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[Clinicopathologic study of angiogenesis in human hepatocellular carcinoma].

Jun Ma, Xiaohua Zhou, T Zhang, Guangxi Sun, K Meng

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Abstract

OBJECTIVE: To study clinicopathologic significance of microvessel density (MVD) and the expression of vascular endothelial growth factor (VEGF) in human hepato-cellular carcinoma (HCC). METHODS: 30 HCC cases with neighboring noncancerous tissues, 10 liver cirrhosis cases, 5 mild chronic hepatitis cases and 4 normal liver tissue samples were stained with CD34, VEGF by immunohistochemistry method. Quantitation of sinusoid-like vessels and semi-quantitation of VEGF expression were performed and analyzed in conjunction with the clinico-pathological features of HCC. RESULTS: All HCC tissues showed diffuse CD34 expression and its site of distribution was somewhat corresponding to the original structure of sinusoid-like pattern, while CD34 was negative in the "sinusoid" regions of normal and chronic liver disease. Both MVD and VEGF were correlated to portal vein invasion of HCC, MVD was also correlated to the tumor size. The MVD of tumor less than 2 cm in diameter was significantly lower than that of tumors with a diameter of 2 similar 5 cm. The positive rate of VEGF in HCC was 83.3%. The expression of VEGF was also remarkable in the neighboring noncancerous tissues in which inflammatory cell infiltration was apparent. CONCLUSIONS: MVD and expression of VEGF were remarkably increased in HCC. Both were correlated with portal vein invasion. VEGF derived from tumor cells and noncancerous tissues may be associated with the angiogenesis of HCC.

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OBJECTIVE: To study clinicopathologic significance of microvessel density (MVD) and the expression of vascular endothelial growth factor (VEGF) in human hepato-cellular carcinoma (HCC). METHODS: 30 HCC cases with neighboring noncancerous tissues, 10 liver cirrhosis cases, 5 mild chronic hepatitis cases and 4 normal liver tissue samples were stained with CD34, VEGF by immunohistochemistry method. Quantitation of sinusoid-like vessels and semi-quantitation of VEGF expression were performed and analyzed in conjunction with the clinico-pathological features of HCC. RESULTS: All HCC tissues showed diffuse CD34 expression and its site of distribution was somewhat corresponding to the original structure of sinusoid-like pattern, while CD34 was negative in the "sinusoid" regions of normal and chronic liver disease. Both MVD and VEGF were correlated to portal vein invasion of HCC, MVD was also correlated to the tumor size. The MVD of tumor less than 2 cm in diameter was significantly lower than that of tumors with a diameter of 2 similar 5 cm. The positive rate of VEGF in HCC was 83.3%. The expression of VEGF was also remarkable in the neighboring noncancerous tissues in which inflammatory cell infiltration was apparent. CONCLUSIONS: MVD and expression of VEGF were remarkably increased in HCC. Both were correlated with portal vein invasion. VEGF derived from tumor cells and noncancerous tissues may be associated with the angiogenesis of HCC.

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Available abstract

OBJECTIVE: To study clinicopathologic significance of microvessel density (MVD) and the expression of vascular endothelial growth factor (VEGF) in human hepato-cellular carcinoma (HCC). METHODS: 30 HCC cases with neighboring noncancerous tissues, 10 liver cirrhosis cases, 5 mild chronic hepatitis cases and 4 normal liver tissue samples were stained with CD34, VEGF by immunohistochemistry method. Quantitation of sinusoid-like vessels and semi-quantitation of VEGF expression were performed and analyzed in conjunction with the clinico-pathological features of HCC. RESULTS: All HCC tissues showed diffuse CD34 expression and its site of distribution was somewhat corresponding to the original structure of sinusoid-like pattern, while CD34 was negative in the "sinusoid" regions of normal and chronic liver disease. Both MVD and VEGF were correlated to portal vein invasion of HCC, MVD was also correlated to the tumor size. The MVD of tumor less than 2 cm in diameter was significantly lower than that of tumors with a diameter of 2 similar 5 cm. The positive rate of VEGF in HCC was 83.3%. The expression of VEGF was also remarkable in the neighboring noncancerous tissues in which inflammatory cell infiltration was apparent. CONCLUSIONS: MVD and expression of VEGF were remarkably increased in HCC. Both were correlated with portal vein invasion. VEGF derived from tumor cells and noncancerous tissues may be associated with the angiogenesis of HCC.

Key concepts: Hepatocellular carcinoma, CD34, Pathology, Angiogenesis, Cirrhosis, Immunohistochemistry, Sinusoid, Microvessel

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[Clinicopathologic study of angiogenesis in human hepatocellular carcinoma]. — Research Paper | ScholarLens