Background. Barrett's esophagus is a histologically defined premalignant lesion of the esophagus in which normal squamous epithelium is replaced by intestinalized columnar epithelium. In a multistep progression from Barrett's esophagus to fully developed carcinoma, accelerated proliferation may indicate or precede genomic instability and, therefore, may be an important factor in the pathogenesis and/or prediction of malignant transformation. Ki‐67 is a nuclear antigen expressed in proliferating cells, (G1, S, G2, and M phases) but not in resting cells (G0 phase). This study was undertaken to determine if Ki‐67 expression correlates with the degree of dysplasia and if Ki‐67 expression can help to differentiate those patients with or without dysplasia. Methods. The Ki‐67 proliferation fraction in 87 paraffin embedded esophageal biopsies from 43 patients with the Ki‐67 antibody (MIB‐1) was analyzed using immunohistochemistry. Using a computerized proliferation index program (QNA v2.54, Becton Dickinson Cellular Imaging Systems, Inc., Elmhurst, IL), a Ki‐67 score was derived for the luminal surface, upper esophageal crypt, lower crypt, and underlying glandular zone of the columnar‐lined esophagus. Results. Significant differences in Ki‐67 scores were noted in each zone among different histologic categories: normal gastric ([NG] n = 17); Barrett's without dysplasia ([ND] n = 17); low grade dysplasia ([LG] n = 21); high grade dysplasia ([HG] n = 14); and adenocarcinoma ([CA] n = 5). The pattern of Ki‐67 expression was associated strongly with each histologic category. The percentage of Ki‐67 positive nuclei in each mucosal zone statistically separated high grade from low grade dysplasia (P < 0.001). In high grade dysplastic tissues, the Ki‐67 positive nuclei were found predominantly on the surface epithelium and upper crypt zones, whereas in low grade dysplasia, the majority of Ki‐67 positive nuclei were found in the lower crypt zone. The number of Ki‐67 positive nuclei in each mucosal component also was significantly different in Barrett's esophagus without dysplasia when compared with Barrett's esophagus with low grade dysplastic tissues. (P < 0.001) Staining patterns of indefinite for dysplasia by H & E staining separated into several distinct patterns (five LG, seven ND, one NG) whereas six biopsies with low grade dysplasia had a Ki‐67 expression pattern more consistent with that of high grade dysplasia. Conclusion. The Ki‐67 staining pattern correlated with histologic findings in Barrett's esophagus and may represent an additional parameter for differentiating patients with or without dysplasia. Cancer 1995;75:423–9.

ASGPR, GPC3, and CK may be valuable HCC biomarkers for CTC detection; the expression of ASGPR and GPC3 might be helpful for understanding patients' OS.

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