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Expression and mutual relationship of tumor suppression gene and apoptosis regulating gene in gastric carcinoma and paracancerous tissues

Peng Yan-shen

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Abstract

Objective To investigate the expression and mutual relationship of tumor suppression gene and apoptosis regulating gene in gastric carcinoma and paracancerous tissues. Methods 30 cases of gastric carcinoma patients underwent surgical resection. Samples were taken from tumor site and paracancerous tissues. ABC immunohistochemical staining was used to detect the expression of p53、p16、bcl 2 proteins. Results No correlation between p53, p16, or bcl 2 expression and grade of pathologic stage, grade of differentiation, or lymph node status was observed ( P 0.05), there was significant correlation between bcl 2 and type of gastric carcinoma ( P 0.05). The positive rate of p53 gene expression in gastric carcinoma was significantly higher than that in moderate and severe dysplasia ( P 0.05). The positive rate of p16 gene expression in chronic gastritis was significantly higher than that in gastric cancer ( P 0.01), in incomplete intestinal metaplasia or dysplasia ( P 0.05). There was no significant difference for the positive rate of bcl 2 gene expre ssion between dysplasia and gastric cancer or incomplete intestinal metaplasia ( P 0.05), The positive rate of bcl 2 expression in dysplasia or gastric cancer was significantly higher than that in chronic gastritis (P 0.001). There was no significant correlation between p53 and p16, nor between p16 and bcl 2 ( P 0.05), whereas there was significant correlation between p53 and bcl 2 ( P 0.05). Conclusions The p53 gene overexpression is relatively late event in stomach tumorigenesis and mainly relate to the progression. p16 or bcl 2 protein expression alteration might play a role in the early development/promotion of gastric carcinoma but not in tumor progression and aberrant bcl 2 protein expression appears to be preferentially associated with the intestinal type tumors. p53, p16 and bcl 2 play both independant and synergetic role in the course and development of gastric cancer.

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Objective To investigate the expression and mutual relationship of tumor suppression gene and apoptosis regulating gene in gastric carcinoma and paracancerous tissues. Methods 30 cases of gastric carcinoma patients underwent surgical resection. Samples were taken from tumor site and paracancerous tissues. ABC immunohistochemical staining was used to detect the expression of p53、p16、bcl 2 proteins. Results No correlation between p53, p16, or bcl 2 expression and grade of pathologic stage, grade of differentiation, or lymph node status was observed ( P 0.05), there was significant correlation between bcl 2 and type of gastric carcinoma ( P 0.05). The positive rate of p53 gene expression in gastric carcinoma was significantly higher than that in moderate and severe dysplasia ( P 0.05). The positive rate of p16 gene expression in chronic gastritis was significantly higher than that in gastric cancer ( P 0.01), in incomplete intestinal metaplasia or dysplasia ( P 0.05). There was no significant difference for the positive rate of bcl 2 gene expre ssion between dysplasia and gastric cancer or incomplete intestinal metaplasia ( P 0.05), The positive rate of bcl 2 expression in dysplasia or gastric cancer was significantly higher than that in chronic gastritis (P 0.001). There was no significant correlation between p53 and p16, nor between p16 and bcl 2 ( P 0.05), whereas there was significant correlation between p53 and bcl 2 ( P 0.05). Conclusions The p53 gene overexpression is relatively late event in stomach tumorigenesis and mainly relate to the progression. p16 or bcl 2 protein expression alteration might play a role in the early development/promotion of gastric carcinoma but not in tumor progression and aberrant bcl 2 protein expression appears to be preferentially associated with the intestinal type tumors. p53, p16 and bcl 2 play both independant and synergetic role in the course and development of gastric cancer.

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Available abstract

Objective To investigate the expression and mutual relationship of tumor suppression gene and apoptosis regulating gene in gastric carcinoma and paracancerous tissues. Methods 30 cases of gastric carcinoma patients underwent surgical resection. Samples were taken from tumor site and paracancerous tissues. ABC immunohistochemical staining was used to detect the expression of p53、p16、bcl 2 proteins. Results No correlation between p53, p16, or bcl 2 expression and grade of pathologic stage, grade of differentiation, or lymph node status was observed ( P 0.05), there was significant correlation between bcl 2 and type of gastric carcinoma ( P 0.05). The positive rate of p53 gene expression in gastric carcinoma was significantly higher than that in moderate and severe dysplasia ( P 0.05). The positive rate of p16 gene expression in chronic gastritis was significantly higher than that in gastric cancer ( P 0.01), in incomplete intestinal metaplasia or dysplasia ( P 0.05). There was no significant difference for the positive rate of bcl 2 gene expre ssion between dysplasia and gastric cancer or incomplete intestinal metaplasia ( P 0.05), The positive rate of bcl 2 expression in dysplasia or gastric cancer was significantly higher than that in chronic gastritis (P 0.001). There was no significant correlation between p53 and p16, nor between p16 and bcl 2 ( P 0.05), whereas there was significant correlation between p53 and bcl 2 ( P 0.05). Conclusions The p53 gene overexpression is relatively late event in stomach tumorigenesis and mainly relate to the progression. p16 or bcl 2 protein expression alteration might play a role in the early development/promotion of gastric carcinoma but not in tumor progression and aberrant bcl 2 protein expression appears to be preferentially associated with the intestinal type tumors. p53, p16 and bcl 2 play both independant and synergetic role in the course and development of gastric cancer.

Key concepts: Intestinal metaplasia, Dysplasia, Immunohistochemistry, Atrophic gastritis, Carcinogenesis, Cancer, Carcinoma, Pathology

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