BARRETTS-ESOPHAGUS, MARKERS TO DISTINGUISH RISK GROUPS

Citation
I. Ferrando et al., BARRETTS-ESOPHAGUS, MARKERS TO DISTINGUISH RISK GROUPS, Revista espanola de enfermedades digestivas, 90(6), 1998, pp. 436-440
Citations number
62
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
11300108
Volume
90
Issue
6
Year of publication
1998
Pages
436 - 440
Database
ISI
SICI code
1130-0108(1998)90:6<436:BMTDRG>2.0.ZU;2-C
Abstract
BACKGROUND: as compared to the general population, patients with Barre tt's esophagus (BE) present a 30 to 40 times higher risk of developing cancer. Their prognosis is poor and it will only be changed trying to recognize and detect preneoplastic changes early in order to provide these patients with an effective surgical therapy. Although epithelial dysplasia is still the ''gold standard'' as a marker of increased ris k for malignancy, in view of the inter and intraobserver differences f or interpreting it, both as regards its existence and grade, we have i nvestigated other markers which can show this increased cancer risk. O BJECTIVE: our aim has been to analyze which parameters, in addition to dysplasia, can distinguish groups with a higher or lower risk of prog ression to malignancy for a differentiated follow-up, so that the cost -benefit ratio is adequate and a sufficiently early diagnosis can be a chieved which allows for a healing surgical therapy in most patients. PATIENTS AND METHODS: twenty-seven patients have been studied, 9 with BE wi- thout dysplasia (control group), 9 with Barrett's esophagus wit h dysplasia, and 9 adenocarcinomas over BE, in all of which the presen ce of p53, cerb-2, PCNA and CEA was established by histochemistry and the existence of aneuploidy by static cytometry. RESULTS: PCNA was pos itive in the three groups, though it was not at the surface epithelium in 55.5% of the control cases. C-erb-2 was negative in all control ca ses and positive in 5 cases with dysplasia, and 2 with adenocarcinoma. Protein p53 was positive in one control case, in 2 with dysplasia, an d 4 with adenocarcinoma. CEA was positive in 7 control cases and in al l cases with dysplasia and adenocarcinoma. Finally, aneuploidy was fou nd by static cytometry in 5 of 9 control cases, in 4 of 9 with dysplas ia, and in all adenocarcinomas. From the analysis of the results obtai ned, it can be concluded that a positive marker, even in the absence o f dysplasia, suggests the presence of a ''genomic instability'' which may lead to progression to malignancy. CONCLUSIONS: this study allows us to establish three risk groups (high, low and intermediate) for a d ifferentiated follow-up which allows an early diagnosis, with an adequ ate cost-benefit ratio.