본문으로 건너뛰기
← 뒤로

Targeting STING to generate therapeutic anti-tumor immunity.

1/5 보강
Cancer cell 📖 저널 OA 38.1% 2024: 2/4 OA 2025: 7/18 OA 2026: 15/41 OA 2024~2026 2026 Vol.44(2) p. 260-280
Retraction 확인
출처

Fahey CG, Cordova AF, Gedeon PC, Barbie DA

📝 환자 설명용 한 줄

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway bridges cytosolic DNA sensing with type I interferon activation in cancer.

이 논문을 인용하기

↓ .bib ↓ .ris
APA Fahey CG, Cordova AF, et al. (2026). Targeting STING to generate therapeutic anti-tumor immunity.. Cancer cell, 44(2), 260-280. https://doi.org/10.1016/j.ccell.2025.12.002
MLA Fahey CG, et al.. "Targeting STING to generate therapeutic anti-tumor immunity.." Cancer cell, vol. 44, no. 2, 2026, pp. 260-280.
PMID 41448179 ↗

Abstract

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway bridges cytosolic DNA sensing with type I interferon activation in cancer. Despite promising preclinical results, generating clinically meaningful anti-tumor immunity with STING agonists has faced substantial challenges, highlighting gaps in model systems and the biologic complexity of STING signaling. In the tumor microenvironment (TME), STING activation elicits highly context- and cell type-dependent outcomes, with divergent effects on tumor cells, myeloid cells, T cells, and other cell types. Furthermore, the downstream induction of type I interferon and other cytokines in the TME can have both pro- and anti-tumorigenic consequences, with emerging interferon-independent functions of STING signaling adding further complexity. In this review, we chart the diverse impact of STING activation across the TME and discuss how recent insights can inform the design of next-generation therapeutic strategies that more effectively harness STING-driven innate immunity to promote durable anti-tumor activity in humans.

🏷️ 키워드 / MeSH 📖 같은 키워드 OA만

🏷️ 같은 키워드 · 무료전문 — 이 논문 MeSH/keyword 기반

🟢 PMC 전문 열기