Abstract
Tumor cell plasticity exhibited as an epithelial-mesenchymal transition (EMT) has been identified as a major obstacle for the effective treatment of many cancers. This process, which involves the dedifferentiation of epithelial tumor cells towards a motile, metastatic, and mesenchymal tumor phenotype, mediates resistance to conventional therapies and small-molecule targeted therapies. In this review, we highlight current research correlating the role of tumor plasticity with resistance to current immunotherapy approaches and discuss future and ongoing combination immunotherapy strategies to reduce tumor cell plasticity-driven resistance in cancer.
Keywords:
EMT; IL-8; TGF-β; immunotherapy resistance; tumor plasticity.
Published by Elsevier Inc.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Combined Chemotherapy Protocols / pharmacology
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Cancer Vaccines / administration & dosage
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Cell Line, Tumor
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Cell Plasticity / drug effects
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Cell Plasticity / immunology*
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Clinical Trials, Phase I as Topic
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Clinical Trials, Phase II as Topic
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Combined Modality Therapy / methods
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Disease Models, Animal
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Drug Resistance, Neoplasm / drug effects
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Drug Resistance, Neoplasm / immunology
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Drug Synergism
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Epithelial-Mesenchymal Transition / drug effects
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Epithelial-Mesenchymal Transition / immunology*
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Humans
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Immune Checkpoint Inhibitors / pharmacology
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Immune Checkpoint Inhibitors / therapeutic use
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Immunotherapy / methods*
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Molecular Targeted Therapy / methods
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Neoplasms / immunology
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Neoplasms / pathology
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Neoplasms / therapy*
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Treatment Outcome
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Tumor Escape / drug effects
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Tumor Escape / immunology
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Xenograft Model Antitumor Assays
Substances
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Cancer Vaccines
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Immune Checkpoint Inhibitors