Journal
CANCER DRUG RESISTANCE
Volume 3, Issue 4, Pages 832-853Publisher
OAE PUBLISHING INC
DOI: 10.20517/cdr.2020.41
Keywords
Epithelial-to-mesenchymal transition; epithelial-mesenchymal plasticity; immune evasion; tumor immune microenvironment; intrinsic and extrinsic mechanisms of resistance to immune checkpoint blockade; therapeutic opportunity
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Funding
- Research Council of Norway [223250]
- Norwegian Research Council [240130]
- Norwegian Cancer Society [190330]
- FRIPRO Mobility Grant Fellowship from the Research Council of Norway
- EU's 7th Framework Programme's Marie Sklodowska Curie Actions (MSCA COFUND) [608695]
- Legat for Forskning av Kreftsykdommer fund at UIB
- Familien Blix fund
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Epithelial-mesenchymal plasticity (EMP) of cancer cells contributes to cancer cell heterogeneity, and it is well established that EMP is a critical determinant of acquired resistance to cancer treatment modalities including radiation therapy, chemotherapy, and targeted therapies. Here, we aimed to explore how EMP contributes to cancer cell camouflage, allowing an ever-changing population of cancer cells to pass under the radar of our immune system and consequently compromise the effect of immune checkpoint blockade therapies. The ultimate clinical benefit of any combination regimen is evidenced by the sum of the drug-induced alterations observed in the variety of cellular populations composing the tumor immune microenvironment. The finely-tuned molecular crosstalk between cancer and immune cells remains to be fully elucidated, particularly for the spectrum of malignant cells along the epithelial to mesenchymal axis. High-dimensional single cell analyses of specimens collected in ongoing clinical studies is becoming a key contributor to our understanding of these interactions. This review will explore to what extent targeting EMP in combination with immune checkpoint inhibition represents a promising therapeutic avenue within the overarching strategy to reactivate a halting cancer-immunity cycle and establish a robust host immune response against cancer cells. Therapeutic strategies currently in clinical development will be discussed.
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