NRF2 participates in the suppressive tumor immune microenvironment of KRAS/KEAP1 co-mutant non-small cell lung cancer by inhibiting the STING

作     者：Sun Xiaodan Zhao Peiyan Li Hui Liu Yan Cheng Ying Sun Xiaodan;Zhao Peiyan;Li Hui;Liu Yan;Cheng Ying

作者机构：Postdoctoral Research WorkstationJilin Cancer HospitalChangchunJilin 130012China Translational Cancer ResearchJilin Cancer HospitalChangchunJilin 130012China Department of Medical Thoracic OncologyJilin Cancer HospitalChangchunJilin 130012China 

出 版 物：《Genes & Diseases》 (基因与疾病（英文）)

年 卷 期：2023年第10卷第5期

页      面：1727-1730页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：financially supported by the project of lung cancer targeted therapy research of Beijing CSCO(No.Y-2021AST/qn-0013) the National Natural Science Foundation of China(No.82103343) 

主　　题：KRAS inhibiting cancer 

摘      要：Kirsten rat sarcoma(KRAS)mutant non-small cell lung cancer(NSCLC)has distinct co-mutational *** 20%of KRAS mutant NSCLC cases underwent loss-of-function mutation of Kelch-like ECH-associated protein 1(KEAP1)gene,namely KRAS-KEAP1 comutation(KK)type,which exhibited a poorer immune checkpoint inhibitor(ICl)response compared with individual KRAS mutation(K)type tumors.i Recent studies suggest that K-type tumors are referred to ashot tumorswhile KK-type tumors are ascold tumors.Therefore,clarifying the molecular mechanism of the poor IClresponsive phenotype of KK-type tumors is the key to improving the clinical efficacy and breaking through the therapy ***-mutations could regulate the immune contexture to reshape the tumor immune microenvironment(TIME)。