PD-1
Aged
Animals
Antineoplastic Agents, Immunological
/ adverse effects
CTLA-4 Antigen
/ metabolism
Disease Progression
Humans
Lymphocytes, Tumor-Infiltrating
/ drug effects
Male
Mice
Nivolumab
/ adverse effects
Programmed Cell Death 1 Receptor
/ antagonists & inhibitors
Stomach Neoplasms
/ drug therapy
T-Lymphocytes, Regulatory
/ drug effects
PD-1
hyperprogressive disease
immune-checkpoint blockade
regulatory T cells
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
14 05 2019
14 05 2019
Historique:
pubmed:
28
4
2019
medline:
31
3
2020
entrez:
28
4
2019
Statut:
ppublish
Résumé
PD-1 blockade is a cancer immunotherapy effective in various types of cancer. In a fraction of treated patients, however, it causes rapid cancer progression called hyperprogressive disease (HPD). With our observation of HPD in ∼10% of anti-PD-1 monoclonal antibody (mAb)-treated advanced gastric cancer (GC) patients, we explored how anti-PD-1 mAb caused HPD in these patients and how HPD could be treated and prevented. In the majority of GC patients, tumor-infiltrating FoxP3
Identifiants
pubmed: 31028147
pii: 1822001116
doi: 10.1073/pnas.1822001116
pmc: PMC6525547
doi:
Substances chimiques
Antineoplastic Agents, Immunological
0
CTLA-4 Antigen
0
Programmed Cell Death 1 Receptor
0
Nivolumab
31YO63LBSN
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
9999-10008Informations de copyright
Copyright © 2019 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
Conflict of interest statement: The Sponsor declares a conflict of interest. Y. Togashi has received honoraria and grants from Ono Pharmaceutical as to this work, honoraria and grants from Bristol-Myers Squibb and AstraZeneca, and honoraria from Chugai Pharmaceutical and Merck Sharp & Dohme (MSD) outside of this study. K.S. received honoraria and grants from Ono Pharmaceutical and Bristol-Myers Squibb and grants from MSD outside of this study. H.N. received honoraria and grants from Ono Pharmaceutical as to this work, honoraria and grants from Bristol-Myers Squibb and Chugai Pharmaceutical, and grants from Taiho Pharmaceutical, Daiichi-Sankyo, Kyowa-Hakko Kirin, Zenyaku Kogyo, Astellas Pharmaceutical, Sysmex, and BD Japan outside of this study. Other authors declare no competing financial interests.
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