Esophageal adenocarcinoma (EAC) has increased dramatically in the past 3 decades, making its precursor lesion Barrett’s esophagus (BE) an important clinical problem. Effective interventions are available, but overall outcomes remain unchanged. Most of the BE population remains undiagnosed; most EACs are diagnosed late, and most BE patients will never progress to cancer. These epidemiologic factors make upper endoscopy an inefficient and ineffective strategy for BE diagnosis and risk stratification. In the current review, biomarkers for diagnosis, risk stratification, and predictors of response to therapy in BE are discussed.
Key points
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Molecular diagnosis of Barrett’s esophagus (BE) can now be performed on nonendoscopic cytology specimens. Trefoil factor 3 is promising. Other markers to test further are microRNA and methylated genes.
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BE can be risk-stratified by measuring global (eg, aneuploidy, multiple gains) or specific (eg, p53 expression) markers. A biomarker panel is likely to be needed.
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Limited data are available on markers that can predict response to therapy. Chromosome and gene loss/gain by fluorescent in situ hybridization may be of value.
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P53 mutational analysis on nonendoscopic cytology specimens can detect prevalent high-grade dysplasia. Thus, the same sample can be used to screen for and risk-stratify BE.
Related posts:
Forthcoming Issues
Screening for Barrett’s Esophagus
Cost-Analyses Studies in Barrett’s Esophagus
Epidemiology of Barrett’s Esophagus and Esophageal Adenocarcinoma
Challenges with Endoscopic Therapy for Barrett’s Esophagus
Genetic and Epigenetic Alterations in Barrett’s Esophagus and Esophageal Adenocarcinoma
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