Diagnostic and prognostic value of circulating miR-18a in the plasma of patients with gastric cancer.

The aim of this manuscript is to analyze the diagnostic and prognostic value of circulating miR-18a in the plasma of patients with gastric cancer. In this study, 82 patients with gastric cancer and 65 healthy controls were enrolled in the study, and 10 ml of peripheral venous blood was collected for RNA extraction. miR-18a expression was determined using TaqMan quantitative real-time polymerase chain reaction assay and was further correlated with patients' clinicopathological parameters and the follow-up data. The results indicated that plasma miR-18a was upregulated in gastric cancer patients compared with healthy controls (P < 0.001). miR-18a yielded an area under the receiver-operating characteristic curve of 0.907 with 80.5 % sensitivity and 84.6 % specificity in discriminating gastric cancer from healthy controls. Plasma miR-18a expression was significantly associated with pathological grade (P = 0.036) and lymph node status (P = 0.025), but not with tumor stage (P = 0.075). Both log-rank test and univariate Cox regression analysis showed that the higher miR-18a expression in plasma was associated with shorter disease-free survival and disease-specific survival of the patients with gastric cancer (P = 0.023 and P = 0.027; P = 0.036 and P = 0.043, respectively), which was also not proven by multivariate Cox regression analysis (P = 0.238 and P = 0.160, respectively). In conclusion, this study showed that miR-18a may be a promising biomarker for the detection of gastric cancer and its upregulation may be potentially associated with unfavorable prognosis of bladder cancer, suggesting that miR-18a might serve as a potential biological marker for further risk stratification in the management of gastric cancer.

Upregulation of microRNA-25 associates with prognosis in hepatocellular carcinoma.

BACKGROUND: Accumulating evidence has shown that up-regulation of microRNA-25(miR-25) is associated with the prognosis of several types of human malignant solid tumors. However, whether miR-25 expression has influence on the prognosis of hepatocellular carcinoma (HCC) is still unknown. METHODS: The differentially expressed amount of the miR-25 was validated in triplicate by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Survival rate was analyzed by log-rank test, and survival curves were plotted according to Kaplan-Meier. Multivariate analysis of the prognostic factors was performed with Cox regression model. RESULTS: The expression of miR-25 was significantly upregulated in HCC tissues when compared with adjacent normal tissues (p<0.0001). Patients who had high miR-25 expression had a shorter overall survival than patients who had low miR-25 expression (median overall survival, 31.0 months versus 42.9 months, p=0.0192). The multivariate Cox regression analysis indicated that miR-25 expression (HR=2.179; p=0.001), TNM stage (HR=1.782; p=0.014), and vein invasion (HR=1.624; p=0.020) were independent prognostic factors for overall survival. CONCLUSION: Our data suggests that the overexpression of miR-25 in HCC tissues is of predictive value on poor prognosis. VIRTUAL SLIDE: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1989618421114309.

[Effect of glucocorticoid on glucocorticoid-resistant children with primary nephrotic syndrome].

OBJECTIVE: Glucocorticoid (GC) is the first therapeutic choice of primary nephrotic syndrome (PNS). The response to GC treatment is an important indicator for the outcome of PNS children. Children with GC-resistant PNS present with incomplete or no response to GC, and may herald the progression to end-stage renal failure. However, the detailed mechanism of GC-resistance or GC-sensitive effect in these PNS children has not been clearly elucidated. The previous study by the authors indicated that there was increased expression of GR beta in PBMCs in GC-resistant children with PNS, and the over expression of GR beta resulted in GC resistance via influencing the ability of GR alpha nuclear translocation. To elucidate the relationship between GR beta expression in renal and in PBMCs and the effect of glucocorticoid on glucocorticoid-resistance children with PNS, the expression of GR alpha and GR beta in renal tissue and in PBMCs were detected by immunohistochemistry. METHODS: Forty children with PNS were divided into two groups, GC-resistant group(20) and GC-sensitive group(20), the expression of GR alpha and GR beta in renal intrinsic cells and in PBMCs were measured with the immunohistochemistry technique. A semiquantitative score was used to evaluate the injury degree of the glomeruli and tubulointerstitium. RESULTS: Compared with GC-sensitive group, the glomerular pathologic scores (6.91 +/- 1.98) and renal tubular pathologic scores (7.12 +/- 1.62) in GC- resistant group were significantly different (P < 0.01, respectively). GR alpha expressions of renal tissue and PBMCs were higher in the control group (58.3 +/- 2.6, 59.1 +/- 7.2) than those in the GC-sensitive group (40.2 +/- 7.2 and 36.6 +/- 5.1, P < 0.01, respectively) and GC-resistant group (35.0 +/- 8.2 and 36.4 +/- 6.6, P < 0.01, respectively). GR beta expressions of renal tissue and PBMCs were higher in the GC-resistant group (13.8 +/- 3.0 and 12.1 +/- 4.1) and in the GC-sensitive group (6.5 +/- 1.9 and 5.9 +/- 1.0) than that in control group (2.3 +/- 0.4 and 3.2 +/- 1.1, P < 0.01, respectively). GR beta expressions in renal tissue and PBMCs were higher in the GC-resistant group than that in the GC-sensitive group (P < 0.01). Compared with control group, GR beta expressions in PBMCs and in renal tissue were lower than those in mild renal lesion group (5.4 +/- 2.8, 6.46 +/- 2.50), midmedium renal lesion group (8.7 +/- 2.4 and 11.4 +/- 3.7) and (17.1 +/- 0.4 and 18.7 +/- 0.7) in severe renal lesion group (F = 5.8, 15.6, P < 0.01, respectively). GR beta expression of PBMCs had a positive correlation with GR beta expression of renal intrinsic cells (r = 0.651, P < 0.01). GR beta expressions by PBMCs and renal intrinsic cells were positively correlated with renal pathologic scores (r = 0.579 and 0.623, P < 0.01, respectively). CONCLUSION: GC-resistant children with PNS were related to the increased GR beta expression in PBMCs and renal intrinsic cells. There was no correlation between the GR alpha expressions in PBMCs and in renal intrinsic cells. Increased GR beta expression might decrease the effect of GC via inhibiting the activity of GR alpha.