Chemotherapy-induced peripheral neuropathy in breast cancer: a narrative review.

Abstract

Background and objective: Chemotherapy-induced peripheral neuropathy (CIPN) remains a major, unresolved complication of breast cancer therapy, often leading to treatment modifications and enduring functional impairment. This review addresses the complex pathogenesis of CIPN, as well as the clinical presentation and impact of CIPN on patient quality of life. The primary objective of this review is to highlight the pathophysiology and pathogenesis of CIPN, as well as detail current strategies and future targets to prevent and treat CIPN in breast cancer patients.

Methods: We conducted a narrative review using the PubMed/Medline, Cochrane, and Embase databases from database inception to July 2025. We used keyword searches including 'breast cancer', 'chemotherapy-induced peripheral neuropathy/CIPN', 'taxane', 'taxane induced peripheral neuropathy/TIPN', 'platinum', 'alkaloids', 'antibody drug conjugates', 'CIPN prevention', 'CIPN treatment', 'biomarkers', 'microbiome', 'racial disparities', 'genetics', 'quality of life', 'inflammation'. Inclusion criteria included clinical and translational English-language studies addressing CIPN in breast cancer, CIPN biomarkers, and the microbiome in oncology research. Exclusion criteria included non-English language studies and clinical studies unrelated to breast cancer.

Key content and findings: In this paper, we synthesize the pathophysiology of CIPN and the growing body of research implicating systemic inflammation and gut microbiome composition in modulating CIPN pathogenesis, suggesting a biological basis for interindividual variability in susceptibility. We also summarize emerging evidence on the role of racial disparities in CIPN. Finally, we explore commonly studied biomarkers that have shown promise as potential predictive markers of CIPN onset as well as potential therapeutic strategies.

Conclusions: CIPN remains a common, dose-limiting toxicity in breast cancer care. Preventive strategies and symptomatic management with consistent clinical benefits are lacking. Duloxetine has strongest scientific evidence for pain reduction; other pharmacologic and non-pharmacologic approaches are promising but heterogeneous and should be framed as adjunctive. Biomarker driven trial designs that test anti-inflammatory strategies, as well as microbiome-targeted interventions, may accelerate treatment breakthroughs. Finally, attention to race as a factor in CIPN susceptibility can help to identify high-risk patients and reduce disparities in CIPN burden.