TY - JOUR
T1 - Mechanistic insights into lethal hyper progressive disease induced by PD-L1 inhibitor in metastatic urothelial carcinoma
AU - Nishimura, Kazuki
AU - Takahara, Kiyoshi
AU - Komura, Kazumasa
AU - Ishida, Mitsuaki
AU - Hirosuna, Kensuke
AU - Maenosono, Ryoichi
AU - Ajiro, Masahiko
AU - Sakamoto, Moritoshi
AU - Iwatsuki, Kengo
AU - Nakajima, Yuki
AU - Tsujino, Takuya
AU - Taniguchi, Kohei
AU - Tanaka, Tomohito
AU - Inamoto, Teruo
AU - Hirose, Yoshinobu
AU - Ono, Fumihito
AU - Kondo, Yoichi
AU - Yoshimi, Akihide
AU - Azuma, Haruhito
N1 - Publisher Copyright:
© The Author(s) 2024.
PY - 2024/12
Y1 - 2024/12
N2 - Hyper progressive disease (HPD) is a paradoxical phenomenon characterized by accelerated tumor growth following treatment with immune checkpoint inhibitors. However, the pathogenic causality and its predictor remain unknown. We herein report a fatal case of HPD in a 50-year-old man with metastatic bladder cancer. He had achieved a complete response (CR) through chemoradiation therapy followed by twelve cycles of chemotherapy, maintaining CR for 24 months. Three weeks after initiating maintenance use of a PD-L1 inhibitor, avelumab, a massive amount of metastases developed, leading to the patient’s demise. Omics analysis, utilizing metastatic tissues obtained from an immediate autopsy, implied the contribution of M2 macrophages, TGF-β signaling, and interleukin-8 to HPD pathogenesis.
AB - Hyper progressive disease (HPD) is a paradoxical phenomenon characterized by accelerated tumor growth following treatment with immune checkpoint inhibitors. However, the pathogenic causality and its predictor remain unknown. We herein report a fatal case of HPD in a 50-year-old man with metastatic bladder cancer. He had achieved a complete response (CR) through chemoradiation therapy followed by twelve cycles of chemotherapy, maintaining CR for 24 months. Three weeks after initiating maintenance use of a PD-L1 inhibitor, avelumab, a massive amount of metastases developed, leading to the patient’s demise. Omics analysis, utilizing metastatic tissues obtained from an immediate autopsy, implied the contribution of M2 macrophages, TGF-β signaling, and interleukin-8 to HPD pathogenesis.
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U2 - 10.1038/s41698-024-00707-6
DO - 10.1038/s41698-024-00707-6
M3 - Article
AN - SCOPUS:85204310821
SN - 2397-768X
VL - 8
JO - npj Precision Oncology
JF - npj Precision Oncology
IS - 1
M1 - 206
ER -
