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 alter...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.展开更多
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)
文摘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.
