In this early experience, EMD appears to be a feasible and minimally invasive treatment for some patients with upper-GI SETs originating from the muscularis propria. Although there is a higher risk of perforation than with ESD, this will improve with extended practice, and perforations have become manageable endoscopically.

tEMD appears to be a feasible minimally invasive and effective treatment for patients with SETs originating from the MP layer of the esophagus and cardia.

No abstract

This study aimed to investigate the impact of the combined use of the nuclear factor-κB (NF-κB) inhibitors pyrrolidine dithiocarbamate (PDTC), bortezomib or SN50, and the chemotherapy agents arsenic acid (As2O3), fluorouracil (5FU), oxaliplatin or paclitaxel on the growth and apoptosis of HT-29 cells. Cell morphology was observed using inverted microscopy, and cell viability and apoptosis were assessed using the MTT assay and flow cytometry, respectively. The activities of NF-κB were analyzed by western blotting and electrophoretic mobility shift assay (EMSA). Cell growth was significantly inhibited by As2O3, oxaliplatin and paclitaxel in a time- and concentration-dependent manner (P<0.05), while 5FU inhibited cell growth in a time-dependent manner only (P<0.05). The growth inhibition rate and apoptosis induction ratio were increased following the combined treatment of the chemotherapy agent and NF-κB inhibitor. The expression of NF-κB p65 was upregulated when cells were treated with a chemotherapy drug, however it was downregulated following combined treatment or treatment with an NF-κB inhibitor alone. In conclusion, an NF-κB inhibitor combined with a chemotherapy drug effectively inhibited cell proliferation, induced cell apoptosis and inhibited NF-κB activity to enhance the chemotherapeutic sensitivity of HT-29 cells.

Decreasing hepatic fibrosis remains one of the major therapeutic challenges in hepatology. The present study aims to evaluate the effect of Endostar on both CCl-induced liver fibrosis in mice and a hepatic stellate cell (HSC) line. Two main models were studied: (i) a liver fibrosis model was induced in BALB/c mice using CCl by intraperitoneal injection for six weeks. Six animal groups were studied: group 1: normal animals; group 2: CCl-induced liver fibrosis; group 3: CCl + Endostar 20 mg/kg/d, six weeks; group 4: CCl + Endostar 10 mg/kg/d, six weeks; group 5: CCl + Endostar 20 mg/kg/d, four weeks; group 6: CCl + Endostar 10 mg/kg/d, four weeks corresponded to different Endostar doses and duration of administration. Liver fibrosis was evaluated by histopathological staining and liver hydroxyproline content. Expressions of collagen type I, α-smooth muscle actin (α-SMA), TGF-β1 and VEGFR were measured by real-time polymerase chain reaction (PCR). (ii) A liver cell model. HSC-T6 cells were cultured with or without Endostar for 12 h or 24 h. Expressions of collagen type I, α-SMA, and TGF-β1 were measured by real-time PCR. Collagen I and transforming growth factor β1 (TGF-β1) contents in cell supernatant were measured by enzyme-linked immunosorbent assay. As compared to the group without Endostar, liver fibrosis scores and hydroxyproline content were decreased in both Endostar groups (P < 0.05). Moreover, Endostar inhibited the hepatic expression of α-SMA, TGF-β1, Collagen-1, VEGFR1, and VEGFR2 mRNA (P < 0.05). In the HSC-T6 cell line model, Endostar profoundly inhibited the expression of α-SMA, Collagen-1, and TGF-β1 mRNA. Expressions of Collagen-1 and TGF-β1 protein were decreased in the Endostar group as compared to the normal controls in the supernatant of HSC-T6 cells (P < 0.05). Endostar decreased both liver fibrosis in CCl-induced mice and collagen synthesis in HSCs in vitro. Therefore, this recombinant human endostatin is a promising compound for counteracting liver fibrosis.