Oxidative stress

Scientific explanation

Reactive oxygen species are both signalling molecules and sources of damage. Tumours often upregulate antioxidant programmes to live with higher ROS set-points.

Cancers where relevant

Compounds that intersect this pathway

Melatonin

MT1/MT2 circadian with antioxidant chemistry. Adjunctive oncology hypotheses exist; circadian and redox effects should not be read as anticancer proof.

Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible

N-acetylcysteine

Cysteine donor replenishing glutathione. Redox buffering can be protective or, in some models, support tumour antioxidant capacity. Dual-edged; not an antineoplastic.

Evidence in mapped cancers: In Vitro · Mechanistically Plausible · Hypothesis-Generating

Disulfiram

ALDH ; copper-complexed forms can inhibit proteasome and NF-κB-related survival programmes in models. Clinical oncology evidence remains limited.

Evidence in mapped cancers: In Vitro · In Vivo · Early Clinical

Curcumin

Polyphenol with promiscuous in-vitro NF-κB, and ROS effects. Bioavailability is poor; dish activity does not establish clinical anticancer efficacy.

Sulforaphane

Isothiocyanate that can activate NRF2 via KEAP1 modification and has epigenetic HDAC-related reports in models. Chemoprevention hypotheses exceed proven oncology treatment.

Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible

EGCG

Green-tea catechin with in-vitro effects on RTKs, epigenetic enzymes and redox. Clinical anticancer efficacy is not established.

Resveratrol

Stilbene with sirtuin/-related and anti-inflammatory reports in models. Pharmacokinetic limits and mixed trials caution against efficacy claims.

Quercetin

Flavonol with -related and antioxidant in-vitro activity. Not a clinical oncology agent.

Convergence partners

Other pathways that co-occur with Oxidative stress on mapped adjunct records: Apoptosis, Cancer stemness, NF-κB, NRF2, Ferroptosis.

This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.