Review highlights cGAS–STING pathway modulation in turning cold tumors hot, suggesting targeted delivery platforms can overcome checkpoint inhibitor resistance.
Key Points
To synthesize the molecular mechanisms of the cGAS–STING axis and propose translational strategies that harness pathway activation to overcome immunotherapy resistance.
Narrative review examining the dual immunostimulatory and pro-tumorigenic roles of cGAS–STING signaling across diverse malignancies.
Comparative analysis of first-generation STING agonists versus next-generation delivery platforms, including antibody-drug conjugates and nanoparticles.
Distinguishes acute immunostimulatory antitumor activation from chronic, pro-tumorigenic inflammation fueled by chromosomal instability.
Identifies next-generation delivery platforms (nanoparticles and antibody-drug conjugates) as solutions to the pharmacological failures of first-generation STING agonists.
Establishes a therapeutic framework mapping STING-targeted interventions to specific tumor microenvironment phenotypes, including immune-desert, immune-excluded, and exhausted-inflamed states.