Science· 2018Q1
Cancer immunotherapy using checkpoint blockade
- 6,782citations
- Q1SCImago
- 2018year
Short summary
Blocking immune checkpoints like CTLA-4 and PD-1 with antibodies elicits long-lasting tumor responses in many cancer patients by releasing negative regulators of immune activation.
AI-generated from the title and abstract; the full text is not read.
Key points
- Immune checkpoint blockade (CTLA-4, PD-1) achieves unprecedented long-lasting tumor responses.
- Therapy requires pre-existing anti-tumor T cells limited by specific checkpoints.
- Most responders maintain long-term disease control, but one-third relapse.
- Acquired resistance may involve antigen presentation and interferon-γ signaling pathways.
- New combinatorial therapies are needed to overcome resistance.
AI-generated from the title and abstract; the full text is not read.
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.
The authors' abstract, as published at the source. Science, 2018 · DOI ↗
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Field: Oncology
OncologyMedicine