Mechanisms and Management of Albumin-Paclitaxel-Induced Peripheral Neuropathy in Breast Cancer

Breast cancer incidence continues to rise globally, with molecular subtyping now playing a critical role in prognosis and treatment selection. The main subtypes-Luminal A, Luminal B, HER2-enriched, and triple-negative breast cancer (TNBC)-exhibit distinct clinical behaviors and treatment responses, with respective molecular characteristics. Chemotherapy plays a pivotal role in the comprehensive treatment of breast cancer, being widely used in neoadjuvant, adjuvant, and metastatic systemic therapy. Albumin-Paclitaxel based regimens remain the cornerstone of clinical treatment, particularly for highly aggressive subtypes like triple-negative breast cancer (TNBC) and HER2-positive breast cancer. However, 30-60% of breast cancer patients receiving chemotherapy develop chemotherapy-induced peripheral neuropathy (CIPN). Approximately 35% experience severe (≥grade 2) symptoms, often requiring dose modification or treatment discontinuation. Albumin-Paclitaxel's neurotoxicity primarily involves two mechanisms: microtubule stabilization disruption causing axonal transport impairment, and sensory neuron mitochondrial dysfunction. For younger patients, this presents dual clinical challenges: controlling tumor progression while managing neuropathic pain and functional impairment that significantly affect quality of life and work capacity. Treatments are constantly evolving and currently, the most effective treatments (eg duloxetine, cold therapy). Understanding CIPN pathogenesis, diagnostic approaches, and developing effective prevention/treatment strategies is clinically crucial. This maintains treatment adherence and efficacy while improving long-term quality of life for breast cancer patients.