| Objective: Esophageal carcinoma had high incidence rate in our country, especially in our Northern areas. But up to now, it was not clear about its exact causes. So, precancerious finding, precancerious diagnosis and precancerious therapy had very importent significance to the field of prevention and cure of esophageal carcinoma. In the process of occurrence and development of esophageal carcinoma, precancerious lesions were active and unstable stage, and may develop to different directions. In order to investigate the change of gene protein expression in different precancerious lesion stages, and to study the molecule mechanism of their occurrence, we took biopsies from unstained areas and analyzed the expression of FHIT and p16 protein by pathology, flow cytometry analysis and immunohistochemical method. Our aim was to find the relationship of FHIT and/or p16 expression and the clinical characteristic behavior of esophageal precancerous carcinoma. Methods: 1. After carefully observing the whole picture of esophagus, we sprayed 1.5% Lugol's solution through endoscope to esophageal mucosa different from normal epithelium. The position, size, shape and boundary of all visible unstained lesions were recorded. 2. Multiple biopsies were taken from unstained areas. Histological diagnosis was conformed by two pathological experts at the same time. 3. Expression of p16 and FHIT protein was detected and analyzed by flow cytometry and immunohistochemical method respectively.Results: 1 Endoscope appearance: The normal esophageal mucosa was appeared brown or green after iodine staining, while the atypical hyperplasia lesions were showed unstained or less staining in different degrees. Carcinomatous changed squamous epithelium usually had clear-cut margins. In this paper, before staining, 136 doubtful esophageal mucosa lesions were observed. While after staining, abnormal stained lesions in 115 cases were detected. Among them, 35 cases were confirmed moderate and severe dysplasia by histology, occupying 25.74% of all stained individuals. 10 cases were carcinoma in situ in 12 esophageal squamous cell carcinoma.2 The result of pathology: Normal squamous epithelium cells arrayed in order. Normal nucleus had regular shape, showed light purple after haematine and eosin staining and their cytoplasm are red. Atypia could be seen in esophageal precancerous lesions: different sizes of hyperplastic cells, larger and deeper staining nucleus, increased mitotic figures (but no pathological mitotic figures), increased cell layers, disorderly arrangment and no polarity. According to the degree and (or) coverage, atypia could be divided into three grades: mild, moderate and severe dysplasia.3 The result of immunohistochemical method: The expression of p16 protein was negative in 61.11%(11/18)cases of esophageal infiltrating carcinomas and in 5.88%(1/17) cases of normal epithelial tissue. The negative expression of p16 protein in mild, moderate, severe dysplasia and carcinoma in situ was 18.75%(3/16),37.50%(6/16),58.82%(10/17) and 70%(7/10) respectively. The negtive expression of p16 protein from normal epithelium, atypical hyperplasia, carcinoma in situ to infiltrating carcinomas was increasing gradually. There was significant difference between normal and moderate dysplasia groups, between mild and severe dysplasia groups(p<0.05). But no statistic significance was showed between normal and mild dysplasia(p>0.05). Among moderate, severe dysplasia, carcino-ma in situ, infiltrating carcinomas groups,no statistic significance could be found through two-two Comparison (p>0.05).The expression of FHIT protein was negative in 66.67%(12/18) cases of esophageal infiltrating carcinomas and in 17.65%(3/17) cases of normal epithelial tissue. The negative expression of p16 protein in mild, moderate, severe dysplasia and carcinoma in situ was 25%(4/16), 56.25%(9/16), 64.71% (11/17) and 70%(7/10) respectively. Significant difference was showed between normal and moderate dysplasia , between mild and severe dysplasia group... |
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