Nakano-Narusawa Yuko, Yokohira Masanao, Yamakawa Keiko, Ye Juanjuan, Tanimoto Misa, Wu Linxuan, Mukai Yuri, Imaida Katsumi, Matsuda Yoko
Oncology Pathology, Department of Pathology and Host-Defense, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan.
Cancers (Basel). 2021 Jun 10;13(12):2910. doi: 10.3390/cancers13122910.
Lung cancer remains the leading cause of cancer-related deaths, with an estimated 1.76 million deaths reported in 2018. Numerous studies have focused on the prevention and treatment of lung cancer using rodent models. Various chemicals, including tobacco-derived agents induce lung cancer and pre-cancerous lesions in rodents. In recent years, transgenic engineered rodents, in particular, those generated with a focus on the well-known gene mutations in human lung cancer (, , and mutations) have been widely studied. Animal studies have revealed that chronic inflammation significantly enhances lung carcinogenesis, and inhibition of inflammation suppresses cancer progression. Moreover, the reduction in tumor size by suppression of inflammation in animal experiments suggests that chronic inflammation influences the promotion of tumorigenesis. Here, we review rodent lung tumor models induced by various chemical carcinogens, including tobacco-related carcinogens, and transgenics, and discuss the roles of chronic inflammation in lung carcinogenesis.
肺癌仍然是癌症相关死亡的主要原因,2018年估计有176万人死亡。许多研究致力于使用啮齿动物模型来预防和治疗肺癌。包括烟草衍生剂在内的各种化学物质会在啮齿动物中诱发肺癌和癌前病变。近年来,转基因工程啮齿动物,特别是那些针对人类肺癌中著名基因突变(、和突变)而产生的啮齿动物,受到了广泛研究。动物研究表明,慢性炎症会显著增强肺癌的发生,而抑制炎症则会抑制癌症进展。此外,在动物实验中通过抑制炎症使肿瘤大小减小,这表明慢性炎症会影响肿瘤发生的促进过程。在此,我们综述了由各种化学致癌物(包括烟草相关致癌物)和转基因诱导的啮齿动物肺肿瘤模型,并讨论了慢性炎症在肺癌发生中的作用。