Clinical Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 1, 2004; 10(1): 132-135
Published online Jan 1, 2004. doi: 10.3748/wjg.v10.i1.132
Alteration of somatostatin receptor subtype 2 gene expression in pancreatic tumor angiogenesis
Ren-Yi Qin, Ru-Liang Fang, Manoj Kumar Gupta, Zheng-Ren Liu, Da-Yu Wang, Qing Chang, Yi-Bei Chen
Ren-Yi Qin, Ru-Liang Fang, Manoj Kumar Gupta, Zheng-Ren Liu, Da-Yu Wang, Qing Chang, Yi-Bei Chen, Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
Supported by National Natural Science Foundation of China, No. 30271473
Correspondence to: Professor Ren-Yi Qin, Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, Province, China. ryqin@tjh.tjmu.edu.cn
Telephone: +86-27-83662389 Fax: +86-27-83662389
Received: June 4, 2003
Revised: July 20, 2003
Accepted: July 30, 2003
Published online: January 1, 2004
Abstract

AIM: To explore the difference of somatostatin receptor subtype 2 (SST2R) gene expression in pancreatic cancerous tissue and its adjacent tissue, and the relationship between the change of SST2R gene expression and pancreatic tumor angiogenesis related genes.

METHODS: The expressions of SST2R, DPC4, p53 and ras genes in cancer tissues of 40 patients with primary pancreatic cancer, and the expression of SST2R gene in its adjacent tissue were determined by immunohistochemiscal LSAB method and EnVisionTM method. Chi-square test was used to analyze the difference in expression of SST2R in pancreatic cancer tissue and its adjacent tissue, and the correlation of SST2R gene expression with the expression of p53, ras and DPC4 genes.

RESULTS: Of the tissue specimens from 40 patients with primary pancreatic cancer, 35 (87.5%) cancer tissues showed a negative expression of SST2R gene, whereas 34 (85%) a positive expression of SST2R gene in its adjacent tissues. Five (12.5%) cancer tissues and its adjacent tissues simultaneously expressed SST2R. The expression of SST2R gene was markedly higher in pancreatic tissues adjacent to cancer than in pancreatic cancer tissues (P < 0.05). The expression rates of p53, ras and DPC4 genes were 50%, 60% and 72.5%, respectively. There was a significant negative correlation of SST2R with p53 and ras genes (χ12 = 9.33, χ22 = 15.43, P < 0.01), but no significant correlation with DPC4 gene (χ2 = 2.08, P > 0.05).

CONCLUSION: There was a significant difference of SST2R gene expression in pancreatic cancer tissues and its adjacent tissues, which might be one cause for the different therapeutic effects of somatostatin and its analogs on pancreatic cancer patients. There were abnormal expressions of SST2R, DPC4, p53 and ras genes in pancreatic carcinogenesis, and moreover, the loss or decrease of SST2R gene expression was significantly negatively correlated with the overexpression of tumor angiogenesis correlated p53 and ras genes, suggesting that SST2R gene together with p53 and ras genes may participate in pancreatic cancerous angiogenesis.

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