|Title:||Cyclooxygenase-2 Expression Correlates with Nuclear P53 Accumulation in Gastric Carcinoma||Authors:||SHUN, CHIA-TUNG
|Keywords:||NITRIC-OXIDE SYNTHASE;TUMOR-SUPPRESSOR GENE;COLORECTAL- CANCER;CLINICAL IMPLICATIONS;CYCLO-OXYGENASE-2;OVEREXPRESSION||Issue Date:||2003||Source:||HEPATO-GASTROENTEROLOGY||Journal Volume:||v.50||Journal Issue:||n.52||Start page/Pages:||988-992||Abstract:||
Background/Aims: COX-2 (Cyclooxygenase-2) is the inducible isoform of cyclooxygenase in response to cytokines, mitogens , and growth factors and may induce carcinogenesis through the mechanisms of inhibiting apoptosis, increasing cell proliferation, and enhancing angiogenesis. This study aimed to clarify the relationship of COX-2 and p53, a well-known tumor suppressor gene, in gastric carcinoma. Methodology: Immunohistochemical staining of nuclear,p53 protein and cytoplasmic COX-2 protein were utilized on tumor tissue sections from 65 surgical specimens. Their correlation was further analyzed according to pathologic characteristics. Results: There were 47% (16/34) of high COX-2 expression in the high p53 immunoreactivity group but only 19% (6/31) of high COX-2 expression in,the low p53 immunoreactivity group. COX-2 overexpression significantly correlated with the accumulation of nuclear p53 protein in general (p=0. 035). Analysis based on different pathologic characteristics revealed. that COX-2 correlates with p53 in subsets of advanced, cardiac, and H. pylori (-) gastric carcinomas (p=0 .027, 0.048, 0.036, respectively). But the. relationship does not differ between Lauren's intestinal- and diffuse - type gastric carcinomas. Conclusions: Our work provides evidence linking COX-2 and p53 in gastric carcinogenesis, but the mechanism how they interact to promote tumorigenesis remains to be elucidated.
|Appears in Collections:||法醫學研究所|
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