Changes in screening, prognosis and therapy for esophageal adenocarcinoma in Barrett's esophagus

Abstract

Purpose of review: Significant changes in concepts of managing Barrett's esophagus have led to change in the recommendations concerning screening, surveillance, biomarkers, and therapies in this condition over the past several years. We summarize the important changes in this regard.

Recent findings: Narrow band imaging and esophageal capsule endoscopy are alternative methods to screen for Barrett's esophagus. Narrow band imaging provides clear visualization of the mucosal pit patterns and vascular patterns, which improve the diagnostic value for specialized intestinal mataplasia. Esophageal capsule endoscopy is a new potential tool that allows a direct noninvasive visualization of esophagus. Research efforts are currently directed towards risk stratification of patients and biomarkers have been developed to predict development of esophageal adenocarcinoma. Recent studies have reported that frequent loss of heterozygosity (LOH) as well as allelic imbalances in chromosomes in esophageal adenocarcinoma. Fluorescent in-situ hybridization technique, which uses fluorescently labeled DNA probes to detect chromosomal alterations in cells, obtained from cytology specimens has been developed. It showed more sensitive and specific for abnormalities than PCR based techniques. Currently, many studies support the concept of endoscopic elimination of dysplastic lesions in the esophagus by a mucosal ablation therapy. Photodynamic therapy and radiofrequency ablation are recently developed, emerging techniques.

Summary: Recent advances in screening; prognostication and therapy for esophageal adenocarcinoma in Barrett's esophagus have brought a significant new insight in clinical practices and will eventually ensure better patients outcomes.

Figure 1

Lead time bias refers to two patients, A and B, who are develop cancer and are develop cancer at the same time and are destined to die at the same time. If one is detected earlier through screening, even though the disease runs the same course, it leads to an apparent increase in survival. Screening programs are susceptible to this bias.

Figure 2

Treatment algorithm for Barrett’s esophagus. Non-dysplastic Barrett’s esophagus rarely has genetic abnormalities and is unlikely to progress. It would be beneficial to conduct surveillance in these patients only if there were reasonable expectations for good quality of life. Low-grade dysplasia should be confirmed by another expert pathologist. There are no good studies to demonstrate efficacy of therapy and treatment should probably be done at this time in the context of clinical trials. Surveillance is more reasonable in this group given the higher risk of cancer. High-grade dysplasia should be evaluated carefully for evidence of cancer with endoscopic mucosal resection of any mucosal abnormalities. Treatment options are open to the needs of the patient, the experience of the physicians, and the length of the Barrett’s esophagus. Further surveillance, endoscopic ablation, and esophagectomy would be reasonable options.

Fig 3

simplified schema of molecular alterations in metaplasia-dysplasia-carcinoma sequences of Barrett’s esophagus