Histopathology · 2013
Value of α-methylacyl-CoA racemase immunochemistry for predicting neoplastic progression in Barrett's oesophagus.
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Kastelein Florine, Biermann Katharina, Steyerberg Ewout W, Verheij Joanne, Kalisvaart Marit, Looijenga Leendert H J, Stoop Hans A, Walter Laurens, Kuipers Ernst J, Spaander Manon C W, Bruno Marco J, ProBar study group
Аннотация
AIM: To investigate the value of α-methylacyl-CoA racemase (AMACR) immunohistochemistry for predicting neoplastic progression in Barrett's oesophagus (BO).
METHODS AND RESULTS: We conducted a case-control study within a prospective cohort of 720 BO patients. Patients who developed high-grade dysplasia or oesophageal adenocarcinoma were classified as cases, and patients without neoplastic progression as controls. AMACR expression was determined by immunohistochemistry in 12 127 biopsies from 635 patients, and was scored independently by two expert pathologists. Relative risks adjusted for age, gender, BO length and oesophagitis (RR(a)) were calculated in log-linear models. During a median follow-up of 6.6 years, 49 patients (8%) developed high-grade dysplasia or oesophageal adenocarcinoma. Although mild AMACR expression was associated with a trend towards an increased risk of neoplastic progression (RR(a) 1.6, 95% CI 0.9-3.1), the risk was especially elevated with strong AMACR expression (RR(a) 4.8, 95% CI 1.9-12.6). The positive predictive value of strong AMACR expression was slightly higher than that of low-grade dysplasia (22% versus 15%); the negative predictive value was slightly lower (91% versus 93%).
CONCLUSIONS: Strong AMACR expression is associated with an increased risk of neoplastic progression in BO. However, AMACR expression appears to be a less powerful predictor for neoplastic progression than low-grade dysplasia.
METHODS AND RESULTS: We conducted a case-control study within a prospective cohort of 720 BO patients. Patients who developed high-grade dysplasia or oesophageal adenocarcinoma were classified as cases, and patients without neoplastic progression as controls. AMACR expression was determined by immunohistochemistry in 12 127 biopsies from 635 patients, and was scored independently by two expert pathologists. Relative risks adjusted for age, gender, BO length and oesophagitis (RR(a)) were calculated in log-linear models. During a median follow-up of 6.6 years, 49 patients (8%) developed high-grade dysplasia or oesophageal adenocarcinoma. Although mild AMACR expression was associated with a trend towards an increased risk of neoplastic progression (RR(a) 1.6, 95% CI 0.9-3.1), the risk was especially elevated with strong AMACR expression (RR(a) 4.8, 95% CI 1.9-12.6). The positive predictive value of strong AMACR expression was slightly higher than that of low-grade dysplasia (22% versus 15%); the negative predictive value was slightly lower (91% versus 93%).
CONCLUSIONS: Strong AMACR expression is associated with an increased risk of neoplastic progression in BO. However, AMACR expression appears to be a less powerful predictor for neoplastic progression than low-grade dysplasia.