A high incidence of esophageal cancer exists in China. Surgical resection remains the dominant therapeutic intervention for patients with operable esophageal carcinoma. However, alternative strategies are actively applied to reduce the frequency of post-op-erative local or distant disease recurrence and to prolong survival. These strategies include neoadjuvant and adjuvant therapies. This review discusses the current knowledge, as well as available data and information, with regard to neoadjuvant and adjuvant therapies for patients with locally advanced esophageal cancer.

AIM: To observe the effects of Cidan Capsule and Shenyi Capsule(ginsenoside Rg_3) with intraarterial therapy for advanced primary liver cancer. METHODS: Sixty cases with advanced primary liver cancer patients were randomly divided into two groups,30 cases of the treatment groups were treated with Cidan Capsule and Shenyi Capsule with intraarterial therapy,30 cases of the controls were only treated with intraarterial therapy.(RESULTS:)(1) The two groups(CR + PR) efficiency were 70%(21/30) and 33.3%(10/30) respectively.The statistical analysis was significantly different(P

Objective To study the effect of Bortezomib on proliferation, apoptosis, cell cycles and activation of NF-?B of non-small cell lung cancer cells (NSCLC) in vitro. Methods The inhibitory action of Bortezomib on cellular growth was determined by MTT. The effects of Bortezomib on cell cycle and apoptosis were assessed by flow cytometry. The influence of Bortezomib on the expressions of NF-?B, I?B and Bcl-2 were detected with Western blotting. Results The inhibitory effects of Bortezomib on the proliferation of NSCLC cells showed a time-and concentration-dependent manner. The growth of NSCLC cells was arrested at G2/M stage after treatment with Bortesomib at 25nmol/L for 48h. Basal expression of NF-?B was found to exist in all the 6 cell lines, with NF-?B expression in nucleus showing an inverse correlation with I?B expression in cytoplasm. Bortezomib threw no significant influence on the basal expression of NF-?B, but significantly blocked the TNF-?-induced nuclear translocation of NF-?B and down-regulated the expression of anti-apoptosis protein Bcl-2 in a time-and concentration-dependent manner. Conclusion With NF-?B-dependent pathway, Bortezomib may inhibit the proliferation of NSCLC cells and induce apoptosis.

Objective To investigate the expressions of tissue factor pathway inhibitor-2 (TFPI-2 ) and matrix metalloproteinase-9 (MMP-9)in esophageal squamous cell carcinoma(ESCC)tissue and their relationship with vasculogenic mimicry (VM).Methods 162 cases of esophageal squamous cell carcinoma tissues were collected. CD34/periodic acid-schiff double staining was performed to observe the distribution of VM in ESCC tissue,and immunohistochemical staining was used to detect the expressions of TFPI-2 and MMP-9 in ESCC tissue. The relationship between VM and the clinicopathologic parameters of ESCC, the expressions of TFPI-2 and MMP-9 were analyzed.Results The positive rate of VM in ESCC tissue was 20.37%.The positive rate of VM in poorly differentiated group(40.38%)was significantly higher than those in moderately differentiated group(11.76%)and well differentiated group (7.14%)(χ2 = 20.915, P < 0.01 ). The positive rate of VM in TNM Ⅰ-Ⅱ(11.59%)group was significantly lower than that in TNM Ⅲ group(26.88%)(χ2=5.707,P=0.017).The positive rate of TFPI-2 in VM(+)group(33.34%)was significantly higher than that in VM(-)group(6.45%) (χ2=4.582,P=0.032)in poorly differentiated ESCC.The positive rate of MMP-9 in VM(+)group(78.79%) was significantly higher than that in VM(-)group(44.96%)(χ2=12.05,P=0.001).The expression level of TFPI-2 in poorly differentiated group was positively correlated with VM (r= 0.166,P= 0.032 ), and the expression level of MMP-9 was positively correlated with the VM(r=0.183,P=0.018).The five-year survival rate in VM (-) group was significant higher than that in VM (+) group (χ2 = 22.84, P < 0.001 ). Conclusion VM exists in ESCC tissue,especially in poorly differentiated and advanced ESCC tissue.VM is related to poor prognostis of ESCC.TFPI-2 and MMP-9 might involve in the formation of VM in ESCC.

Objective To investigate the correlation between hope level and self-management behaviors among patients with type 2 diabetes.Method One hundred and ninety-eight hospitalized patients with type 2 diabetes were recruited in the investigation by convenience sampling in a first-class grade I hospital from December 2015 to April 2016 to understand the status of hope and self-management behaviors as well as the correlation between them.Results The score on hope level was (35.0±3.6),which was in a medium or above level.The total score of self-management behaviors was (84.1 ±13.0),which indicated their self-management remained in the middle level.The total score on the hope level and its all dimensions were positively correlated with the total score on self-management behaviors and the dimensions such as drug compliance,foot care,high and low blood sugar processing (all P ＜0.05).There was a positive relationship between maintain close relationship with others and regular exercise (P＜0.05).The average score on hope and each dimension were insignificantly correlated with diet control and blood glucose monitoring (all P＞0.05).Conclusions The hope of 2 diabetic patients is in a medium or above level.The hope level is closely related to their self-management behaviors.The nurses should pay attention to the hope level of patients.Effective nursing interventions should be adopted to improve the self-management ability and quality of life in patients with type 2 diabetes.

OBJECTIVETo explore the role of S100A4 in the epithelial-mesenchymal transition (EMT) in esophageal squamous cell carcinoma and its possible molecular mechanism.

METHODSThree chemically synthesized S100A4 siRNA sequences were transiently transfected into esophageal carcinoma EC9706 cells. EC9706 cells transfected with negative siRNA, lipofectamine 2000, and vacant EC9706 cells were used as control. Fluorescence quantitative RT-PCR and Western blot were used to detect the inhibition rate of S100A4 siRNA. S100A4 siRNA2 with the best inhibition rate was chosen to transiently transfect into EC9706 cells under the same conditions. The EC9706 cells transfected with negative siRNA, lipofectamine 2000 and vacant EC9706 cells were also used as control. Fluorescence quantitative RT-PCR and Western blot were used to detect the mRNA and protein expressions of E-cadherin, vimentin and snail. The morphology of EC9706 cells was observed under an inverted microscope. Boyden chamber and scratch test were used to detect the invasion and migration ability of EC9706 cells, and CCK8 assay was used to detect the proliferation ability of EC9706 cells. EC9706 cells transfected with S100A4 siRNA2 were further transfected with snail eukaryotic expression vector. The EC9706 cells transfected with S100A4 siRNA, EC9706 cells transfected with snail eukaryotic expression vector and vacant EC9706 cells were used as control. The above indexes of all the groups were observed, too.

RESULTSThe S100A4 mRNA and protein expression levels of the S100A4 siRNA2 group were 0.417 ± 0.041 and 0.337 ± 0.039, the transmembrane cell number was 61.608 ± 8.937, the scratch healing distance was (0.216 ± 0.064) mm, the A value was 0.623 ± 0.084, the E-cadherin mRNA and protein levels were 0.619 ± 0.032 and 0.495 ± 0.034, the vimentin mRNA and protein levels were 0.514 ± 0.032 and 0.427 ± 0.028, the snail mRNA and protein levels were 0.573 ± 0.029 and 0.429 ± 0.041. These data were significantly different with the liposome group, the negative control group and the blank group (P < 0.05 for all). After the S100A4 siRNA2 treatment for 24 h, the appearance of EC9706 cells changed to epithelial cell morphology. The transmembrane cell number and the scratch healing distance of the S100A4 siRNA2+snail eukaryotic expression vector group were (69.382 ± 9.666) cells and (0.274 ± 0.029) mm, the A value was 0.823 ± 0.101, the snail mRNA and protein levels were 0.704 ± 0.037 and 0.625 ± 0.031, the vimentin mRNA and protein levels were 0.712 ± 0.046 and 0.609 ± 0.038, and these data were significantly higher than those of the Sl00A4 siRNA2 group (P < 0.05 for all). The E-cadherin mRNA and protein levels of the S100A4 siRNA2+eukaryotic expression vector group were 0.437 ± 0.038 and 0.381 ± 0.031, significantly lower than those of the S100A4 siRNA2 group (P < 0.05 for all). However, snail had no effect on the morphology of EC9706 cells.

CONCLUSIONSS100A4 may be involved in the EMT process of esophageal squamous-cell carcinoma by regulating the expression of snail and then plays a role in the invasion and metastasis of esophageal carcinoma.

Cadherins ; analysis ; Carcinoma, Squamous Cell ; metabolism ; pathology ; physiopathology ; Cell Line, Tumor ; Epithelial Cells ; Epithelial-Mesenchymal Transition ; Esophageal Neoplasms ; metabolism ; pathology ; physiopathology ; Humans ; Indicators and Reagents ; Lipids ; RNA, Messenger ; analysis ; RNA, Small Interfering ; analysis ; physiology ; S100 Calcium-Binding Protein A4 ; S100 Proteins ; antagonists & inhibitors ; genetics ; physiology ; Snail Family Transcription Factors ; Transcription Factors ; analysis ; genetics ; Transfection ; Vimentin ; analysis ; genetics

Background and purpose:More and s’more evidence has demonstrated that DNMT1 was expressed at high levels in many different kinds of human tumor tissues or cells,suggesting that high expression of DNMT1 was closely associated with occurrence and development of tumors.In this study,effect of down-regulation of DNMT1 on cell proliferation and migration ability of esophageal squamous cell carcinoma(ESCC) cell line EC9706 cells was studied and its related mechanism was explored.Methods:Cell proliferation assay was investigated using CCK-8 Kit,cell migration ability was analyzed using Boyden chamber and the expressions of DNMT1 and MMP-2 were detected by Real-time PCR and Western blotting methods.Results:The result of cell proliferation experiment showed that down-regulation of DNMT1 could markedly inhibit cell proliferation in EC9706 cells.After transfection with DNMT1 siRNA,invasiveness and metastasis ability of EC9706 cells displayed an obvious decrease(P

Objective To observe the effects of all-trans retinoic acid (ATRA) and oxaliplatin (L-OHP) on the proliferation of human gastric cancer BGC-823 cells. Methods Human gastric cancer cells BGC-823 were treated with ATRA and/or L-OHP,respectively. The cell proliferative activity was assessed by MTT assay. Cell morphological changes were observed under inverted microscope while apoptosis rate and cell cycle were assayed by flow cytometry. The expressions of Bcl-2 and Survivin protein were detected by immunocytochemistry. Results The proliferation of the cells treated with ATRA was inhibited obviously and the morphology of the cells changed. The apoptosis rate of BGC-823 cells increased gradually and the effect was enhanced when ATRA was combined with L-OHP. After treatment with ATRA,the expressions of Bcl-2 and Survivin protein in BGC-823 cells were both down-regulated obviously. With the combination of ATRA and L-OHP,the expressions both further decreased. Conclusion ATRA can inhibit the proliferation of human gastric cancer BGC-823 cells,and the inhibitory effect is synergistic when ATRA is combined with L-OHP. The mechanism might be related to the down-regulation of Bcl-2 and Survivin protein expressions.

Objective To study the inhibitory effect of arsenic trioxide(AS2O3)on the tumor growth of breast cancer line MDA-MB-435s implanted subcutaneously in nude mice and its mechanism.Methods BALB/C-nu/nu nude mice were subcutaneously injected with MDA-MB-435s breast cancer cells that are ER-positive,and treated with intraperitoneal injection of AS2O3 and DDP in different concentrations.The implanted tumor was weighed,and tumor inhibition rates were calculated.The expression of PTEN and Caspase-7 induced by AS2 03 were examined by immunohistochemical method.Results The growth of implanted tumor was markedly inhibited with DDP,low dose and high dose AS2O3,and the inhibitory rates were 48.68%,32.80%,66.67%respectively.The immunohisto chemical staining showed that the number of PTEN and Caspase-7 protein increased markedly(P＜0.05).Conclu sions AS2O3 inhibits the growth of human breast cancer cell implanted tumor.The molecular mechanism of AS2O3 on induction of apoptosis of breast cancer cells may be throush increasing the expression of PrrEN and Caspase-7(P ＜0.05).

Objective:To investigate the expression of tissue factor pathway inhibitor-2 (TFPI-2) and synuclein gamma (SNCG) in esophageal cancer and their correlation with local invasion, lymph node metastasis and apoptosis. Methods:The expression of TFPI-2, SNCG, and matrix metalloproteinase-9 (MMP-9) was detected by immunohistochemical SP methods in 82 cases of esophageal cancer tissues, 20 cases of atypical hyperplasia tissues, and 54 cases of para-cancerous tissues. The apoptosis of esophageal cancer cells was detected by TUNEL staining and apoptosis index (AI) was calculated. Results:The positive rates were 30.4%, 60.0%, and 87.0% for TFPI-2 protein and 63.4%, 30.0%, and 3.7% for SNCG protein in the tumor tissues, atypical hyperplasia tissues,and tumor-adjacent normal tissues, respectively. There was a significant difference between the three groups(P<0.01). The positive expression of TFPI-2 and SNCG correlated with the lymph node metastasis, invasion depth, TNM staging, and differentiation degree of esophageal cancer (P<0.01), but did not correlate with age at surgery, gender, tumor location, and pathologic classification(P>0.05). The expression of TFPI-2 and MMP-9 was negatively correlated (r=-0.636, P=0.000). The expression of SNCG and MMP-9 was positively correlated(r=0.393,P=0.000). AI was related with TFPI-2 and SNCG expression (P<0.05). Conclusion:TFPI-2 not only inhibited the expression of MMP-9 but also induces apoptosis of esophageal cancer to prevent tumor invasion and metastasis, however, SNCG plays a contradictory role in cancer development. TFPI-2 and SNCG might serve as new tumor markers and the new targets for tumor gene therapy.