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Published on: November 19, 2019
Programmed death 1 pathway inhibition in metastatic renal cell cancer and prostate cancer
Patricia A Tang1, Daniel Y C Heng
1Tom Baker Cancer Center, University of Calgary, Calgary, AB, Canada.
Abstract:
Programmed death 1 (PD-1) is a T cell co-inhibitory receptor with two ligands, PD-L1 and PD-L2. In cancer, this pathway plays a major role in immune resistance in the tumor environment. Blockade of this pathway can enhance antitumor immune responses. This review discusses the preclinical rationale for PD-1 pathway inhibition in advanced renal cell carcinoma and prostate cancer, in addition to the clinical activity and toxicity of the anti-PD-L1 antibody BMS-936559, as well as anti-PD-1 antibodies MK-3475 and BMS-936558.
Insights
Programmed death 1 (PD-1) pathway blockade enhances antitumor immunity. This review covers PD-1 inhibition in renal cell and prostate cancers, detailing clinical data for specific antibodies.
Area of Science:
- Immunology
- Oncology
- Pharmacology
Background:
- Programmed death 1 (PD-1) is a T cell receptor that inhibits immune responses.
- Its ligands, PD-L1 and PD-L2, are crucial in tumor immune evasion.
- Targeting the PD-1 pathway can overcome cancer-induced immune suppression.
Purpose of the Study:
- To review the preclinical basis for inhibiting the PD-1 pathway in advanced cancers.
- To discuss the clinical efficacy and safety of PD-1/PD-L1 inhibitors in renal cell and prostate cancers.
Main Methods:
- Literature review of preclinical studies on PD-1 pathway inhibition.
- Analysis of clinical trial data for anti-PD-L1 (BMS-936559) and anti-PD-1 (MK-3475, BMS-936558) antibodies.
Main Results:
- Preclinical data support PD-1 pathway blockade for enhancing antitumor immunity.
- Clinical studies demonstrate activity of PD-1/PD-L1 inhibitors in advanced renal cell and prostate cancers.
- Specific antibodies show varying efficacy and toxicity profiles.
Conclusions:
- PD-1 pathway inhibition is a promising strategy for treating advanced renal cell and prostate cancers.
- Further investigation into the clinical activity and toxicity of these agents is warranted.
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