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Min Young Park 2 Articles
Synergistic Apoptotic Effect of Combination Treatment with Troglitazone and COX-2 Inhibitor in Glioma Cells.
Kyung Ryoul Kim, Min Young Park, Ho Sung Park, Kyu Yun Jang, Woo Sung Moon, Dong Geun Lee, Myoung Jae Kang
Korean J Pathol. 2007;41(1):1-6.
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AbstractAbstract PDF
BACKGROUND
The use of troglitazone (a PPARgamma ligand) and COX-2 inhibitor have been intensively studied for inhibition of tumor growth in cancer treatment, but the anti-tumor effect with a combination of these agents for cancer has not yet been studied. The aim of this study was to determine if low concentrations of troglitazone with COX-2 inhibitor in combination would cause significant cytotoxicity in glioma cells.
METHODS
The effects of co-treatment with troglitazone and COX-2 inhibitor on cell growth and apoptosis were assessed by use of trypan blue exclusion and a DNA fragmentation assay. A western blot was used to analyze the apoptotic signaling for the expression of bcl-2, bax, PARP and p21 proteins.
RESULTS
A low dose of troglitazone (5micrometer) and COX-2 inhibitor (5micrometer) strongly enhanced the cell growth inhibition and apoptosis in glioma cells when compared to a low dose of each drug alone. Western blotting analysis showed a decreased expression of bcl-2 and PARP proteins. In contrast, the bax protein level was increased.
CONCLUSIONS
The combination of troglitazone and COX-2 inhibitor in a low dose elicits synergistic cytotoxicity in glioma cells. Our study also demonstrates that down regulation of bcl-2, fragmentation of PARP protein and increased expression of bax protein were accompanied by co-treatment with troglitazone and the COX-2 inhibitor.
Rarity of EGFR and c-ErbB-2 Overexpressions in Hepatocellular Carcinoma: An Immunohistochemical Study.
Woo Sung Moon, Hyun Jin Son, Ho Sung Park, Min Young Park
Korean J Pathol. 2004;38(4):244-248.
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AbstractAbstract PDF
BACKGROUND
The overexpression of epidermal growth factor receptor (EGFR) and c-erbB-2 oncogenes has been implicated in the development of many types of cancer. However, the role of EGFR and c-erbB-2 overexpression in hepatocellular carcinoma (HCC) has not been fully elucidated.
METHODS
The aim of this study was to evaluate the immunohistochemical expression of EGFR and c-erbB-2 oncoprotein in a series of 52 HCCs.
RESULTS
All but one of the HCC tumor tissues were negative for EGFR monoclonal antibody, clone H11. All of the HCC tumor tissue samples were negative for EGFR monoclonal antibody, clone 29.1.1. However, strong EGFR immunoreactivity was detected in sinusoidal endothelial cells of HCC in 25 tumors (48%) using EGFR 29.1.1 antibody. The expression of c-erbB-2 was observed in 6% (3/52) of the HCCs. No significant correlation was found between p53 mutation and the expression of c-erbB-2.
CONCLUSION
Our results suggest that both EGFR and c-erbB-2 oncoprotein overexpressions in tumor cells are rare and do not seem to predominantly contribute to the malignant phenotype in HCC.

J Pathol Transl Med : Journal of Pathology and Translational Medicine