Transcriptome dysregulation in hyper-progressive disease samples with immune checkpoint blockade  

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作  者:Dan Xue Tengteng Zhu Hongguang Lin Peilin Guo Mengling Li Mei’e Yu Fan Yang Sheng Yang Xiangqi Chen 

机构地区:[1]Department of Respiratory Medicine,Fujian Medical University Union Hospital,Fuzhou,Fujian 350000,China [2]Department of Geriatrics,Fujian Medical University Union Hospital,Fuzhou,Fujian 350000,China [3]Hongqiao International Institute of Medicine,Shanghai Tongren Hospital/Clinical Research Institute,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China [4]Department of Oncology,Fujian Medical University Union Hospital,Fuzhou,Fujian 350000,China [5]Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases,Fuzhou,Fujian 350122,China

出  处:《Chinese Medical Journal》2023年第24期3019-3021,共3页中华医学杂志(英文版)

基  金:supported by the Joint Funds for the Innovation of Science and Technology,Fujian Province,China(Nos.2016Y9028,2019Y9055 and 2020Y9090);Fujian provincial health technology project(No.2020CXB016);the Natural Science Foundation of Fujian Province(No.2021J01772)

摘  要:To the Editor:Tumor immunotherapy has made rapid progress in recent years.However,immune checkpoint blockade(ICB)therapy may cause clinical symptoms of hyper-progressive disease(HPD),especially for patients with alterations or amplifications in driver genes,such as mouse double minute 2(MDM2),epidermal growth factor receptor(EGFR),and fibroblast growth factor 4(FGF4).Recently,Kamada et al[1]investigated the molecular mechanism of HPD to explore whether immune checkpoint inhibition caused HPD in patients in clinical trials.Ki67+effector regulatory T cells(eTregs)in HPD patients were found to be increased after PD-1 monoclonal antibody treatment.Other studies have also found that immune cells in the tumor microenvironment of patients with HPD show obvious changes before and after treatment.[2]Tumor microenvironment changes in HPD imply the potential presence of unknown gene interactions that promote rapid growth of tumor cells after cancer immunotherapy.

关 键 词:alterations clinical patients 

分 类 号:R730.51[医药卫生—肿瘤]

 

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