Abstract

Abstract Objective Barrett’s esophagus (BE) is an established precursor to esophageal adenocarcinoma, which has a poor prognosis unless detected at an early stage. The progression of BE to adenocarcinoma is slow and unpredictable. Currently, the best predictor of adenocarcinoma is histological detection of dysplasia. Accurate grading of dysplasia and especially discriminating low-grade dysplasia LGD from high-grade dysplasia HGD is important for management. Marked variability exists when diagnosing dysplasia in BE. This highlights the need for a diagnostic adjunct, especially in histologically challenging cases. This study aims at evaluating the role of immunohistochemical expression of (p53, IMP3, AMCAR and CDx2) in Barrett’s oesophagus spectrum, to increase the diagnostic accuracy of grading dysplasia and predicting progression risk. Methods This is a retrospective immunohistochemical study, performed on selected 52 cases of esophageal biopsies. Results The p53 was negative in nondysplastic Barrett’s esophagus (ND-BE) and LGD and strong positivity towards HGD/esophageal adenocarcinoma (EAC). CDX2 showed highest expression among ND-BE and decreased towards EAD. IMP3 and AMCAR were negative in all cases of ND-BE with gradual increase among HGD/esophageal adenocarcinoma cases. IMP3, AMCAR, and CDX2 were found to be more sensitive in detecting HGD (80%, 70% & 70%). Meanwhile, p53 is more specific (100%), IMP3 and AMCAR are more sensitive discriminating LGD from HGD (80%) than p53 and CDX2 (60%, 70%). Conclusion This combined panel of p53, CDX2, IMP3, and AMACR could be used in conjunction with histology as a promising tool to accurately predict progression form BE to HGD/adenocarcinoma with a great value for early detecting high grade dysplasia, discriminating it from LGD, improving risk stratification in BE, and optimizing patient care.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.