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Purpose: The aim of this study was to evaluate the diagnostic value of FNA-Tg for detecting lymph node metastases in patients with a history of differentiated thyroid cancer (DTC). Materials and Methods: A total of 58 patients with DTC diagnosis and evidence of single or multiple suspicious cervical lymph nodes were assessed. All underwent total or near-total thyroidectomy with (35 cases) or without (23 cases) radioiodine (RAI) ablation, followed by thyroid stimulating hormone (TSH) suppression therapy. A total of 68 lymph nodes were examined by ultrasound-guided fine needle aspiration (US-FNA) for both cytological examination and FNA-Tg measurement. Serum Tg and anti-thyroglobulin antibody (TgAb) levels were also measured. Diagnostic performance including sensitivity, specificity , accuracy, positive (PPV) and negative predictive value (NPV) of FNAC and FNA-Tg were calculated and compared. The Spearman’s rank correlation coefficient was used to estimate the relationship between FNA-Tg and serum TgAb. Results: The FNA-Tg levels were significantly higher with DTC metastatic lymph nodes (median 927.7 ng/mL, interquartile range 602.9 ng/mL) than non-metastatic lymph nodes (median 0.1 ng/mL, interquartile range 0.4 ng/mL) (p

Background Previous studies indicated that microRNA-338-5p (miR-338-5p) functions as tumor suppressor in some cancer types including glioma. However, the clinical significance and biological function of miR-338-5p in glioma still need to be explored. Methods We used quantitative real time PCR (qRT-PCR) to detect the miR-338-5p expression in the 44 cases of glioma tissues and adjacent normal tissues. In vitro, CCK8 cell proliferation, cell colony formation, transwell invasion assay and flow cytometry analysis were performed to explore the effects of miR-338-5p on cell proliferation, cell invasion and cell cycle distribution. Dual luciferase assay, qRT-PCR and western blot analysis were applied to validate CTBP2 was a direct target of miR-338-5p in glioma cells. Results we demonstrated that miR-338-5p was significantly lower expression in 44 glioma patients, compared with adjacent normal tissues. MiR-338-5p expression was significantly correlated with glioma grades and Karnofsky Performance Status in patients. We then validated that increased miR-338-5p significantly inhibited the cell proliferation, cell invasion and epithelial-mesenchymal transition (EMT) in vitro. Moreover, Dual luciferase assay results indicated that CTBP2 was direct target of miR-338-5p in glioma cells. Meanwhile, CTBP2 silencing can rescued the phenotype changes induced by miR-338-5p inhibitor on cell proliferation and invasion in glioma. Conclusion Our results suggested that miR-338-5p acts as tumor suppressor and could be a potential therapeutic target for glioma.

Aim: To investigate the transforming growth factor β1 (TGF-β1) and basic fibroblast growth factor (bFGF) expressions in benign prostatic hyperplasia (BPH) and the effect of β-radiation. Methods: TGF-β1 and bFGF expression was studied by means of an immunohistochemical method in nine normal prostatic (NP) tissues, 15 hyperplastic prostatic tissues and 35 hyperplastic prostatic tissues treated with 90 Sr/ 90 Y. Results: The TGF-β1 expression in the epithelium and stroma of normal prostatic tissues was 68.2 % ± 10.5 % and 29.7 % ± 4.6 %, respectively, while it was 64.8 % ± 9.3 % and 28.6 % ± 4.1 %, respectively, in hyperplastic prostatic tissues. Compared with the controls, TGF-β1 expression in the epithelia and stroma of BPH treated with 90 Sr/ 90 Y increased significantly (P < 0.01). The bFGF expression in epithelia and stroma of normal prostatic tissues was 17.4 % ± 3.7 % and 42.5 % ± 6.8 %, respectively, and was 46.3 % ± 8.2 % and 73.2 % ± 12.1 %, respectivley, in hyperplastic prostatic tissues. Compared with the controls, expressions of bFGF in the epithelia and stroma of BPH treated with a 90 Sr/ 90 Y prostatic hyperplasia applicator decreased significantly (P < 0.01). Conclusion: Exposure of β-rays had noticeable effects on BPH tissues, enhancing TGF-β1 expression and inhibiting bFGF expression. (Asian J Androl 2005 Mar; 7: 49–54)