Activating the Nucleic Acid-Sensing Machinery for Anticancer Immunity.

Authors

Terry R Medler, Earle A. Chiles Research Institute, Providence Portland Medical CenterFollow
Jaina M Patel, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, Portland, OR, United StatesFollow
Alejandro Alice, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, Portland, OR, United StatesFollow
Jason R Baird, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, Portland, OR, United StatesFollow
Hong-Ming Hu, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, Portland, OR, United StatesFollow
Michael J Gough, Earle A. Chiles Research Institute, Robert W. Franz Cancer Center, Providence Portland Medical Center, Portland, OR, United StatesFollow

Document Type

Article

Publication Date

1-1-2019

Publication Title

Int Rev Cell Mol Biol

Keywords

Cancer; Innate immunity; RIG-I; STING; TLR; Tumor; Vaccine

Abstract

Nucleic acid sensing pathways have likely evolved as part of a broad pathogen sensing strategy intended to discriminate infectious agents and initiate appropriate innate and adaptive controls. However, in the absence of infectious agents, nucleic acid sensing pathways have been shown to play positive and negative roles in regulating tumorigenesis, tumor progression and metastatic spread. Understanding the normal biology behind these pathways and how they are regulated in malignant cells and in the tumor immune environment can help us devise strategies to exploit nucleic acid sensing to manipulate anti-cancer immunity.

Clinical Institute

Cancer

Department

Earle A. Chiles Research Institute

Department

Oncology

Recommended Citation

Medler, Terry R; Patel, Jaina M; Alice, Alejandro; Baird, Jason R; Hu, Hong-Ming; and Gough, Michael J, "Activating the Nucleic Acid-Sensing Machinery for Anticancer Immunity." (2019). Articles, Abstracts, and Reports. 1148.
https://digitalcommons.providence.org/publications/1148