The Kirsten rat sarcoma viral oncogene homologue (KRAS) mutation is one of the most prevailing mutations in various tumors and is difficult to cure. Long-term proliferation in carcinogenesis is primarily initiated by oncogenic KRAS-downstream signaling. Recent research suggests that it also activates the autocrine effect and interplays the tumor microenvironment (TME). Here, we discuss the emerging research, including KRAS mutations to immune evasion in TME, which induce immunological modulation that promotes tumor development. This review gives an overview of the existing knowledge of the underlying connection between KRAS mutations and tumor immune modulation. It also addresses the mechanisms to reduce the effect of oncogenes on the immune system and recent advances in clinical trials for immunotherapy in KRAS-mutated cancers.
克尔斯滕大鼠肉瘤病毒癌基因同源物(KRAS)突变是多种肿瘤中最普遍的突变之一,且难以治愈。致癌过程中长期增殖主要由致癌性KRAS下游信号通路启动。最新研究表明,KRAS突变还能激活自分泌效应并与肿瘤微环境相互作用。本文系统探讨了KRAS突变导致肿瘤微环境中免疫逃逸的新兴研究,揭示了其诱导免疫调节促进肿瘤发展的机制。本综述全面阐述了KRAS突变与肿瘤免疫调节的内在联系,解析了降低癌基因对免疫系统影响的机制,并总结了KRAS突变癌症免疫治疗临床试验的最新进展。