Pancreatic cancer is characterized by late diagnosis, therapy resistance, and poor prognosis, necessitating the exploration of early carcinogenesis and prevention methods. Preclinical mouse models have evolved from cell line-based to human tumor tissue- or organoid-derived xenografts, now to humanized mouse models and genetically engineered mouse models (GEMMs). GEMMs, primarily driven by oncogenic Kras mutations and tumor suppressor gene alterations, offer a realistic platform for investigating pancreatic cancer initiation, progression, and metastasis. The incorporation of inducible somatic mutations and CRISPR-Cas9 screening methods has expanded their utility. To better recapitulate tumor initiation triggered by inflammatory cues, common pancreatic risk factors are being integrated into model designs. This approach aims to decipher the role of environmental factors as secondary or parallel triggers of tumor initiation alongside oncogenic burdens. Emerging models exploring pancreatitis, obesity, diabetes, and other risk factors offer significant translational potential. This review describes current mouse models for studying pancreatic carcinogenesis, their combination with inflammatory factors, and their utility in evaluating pathogenesis, providing guidance for selecting the most suitable models for pancreatic cancer research.
胰腺癌以诊断晚、治疗抵抗和预后差为特征，因此亟需探索其早期癌变机制与预防策略。临床前小鼠模型已从基于细胞系的异种移植，发展到人源肿瘤组织或类器官来源的异种移植，进而演进至人源化小鼠模型与基因工程小鼠模型（GEMMs）。以致癌性Kras突变和抑癌基因改变为主要驱动因素的GEMMs，为研究胰腺癌的发生、进展和转移提供了高度仿真的研究平台。通过引入可诱导的体细胞突变及CRISPR-Cas9筛选技术，其应用范围得到进一步拓展。为更真实模拟炎症信号触发的肿瘤发生过程，当前模型设计正整合常见的胰腺癌风险因素。该方法旨在解析环境因素如何作为致癌负荷之外的次级或平行触发因素参与肿瘤发生。新兴模型通过探索胰腺炎、肥胖、糖尿病等风险因素，展现出重要的转化研究潜力。本综述系统阐述了当前用于研究胰腺癌发生的小鼠模型、其与炎症因素的整合策略，以及这些模型在评估发病机制中的应用价值，为选择最适合胰腺癌研究的模型提供指导。
肿瘤(癌症)患者之家