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PubMed2026

Is random biopsy necessary for normal esophageal mucosa during chromoendoscopy? Evidence from a population-based cohort study.

BACKGROUND: Esophageal squamous intraepithelial neoplasia could be detected in normally stained mucosa under Lugol's chromoendoscopy. We aim to determine whether an active biopsy should be performed on such mucosa. METHODS: This study was based on a population-based screening cohort where participants underwent Lugol's chromoendoscopy with biopsies taken from abnormal-unstaining areas and normally stained standard site. A total of 641 participants with esophageal squamous intraepithelial neoplasia or more severe lesions were included in the analysis. The cumulative incidence of high-grade intraepithelial neoplasia/esophageal squamous cell carcinoma (HGIN/ESCC) and ESCC-specific mortality were compared between participants biopsied from iodine unstained and stained areas. Additionally, paired eligible tissues were utilized for comparative genomic analysis. RESULTS: For participants diagnosed with low-grade intraepithelial neoplasia (LGIN), HGIN, and ESCC, 292 (54.8%), 11 (14.9%), and 1 (2.9%) cases, respectively, were biopsied from normal-staining mucosa. Over a median 9.5-year follow-up, no incident HGIN/ESCC cases were identified among individuals with LGIN diagnosed from normal-staining esophageal mucosa. In contrast, LGIN cases detected in unstained lesions exhibited a cumulative incidence of HGIN/ESCC of 15.8 (95% CI, 11.4-21.0) per 100 persons. No ESCC-related deaths occurred in patients having normal-staining lesions, irrespective of pathological grade. Contrastingly, cumulative ESCC-specific mortality per 100 persons for LGIN, HGIN, and ESCC patients of unstained lesions were 2.1 (95% CI, 0.7-4.8), 14.3 (95% CI, 6.7-25.4), and 36.4 (95% CI, 20.4-54.9), respectively. Genomic analysis revealed minimal copy number variants in normally stained lesions compared to substantial alterations in unstained lesions. CONCLUSIONS: Random biopsies of normally stained esophageal mucosa under Lugol's chromoendoscopy should be unnecessary for population-level ESCC screening.

Humans↗
PubMed2024

Molecular Analysis of Persistent and Recurrent Barrett's Esophagus in the Setting of Endoscopic Therapy.

INTRODUCTION: Early neoplastic progression of Barrett's esophagus (BE) is often treated with endoscopic therapy. Although effective, some patients are refractory to therapy or recur after apparent eradication of the BE. The goal of this study was to determine whether genomic alterations within the treated BE may be associated with persistent or recurrent disease. METHODS: We performed DNA sequencing on pre-treatment esophageal samples from 45 patients who were successfully treated by endoscopic therapy and did not recur as well as pre-treatment and post-treatment samples from 40 patients who had persistent neoplasia and 21 patients who had recurrent neoplasia. The genomic alterations were compared between groups. RESULTS: The genomic landscape was similar between all groups. Patients with persistent disease were more likely to have pre-treatment alterations involving the receptor tyrosine kinase pathway ( P = 0.01), amplifications of oncogenes ( P = 0.01), and deletions of tumor suppressor genes ( P = 0.02). These associations were no longer significant after adjusting for patient age and BE length. More than half of patients with persistent (52.5%) or recurrent (57.2%) disease showed pre-treatment and post-treatment samples that shared at least 50% of their driver mutations. DISCUSSION: Pre-treatment samples were genomically similar between those who responded to endoscopic therapy and those who had persistent or recurrent disease, suggesting there is not a strong genomic component to treatment response. Although it was expected to find shared driver mutations in pre-treatment and post-treatment samples in patients with persistent disease, the finding that an equal number of patients with recurrent disease also showed this relation suggests that many recurrences represent undetected minimal residual disease.

Humans↗