Journal of Pathology and Translational Medicine

Original Articles

An Immunohistochemical Study of Angiogenesis in Tumor Emboli.: Jo Heon Kim, Chan Choi, Jae Hyuk Lee, Ji Shin Lee, Sung Sun Kim, Chang Woo Han, Sang Woo Juhng; Korean J Pathol. 2007;41(4):252-257.

Abstract PDF: BACKGROUND
Angiogenesis, which is essential for tumor growth, is known to occur in the extravascular stroma. However, vascular structures were noted in intravascular tumor emboli in surgical specimens. This prompted our investigation of the frequency and morphology of angiogenesis in tumor emboli.
METHODS
Hematoxylin-eosin stained specimens were reviewed for tumor emboli, in 21 cases of stomach adenocarcinoma and 22 cases of colon adenocarcinoma. The cases were examined with immunohistochemistry using antibodies against epithelial antigen (cytokeratin), endothelial antigens (CD31, CD34), lymphatic endothelial antigen (D2-40), and proliferation-associated antigen (MIB1).
RESULTS
Endothelial cells were observed in 16 tumor emboli among four (19.1%) of the 21 cases of stomach adenocarcinoma and in 32 tumor emboli among four (18.2%) of the 22 cases of colon adenocarcinoma. The endothelial cells in the tumor emboli showed papillary ingrowth from the vessel wall, formation of vascular lumens, scattered distribution, or surface coating of the emboli. Some of the endothelial cells in the tumor emboli were D2-40-positive, and some were MIB1- positive.
CONCLUSIONS
These findings demonstrated that angiogenesis occurs in intravascular tumor emboli as well as in the extravascular stroma. Angiogenesis in the tumor emboli may reflect an active process and may facilitate tumor growth.

Changes of the Kupffer Cell Number in the Course of Metastasis of Hepatocellular Carcinoma.: Chan Il Park, Yee Jeong Kim, Young Nyun Park, Sun Hee Sung; Korean J Pathol. 1992;26(3):247-252.

Abstract PDF: The number of Kupffer cells was evaluated in hepatocellular carcinomas, including 18 primary lesions, 3 tumor emboli within the portal vein radicles and 4 metastatic lesions and in non-neoplastic liver adjacent to the primary lesions, to persue the origin of Kupffer cells dwelling in hepatocellular carcinoma. Hepatocellular carcinomas of the sinusoidal(trabecular) type were carefully selected, and excluded were those carcinomas which showed inflammation or other changes evoking inflammation. The immunohistochemical stains for CD 68 and lysozyme were done to identify Kupffer cells and to draw the mean Kupffer cell number per high power microscopic field of each lesion. Kupffer cell was most numerous in primary lesions followed by tumor emboli and still fewer in metastatic lesions. The Kupffer cell number in the primary lesions of hepatocellular carcinoma was in turn smaller than that of the adjacent non-neoplastic liver. The results suggest that, during the early neoplastic transformation, sinusoids of the non-neoplastic liver could creep into the carcinomatous tissue accompanying Kupffer cells.

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