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Targeting apoptosis to manage acquired resistance to third generation EGFR inhibitors
《医学前沿(英文)》 2022年 第16卷 第5期 页码 701-713 doi: 10.1007/s11684-022-0951-0
关键词: acquired resistance EGFR inhibitor apoptosis lung cancer
Mechanisms of resistance to third-generation EGFR tyrosine kinase inhibitors
null
《医学前沿(英文)》 2016年 第10卷 第4期 页码 383-388 doi: 10.1007/s11684-016-0488-1
The tyrosine kinase inhibitors (TKI) of the epidermal growth factor receptor (EGFR) are becoming the first line of therapy for advanced non-small cell lung cancer (NSCLC). Acquired mutations in EGFR account for one of the major mechanisms of resistance to the TKIs. Three generations of EGFR TKIs have been used in clinical applications. AZD9291 (osimertinib; Tagrisso) is the first and only FDA approved third-generation EGFR TKI for T790M-positive advanced NSCLC patients. However, resistance to AZD9291 arises after 9–13 months of therapy. The mechanisms of resistance to third-generation inhibitors reported to date include the EGFR C797S mutation, EGFR L718Q mutation, and amplifications of HER-2, MET, or ERBB2. To overcome the acquired resistance to AZD9291, EAI045 was discovered and recently reported to be an allosteric EGFR inhibitor that overcomes T790M- and C797S-mediated resistance. This review summarizes recent investigations on the mechanisms of resistance to the EGFR TKIs, as well as the latest development of EAI045 as a fourth-generation EGFR inhibitor.
Growth suppression of colorectal cancer expressing S492R EGFR by monoclonal antibody CH12
Qiongna Dong, Bizhi Shi, Min Zhou, Huiping Gao, Xiaoying Luo, Zonghai Li, Hua Jiang
《医学前沿(英文)》 2019年 第13卷 第1期 页码 83-93 doi: 10.1007/s11684-019-0682-z
Colorectal cancer (CRC) is a common malignant tumor in the digestive tract, and 30%–85% of CRCs express epidermal growth factor receptors (EGFRs). Recently, treatments using cetuximab, also named C225, an anti-EGFR monoclonal antibody, for CRC have been demonstrated to cause an S492R mutation in EGFR. However, little is known about the biological function of S492R EGFR. Therefore, we attempted to elucidate its biological function in CRC cells and explore new treatment strategies for this mutant form. Our study indicated that EGFR and S492R EGFR accelerate the growth of CRC cells in vitro and in vivo and monoclonal antibody CH12, which specifically recognizes an EGFR tumor-specific epitope, can bind efficiently to S492R EGFR. Furthermore, mAb CH12 showed significantly stronger growth suppression activities and induced a more potent antibody-dependent cellular cytotoxicity effect on CRC cells bearing S492R EGFR than mAb C225. mAb CH12 obviously suppressed the growth of CRC xenografts with S492R EGFR mutations in vivo. Thus, mAb CH12 may be a promising therapeutic agent in treating patients with CRC bearing an S492R EGFR mutation.
关键词: S492R EGFR ectodomain mutation colorectal cancer mAb CH12 immunnotherapy
LI Yanhua, BI Zhigang
《医学前沿(英文)》 2007年 第1卷 第1期 页码 79-86 doi: 10.1007/s11684-007-0016-4
CD47 blockade improves the therapeutic effect of osimertinib in non-small cell lung cancer
《医学前沿(英文)》 2023年 第17卷 第1期 页码 105-118 doi: 10.1007/s11684-022-0934-1
关键词: osimertinib anti-CD47 antibody combination strategy ADCP EGFR
标题 作者 时间 类型 操作
Growth suppression of colorectal cancer expressing S492R EGFR by monoclonal antibody CH12
Qiongna Dong, Bizhi Shi, Min Zhou, Huiping Gao, Xiaoying Luo, Zonghai Li, Hua Jiang
期刊论文
Ultraviolet-B induced expression of hypoxia-inducible factor 1α, transferrin receptor through EGFR/PI3K
LI Yanhua, BI Zhigang
期刊论文