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IL-17 mediates resistance to anti-VEGF therapy

Eleni Maniati1, Thorsten Hagemann

  • 1Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, London, UK.

Nature Medicine
|September 10, 2013
PubMed

Insights

Interleukin-17 (IL-17) released during anti-angiogenic therapy promotes inflammation and blood vessel growth, leading to cancer drug resistance. This IL-17 activity drives resistance to vascular endothelial growth factor (VEGF) targeted treatments.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Anti-angiogenic therapy targeting vascular endothelial growth factor (VEGF) is a key cancer treatment strategy.
  • Tumor refractoriness to anti-angiogenic drugs is a significant clinical challenge.
  • The tumor microenvironment's role in mediating drug resistance requires further elucidation.

Discussion:

  • Interleukin-17 (IL-17) in the tumor microenvironment promotes inflammation.
  • IL-17 activates VEGF-independent angiogenic programs, bypassing anti-angiogenic drug effects.
  • This IL-17 mediated pathway contributes to acquired resistance in cancers treated with VEGF inhibitors.

Key Insights:

  • IL-17 release is a critical mechanism underlying resistance to VEGF-targeted therapies.
  • Stromal-derived inflammatory programs induced by IL-17 are crucial for resistance.
  • The findings highlight a novel pathway driving refractory cancer phenotypes.

Outlook:

  • Targeting IL-17 or associated inflammatory pathways may overcome anti-angiogenic drug resistance.
  • Developing combination therapies involving IL-17 inhibition could enhance treatment efficacy.
  • Further research into IL-17's role in diverse cancer types is warranted.

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