Evidence map›Paper›PMID 42144521›Full record

ReviewCancer treatment and research2026

The Role of Oxidative Stress and Redox Regulation in Cancer.

Nahid Nafissi, Pedram Fadavi, Farzad Taghizadeh-Hesary

Abstract readReview
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In one paragraph

Review in Cancer treatment and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Nahid Nafissi *Breast Cancer Research Center, Iran University of Medical Sciences, Tehran, Iran.
Pedram Fadavi *Breast Cancer Research Center, Iran University of Medical Sciences, Tehran, Iran.
Farzad Taghizadeh-HesaryBreast Cancer Research Center, Iran University of Medical Sciences, Tehran, Iran. taghizadeh_hesary.f@iums.ac.ir.ORCID https://orcid.org/0000-0002-6195-2203

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is a pivotal regulator of cancer biology, influencing both the initiation and progression of malignancy. Oxidative stress results from an imbalance between the generation of reactive oxygen species (ROS) and the ability of antioxidant systems to detoxify them. While physiological levels of ROS are essential for cellular homeostasis, excessive ROS can damage DNA, proteins, and lipids, leading to cellular death. Paradoxically, cancer cells rely on moderately elevated ROS levels to sustain proliferative signaling, metabolic reprogramming, and invasion. To prevent oxidative damage, they rewire their redox networks by simultaneously increasing ROS production and enhancing antioxidant defense lines. Meanwhile, cancer stem cells (CSCs) keep even tighter redox control by preserving intrinsically low ROS levels through metabolic adaptation and robust antioxidant capacity. Elevated ROS not only promotes tumor growth but also modulates the tumor microenvironment (TME), inducing immune evasion, epithelial-mesenchymal transition, and therapy resistance. Clinically, targeting redox balance has become a promising approach for cancer diagnosis and treatment. This Chapter is dedicated to provide a practical summary of current knowledge on oxidative stress in cancer cells and how it contributes to cancer formation and progression.

Indexed as

NeoplasmsOxidative StressAnimalsAntioxidantsHumansMetabolic ReprogrammingNeoplastic Stem CellsOxidation-ReductionReactive Oxygen SpeciesTumor MicroenvironmentAntioxidantsReactive Oxygen SpeciesCancerMetabolismMitochondriaOxidative stressRedox

Identifiers

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Registered trials

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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.