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Original Articles
- The Expression of Transforming Growth Factor-1 and Its Signaling Receptors in Human Colorectal Carcinoma.
- Gyeong Seon Kim, Joo Heon Kim, Woo Sung Moon, Myoung Ja Chung, Dong Geun Lee, Myoung Jae Kang
- Korean J Pathol. 2001;35(2):115-122.
- 1,662 View
- 13 Download
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Abstract
PDF - BACKGROUND
Resistance to the potent growth inhibitory effects of TGF- (transforming growth factor-) is a characteristic of many malignancies. TGF- insensitivity has been attributed to alterations in the number and function of the TGF- receptors as well as disturbances of downstream signal transduction. The aim of this study was to examine the expression of TGF-1 and its receptors in human colorectal cancer tissue and determine its relationship with cancer growth and with prognostic factors.
METHODS
Immunohistochemical staining of TGF-1, TGF-RI, and TGF-RII was performed on 20 human colorectal adenomas, 30 carcinomas and 10 normal mucosas as a control.
RESULTS
The staining indices of TGF-1, TGF-RI, and TGF-RII increased in adenomas and carcinomas compared with normal mucosas and adenomas, respectively. In adenomas the staining index of TGF-1 significantly increased with the severity of atypism. The staining index of TGF-RII increased in the carcinomas in the right colon and rectum, compared with those in the left colon.
CONCLUSION
The enhanced expression of TGF-1, TGF-RI and II in the colorectal carcinoma suggests an important role of colorectal carcinogenesis and tumor progression.
- Expression of Cyclin D1, Cyclin E, p21Cip1 and p27Kip1 in Chemically Induced Rat Mammary Tumor Treated with Tamoxifen and Transforming Growth Factor-1.
- Tae Jung Jang, Jae Hum Park, Mee Yon Cho, Ki Kwon Kim, Jung Ran Kim
- Korean J Pathol. 2001;35(2):151-157.
- 1,488 View
- 12 Download
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Abstract
PDF
- BACKGROUND
Tamoxifen (TAM) inhibits the action of estrogen by binding to estrogen receptors, and also has non-estrogen receptor mediated cytostatic activities. Transforming growth factor-1 (TGF-1) inhibits the proliferation of many other cell types, such as epithelial, hematopoietic and endothelial cells.
METHODS
We investigated the effects of tamoxifen on the growth of 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumors and the expression of cyclin D1, cyclin E, p21Cip1, and p27Kip1 by performing immunohistochemistry and Western blot analysis, and studied whether TGF-1 injection amplified the effects of TAM. When tumor size reached between 10-15 mm in the largest dimension, the rats were divided into 3 groups: DMBA-control group (n=12), DMBA-TAM group (n=14) and DMBA-TAM plus TGF-1 group (n=5).
RESULTS
The consecutive administration of TAM markedly decreased the tumor development compared with the DMBA-control group. The DMBA-TAM and DMBA-TAM plus TGF-1 groups showed decreased expression of bromodexoyuridine, cyclin D1, cyclin E, and p21Cip1 when compared with those of the DMBA-control group. On the other hand, the labeling index of p27Kip1 was higher in the DMBA-TAM plus TGF-1 group than in the DMBA-control group.
CONCLUSION
TAM suppresses tumor development, which may be associated with down-expression of cyclin D1 and cyclin E, and overexpression of p27Kip1, and addition of TGF-1 does not influence tumor development treated by TAM.
- The Effect of Antibody and Gene Therapy for Transforming Growth Factor- 1 on Scar Formation.
- Jun Hyung Kim, Ki Hwan Han, Jong Duck Ahn, In Kyu Lee, Eun Joo Kim, Mee Yul Hwang, Kwan Kyu Park
- Korean J Pathol. 2001;35(5):424-432.
- 1,450 View
- 12 Download
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Abstract
PDF
- BACKGROUND
Transforming growth factor (TGF)- has a large variety of biological functions, including the modulation of inflammation and the immune system, and is presumed to play important roles in repairing wounds and reducing scarring. The objective of this study is to examine the effects of TGF-1 on healing wounds and reducing scarring. We have also analysed the ability of the hemagglutinating virus of Japan (HVJ) liposome mediated antisense oligodeoxynucleotides (ODNs) to specifically inhibit wound-induced expressions of TGF-1 proteins and mRNA in the rat skin.
METHODS
Skin wounds were created on the backs of 80 anesthetized rats. The first group of wounds, as the controls, was unmanipulated. The second group of wounds, as positive controls or an excessive scarring model, was injected with TGF-1 subcutaneously. The third group of wounds was injected with anti-TGF-1 antibody subcutaneously. The fourth group of wounds was injected with HVJ liposome mediated antisense ODNs for TGF-1 subcutaneously. The wounds of all groups were bisected and analysed histologically 5, 10, 15, 30, and 50 days after the wounds were made.
RESULTS
All control wounds (TGF-1 or no injection) healed with scarring, whereas the wounds treated with the antibody or antisense ODNs healed with less scar formation compared to the control group. The wounds treated with the antibody or antisense ODNs had fewer macrophages, less collagen and fibronectin contents than the other wounds. Northern blotting and in situ hybridization analysis showed that wound sites treated with HVJ liposome mediated antisense ODNs for TGF-1 exhibited decreased levels of TGF-1 mRNA after injury.
CONCLUSIONS
These findings suggest an important new approach to controlling scarring in normal wound healing, complementing the practice of adding exogenous growth factors to chronic wounds in the attempt to inhibit collagen deposition.
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