Multiparametric CT features for prediction of the risk classification of gastric stromal tumor / 实用放射学杂志

Objective To investigate the value of multiparametric CT features for predicting the risk classification of gastric stro-mal tumor(GST).Methods The clinical data from 139 patients with GST were retrospectively collected.According to the patho-logical risk results,the patients were divided into two groups:a low-risk GST group(including very low-and low-risk)with 75 patients and a high-risk GST group(including medium and high-risk)with 64 patients.The CT features between low-risk GST group and high-risk GST group were compared using chi-squared test or t-test.The risk factors of high-risk GST were identified by univariate analysis.The prediction models were built by multivariate logistic regression.The performance of models were evaluated by receiver oper-ating characteristic(ROC)curve.Results There were significant differences in the maximum tumor diameter,minimum tumor diameter,arterial phase enhancement degree,venous phase enhancement rate,arterial phase enhancement degree rate,venous phase enhance-ment degree rate,cystic,and necrosis between low-risk GST group and high-risk GST group,which were associated with the risk classification of GST.The area under the curve(AUC)of the quantitative features-based model that combined maximum tumor diam-eter,minimum tumor diameter,arterial phase enhancement degree,venous phase enhancement rate,arterial phase enhancement degree rate and venous phase enhancement degree rate,showed a significantly higher performance than the qualitative features-based model that incorporated cystic and necrosis(0.981 vs 0.850,P<0.001).Conclusion Maximum tumor diameter,minimum tumor diameter,arterial phase enhancement degree,venous phase enhancement rate,arterial phase enhancement degree rate,venous phase enhance-ment degree rate,as well as cystic and necrosis,are associated with the risk classification of GST and can predict the high-risk GST.

CRKL promotes lung cancer cell invasion through ERK-MMP9 pathway.

CRKL is recently defined as a new oncogene, which plays a role in the lung cancer progression. However, the potential mechanism of CRKL in human non-small cell lung cancer cell invasion is obscure. We investigated the potential mechanism of CRKL in lung cancer cell invasion using immunohistochemistry, plasmid transfection, Western blotting, real-time PCR, matrigel invasion assay, chromatin immunoprecipitation assay, and luciferase reporter assay. CRKL expression is higher in lymph node metastatic tumor compared with primary tumor. CRKL overexpression enhanced cell invasion and MMP9 expression in both HBE and H1299 cell lines. There was a significant correlation between CRKL overexpression and high MMP9 expression in primary tumors. MMP-9 antibody treatment significantly blocked cell invasion. CRKL overexpression also activated AP-1 luciferase reporter activity, ERK phosphorylation and association of c-fos to MMP9 promoter. Treatment with ERK inhibitor PD98059 in cells with CRKL transfection inhibited ERK activity, cell invasion, and MMP9 expression. These results suggested that overexpression of CRKL promoted cell invasion through upregulation of MMP9 expression and activation of ERK pathway.

Loss of β-catenin inhibits Stat-5α phosphorylation in bcr-abl induced leukemia cells / 白血病·淋巴瘤

Objective To investigate the influence of β-catenin gene deletion on Stat-5α phosphorylation in bcr-abl induced leukemia cells. Methods The established conditonal hematopoitic β-catenin knockout mice were used to isolate bone marrow cells. Exogenous bcr-abl fusion gene was transduced to these bone marrow cells by retroviral infection with intent to transfom them to leukemia cells.Immunofluorescence was performed to detect the phosphorylation status of Stat-5α in both β-catenin deletion cells and control cells. bcr-abl transcription and protein levels were evaluated with real-time PCR and western blotting. Results Phosphorylation of Stat-5α was reduced significantly in β-catenin deletion leukemia cells on comparison with control cells despite that total Stat-5α protein showed no obvious changes. Total tyrosine phosphorylation and bcr-abl protein expression were reduced in bcr-abl induced β-catenin deletion CML cells,on the contrary, both of the reduction were not seen in bcr-abl induced β-catenin deletion ALL cells.Conclusion Loss of β-catenin inhibits both Stat-5α phosphorylationin and bcr-abl expression in bcr-abl induced leukemia cells.

Expression of MMP-2, MMP-9, TIMP-1 and their relationship with prognosis in NSCLC / 中国肺癌杂志

<p><b>BACKGROUND</b>To study the expression of MMP-2, MMP-9, TIMP-1 proteins and mRNA in NSCLC and to analyse their relations with prognosis.</p><p><b>METHODS</b>Immunohistochemistry (IHC) and in situ hybridization (ISH) were used to detect the expression of MMP-2, MMP-9, TIMP-1 proteins and mRNA in pa-raffin-embedded NSCLC specimens.</p><p><b>RESULTS</b>There were no significant differences among the MMP-2, MMP-9, TIMP-1 expression and age, sex, histological type and differentiation. There was statistical relationship between expression of MMP-2, MMP-9, TIMP-1 and lymph node metastasis. Multivariate Cox model analysis suggested that the survival time was significantly related to lymph node metastasis, expression of MMP-2 and MMP-9. The results of IHC and ISH suggested that the concordant rates of MMP-2, MMP-9, TIMP-1 proteins and mRNA were of statistical significance (P < 0.01,P < 0.005,P < 0.025).</p><p><b>CONCLUSIONS</b>MMP-2 and MMP-9 are independent factors that affect prognosis, TIMP-1 is an useful parameter to the prognosis of NSCLC.</p>