Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas.
- Author:
Young Eun JOO
1
;
Young Hae SOHN
;
Wan Sik LEE
;
Chang Hwan PARK
;
Sung Kyu CHOI
;
Jong Sun REW
;
Chang Soo PARK
;
Sei Jong KIM
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
- Publication Type:Original Article
- Keywords:
VEGF;
Angiogenesis;
Genes;
p53;
Carcinoma;
Pancreatic ductal;
Immunohistochemistry
- MeSH:
Adenocarcinoma/*genetics/pathology;
Adult;
Aged;
Aged, 80 and over;
Endothelial Growth Factors/*genetics;
Female;
*Genes, p53;
Human;
Male;
Middle Age;
Mutation;
Neovascularization, Pathologic/genetics;
Pancreatic Neoplasms/*genetics/pathology;
Prognosis
- From:The Korean Journal of Internal Medicine
2002;17(3):153-159
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Angiogenesis has been shown to be a critical aspect of tumor growth and progression. Vascular endothelial growth factor (VEGF) has potent angiogenic activity and has been identified in a wide variety of malignancies, including pancreatic carcinoma. The tumor-suppressor gene p53 has been thought to regulate VEGF in angiogenesis. The aim of the current study was conducted to investigate the association between p53 mutation and VEGF expression and the prognostic value of these factors in pancreatic carcinoma. METHODS: Formalin-fixed, paraffin-embedded tissue specimens were obtained from 30 patients who underwent surgery for pancreatic carcinoma. We used an immunohistochemical technique to localize VEGF and p53 in pancreatic carcinoma tissues. RESULTS: Positive expression of VEGF was detected in 17 out of 30 (56.7%) tumors. Positive expression of VEGF correlated with the depth of tumor invasion (p=0.002). There was a trend towards an association between positive expression of VEGF and distant metastasis, although these associations were not statistically significant (p=0.070). p53 mutations were identified in 18 out of 30 (60.0%) tumors. However, no significant correlation was found between p53 expression and various clinicopathological parameters. The correlation between p53 mutation and VEGF expression was statistically significant (p=0.004). CONCLUSION: VEGF, a key factor for the induction of tumor-associated angiogenesis, may be involved in tumor characteristics, including tumor invasion and metastasis. And p53 mutation may be implicated in the regulation of angiogenesis through a VEGF up-regulation.
