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Tumor Plasticity and Resistance to Immunotherapy

Lucas A Horn1, Kristen Fousek1, Claudia Palena1

  • 1Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Trends in Cancer
|April 30, 2020
PubMed

Insights

Tumor cell plasticity, or epithelial-mesenchymal transition (EMT), drives cancer treatment resistance. This review explores how EMT impacts immunotherapy effectiveness and proposes combination strategies to overcome this challenge.

Area of Science:

  • Oncology
  • Cancer Biology
  • Immunotherapy

Background:

  • Tumor cell plasticity, characterized by epithelial-mesenchymal transition (EMT), is a key mechanism enabling cancer cells to acquire migratory and invasive properties.
  • EMT-induced dedifferentiation confers resistance to conventional and targeted cancer therapies, posing a significant clinical challenge.
  • Understanding the interplay between tumor plasticity and treatment response is crucial for developing more effective cancer interventions.

Purpose of the Study:

  • To review current research on the role of tumor plasticity in mediating resistance to cancer immunotherapies.
  • To discuss the implications of epithelial-mesenchymal transition (EMT) in the context of immunotherapy resistance.
  • To explore potential combination immunotherapy strategies aimed at overcoming plasticity-driven resistance.

Main Methods:

  • Literature review of current research findings.
  • Analysis of studies investigating tumor plasticity and immunotherapy response.
  • Synthesis of information on combination therapy approaches.

Main Results:

  • Tumor cell plasticity, including EMT, is increasingly recognized as a mechanism of resistance to various immunotherapy modalities.
  • The dedifferentiated, mesenchymal phenotype associated with EMT can alter tumor immunogenicity and the tumor microenvironment, impacting immune cell infiltration and function.
  • Evidence suggests that targeting EMT or combining therapies may enhance anti-tumor immune responses.

Conclusions:

  • Tumor plasticity represents a significant hurdle for effective cancer immunotherapy.
  • Combination immunotherapy strategies that address or overcome tumor cell plasticity are essential for improving treatment outcomes.
  • Further research into targeting EMT and its downstream effects is warranted to enhance immunotherapy efficacy in resistant cancers.
Keywords:
EMTIL-8TGF-βimmunotherapy resistancetumor plasticity

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