- 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.
- Expression of Vascular Endothelial Growth Factors A,C and D in Gastric Adenocarcinoma.
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Myoung Ja Chung, Jin Wook Lee, Ki Hoon Yu, Doo Hyun Yang, Kyu Yun Jang, Woo Sung Moon, Myoung Jae Kang, Dong Geun Lee
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Korean J Pathol. 2005;39(2):99-105.
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Abstract
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- BACKGROUND
Vascular endothelial growth factor (VEGF)-C and VEGF-D are novel growth factors that regulate lymphatic vessel growth. This study was designed to examine whether the expression of three VEGF family members, VEGF-A, VEGF-C and VEGF-D are associated with the clinicopathologic parameters, especially with lymph node metastasis, in advanced gastric carcinomas.
METHODS
Immunohistochemical staining was performed for VEGF-A, VEGF-C, and VEGF-D in the surgically resected specimens from 102 patients with advanced gastric carcinoma.
The mRNA expressions of the three VEGF family members were assessed in 16 cases of tumor tissues and their corresponding non-neoplastic tissues.
RESULTS
Of the 102 gastric carcinomas, 74 (73%), 82 (80%), and 34 (33%) cases showed cytoplasmic immunoreactivity for VEGF-A, VEGF-C and VEGF-D, respectively. Both VEGF-A and VEGF-C expressions were associated with lymphatic invasion and lymph node metastasis (p<0.05), but the VEGF-D expression was not associated with them (p>0.05). In the tumor tissue, VEGF-C mRNA expression was greater, while VEGF-D mRNA expression was lower than in the nonneoplatic tissue adjacent to the tumor.
CONCLUSIONS
VEGF-A and VEGF-C may play important roles for the lymphatic spread of gastric carcinoma. We suggest that neutralizing both VEGF-A and VEGF-C may be reguired to block lymph node metastasis.
- Expression of Transforming Growth Factor-beta and Its Receptors during Acetic Acid-induced Duodenal Ulcer Healing in Rats.
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Kyu Yun Jang, Han Sang Yoon, Ki Hoon Yu, Myung Ja Chung, Dong Geun Lee, Jae Kang Myoung
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Korean J Pathol. 2003;37(2):108-114.
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Abstract
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- BACKGROUND
Many works have been written about the transforming growth factor-beta 1 (TGF-beta1) which is closely associated with fibrosis in the inflammatory conditions of different organs. TGF-beta1 exerts its biological effects by interacting with specific cell surface receptors, namely, transforming growth factor-beta receptor type I and II (TGFbetaRI and TGFbetaRII).
METHODS
To investigate the temporal expressions and localizations of TGF-beta1, TGFRbetaI, and TGFbetaRII in acetic acid-induced duodenal ulcerated tissues, we performed in situ hybridization and immunohistochemical techniques.
RESULTS
Under in situ hybridization, TGF-beta1, TGFbetaRI, and TGFbetaRII mRNA signals increased in the experimental groups (1, 3, 7, and 14 day groups) compared to those of the control group. The signals on day 14 decreased slightly compared to those of days 1, 3, and 7, but they were higher than those of the control group. Under immunohistochemical study, TGF-beta1, TGFbetaRI, and TGFbetaRII were localized in the mucosal epithelial cells and in the macrophages, vascular endothelial cells, and fibroblasts of the lamina propria and granulation tissue. As in the case of the in situ hybridization, it revealed that the expression of three proteins increased in the experimental groups compared to that of the control group. The expression on day 14 decreased compared to those of days 1, 3, and 7, but it was more intense than that of the control group.
CONCLUSIONS
This study suggests that TGF-beta1, TGFbetaRI, and TGFbetaRII contribute to the early stage healing of duodenal ulcer.
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