BACKGROUND: As compared to the general population, patients with Barrett'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 risk for malignancy, in view of the inter and intraobserver differences for interpreting it, both as regards its existence and grade, we have investigated other markers which can show this increased cancer risk. OBJECTIVE: Our aim has been to analyze which parameters, in addition to dysplasia, can distinguish groups with a higher or lower risk of progression to malignancy for a differentiated follow-up, so that the cost-benefit ratio is adequate and a sufficiently early diagnosis can be achieved which allows for a healing surgical therapy in most patients. PATIENTS AND METHODS: Twenty-seven patients have been studied, 9 with BE without dysplasia (control group), 9 with Barrett's esophagus with dysplasia, and 9 adenocarcinomas over BE, in all of which the presence of p53, c-erb-2, PCNA and CEA was established by histochemistry and the existence of aneuploidy by static cytometry. RESULTS: PCNA was positive 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 cases and positive in 5 cases with dysplasia, and 2 with adenocarcinoma. Protein p53 was positive in one control case, in 2 with dysplasia, and 4 with adenocarcinoma. CEA was positive in 7 control cases and in all cases with dysplasia and adenocarcinoma. Finally, aneuploidy was found by static cytometry in 5 of 9 control cases, in 4 of 9 with dysplasia, and in all adenocarcinomas. From the analysis of the results obtained, it can be concluded that a positive marker, even in the absence of 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 differentiated follow-up which allows an early diagnosis, with an adequate cost-benefit ratio.
BACKGROUND: As compared to the general population, patients with Barrett'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 risk for malignancy, in view of the inter and intraobserver differences for interpreting it, both as regards its existence and grade, we have investigated other markers which can show this increased cancer risk. OBJECTIVE: Our aim has been to analyze which parameters, in addition to dysplasia, can distinguish groups with a higher or lower risk of progression to malignancy for a differentiated follow-up, so that the cost-benefit ratio is adequate and a sufficiently early diagnosis can be achieved which allows for a healing surgical therapy in most patients. PATIENTS AND METHODS: Twenty-seven patients have been studied, 9 with BE without dysplasia (control group), 9 with Barrett's esophagus with dysplasia, and 9 adenocarcinomas over BE, in all of which the presence of p53, c-erb-2, PCNA and CEA was established by histochemistry and the existence of aneuploidy by static cytometry. RESULTS:PCNA was positive 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 cases and positive in 5 cases with dysplasia, and 2 with adenocarcinoma. Protein p53 was positive in one control case, in 2 with dysplasia, and 4 with adenocarcinoma. CEA was positive in 7 control cases and in all cases with dysplasia and adenocarcinoma. Finally, aneuploidy was found by static cytometry in 5 of 9 control cases, in 4 of 9 with dysplasia, and in all adenocarcinomas. From the analysis of the results obtained, it can be concluded that a positive marker, even in the absence of 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 differentiated follow-up which allows an early diagnosis, with an adequate cost-benefit ratio.