Ferroptosis is a regulated form of cell death driven by iron accumulation and lipid peroxidation. Since its recognition as a modality of regulated cell death, ferroptosis has attracted increasing attention in cancer research for its distinct metabolic and redox dependencies. Recent evidence suggests that ferroptosis arises from systems-level regulation integrating metabolic reprogramming, gene and RNA control, and inter-organelle communication, while simultaneously influencing immune remodeling and the tumor microenvironment. These processes collectively determine ferroptosis susceptibility and therapeutic response. Ferroptosis-related genes and pathways have also emerged as potential biomarkers for risk stratification, treatment prediction, and imaging-based assessment. Moreover, small-molecule inducers, targeted inhibitors, and delivery systems capable of modulating ferroptosis demonstrate translational potential to overcome therapeutic resistance across multiple malignancies, including pancreatic cancer. This review synthesizes recent mechanistic and translational advances, highlighting ferroptosis as a conceptual bridge between cellular metabolism and tumor therapy, and outlining perspectives for precision diagnostics and personalized interventions.
