Pancreatic ductal adenocarcinoma (PDAC) remains an aggressive malignancy with a 5-year survival rate below 10%. Its unique genetic makeup and tumor microenvironment produce a lack of response to current treatments, including chemotherapy, radiotherapy, and immunotherapy. Recent preclinical studies have revealed that ferroptosis, an iron-dependent form of nonapoptotic cell death driven by unrestricted lipid peroxidation, may be an attractive therapeutic goal in PDAC. Understanding the dual role of ferroptotic cell death in both promoting and suppressing tumor immunity, as well as its integrated regulatory mechanisms and signaling pathways, may lead to more effective treatment designs for clinical trials of PDAC and may minimize or delay the emergence of drug resistance or side effects.

胰腺导管腺癌 (PDAC) 仍然是一种侵袭性恶性肿瘤，其 5 年生存率低于 10%。其独特的基因组成和肿瘤微环境导致对目前的治疗缺乏反应，包括化学疗法、放射疗法和免疫疗法。最近的临床前研究表明，铁死亡，一种由不受限制的脂质过氧化驱动的铁依赖性非凋亡性细胞死亡形式，可能是 PDAC 中一个有吸引力的治疗目标。了解铁死亡细胞死亡在促进和抑制肿瘤免疫中的双重作用，以及其整合的调节机制和信号通路，可能会为 PDAC 的临床试验带来更有效的治疗设计，并可能最大限度地减少或延缓耐药性的出现或副作用。