Objective To evaluate the value of MRI and MDCT in detecting both inferior vena cava tumor thrombus and vena cava wall invasion in renal cell carcinoma. Methods Databases including PubMed, EMbase, The Cochrane Library, MEDLINE (Ovid), CBM, CNKI, VIP and WanFang Data were searched from January 2000 to February 2012. Relevant studies were screened on the basis of the inclusion and exclusion criteria, and then quality assessment and data extraction were conducted. Then heterogeneity test and meta-analysis were conducted using RevMan 5 and Meta-disc 1.4. Results A total of 6 trials involving 244 patients and 246 cases of renal cell carcinoma were included. The results of meta-analysis showed that, for the MRI group and the MDCT group, the sensitivity was 0.963 and 0.952, the specificity was 0.969 and 0.979, the value of +LR was 9.759 and 15.57, the value of −LR was 0.091 and 0.108, and the dOR was 198.71 and 251.54, respectively. There were no significant differences in pooled effect-size among groups (Pgt;0.05). The area under curve (AUC) of summary ROC curve analysis as well as Q index of the MDCT group were 0.981 8 and 0.940 7, respectively. Conclusion There is no significant difference in the value of MRI and MDCT in detecting inferior vena cava tumor thrombus induced by renal cell carcinoma. More original studies on vena cava wall invasion by tumor thrombus should be conducted in the future due to the limitation of current materials.
ObjectiveTo investigate the effect of the femoral tunnel angle on the femoral tunnel after anterior cruciate ligament (ACL) reconstruction in rabbits. MethodsFifty-four healthy 4-5 months old rabbits (weighing, 1.8-2.3 kg, male or female) were randomly divided into 3 groups (n=18). The ACL reconstruction models of the right knee were established in 3 experimental groups using its Achilles tendons, and the left knee served as the control group. On the coronal position, the angle between the femoral tunnel and the femoral shaft axis was 30°, 45°, and 60°. The level of tumor necrosis factor α (TNF-α) in the synovial fluid at 1, 2, and 4 weeks, the maximum load of the ligament and the rate of bone tunnel enlargement at 4, 8, and 12 weeks were detected. ResultsThe level of TNF-α significantly increased, and the maximum load of the ligament significantly decreased in the 3 experimental groups when compared with ones in the control group (P<0.05), but no significant difference was found among 3 experimental groups (P>0.05). The bone tunnel enlargement was observed in 3 experimental groups at each time point and reached the peak at 4 weeks, but no significant difference was shown among 3 groups (P>0.05). ConclusionThe 30-60° angle between the femoral tunnel and the femoral shaft axis in the coronal position has no significant effect on the femoral tunnel enlargement after ACL reconstruction in rabbits.
ObjectiveTo investigate the expression of tumor metastasis associated genes-1 (MTA1) and vascular endothelial growth factor-C (VEGF-C) in esophageal squamous cell carcinoma (ESCC) and the relationship between them and lymphangiogenesis. MethodA total of 107 patients who received excision for ESCC in the Cardiothoracic Surgery Department of Suining Central Hospital from March 2013 through January 2014 were enrolled. And the paraffinembedded esophageal tissues in 56 healthy persons were collected. The expression of MTA1 and VEGF-C in ESCC was detected using the immunohistochemical method. And D2-40 was used to label the micro-lymphatic endothelial cells of the tumor tissues while the micro-lymphatic vessel density (LVD) was counted. Meanwhile, a statistical analysis was performed for the relationship between MTA1 with VEGF-C and clinical pathological parameters. ResultsThe expression rates of MTA1 protein and VEGF-C protein in ESCC (50.4% and 58.8%, respectively) were higher than those in normal esophageal tissues with a statistical difference (P<0.05). Besides, their high expression rates in stage T3/T4 ESCC and lymph node metastasis group were significantly higher than those in stage T1/T2 ESCC and metastasisfree group, with statistical differences (P<0.05). The high expression rates of MTA1 and VEGF-C protein in ESCC with different TNM stages were compared using Kruskal-Wallis test with statistical differences (P<0.05). Moreover, a positive correlation existed in the expression level between MTA1 protein and VEGF-C protein of ESCC (Spearman coefficient r=0.512, P=0.000). And LVD of the high expression group for MTA1 protein and VEGF-C protein was statistically different from that of the low expression group (P<0.05). ConclusionThe expression of MTA1 is positively correlated with the expression of VEGF-C in ESCC. And they may co-promote lymphangiogenesis and lymphatic metastasis in ESCC. Therefore, both can be used as the laboratory indicators to determine the prognosis of ESCC.
Objective To review the clinical evidence of Pingxiao Capsule for tumor adjuvant treatment so as to provide some decision-making references for clinical practice. Methods We electronically searched CBM, CNKI, VIP, WanFang Data and MEDLINE (from inception to Feb, 2013) to collect the randomized controlled trials (RCTs) and non-randomized controlled trials (non-RCTs) about Pingxiao Capsule for tumor adjuvant treatment. Then, the included studies were summarized and evaluated according to the classification of diseases. Results 1 097 potential relevant articles were searched. We included 41 RCTs and 15 non-RCTs. The results showed that Pingxiao Capsule used as an adjuvant therapy in treating tumor improved the efficacy and reduced the side effects of radiation and chemotherapy, and also improved the quality of survival. Conclusion Current evidence showed that the effectiveness and safety of Pingxiao Capsule combined with radiation or chemotherapy in the tumor treatment is superior to radiation monotherapy or chemotherapy monotherapy. But due to the limited quality of the included studies, the results needed to be further verified by high-quality studies.
ObjectiveTo investigate the expressions of IL-10,tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in serum and lung tissue of COPD rats in order to elucidate the potential mechanism of airway inflammation. MethodsForty-five healthy adult male SD rats were randomly divided into a COPD model group (n=30) and a normal control group (n=15). The COPD rat model was established by intratracheal instillation of lipopolysaccharide (LPS) and exposure to cigarette smoke for 28 days. The concentrations of IL-10,TNF-α and IFN-γ in serum and lung tissue were measured by ELISA. ResultsTNF-α level of serum and lung tissue in the COPD model group increased significantly compared with the control group(P<0.05),while the levels of IFN-γ and IL-10 decreased significantly[serum:(44.68±8.67) ng/L vs. (75.96±10.59) ng/L;lung tissue:(64.55±9.03) ng/L vs. (94.06±8.71) ng/L,P<0.01]. The level of IL-10 in serum and lung tissue was negatively correlated with TNF-α (serum:r=-0.67,lung tissue:r=-0.80,P<0.01). The level of IL-10 in serum and lung tissue was positively correlated with IFN-γ (serum:r=0.64,lung tissue:r=0.72,P<0.01). The level of IL-10 in serum and lung tissue was negatively correlated with the percentage of neutrophils(serum:r=-0.70,lung tissue:r=-0.67,P<0.01). ConclusionIn COPD rats,down regulation of IL-10 plays an important role in regulation of airway inflammation.
Objective To summarize the roles of tumor initiating cells （TICs） and epithelial-mesenchymal transition （EMT） in tumor metastasis and drug resistance. Methods Domestic and international publications online which involving TICs，EMT，and its roles in tumor metastasis and drug resistance in recent years were reviewed. Results TICs were self-renewal cells and had the ability to give rise to more differentiated cell types，and played an important role in tumor metastasis and drug resistance. Various markers had been used to identify TICs，such as CD133，CD44，and so on. EMT was the process by which epithelial cells losed polarity and detach from the epithelial sheet， and acquired a motile mesenchymal phenotype，usually observed in embryo development and wound healing. It also could promote tumor progression and metastasis，and may also be responsible for the ability of tumors to evade the body’s immune response. EMT may be the reasons of TICs that drived tumor metastasis and recurrence. TICs or EMT as a target for treatments may effectively prevent tumor recurrence and improve patient’s survival. Conclusions EMT is probably the mechanism that TICs promote tumor metastasis and drug resistance. More effective target therapies for cancer may be found if we know more about TICs and EMT.
Objective To investigate the effect of tumor associated glycoprotein-72 （TAG-72） redirected T lymphocytes on breast cancer cells. Methods Peripheral blood mononuclear cells （PBMCs）were isolated from healthy volunteers. The recombinant vector anti-TAG-72-scFv-CD3ζ-pcDNA 3.0 were transfected into PBMCs by lipofectamineTM2000 （transfection group）， PBMCs transfected with plasmid pcDNA 3.0 as control group. MCF-7 and Bcap37 cells were cocultivated with PBMCs of transfection group and control group， respectively， and antitumor response of G1 block was observed. Results G1 block rate of MCF-7 cells in transfection group was （82.3±6.9）%， which was significantly higher than that in control group 〔（43.4±3.9）%， P＜0.05〕. G1 block rate of Bcap37 cells in transfection group was （51.3±4.7）%， and not differed from that in control group 〔（45.6±2.5）%， P＞0.05〕. Conclusion TAG-72 redirected T lymphocytes can inhibit the cell proliferation of TAG-72 positive breast cancer cells， and it may provide valuable tools for the cellular immunotherapy.
Objective To summarize the research progress of CO2 pneumoperitoneum impacts on invasiveness of cancer cells. Methods Currently published experimental and clinical researches related to the effect of CO2 pneumoperitoneum on invasiveness of cancer cells were reviewed. Results CO2 pneumoperitoneum may affect the invasiveness of cancer cell through several ways， such as changing the structure and function of mesothelial cell， changing microenvironment of peritoneum， influencing the expression of oncogen， affecting the secretion of cell factor， and changing the adhesion of cancer cell. Conclusions The consequences of these alterations to cancer cell and the microenvironment are not well understood， but they may facilitate tumor invasion and implantation. Further investigations in this area are very urgent.
Objective To review the role of mTOR signal pathway in chemo-resistance of gastric cancer. Methods Domestic and international publications related mTOR signal pathway in chemo-resistance of gastric cancer in recent years were collected and reviewed. Results mTOR was a central signaling molecule of mTOR signal pathway， which regulated key cellular processes such as cell growth， cell proliferation， cell metabolism， and angiogenesis. Signaling molecules of mTOR signal pathway were overexpressed in gastric cancer. Moreover， mTOR signal pathway might play an important role in chemo-resistance of gastric cancer， and tumor stem cells were involved in it too. Conclusion As mTOR signal pathway plays an important role in chemo-resistance of gastric cancer， the combination of mTOR inhibitors and chemotherapy drugs may overcome the chemo-resistance of gastric cancer.
ObjectiveTo detect the expressions of CD133 in four gastric cancer cell lines (KATO-Ⅲ, SGC7901, AGS, and MKN-45) and investigate the different biological characteristics of CD133 positive (CD133+) cells and CD133 negative (CD133-) cells in the KATO-Ⅲ cell lines. MethodsThe CD133 gene and protein expressions of four gastric cancer cell lines were evaluated by semiquantitative RT-PCR and Western blot, respectively. CD133+ cells in KATO-Ⅲ cell lines were isolated by magnetic activated cell sorting (MACS) and examined in morphology, growth characteristics, proliferation, and differentiation in vitro. The sensitivity of different concentrations (0.05, 0.10, 0.20, 0.50, and 1.00 mg/ml) 5-fluoropyrimidinedione (5-FU) were contrasted by drug sensitivity testing in vitro (Cell Counting Kit 8-assay) between CD133+ cells and CD133- cells. ResultsThe expressions of CD133 gene and protein in the KATO-Ⅲ cell lines were significantly higher than those in the other three cell lines (Plt;0.05). CD133+ cells produced spheroid colonies in serum-free medium culture and were ber abilities of proliferation and differentiation than those of CD133- cells in vitro. The inhibitor rate of the CD133+ cells at concentration of 0.50 mg/ml was lower than that of CD133- cells (Plt;0.05). ConclusionsCell population with CD133+ in the KATO-Ⅲ cell lines have b ability of cloning, better capability of proliferation and differentiation, as well as anticancer drug resistance to 5-FU. CD133 can be applied as one of surface markers for the detection to gastric cancer initiator cells.