Evidence map›Paper›PMID 34286881›Full record

ReviewCancer science2021

Reactive oxygen species in cancer: Current findings and future directions.

Hajime Nakamura, Kohichi Takada

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 523 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
523citing papers in PubMed, 1 pooled it
39.5field-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

523 citing papers in PubMed, 1 synthesis or guideline pooled it, 882 citations in OpenAlex.

  1. Pooled it
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  17. International journal of molecular sciences · 2026
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463 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 at 1 institution in 1 country.

Hajime NakamuraDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0003-0848-2940
Kohichi TakadaDepartment of Medical Oncology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID https://orcid.org/0000-0002-1393-9442
Sapporo Medical University · JP

Funding

Japan Society for the Promotion of Science C/16K07178Japan Society for the Promotion of Science C/19K08397
6 · The paper itself

Abstract

Reactive oxygen species (ROS), a class of highly bioactive molecules, have been widely studied in various types of cancers. ROS are considered to be normal byproducts of numerous cellular processes. Typically, cancer cells exhibit higher basal levels of ROS compared with normal cells as a result of an imbalance between oxidants and antioxidants. ROS have a dual role in cell metabolism: At low to moderate levels, ROS act as signal transducers to activate cell proliferation, migration, invasion, and angiogenesis. In contrast, high levels of ROS cause damage to proteins, nucleic acids, lipids, membranes, and organelles, leading to cell death. Extensive studies have revealed that anticancer therapies that manipulate ROS levels, including immunotherapies, show promising in vitro as well as in vivo results. In this review, we summarize molecular mechanisms and oncogenic functions that modulate ROS levels and are useful for the development of cancer therapeutic strategies. This review also provides insights into the future development of effective agents that regulate the redox system for cancer treatment.

Indexed as

Antineoplastic AgentsApoptosisAutophagyCell DeathCell MovementCell ProliferationDNA DamageHumansIron OverloadMitochondriaNeoplasm InvasivenessNeoplasmsNeovascularization, PathologicOxidation-ReductionOxidative StressReactive Oxygen SpeciesAntineoplastic AgentsReactive Oxygen Speciescell deathneoplasmsoxidative stressreactive oxygen speciestherapeutics

Identifiers

PMID34286881
PMCPMC8486193
OpenAlexW3185965919

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.