Cited by 2,035Cancer Immunotherapy and BiomarkersImmunotherapy and Immune ResponsesT-cell and B-cell Immunology

Immune checkpoint inhibitors: recent progress and potential biomarkers

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Darvin, Pramod, Toor, Salman M., Sasidharan Nair, Varun, Elkord, Eyad·2018·Experimental & Molecular Medicine

Abstract

Cancer growth and progression are associated with immune suppression. Cancer cells have the ability to activate different immune checkpoint pathways that harbor immunosuppressive functions. Monoclonal antibodies that target immune checkpoints provided an immense breakthrough in cancer therapeutics. Among the immune checkpoint inhibitors, PD-1/PD-L1 and CTLA-4 inhibitors showed promising therapeutic outcomes, and some have been approved for certain cancer treatments, while others are under clinical trials. Recent reports have shown that patients with various malignancies benefit from immune checkpoint inhibitor treatment. However, mainstream initiation of immune checkpoint therapy to treat cancers is obstructed by the low response rate and immune-related adverse events in some cancer patients. This has given rise to the need for developing sets of biomarkers that predict the response to immune checkpoint blockade and immune-related adverse events. In this review, we discuss different predictive biomarkers for anti-PD-1/PD-L1 and anti-CTLA-4 inhibitors, including immune cells, PD-L1 overexpression, neoantigens, and genetic and epigenetic signatures. Potential approaches for further developing highly reliable predictive biomarkers should facilitate patient selection for and decision-making related to immune checkpoint inhibitor-based therapies.

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  • ICI targeting PD-1 and CTLA-4 is clinically effective in enhancing T-cell-mediated antitumor responses.

    “Although proving to be clinically effective in enhancing T-cell-mediated antitumor responses”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [166]

  • Immune therapy studies are limited to particular cancer types and subsets of patients due to differences in mutation load and immune-related adverse effects.

    “However, these studies are limited to particular cancer types and subsets of patients, due to difference in mutation load seen in different cancer types, and immune-related adverse effects of therapy may occur [93][94][95][96].”

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Authors
Darvin, P., Toor, S. M., Sasidharan Nair, V., & Elkord, E.
Affiliations
  • Hamad bin Khalifa University (QA)
  • University of Manchester (GB)
Corresponding author
Elkord, Eyad
Venue
Experimental & Molecular Medicine
Published
2018-12
Volume
50
Issue
12
Pages
1-11
ISSN
  • 1226-3613 (ISSN-L)
  • 2092-6413
OpenAlex
W2903686952
Cited by
2,035
References
79
Citations by year
2026: 77 · 2025: 158 · 2024: 293 · 2023: 347 · 2022: 356 · 2021: 392 · 2020: 321 · 2019: 88 · 2013: 1
FWCI
21.04
Type
journal article
Language
en
Open access
Locations
  • Experimental & Molecular Medicine (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
Funders
Qatar Foundation (VR04)
Topics
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
immune checkpoint inhibitors, predictive biomarkers, PD-1/PD-L1 inhibitors, CTLA-4 inhibitors, immune-related adverse events, tumor immune microenvironment, PD-L1 expression, neoantigens, genetic signatures, epigenetic signatures, immune checkpoint blockade response, patient selection
MeSH terms
Animals, Antibodies, Monoclonal, Humans, Immune Tolerance, Immunity, Immunization, Immunotherapy, Neoplasms, Biomarkers, Tumor, Treatment Outcome, Epigenesis, Genetic, Tumor Microenvironment, B7-H1 Antigen, CTLA-4 Antigen, Programmed Cell Death 1 Receptor

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