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Original Article
- The Expression of TGF-beta1 and TGF-beta Receptor I in Human Lung Cancer.
- Hye Kyung Ahn, Young Hee Choi, Jung Weon Shim, Young Euy Park, Han Kyeom Kim, Jong Sang Choi, Joung Ho Han
- Korean J Pathol. 1998;32(1):9-20.
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Abstract
PDF - A majority of human lung cancer cell lines have developed resistance to growth inhibition via the activation of transforming growth facter-beta (TGF-beta). Previous studies have reported that growth inhibition of TGF-beta is linked to the expression of transforming growth factor-beta receptor type I (TGF-betaRI). Immunohistochemical studies of TGF-beta1 and TGF-betaRI have been carried out in 43 cases of lung neoplasm; including 25 cases of squamous cell carcinoma, 13 cases of adenocarcinoma, 2 cases of adenosquamous cell carcinoma, and 1 case each of undifferentiated carcinoma, small cell carcinoma and neuroendocrine carcinoma. Reverse transcriptase polymerase chain reaction (RT-PCR) for TGF-beta1 mRNA was also performed in 40 cases of tumors and 14 control cases of normal parenchyme. Immunohistochemically, TGF-beta1 and TGF-betaRI expression were noted in the cytoplasm of all type of tumor cells. The staining intensity and areas were examined and scored from 0 to 5. As a whole, TGF-beta1 staining scores in the neoplastic lesions were higher than that of the adjacent normal parenchyme, bronchial epithelium or alveolar epithelium. However, TGF-betaRI staining scores were generally lower than that of the adjacent normal components. The TGF-beta1 mRNA showed a higher percentage of expression in tumors than in normal control. Tumor size, lymph node metastasis, histological differentiation and histological type of tumors did not correlated with the staining score of TGF-beta1 and TGF-betaRI. These results indicate that although various types of human lung carcinoma cells produce TGF-beta1, they show a reduction in TGF-betaRI, resulting in an escape from growth inhibition by TGF-beta1.
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