Density of tumor-associated macrophages correlates with lymph node metastasis in papillary thyroid carcinoma.

BACKGROUND: Tumor-associated macrophages (TAMs) have recently been recognized as being important players in the tumoriogenesis of many cancers, including advanced thyroid cancer. However, a role in papillary thyroid carcinoma (PTC), the most prevalent thyroid cancer, has not been established. We hypothesized that TAMs also facilitate tumor progression in PTC. METHODS: We investigated TAMs density in both benign thyroid lesions and PTC tumors by CD68 immunostaining. CD68-positive cell density was further associated with the clinicopathological characteristics of PTC patients. Finally, TAMs were isolated from PTC tumors and phenotyped by cytokine and receptor profiling. RESULTS: The overall density of TAMs was found to be significantly higher in PTC tumors, compared with thyroid goiter and follicular adenoma. The density of TAMs was positively associated with lymph node metastasis in TNM (tumor-node-metastasis) stages III/VI compared with stages I/II. No association was observed in other common tumor features, including the BRAF mutation. The isolated TAMs presented with high levels of M2-associated cytokine and receptors, making M2 the predominant TAM phenotype. CONCLUSIONS: TAMs may play a functional role in the progression of PTC.

Pharmacokinetic analysis of glaucocalyxin A in rat plasma by liquid-liquid extraction and HPLC.

A validated HPLC method is described for determination of glaucocalyxin A in rat plasma using liquid-liquid extraction and UV absorbance detection. The extraction recovery of glaucocalyxin A ranged from 81.72 % to 79.25 %, the linear range was 0.2-10 microg/mL, and R was 0.9984. A pharmacokinetic analysis of glaucocalyxin A after intravenous administration in rats revealed that glaucocalyxin A followed a two-compartment open model. The values of t (1/2alpha) and t (1/2beta) were 4.327 min and 28.56 min, respectively, and the area under the plasma concentration-time curve (AUC) was 222.744 microg x min x mL (-1). The method developed was simple, rapid and specific, and an accurate way of investigating the pharmacokinetics of a diterpenoid in plasma.

Inhibition effect of Oncostatin M on metastatic human lung cancer cells 95-D in vitro and on murine melanoma cells B16BL6 in vivo.

Oncostatin M (OSM) is a multifunctional regulator of cell growth and differentiation. It inhibits the growth of many types of tumor cells, but its role in metastasis is unknown. We studied the human OSM expressed and purified from reconstructed E. Coli on its activity of inhibiting metastasis of tumor cells by a series of assays in vitro and in vivo. Clone formation assay in soft agar was used to measure the inhibition activity of OSM on the proliferation of high metastatic human lung cancer cells 95-D. Cell attachment assay, cell migration assay and cell invasion assay were used to evaluate inhibition by OSM on 95-D cells of the adhesion ability, the migration ability, and the ability of cells to cross tissue barriers, respectively. Inhibition of OSM on secretion of MMP-2 and -9 secretion in 95-D cells was determined by Western blot. The in vivo inhibitory effect of OSM on metastasis of murine melanoma cells B16BL6 was examined in the pulmonary metastasis model. In vitro studies showed that OSM inhibited the proliferation of 95-D cells at low concentration. OSM also reduced the adhesion and invasion ability of 95-D cells and inhibited the secretion of MMP-2 and MMP-9 in OSM treated cells. In vivo results showed that OSM (20 microg/kg/d for 7 days) inhibited pulmonary metastasis at a rate of 20.7%. There were no differences in animal weights among the groups. These results suggest that OSM has the potential of being a clinical inhibitor on metastasis of some cancer cells.

[Expression of costimulatory molecules on peripheral blood lymphocytes of patients with idiopathic thrombocytopenic purpura].

OBJECTIVE: To investigate the expressions of costimulators on peripheral T and B lymphocytes in patients with idiopathic thrombocytopenic purpura (ITP). METHODS: The expression of B7-CD(28) and CD(40) of peripheral lymphocytes was measured by flow cytometry in 21 ITP patients and 9 normal subjects. The expression of PAIgG was measured by ELISA method. RESULTS: The expression of CD(4)(+)CD(28)(+) was lower in ITP patients than in normal controls, but the expression of CD(86)(+) and CD(86)(+)CD(19)(+) was higher in ITP patients than in normal controls, while the expression of CD(80)(+), CD(40)(+), CD(28)(+), CD(19)(+)CD(86)(+), CD(19)(+)CD(40)(+), CD(4)(+)CD(28)(+)/CD(4)(+), CD(19)(+)CD(80)(+)/CD(19)(+) and CD(19)(+)CD(40)(+)/CD(19)(+) in ITP patients was normal. The PAIgG level was higher in 16 patients with a mean of (184.62 +/- 38.00) ng/10(7) plt. A positive correlation was found between PAIgG and CD(19)(+)CD(86)(+)/CD(19)(+) expression. CONCLUSION: There is no deficiency in expression of CD(28) on CD(4)(+) T lymphocytes in ITP patients. The change of CD(86) expression on B lymphocytes is possibly involved in pathophysiology of ITP, which may provide a theoretical instruction for ITP patients immunological therapy.