BACKGROUND: The G1/S phase proteins of the cell cycle play critical roles in tumorigenesis and tumor progression. Our aim was to investigate the significance of p53, cyclin D1 and c-myc expressions in thyroid tumors. METHODS: The expressions of these proteins were examined in 217 cases of thyroid tumors and tissues using immunohistochemistry. The results were correlated with lymph node metastasis. RESULTS: p53 expression was seen in 75.5, 47.5, 66.7, and 50% of papillary carcinomas (PC), follicular carcinomas (FC), undifferentiated carcinomas (UC) and follicular adenomas (FA), respectively. There was a significant difference between these expressions in these tumors and the results in nodular hyperplasia (NH) and normal tissues. Cyclin D1 expression was noted in 80.0, 68.4, 66.7, 61.1 and 79.5% of PC, FC, UC, FA and NH, respectively. c-myc expression was seen in 80.0, 94.2, 66.7, 66.7 and 52.3% of PC, FC, UC, FA and NH, respectively. There was a significant association between the expressions in these tumors and the results in normal tissues. The expressions of p53, cyclin D1 and c-myc were not correlated with lymph node metastasis. CONCLUSIONS: These findings suggest the expressions of p53, cyclin D1 and c-myc may act in the early stage, and participates in tumorigenesis and promoting cell growth.
Adenoma ; Carcinogenesis ; Carcinoma ; Carcinoma, Papillary ; Cell Cycle ; Cyclin D1* ; Cyclins* ; Hyperplasia ; Immunohistochemistry ; Lymph Nodes ; Neoplasm Metastasis ; Thyroid Gland*

BACKGROUND: Transforming growth factor-beta1 (TGF-beta1) is known to be a potent growth inhibitor of many cell types, including most epithelial cells. However, the mechanism of TGF-beta1 action on cell growth in lymphomas and leukemia still remains to be elucidated. c-myc is a central regulator of cell proliferation and apoptosis, and telomerase is believed to play an important role in carcinogenesis. The aim of the study was to determine the effects of cell growth, c-myc gene expression and telomerase activity due to TGF-beta1 and examine its mechanism of action in lymphomas and leukemia. METHODS: The cell growths of Jiyoye (Burkitt lymphoma), H9 (T cell lymphoma), and CCRF-CEM (acute lymphocytic leukemia, T cell) cell lines due to TGF-beta1 were measured using the MTT assay. RT-PCR was also performed to monitor the expression of the c-myc gene in these cells with the telomerase activity measured using a TRAP assay. RESULTS: There was significant inhibition of cell growth in TGF-beta1 (5ng/mL) treated Jiyoye cells. When treated with TGF-beta1, the Jiyoye cells exhibited marked decreases in the levels of c-myc RNA and telomerase activity. However, TGF-beta1 treated H9 and CCRF-CEM cells showed no cell growth inhibition or reductions in the levels of c-myc mRNA and telomerase activity. The effect of TGF-beta1 on cell growth was noted to closely correlate with c-myc mRNA expression and telomerase activity. CONCLUSION: These results suggest that TGF-beta1 may inhibit cell growth in Jiyoye cells by a mechanism involving down-regulation of the c-myc gene, which in turn, reduces the telomerase activity.
Apoptosis ; Carcinogenesis ; Cell Line* ; Cell Proliferation ; Down-Regulation ; Epithelial Cells ; Genes, myc ; Leukemia* ; Leukemia, T-Cell ; Lymphoma* ; RNA ; RNA, Messenger* ; Telomerase* ; Transforming Growth Factor beta1