Cancer immunotherapy using checkpoint blockade

The release of negative regulators of immune activation (immune checkpoints) that limit antitumor responses has resulted in unprecedented rates of long-lasting tumor responses in patients with a variety of cancers. This can be achieved by antibodies blocking the cytotoxic T lymphocyte-associated pro...

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Published in:	Science (American Association for the Advancement of Science) Vol. 359; no. 6382; p. 1350
Main Authors:	Ribas, Antoni, Wolchok, Jedd D
Format:	Journal Article
Language:	English
Published:	United States 23.03.2018
Subjects:	Antibodies - therapeutic use CTLA-4 Antigen - antagonists & inhibitors Humans Immunotherapy - methods Neoplasms - therapy Programmed Cell Death 1 Receptor - antagonists & inhibitors
ISSN:	1095-9203, 1095-9203
Online Access:	Get more information
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Abstract	The release of negative regulators of immune activation (immune checkpoints) that limit antitumor responses has resulted in unprecedented rates of long-lasting tumor responses in patients with a variety of cancers. This can be achieved by antibodies blocking the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) or the programmed cell death 1 (PD-1) pathway, either alone or in combination. The main premise for inducing an immune response is the preexistence of antitumor T cells that were limited by specific immune checkpoints. Most patients who have tumor responses maintain long-lasting disease control, yet one-third of patients relapse. Mechanisms of acquired resistance are currently poorly understood, but evidence points to alterations that converge on the antigen presentation and interferon-γ signaling pathways. New-generation combinatorial therapies may overcome resistance mechanisms to immune checkpoint therapy.
AbstractList	The release of negative regulators of immune activation (immune checkpoints) that limit antitumor responses has resulted in unprecedented rates of long-lasting tumor responses in patients with a variety of cancers. This can be achieved by antibodies blocking the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) or the programmed cell death 1 (PD-1) pathway, either alone or in combination. The main premise for inducing an immune response is the preexistence of antitumor T cells that were limited by specific immune checkpoints. Most patients who have tumor responses maintain long-lasting disease control, yet one-third of patients relapse. Mechanisms of acquired resistance are currently poorly understood, but evidence points to alterations that converge on the antigen presentation and interferon-γ signaling pathways. New-generation combinatorial therapies may overcome resistance mechanisms to immune checkpoint therapy. The release of negative regulators of immune activation (immune checkpoints) that limit antitumor responses has resulted in unprecedented rates of long-lasting tumor responses in patients with a variety of cancers. This can be achieved by antibodies blocking the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) or the programmed cell death 1 (PD-1) pathway, either alone or in combination. The main premise for inducing an immune response is the preexistence of antitumor T cells that were limited by specific immune checkpoints. Most patients who have tumor responses maintain long-lasting disease control, yet one-third of patients relapse. Mechanisms of acquired resistance are currently poorly understood, but evidence points to alterations that converge on the antigen presentation and interferon-γ signaling pathways. New-generation combinatorial therapies may overcome resistance mechanisms to immune checkpoint therapy.The release of negative regulators of immune activation (immune checkpoints) that limit antitumor responses has resulted in unprecedented rates of long-lasting tumor responses in patients with a variety of cancers. This can be achieved by antibodies blocking the cytotoxic T lymphocyte-associated protein 4 (CTLA-4) or the programmed cell death 1 (PD-1) pathway, either alone or in combination. The main premise for inducing an immune response is the preexistence of antitumor T cells that were limited by specific immune checkpoints. Most patients who have tumor responses maintain long-lasting disease control, yet one-third of patients relapse. Mechanisms of acquired resistance are currently poorly understood, but evidence points to alterations that converge on the antigen presentation and interferon-γ signaling pathways. New-generation combinatorial therapies may overcome resistance mechanisms to immune checkpoint therapy.
Author	Wolchok, Jedd D Ribas, Antoni
Author_xml	– sequence: 1 givenname: Antoni orcidid: 0000-0003-3669-8458 surname: Ribas fullname: Ribas, Antoni email: aribas@mednet.ucla.edu, wolchokj@mskcc.org organization: Department of Medicine, Division of Hematology-Oncology; Department of Surgery, Division of Surgical Oncology; and Department of Molecular and Medical Pharmacology, Jonsson Comprehensive Cancer Center and Parker Institute for Cancer Immunotherapy, University of California, Los Angeles, Los Angeles, CA 90095, USA. aribas@mednet.ucla.edu wolchokj@mskcc.org – sequence: 2 givenname: Jedd D orcidid: 0000-0001-6718-2222 surname: Wolchok fullname: Wolchok, Jedd D email: aribas@mednet.ucla.edu, wolchokj@mskcc.org organization: Weill Cornell Medical and Graduate Colleges, New York, NY 10065, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29567705$$D View this record in MEDLINE/PubMed
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ContentType	Journal Article
Copyright	Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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Snippet	The release of negative regulators of immune activation (immune checkpoints) that limit antitumor responses has resulted in unprecedented rates of long-lasting...
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SubjectTerms	Antibodies - therapeutic use CTLA-4 Antigen - antagonists & inhibitors Humans Immunotherapy - methods Neoplasms - therapy Programmed Cell Death 1 Receptor - antagonists & inhibitors
Title	Cancer immunotherapy using checkpoint blockade
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