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A New Era for High-Risk Gastric Cancer: Early Diagnosis and Personalized Treatment

A research team led by Professor Hye-sung Kim from the Department of Convergence Biomedical Science and Professor Bo-gun Jang from the Department of Pathology at JNU School of Medicine has presented the world's first scientific evidence demonstrating that intestinal metaplasia is a prodromal change that can develop into gastric cancer. This groundbreaking finding opens a new chapter for the early diagnosis and customized treatment of high-risk gastric cancer lesions.

According to the Health Insurance Review and Assessment Service, over 4.8 million people are diagnosed with gastritis in Korea annually. Intestinal epithelial metaplasia is observed in 20-30% of patients who undergo gastroscopy. While atrophic gastritis and intestinal epithelial metaplasia are recognized as pre-stages of gastric cancer, their direct progression to cancer at the molecular level had not yet been definitively proven.

The research team meticulously tracked lesions, identified as precursors to gastric cancer, using spatial transcriptome analysis, single-cell analysis, epigenome analysis, and patient-derived organoid experiments. Historically, intestinal metaplasia has lacked an appropriate animal model to simulate its pathological progression, making it challenging to understand its molecular development into gastric cancer. This study is the first to overcome these limitations, enabling real-time tracking of pre-gastric cancer lesion progression through organoids.

The research team confirmed that incomplete intestinal epithelial metaplasia represents a 'hybrid' cell state, simultaneously expressing genes from both stomach and intestinal cells. This indicates an overall unstable differentiation pattern from stem cells to fully differentiated cells.

Notably, in their research using organoids derived from gastric cancer patients, intestinal metaplasia cells differentiated in both gastric and intestinal directions in response to external stimuli. This revealed an inherent instability in cell fate and epigenetic deregulation.

Furthermore, a comparison with actual gastric cancer tissue showed that 76% of all gastric cancers had a gene profile similar to that of incomplete intestinal epithelial metaplasia.

This study provides the first definitive scientific evidence that incomplete intestinal epithelial metaplasia is not merely a risk signal but a direct prodromal lesion of gastric cancer. The study's results were published online in July 2025 in 'Gut' (IF 25.8), a leading journal in the field of gastroenterology.