Oxidative stress and inflammation in breast cancer: Mechanistic interactions and clinical implications

Table 3 Selected oxidative and inflammatory biomarkers in breast cancer and their clinical implications

Biomarker/signature	Biological process	Clinical association (examples)
Malondialdehyde	Lipid peroxidation	Higher levels associated with increased oxidative stress and more advanced disease
8-hydroxyguanosine	DNA oxidation	Linked to genomic instability and radiotherapy-related toxicity and fatigue
Protein carbonyls	Irreversible protein oxidation	Reflect cumulative oxidative damage, associated with poor prognosis in some cohorts
Antioxidant enzymes (SOD, GPx, CAT)	Endogenous antioxidant defense	Altered activity correlates with tumor stage and treatment response
Myeloperoxidase	Neutrophil-derived oxidant production	Elevated levels related to chronic inflammation and post-treatment fatigue
HDL antioxidant activity	Lipoprotein-associated antioxidant capacity	Increased activity in TNBC as compensatory response to high oxidative stress
Triglyceride-glucose (TyG) index	Insulin resistance, metabolic dysfunction	Higher TyG associated with increased BC risk via oxidative/inflammatory pathways
UHR/NPR	Systemic oxidative stress and inflammation	Related to risk and prognosis; may help refine risk stratification
Ferroptosis-related genes (GPX4, ACSL4)	Iron-dependent lipid peroxidation	Expression patterns associated with TNBC prognosis and potential response to ferroptosis-inducing therapy
Necroptosis-related lncRNA signatures	Regulated necrotic cell death	Risk models predict survival and response to immunotherapy in TNBC

BC: Breast cancer; TNBC: Triple-negative breast cancer; HDL: High-density lipoprotein; SOD: Superoxide dismutase; GPx: Glutathione peroxidase; CAT: Catalase; NPR: Neutrophil-to-platelet ratio; UHR: Uric acid-to-HDL ratio.