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Objective To evaluate endoscopic ultrasonography (EUS) for diagnosis of gastric stromal tumors (GST) by analyzing EUS features of tumors with different invasive capacities.Methods Clinical data of 34 patients with GST were analyzed retrospectively.The tumors were classified according to Fletcher′s GIST biological behavior ranking system and the corresponding EUS features were analyzed.Results The mean maximal diameter of GST in this cohort was 6.7cm.The echo heterogeneity, big tumors size, irregular shape and ulceration were more common in tumors of high risk (P<0.05).Conclusion Tumor size, shape, echo quality and ulceration detected by EUS are useful features for pretreatment evaluation of GST, and can guide the choice of following managements.
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Objective To study the of effets of hFRNK gene transfected by adenoviral vector on human colon cancer cell invasion induced by gastfin.Methods The subjects were divided into three groups:control,G17 and hFRNK group.The G17 group was treated with 100 umol/L gastrin 17 for 12 h to induce Col0320WT cells.As to hFRNK group,Colo320WT cells were infected by pAdhFRNK(MOI:100)for 48 h after transient transfection of pCR3.1-CAR for 48 h and subsequently treated with gastrinl7 for 12 h,and the control group was untreated Colo320WT cells.Expression of phosphorylated FAK(PY397)were assayed by western blot.FAK(PY397)at lamellipoda was observed with a confocal microscope.The influence of hFRNK on formation of signal complex of FAK-Src-p130Cas-Dockl80 was assayed with coimnlunoprecipitation and immunity blotting.Activity of Rac-GTPase was determined by pull down.Results Phosphorylated FAKTyr397 drastically increased with the induction of gastrin.Compared with that of G17 group,FAK (PY397)expression decreased and little FAK(PY397)was found at lamellipoda,at the same time,the signal complex of FAK-Src-p130Cas-Dockl80 did not form,and the activity of Rac decreased.Conclusion hFRNK gene may block gastrin-induced FAK phosphorylation,prevent formation of the signal complex,prevention and treatment of tumor invasion and metastasis.
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AIM: To study the anti-invasive effect of NS-398 on colon cancer cell line HT-29 in vitro an its regulation by CD44v6 and nm23-H1 genes. METHODS: Flow cytometry was used to detect the expression of COX-2 and CD44v6 in HT-29 cells. MTT was used for cell survival rate tests. The modified Boyden chamber model was used for quantitative invasion assay. RT-PCR was used to detect the expression of nm23-H1 mRNA. RESULTS: Flow cytometry analysis showed that COX-2 was positive in HT-29 cells. NS-398 had significant inhibitory effects on invasion of HT-29 cells, which had no relation with its cytotoxicity. NS-398 down-regulated the expression of CD44v6 and up-regulated the expression of nm23-H1 mRNA. CONCLUSION: NS-398 has an anti-invasive effect on HT-29 cells in vitro. Down-regulation of CD44v6 and up-regulation of nm23-H1 may be its underlying mechanisms.
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Objective:To investigate the expressions of S100A4 and MMP- 2 and their correla-tions to invasiveness and metastasis in gastric cancer. Methods:The expressions of S100A4 and MMP- 2 were detected by SP immunohistochemical method in 49 cases of gastric cancer tissue and 20 cases of normal tissue. Results:The positive rate of S100A4 and MMP- 2 (59.18% 、67.35%) was significantly higher in gastric cancer tissue than in normal gastric tissue (0.00% 、20.00% ,P