癌变
肺癌
炎症
克拉斯
肿瘤促进
医学
致癌物
癌症
肺
癌症研究
免疫学
病理
生物
内科学
结直肠癌
遗传学
作者
Yuko Nakano‐Narusawa,Masanao Yokohira,Keiko Yamakawa,Juanjuan Ye,Misa Tanimoto,Linxuan Wu,Yukinori Mukai,Katsumi Imaida,Yoko Matsuda
出处
期刊:Cancers
[Multidisciplinary Digital Publishing Institute]
日期:2021-06-10
卷期号:13 (12): 2910-2910
被引量:8
标识
DOI:10.3390/cancers13122910
摘要
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 (KRAS, EGFR, and p53 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.
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