Tutar Ş, Uçar Çifçi K, Tutar Y. Oxidative stress and inflammation in breast cancer: Mechanistic interactions and clinical implications. World J Clin Cases 2026; 14(24): 122937 [DOI: 10.12998/wjcc.122937]
Corresponding Author of This Article
Yusuf Tutar, Chairman, Dean, Tenured Professor, Division of Medicinal Biochemistry, Department of Basic Medical Sciences, Faculty of Medicine, Recep Tayyip Erdogan University, Islampaşa, Rize 53020, Türkiye. yusuf.tutar@erdogan.edu.tr
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Biochemistry & Molecular Biology
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Tutar Ş, Uçar Çifçi K, Tutar Y. Oxidative stress and inflammation in breast cancer: Mechanistic interactions and clinical implications. World J Clin Cases 2026; 14(24): 122937 [DOI: 10.12998/wjcc.122937]
World J Clin Cases. Aug 26, 2026; 14(24): 122937 Published online Aug 26, 2026. doi: 10.12998/wjcc.122937
Oxidative stress and inflammation in breast cancer: Mechanistic interactions and clinical implications
Şeyma Tutar, Kezban Uçar Çifçi, Yusuf Tutar
Şeyma Tutar, Yusuf Tutar, Division of Medicinal Biochemistry, Department of Basic Medical Sciences, Faculty of Medicine, Recep Tayyip Erdogan University, Rize 53020, Türkiye
Kezban Uçar Çifçi, Division of Basic Sciences and Health, Hemp Research Institute, Yozgat Bozok University, Yozgat 66900, Türkiye
Co-first authors: Şeyma Tutar and Kezban Uçar Çifçi.
Author contributions: Tutar Ş and Uçar Çifçi K contributed equally to this work; Tutar Y and Uçar ÇK conceptualized and designed the study, created the artwork, supervised, and made critical revisions; conducted the literature review; and Tutar Y drafted the original manuscript; all authors prepared the draft and approved the submitted version.
AI contribution statement: The authors used [ChatGPT-5.5] to improve the spelling and clarity of this manuscript.
Conflict-of-interest statement: There is no conflict of interest associated with any of the senior authors or other coauthors who contributed their efforts in this manuscript.
Corresponding author: Yusuf Tutar, Chairman, Dean, Tenured Professor, Division of Medicinal Biochemistry, Department of Basic Medical Sciences, Faculty of Medicine, Recep Tayyip Erdogan University, Islampaşa, Rize 53020, Türkiye. yusuf.tutar@erdogan.edu.tr
Received: May 11, 2026 Revised: June 18, 2026 Accepted: July 28, 2026 Published online: August 26, 2026 Processing time: 110 Days and 0.7 Hours
Abstract
The development and progression of breast cancer (BC) are influenced by genetic, hormonal, and metabolic factors, as well as by signals within the tumor microenvironment. A review of studies on BC biology and treatment outcomes was undertaken. The studies were experimental, translational, and clinical, and were indexed in PubMed and Web of Science. The focus was on the connection between oxidative and inflammatory markers and clinical endpoints, as well as intervention strategies that modify these pathways. Oxidative stress and inflammation promote tumor growth, metastasis, and immune evasion by driving various biological activations. New data suggest that biomarkers could enhance BC assessment, but strategies are limited. Inflammation and oxidative stress are closely connected processes in BC and may offer important opportunities for therapy. In the future, research should combine molecular studies with clinical trials to improve our understanding of this interaction and determine its clinical value for prognosis and treatment.
Core Tip: This review integrates contemporary findings regarding the bidirectional interaction between oxidative stress and inflammation in breast cancer, emphasizing common signaling pathways that facilitate tumor initiation, development, and treatment resistance. This work examines how reactive oxygen species alter the tumor microenvironment, drive genetic instability, and sustain inflammation, while inflammatory mediators exacerbate oxidative damage. Furthermore, it assesses novel biomarkers and tailored therapies that leverage this interaction, providing insights into individualized therapeutic approaches and prospective tactics to improve treatment efficacy and address resistance.
