ABSTRACT
Gastrointestinal stromal tumor (GIST) is one of the most common tumors originating from gastrointestinal mesenchymal tissues,accounting for about 0.2% of all gastrointestinal tumors.It can occur anywhere in the gastrointestinal tract.Because gastrointestinal stromal tumors have the biological characteristics of non-directional differentiation and potential malignancy,it is very important to resect them completely in time.Traditional surgical excision has a good prognosis in the past,but it has some shortcomings,such as large trauma,slow postoperative recovery and more complications.In recent years,with the continuous development of digestive endoscopy technology,many new endoscopic techniques have emerged for the treatment of gastric stromal tumors,such as endoscopic mucosal dissection (ESD),endoscopic fullthickness resection (EFTR),endoscopy and laparoscopic combined surgery,but the safety and effectiveness of endoscopic surgery for gastric stromal tumors are still controversial in the industry.
ABSTRACT
Gastrointestinal stromal tumor (GIST) is one of the most common tumors originating from gastrointestinal mesenchymal tissues, accounting for about 0.2% of all gastrointestinal tumors. It can occur anywhere in the gastrointestinal tract. Because gastrointestinal stromal tumors have the biological characteristics of non-directional differentiation and potential malignancy, it is very important to resect them completely in time.Traditional surgical excision has a good prognosis in the past, but it has some shortcomings, such as large trauma, slow postoperative recovery and more complications. In recent years, with the continuous development of digestive endoscopy technology, many new endoscopic techniques have emerged for the treatment of gastric stromal tumors, such as endoscopic mucosal dissection (ESD), endoscopic full-thickness resection (EFTR), endoscopy and laparoscopic combined surgery, but the safety and effectiveness of endoscopic surgery for gastric stromal tumors are still controversial in the industry.
ABSTRACT
Objective To examine the inhibition effect of zoledronic acid (ZOL) on malignant metastasis of human esophagus squamous cell carcinoma (ESCC) cells and to analyze its molecular mechanisms.Methods EC9706 and EC109 cells were treated with ZOL,and then MTT assay,adhesion and invasion assay were performed to observe the inhibitory effect of As2O3 on proliferation and metastasis of esophagus carcinoma cells.The expression of metastasis-related proteins was detected by Western blotting.Results Exposure to ZOL significantly presented suppressive functions on growth and metastasis of both kinds of cancer cells,in a dose-dependent manner(P< 0.05).Additionally,the expression level of occludin was increased after ZOL treatment by suppressing transcriptional factor Slug.Transfection of Slug could reverse anti-metastasis of ZOL.Conclusion ZOL possesses a significant anti-metastasis function on ESCC cells,mainly through repressing Slug to restore occludin expression.
ABSTRACT
Cyclin-dependent kinase 10 (CDK10) function as a tumor suppressor gene through regulating cell cycle interacting with transcription factor Ets2.Studies demonstrate that the downregulation of CDK10 expression occurs in multiple cancer types,indicating a potential application of CDK10 as a molecular diagnostic marker as well as therapeutic target.
ABSTRACT
Objective To investigate the molecular mechanism of As 2 O3 in suppressing metastasis of esophagus carcinoma cells.Methods The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay, adhesion and invasion assay were performed to observe the inhibitory effect of As 2 O3 on proliferation and metastasis of esophagus carcinoma cells .The expressions of matrix metalloproteinases ( MMP)2, MMP9, E-cadherin, and protein tyrosine phosphatase receptor-type O ( PTPRO) were analyzed with Western blot .Results Exposure to As 2 O3 significantly presented suppressive functions on growth and metastasis of esophagus carcinoma cells in a dose-dependent manner ( P <0.01 ) .Additionally , MMP2 and MMP9 expressions were increased after treatment with casticin ( P <0.01 ) , whereas E-cadherin and PTPRO expressions were down-regulated ( P <0.01 ) .Conclusions As2 O3 had a significant function to inhibit proliferation and metastasis of esophagus carcinoma cells .
ABSTRACT
ObjectiveTo examine the expressions of amplified in breast cancer 1(AIB1) and epithelial cadherin (E-cadherin) in ovarian carcinoma (OC) tissues,and determine the correlation between the expression and clinical pathological features.MethodsThe expression of AIB 1,E-cadherin,estrogen receptor (ER),progesterone receptor (PR) and Ki-67 in tissues of 50OCs and 13 normal ovarians tissues were detected by immunohistochemistry(IHC) EnVision two step process analysis.ResultsPositive expression of AIB1 in OC tissues[68%(34/50) ] was obviously higher than that in normal ovarian tissues [8% (1/13)] (P <0.01).Down-regulation of E-cadherin expression was 60% (30/50).The positive expression of AIB1 was significantly higher in stage Ⅲ and Ⅳ than in stage Ⅰand Ⅱ according to International Federation of Gynecology and Obstetrics (FIGO) stage (P =0.036),in lymph node metastasis group than in none lymph node metastasis group ( P =0.027 ),in stage G3 than in stage G1 and G2 according to Silverberg stage (P =0.003),and in serous adenocarcinoma group than in non-serous adenocarcinoma group (P=0.049);positive rates of ER and Ki-67 were higher than negative rates of ER(P=0.000) and Ki-67 (P =0.009) respectively.Down-regulation of E-cadherin expression was higher in FIGO stage Ⅲ and Ⅳ than in stage Ⅰ and Ⅱ (P =0.044),in serous adenocarcinoma group than in non- serous adenocarcinoma group ( P =0.022) ; positive rates of ER and Ki-67 were higher than negative rates of ER ( P =0.02 1 ) and Ki-67 (P=0.035) respectively.The expression of AIB1 was negatively correlated with E-cadherin expressioh (P =0.026).ConclusionsThe expressions of AIB1 and E-cadherin in OC tissues is closely related to clinical stage.Therefore,AIB1 and E-cadherin may be important moleculars involved in the progression of OC.
ABSTRACT
Esophageal cancer related gene 4 (ECRG4) serves as a tumor suppressor gene through interacting with NF-κB and p53 pathways.Multiple studies have demonstrated that the down-regulated expression of ECRG4 occurs in a variety of cancer types,indicating a potential application of ECRG4 as a molecular diagnostic marker as well as a therapeutic target