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Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas

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...

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Autores principales: Joo, Young Eun, Sohn, Young Hae, Lee, Wan Sik, Park, Chang Hwan, Choi, Sung Kyu, Rew, Jong Sun, Park, Chang Soo, Kim, Sei Jong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Association of Internal Medicine 2002
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531679/
https://www.ncbi.nlm.nih.gov/pubmed/12298426
http://dx.doi.org/10.3904/kjim.2002.17.3.153
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author Joo, Young Eun
Sohn, Young Hae
Lee, Wan Sik
Park, Chang Hwan
Choi, Sung Kyu
Rew, Jong Sun
Park, Chang Soo
Kim, Sei Jong
author_facet Joo, Young Eun
Sohn, Young Hae
Lee, Wan Sik
Park, Chang Hwan
Choi, Sung Kyu
Rew, Jong Sun
Park, Chang Soo
Kim, Sei Jong
author_sort Joo, Young Eun
collection PubMed
description 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.
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spelling pubmed-45316792015-10-02 Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas Joo, Young Eun Sohn, Young Hae Lee, Wan Sik Park, Chang Hwan Choi, Sung Kyu Rew, Jong Sun Park, Chang Soo Kim, Sei Jong Korean J Intern Med Original Article 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. Korean Association of Internal Medicine 2002-09 /pmc/articles/PMC4531679/ /pubmed/12298426 http://dx.doi.org/10.3904/kjim.2002.17.3.153 Text en Copyright © 2002 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Joo, Young Eun
Sohn, Young Hae
Lee, Wan Sik
Park, Chang Hwan
Choi, Sung Kyu
Rew, Jong Sun
Park, Chang Soo
Kim, Sei Jong
Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas
title Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas
title_full Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas
title_fullStr Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas
title_full_unstemmed Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas
title_short Expression of Vascular Endothelial Growth Factor and p53 in Pancreatic Carcinomas
title_sort expression of vascular endothelial growth factor and p53 in pancreatic carcinomas
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4531679/
https://www.ncbi.nlm.nih.gov/pubmed/12298426
http://dx.doi.org/10.3904/kjim.2002.17.3.153
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