Elsevier

Biomedicine & Pharmacotherapy

Volume 110, February 2019, Pages 312-318
Biomedicine & Pharmacotherapy

PD-1/ PD-L1 blockade as a novel treatment for colorectal cancer

https://doi.org/10.1016/j.biopha.2018.11.105Get rights and content
Under a Creative Commons license
open access

Highlights

  • Immune profile of a tumor indicates response to immune checkpoints inhibitors.

  • PD-L1 expression and dMMR genotype would cause better response to PD-1 inhibitors.

  • PD-L1 blockade is not efficient enough by itself.

  • PD-L2 blockade may be considered as a new therapeutic target.

  • Combination therapies may enhance the potential of immunotherapies.

Abstract

Colorectal cancer (CRC), as a prominent cause of cancer-related deaths, has historically been notable worldwide and many attempts have been made to raise the overall survival of CRC patients. Immune response has long been a question of great interest in a wide range of fields such as cancer therapies and anti-tumor immunity through checkpoint inhibitors, specifically anti PD-1/ PD-L1 interaction, is a new line of research for treatment of CRC patients. Following the successful development of anti-PD-1 for melanoma, renal cell carcinoma, and non-small cell lung cancer, several clinical trials have been conducted on monoclonal antibodies (MAbs) against PD-1 in CRC. There is a growing body of literature that recognizes the importance of anti-PD-1 therapy for MSI (Microsatellite instability) tumors among CRC subtypes. We present a comprehensive knowledge of immune therapy through PD-1/PD-L1 blockade that argues how efficient the process is, in colon cancer carcinoma. In this review, we discuss the responsiveness of immunotherapy on PD-1/PD-L1 blockade and various tactics for overcoming weak responses to these checkpoint inhibitors in CRC. More research using controlled trials is required to enable new discoveries to provide continued success with immune-based therapies and grounds for optimism about the future of CRC patients.

Graphical abstract

The mechanism of interaction between PD-1+ T-cells and PD-L1/2+ tumor cells.

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Keywords

Colon cancer
Immune therapy
Programmed death-1 receptor (PD1)
Programmed cell death protein ligand 1 (PD-L1)

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