- Correlation of the Nuclear beta-catenin Expression with the Clinicopathological Parameters of Hepatocellular Carcinoma.
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Hyoung Jong Kwak, Ha Na Choi, Sung Ho Hwang, Keum Ha Choi, Ho Sung Park, Kyu Yun Jang, Myoung Ja Chung, Myoung Jae Kang, Dong Geun Lee, Woo Sung Moon
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Korean J Pathol. 2008;42(4):208-214.
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 Abstract
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- BACKGROUND
Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the human liver. However, the molecular changes and mechanisms that regulate the development and progression of HCC remain unclear.
Beta-catenin is known as a multi-functional protein that acts as a regulator of the cadherin-mediated cell-cell adhesion system and also in the Wingless/Wnt signal transduction pathway. The aim of this study was to investigate the expression of beta-catenin and its possible role in HCC.
METHODS
We investigated the expression of beta-catenin, Ki-67, TP53, alpha-smooth muscle actin and CD34 by performing immunohistochemical staining for 61 specimens of HCC and their adjacent non-tumorous tissue. We also examined the relationship between the nuclear expression of beta-catenin and the clinicopathologic parameters.
RESULTS
The altered expression of beta-catenin was not detected in the nontumorous liver tissue. The nuclear expression of beta-catenin was observed in approximately 16% (10/61) of the HCC specimens. Double immunohistochemical staining for beta-catenin and E-cadherin showed a close relationship between nuclear translocation of beta-catenin and the loss of the membranous E-cadherin expression.
Significant correlation was found between the nuclear translocation of beta-catenin and the tumor size, tumor necrosis and the presence of microvessel invasion and intrahepatic metastasis (p<0.05).
CONCLUSIONS
This data indicates that nuclear translocation of beta-catenin could play a role in the growth and progression of HCC.
- Pseudometastasis in Sentinel Lymph Nodes with Cytokeratin Debris-containing Histiocytes in Breast Cancer Patient: A Case Report.
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Keum Ha Choi, Eun Jung Cha, Ha Na Choi, Woo Sung Moon
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Korean J Pathol. 2007;41(6):427-429.
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Abstract
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- Immunohistochemical staining for cytokeratins can detect false negative nodes in patients with breast carcinoma. We report on a patient with breast carcinoma and pseudometastasis detected by immunohistochemical staining within a negative sentinel lymph node. A 66-year-old woman underwent a simple mastectomy and sentinel lymph node biopsy. Immunohistochemical staining of the sentinel nodes for cytokeratin in permanent sections showed cells with intense cytoplasmic staining in the subcapsular sinus. The cells were negative for epithelial membrane antigen staining, but positive for CD68. In combination with morphologic findings and immunohistochemistry, cytokeratin-positive cells were confirmed as histiocytes with phagocytized cytokeratin debris. Careful correlation with histology and additional IHC could help avoid a misinterpretation of this type of pseudometastasis.
- PPARgamma Ligand-Induced Decrease of in vivo Tumor Growth Accompanied by Increased Cytolytic Activity of Splenocytes.
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Kyu Yun Jang, Ki Hoon Yu, Hak Yong Lee, Kyung Ryoul Kim, Ha Na Choi, Eun Jung Cha, Ho Sung Park, Woo Sung Moon, Myoung Jae Kang, Dong Geun Lee
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Korean J Pathol. 2007;41(1):7-14.
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Abstract
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- BACKGROUND
Recent studies have proposed the use of peroxisome proliferator activated receptor-gamma (PPARgamma) ligands as new chemotherapeutic agents for human malignant tumors. However the in vivo mechanism of PPARgamma ligands on cellular toxicity is not clear. Therefore we examined the anti-tumor effects of the PPARgamma ligand, rosiglitazone (ROS), in animal models.
METHODS
To evaluate the effect of RSO on splenocytes, an in vitro and in vivo study was performed. Cytolytic activity was measured by use of a 51Cr release assay. The splenic natural killer (NK) cell population and effector-target conjugation were measured by flow cytometric analysis.
RESULTS
In 9L glioma bearing rats, 30 mg/kg/d of ROS treatment induced a significant decrease of subcutaneous tumor growth accompanied by an increased cytolytic activity of splenocytes and of the splenic NKR-P1bright/CD3- NK cell population. In normal rats, systemic administration of ROS also increased the cytolytic activity of splenocytes, the splenic NK cell population, and effector-target conjugation.
Moreover, we found that a concentration of 20micrometer ROS caused an increase in the cytolytic activity of splenocytes, and a concentration of 50micrometer ROS increased effector-target conjugation in vitro.
CONCLUSIONS
These results suggest that increased splenic cytolytic activity and NK cell population may contribute to the anti-tumor effects of PPARgamma ligands in vivo.
However, the roles of NK cells in the PPARgamma ligand-induced anti-tumor activity should be further investigated.
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