THYMIDINE PHOSPHORYLASE (PLATELET-DERIVED ENDOTHELIAL-CELL GROWTH-FACTOR), MICROVESSEL DENSITY AND CLINICAL OUTCOME IN HEPATOCELLULAR-CARCINOMA

Citation
A. Yamamoto et al., THYMIDINE PHOSPHORYLASE (PLATELET-DERIVED ENDOTHELIAL-CELL GROWTH-FACTOR), MICROVESSEL DENSITY AND CLINICAL OUTCOME IN HEPATOCELLULAR-CARCINOMA, Journal of hepatology, 29(2), 1998, pp. 290-299
Citations number
46
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
01688278
Volume
29
Issue
2
Year of publication
1998
Pages
290 - 299
Database
ISI
SICI code
0168-8278(1998)29:2<290:TP(EG>2.0.ZU;2-H
Abstract
Background/Aims: Angiogenesis plays an important role in tumor growth and metastasis. It is regulated by angiogenic factors. Thymidine phosp horylase (platelet-derived endothelial cell growth factor) is one such factor. Although the significance of platelet-derived endothelial cel l growth factor has been studied for several types of tumor, the expre ssion of platelet-derived endothelial cell growth factor and its corre lation with microvessel density or clinicopathological factors in hepa tocellular carcinoma are unknown. We evaluated microvessel density and platelet-derived endothelial cell growth factor expression in hepatoc ellular carcinoma to determine whether microvessel density and platele t-derived endothelial cell growth factor expression are correlated wit h the clinicopathological factors of hepatocellular carcinoma. Methods : Using immunohistochemical staining with anti-platelet-derived endoth elial cell growth factor antibody and the ELISA method, we evaluated t he correlation among platelet-derived endothelial cell growth factor e xpression, microvessel density and clinicopathological factors in 84 h epatocellular carcinoma patients, Microvessels were stained with antih uman von Willebrand factor (anti-Factor VIII) and anti-CD34, Results: In the surrounding liver, there was a significant correlation between microvessel density and platelet-derived endothelial cell growth facto r expression (p=0.002), and hepatitis C virus-positive livers had high er microvessel densities than other,vise (p=0.003). However, this corr elation was not found for hepatocellular carcinoma, but hepatitis C vi rus-positive tumors had higher expression of platelet-derived endothel ial cell growth factor (p=0.018). Microvessel density in hepatocellula r carcinoma obtained by Factor VIII staining inversely affected the re currence-free survival rate (p=0.0416), but the microvessel density by CD34 staining was not a significant predictor. Conclusions: This stud y indicates that platelet-derived endothelial cell growth factor may n ot be a major regulator of angiogenesis of hepatocellular carcinoma, b ut this enzyme may play an important role in hepatocarcinogenesis coop erating with hepatitis C virus. Also, the density, not of sinusoid-lik e vessels, but of larger vessels in hepatocellular carcinoma could be a prognostic factor for hepatocellular carcinoma.