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Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo
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STINGing Viral Tumors: What We Know from Head and Neck Cancers

Emma Saulters1, John F Woolley1, Shankar Varadarajan2

  • 1Department of Pharmacology and Therapeutics, University of Liverpool, Liverpool, United Kingdom.

Cancer Research
|April 27, 2021
PubMed

Insights

Viruses impact tumors and immunity. Human papillomavirus (HPV) in head and neck squamous cell carcinomas (HNSCC) activates the STING pathway, potentially explaining better patient outcomes in HPV-positive HNSCC tumors.

Area of Science:

  • Immunology
  • Oncology
  • Virology

Background:

  • Viruses can influence tumor biology and anti-tumor immunity, even if not directly oncogenic.
  • The role of the stimulator of interferon genes (STING) pathway in virus-associated tumor microenvironments is not well understood.
  • Human papillomavirus (HPV) infection in head and neck squamous cell carcinomas (HNSCC) presents a unique clinical profile.

Purpose of the Study:

  • To explore the fundamental question of whether virus-associated tumors should be classified separately from non-virus-associated tumors.
  • To investigate the regulation of the STING pathway within the tumor microenvironment of HPV-positive HNSCC.
  • To understand the mechanisms behind the improved clinical outcomes observed in HPV-positive HNSCC patients.

Main Methods:

  • Review of current literature on viral influence on tumors and innate immune responses.
  • Focus on the STING pathway activation by viral components, particularly in the context of HNSCC.
  • Analysis of HPV's role in modulating the tumor microenvironment and host immune response.

Main Results:

  • Viruses activate innate immune responses, including the STING pathway, via pathogen recognition receptors.
  • HPV-positive HNSCC exhibits a distinct etiology and better patient prognosis (overall survival, reduced recurrence) compared to HPV-negative HNSCC.
  • The improved outcomes in HPV-positive HNSCC may be linked to enhanced immunogenicity driven by HPV-activated innate immune pathways.

Conclusions:

  • HNSCC serves as a valuable model for studying the STING pathway in virus-induced tumors.
  • Understanding STING pathway regulation in HPV-associated HNSCC is crucial for deciphering viral impacts on tumor immunity.
  • Further research into these pathways could reveal novel therapeutic strategies for virus-associated cancers.

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