More than one route to render tumors resistant to cGAS/STING activation

Cherubin Manokaran; Thomas M Roberts; Yubao Wang

doi:10.1016/j.tips.2022.11.002

More than one route to render tumors resistant to cGAS/STING activation

Trends Pharmacol Sci. 2023 Feb;44(2):67-69. doi: 10.1016/j.tips.2022.11.002. Epub 2022 Nov 19.

Authors

Cherubin Manokaran¹, Thomas M Roberts², Yubao Wang³

Affiliations

¹ Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA; Departments of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
² Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA; Departments of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA. Electronic address: thomas_roberts@dfci.harvard.edu.
³ Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA; Departments of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA. Electronic address: yubao_wang@dfci.harvard.edu.

Abstract

STING (stimulator of interferon genes) activation has considerable potential as a new strategy for cancer therapy, but clinical results have not been encouraging. Recent studies by Hong et al. and Li et al. explain why STING agonists often fail to regress human tumors and propose combinatorial strategies to overcome the protumor effects of STING activation.

Keywords: IL35; IL6; chromosome instability; regulatory B cells.

MeSH terms

Humans
Neoplasms* / drug therapy
Nucleotidyltransferases / metabolism
Signal Transduction*

Substances

Nucleotidyltransferases

Grants and funding

R35 CA231945/CA/NCI NIH HHS/United States