Small-molecule Interferon Inducers for Cancer Immunotherapy Targeting Non-T cell-inflamed Tumors

Eunha Kim ,Sang-Hee Lee

doi:10.33696/cancerimmunol.3.037

Abstract

Highlights

IntroductionSince the discovery of escaping mechanism of tumor from negative immune regulation, the paradigm of drug discovery for anti-cancer agents has been dramatically shifted to cancer immunotherapy (e.g., dendritic cell therapy, CAR-T cell therapy, or antibody therapy) by stimulating patient’s immune system to treat cancer [13]
Since the discovery of escaping mechanism of tumor from negative immune regulation, the paradigm of drug discovery for anti-cancer agents has been dramatically shifted to cancer immunotherapy by stimulating patient’s immune system to treat cancer [13]
Patients with tumor-infiltrating T cell appeared as an activation of spontaneous immune response and a benefit with immunotherapy, whereas cancer recurrence was detected in patients with a lack of T cell infiltration

Summary

Introduction

Since the discovery of escaping mechanism of tumor from negative immune regulation, the paradigm of drug discovery for anti-cancer agents has been dramatically shifted to cancer immunotherapy (e.g., dendritic cell therapy, CAR-T cell therapy, or antibody therapy) by stimulating patient’s immune system to treat cancer [13]. Immune checkpoint inhibitors targeting PD-1, PD-L1, and CTLA-4 prevent tumor cells from evading immune surveillance and result in anti-tumor responses [4]. These immunomodulators were considered as a ‘game-changer’ with remarkable clinical achievement [5]. Type I IFN-mediated immune activation is one of the essential parts in the regulation of T cell-infiltration to guide tumor from ‘cold’ to ‘hot’. To facilitate type I IFN signaling for anti-tumor responses, STING (Stimulator of interferon genes) has emerged as an innate immune regulator for the last decade [13].

Objectives

Conclusion