Inflammatory signaling in genomically instable cancers

Francien Talens, Marcel A. T. M. Van Vugt*

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review

10 Citations (Scopus)

Abstract

Recent studies have shown that genomic instability in tumor cells leads to activation of inflammatory signaling through the cGAS/STING pathway. In this review, we describe multiple ways by which genomic instability leads to cGAS/STING-mediated inflammatory signaling, as well as the consequences for tumor development and the tumor microenvironment. Also, we elaborate on how tumor cells have apparently evolved to escape the immune surveillance mechanisms that are triggered by cGAS/STING signaling. Finally, we describe how cGAS/STING-mediated inflammatory signaling can be therapeutically targeted to improve therapy responses.

Original languageEnglish
Number of pages19
JournalCell Cycle
DOIs
Publication statusPublished - 12-Jul-2019

Keywords

  • Genomic instability
  • cytoplasmic DNA
  • cGAS
  • STING
  • interferon response
  • inflammatory signaling
  • AICARDI-GOUTIERES-SYNDROME
  • INNATE IMMUNE SENSOR
  • CYTOSOLIC DNA SENSOR
  • CYCLIC GMP-AMP
  • DEPENDENT ANTITUMOR IMMUNITY
  • I INTERFERON
  • CHROMOSOMAL INSTABILITY
  • INTRACELLULAR DNA
  • TUMOR-REGRESSION
  • BREAST-CANCER

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