Supriya Srivastava1, Florian Kern2, Neel Sharma3, Frank McKeon4, Wa Xian5, Khay Guan Yeoh3, Khek Yu Ho3, Ming Teh6. 1. Cancer Science Institute, National University of Singapore, Singapore. 2. Genome Institute of Singapore, A-STAR, Singapore. 3. Department of Medicine, National University Health System, Singapore. 4. Department of Biological Sciences, National University of Singapore, Singapore. 5. Department of Pathology, Brigham and Women's Hospital, Boston, MA, USA. 6. Department of Pathology, National University Health System, Singapore. Electronic address: ming_teh@nuhs.edu.sg.
Abstract
INTRODUCTION: Barrett's esophagus (BE) is a premalignant condition associated with esophageal adenocarcinoma (EAC). Evidence highlights that EAC is associated with an estimated 5-year survival of approximately 10-15%. Therefore, there is a need to determine which biomarkers are of value in the diagnosis of BE and beyond. The aim of our study was to evaluate the clinical significance of markers known to be expressed across BE and associated neoplasia. METHODS: Retrospective tissues were obtained from columnar lined esophagus (CLE) without goblet cells (n=22), BE (n=29), dysplasia (n=14), and EAC (n=10). Standardised immunohistochemistry for FABP1, Hepar, CDH17, and CDX2 were performed followed by quantitative staining and statistical analysis. RESULTS: FABP1 expression was negligible in CLE and was highest in BE, with a further decrease in expression in dysplasia and EAC. Hepar expression was also negligible in CLE and was highest in dysplasia and BE, with a reduced expression in EAC. CDH17 and CDX2 showed a significantly higher expression in BE, dysplasia, and EAC compared to CLE. CONCLUSION: All 4 markers were excellent diagnostic panels to clearly discriminate BE from CLE. Moreover, as FABP1 and Hepar have different expression levels in dysplasia and EAC, these markers could function as key diagnostic aids in helping to determine the state of disease progression.
INTRODUCTION: Barrett's esophagus (BE) is a premalignant condition associated with esophageal adenocarcinoma (EAC). Evidence highlights that EAC is associated with an estimated 5-year survival of approximately 10-15%. Therefore, there is a need to determine which biomarkers are of value in the diagnosis of BE and beyond. The aim of our study was to evaluate the clinical significance of markers known to be expressed across BE and associated neoplasia. METHODS: Retrospective tissues were obtained from columnar lined esophagus (CLE) without goblet cells (n=22), BE (n=29), dysplasia (n=14), and EAC (n=10). Standardised immunohistochemistry for FABP1, Hepar, CDH17, and CDX2 were performed followed by quantitative staining and statistical analysis. RESULTS:FABP1 expression was negligible in CLE and was highest in BE, with a further decrease in expression in dysplasia and EAC. Hepar expression was also negligible in CLE and was highest in dysplasia and BE, with a reduced expression in EAC. CDH17 and CDX2 showed a significantly higher expression in BE, dysplasia, and EAC compared to CLE. CONCLUSION: All 4 markers were excellent diagnostic panels to clearly discriminate BE from CLE. Moreover, as FABP1 and Hepar have different expression levels in dysplasia and EAC, these markers could function as key diagnostic aids in helping to determine the state of disease progression.