Patient-derived organoids: A new platform for mechanism research and drug development of gastric intestinal metaplasia

Abstract

A recent study identified taurine as a potential drug for suppressing gastric intestinal metaplasia (GIM) in patient-derived organoids and Atp4a-/- mice. Gastric cancer is one of the leading causes of cancer-related deaths worldwide. GIM is a reversible stage in the Correa cascade of gastric carcinogenesis, which is a research hotspot. Previous research models, which included animals and cells, to some extent limited the progress of GIM. Currently, the rapid development of organoid technology has significantly overcome the limitations of the research models in GIM. Organoid technology provides a novel research model for GIM studies that can preserve molecular characteristics of GIM patients with high similarity, thereby offering experimental evidence to support individualized diagnosis and treatment in the clinic. Here, we discuss research models, current therapeutic drugs, and treatment prospects for GIM. Our view is that future research should focus on patient-derived organoids to conduct more accurate studies of GIM pathogenesis and to advance drug development.

Keywords: Gastric intestinal metaplasia; Patient-derived organoids; Helicobacter pylori infection; Bile acids; Transgenic mice

Core Tip: Gastric intestinal metaplasia (GIM) is a precancerous lesion in the process of gastric carcinogenesis. Organoid technology has overcome the limitations of previous models by preserving patient-specific molecular features. A recent study identified taurine as a potential drug for suppressing GIM in patient-derived organoids and mouse models. Future research should prioritize the use of patient-derived organoids to study GIM pathogenesis and advance drug development more precisely.