Barrett's esophagus (BE) is the only recognized precursor to esophageal adenocarcinoma (EAC). Endoscopic monitoring of BE allows for early detection and prevention against advanced cancer, which carries high morbidity and mortality. Over the past two decades, management of early EAC has shifted from esophagectomy toward organ-preserving endoscopic eradication therapy (EET), including endoscopic mucosal resection (EMR), endoscopic submucosal dissection (ESD), and ablative modalities such as radiofrequency ablation, cryotherapy, and hybrid argon plasma coagulation. EMR remains standard for most lesions with pre-invasive neoplasia and small intramucosal EAC, while ESD provides technical advantages for larger or complex neoplasia, though comparative long-term outcome data are limited. Ablation after resection achieves durable clearance of dysplasia and intestinal metaplasia, with emerging therapies showing promise in refractory or high-risk cases. Structured post-EET surveillance is critical, as recurrence risk is highest within 1-2 years of achieving remission, but persists at lower levels long-term. The risk of recurrence is influenced by lesion characteristics, treatment strategy, and center experience. Personalized, risk-adapted surveillance is increasingly supported, incorporating clinical factors such as BE length, baseline histology and prior treatment. More recently, molecular biomarkers and artificial intelligence (AI)-driven integration of clinical and genomic features have shown promising results. Future research should optimize tissue acquisition, refine biomarker panels, and validate AI-enabled predictive models to improve patient selection, minimize recurrence, and guide cost-effective, individualized care.
Abstract The role of postoperative radiotherapy after resection of esophageal small-cell neuroendocrine carcinoma remains uncertain. We evaluated associations with survival and recurrence while addressing treatment timing, confounding, and treatment-effect heterogeneity. We retrospectively analyzed 127 patients from three centers. Diagnosis required small-cell morphology plus synaptophysin and CD56 positivity. Radiotherapy and adjuvant chemotherapy were modeled as time-dependent exposures. Sensitivity analyses included a 90-day landmark design and propensity-score overlap weighting. Treatment-effect heterogeneity was assessed using interaction terms with Holm correction, and recurrence was analyzed using competing-risk methods. A cohort of 43 patients was analyzed descriptively. Radiotherapy was not associated with overall survival in the adjusted time-dependent model (hazard ratio, 1.472; 95% confidence interval, 0.820–2.641; P = 0.195), the 90-day landmark model (hazard ratio, 1.734; 95% confidence interval, 0.934–3.221; P = 0.081), or the overlap-weighted model (hazard ratio, 1.001; 95% confidence interval, 0.550–1.820; P = 0.999). Adjuvant chemotherapy showed a protective direction without statistical significance after adjustment (hazard ratio, 0.569; 95% confidence interval, 0.230–1.407; P = 0.222). No clinicopathological or biomarker-defined factor significantly modified the radiotherapy–survival association after Holm correction. First-failure patterns differed by radiotherapy status, with lower locoregional and higher distant-failure incidence among treated patients; these associations were descriptive because of residual treatment-selection bias. External-cohort estimates were nonsignificant and nonconfirmatory. This study did not demonstrate an overall survival benefit from postoperative radiotherapy and does not provide evidence supporting its routine use or patient selection based on nodal or biomarker status.
