Delhi, New Delhi 110021, India.ORCID 0000-0003-2133-8847
Dhruv KumarAmity Institute of Molecular Medicine and Stem Cell Research (AIMMSCR), Amity University Uttar Pradesh, Sec 125, Noida 201303, India.ORCID 0000-0003-2586-9397
Aalto University · FIAmity University · INSharda University · INAssam University · INUniversity of Delhi · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) are important in regulating normal cellular processes whereas deregulated ROS leads to the development of a diseased state in humans including cancers. Several studies have been found to be marked with increased ROS production which activates pro-tumorigenic signaling, enhances cell survival and proliferation and drives DNA damage and genetic instability. However, higher ROS levels have been found to promote anti-tumorigenic signaling by initiating oxidative stress-induced tumor cell death. Tumor cells develop a mechanism where they adjust to the high ROS by expressing elevated levels of antioxidant proteins to detoxify them while maintaining pro-tumorigenic signaling and resistance to apoptosis. Therefore, ROS manipulation can be a potential target for cancer therapies as cancer cells present an altered redox balance in comparison to their normal counterparts. In this review, we aim to provide an overview of the generation and sources of ROS within tumor cells, ROS-associated signaling pathways, their regulation by antioxidant defense systems, as well as the effect of elevated ROS production in tumor progression. It will provide an insight into how pro- and anti-tumorigenic ROS signaling pathways could be manipulated during the treatment of cancer.

Indexed as

angiogenesisapoptosisautophagycancer metabolismdrug resistancemetastasismitochondrial ROSNFκB pathwayoxidative stresstumor adaptationtumor progressiontumor targetingwarburg effect

Identifiers

PMID33922139
PMCPMC8143540
OpenAlexW3153831334

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.