Esophageal abnormalities and the risk for gastroesophageal cancers—a histopathology-register-based study in Sweden

Abstract

Background The poor survival of patients with gastroesophageal cancers may improve if additional esophageal precursor lesions to Barrett’s esophagus and squamous dysplasia are identified. We estimated the risk for gastroesophageal cancers among patients with various histopathological abnormalities in the esophagus, including Barrett’s esophagus, subdivided by histopathological types. Methods Histopathology data from esophageal biopsies obtained 1979–2014 were linked with several national population-based registers in Sweden. Patients were followed from 2 years after the first biopsy date until cancer, death, emigration, esophagectomy/gastrectomy or end of follow-up, 31st of December 2016, whichever came first. We estimated standardized incidence ratios (SIRs) as measures of relative risk with the Swedish general population as reference. Results In total 367 esophageal adenocarcinoma (EAC) cases were ascertained during 831,394 person-years of follow-up. The incidence rate (IR) for EAC was 0.1 per 1000 person-years for normal morphology, 0.2–0.5 for inflammatory changes, and 0.8–2.9 for metaplasia. The IR was 1.0 per 1000 person-years (95% confidence interval 0.7–1.3) among patients with non-dysplastic intestinal metaplasia, 0.9 (0.8–1.1) in non-dysplastic gastric/glandular metaplasia and 2.9 (2.0–4.2) among columnar metaplasia patients with low-grade dysplasia. The SIRs were 11.7 (95% confidence interval 8.6–15.5), 12.0 (10.0–14.2) and 30.2 (20.5–42.8), respectively. The SIRs for gastric cardia adenocarcinoma (GCA) were moderately elevated. Conclusions For the first time, we demonstrate that patients with esophageal inflammatory and other metaplastic abnormalities than Barrett’s esophagus have an increased risk of EAC and GCA compared to the general population. Moreover, patients with different histopathologic subtypes of Barrett’s esophagus have a comparable risk for EAC.

4‑Methoxydalbergione inhibits esophageal carcinoma cell proliferation and migration by inactivating NF‑κB

“…Furthermore, it has been suggested that inflammation triggered by infections is a notable cause of cancer (40,41). Increasing evidence has shown that inflammation is the main cause of EC induction (19). In the present study, the inflammatory inducer LPS (42,43) was used to promote inflammation in EC cells, which simulated the inflammatory response of EC cells.…”

“…It has been reported that the development of EC is a multistep pathogenic process from inflammation to cancer (18,19). The malignant degree of EC is positively associated with inflammatory factors, such as tumor necrosis factor α (TNF-α) (20), and the survival time of patients with EC has been confirmed to be negatively correlated with inflammation (21,22).…”