Comparison of reverse puncture device and overlap in laparoscopic total gastrectomy for gastric cancer.

BACKGROUND: Intracorporeal oesophagojejunostomy is one of the key steps in laparoscopic total gastrectomy (LTG). At present, there is no widely accepted anastomosis technique in oesophagojejunostomy. MATERIALS AND METHODS: We retrospectively studied 63 patients with gastric cancer who underwent LTG. Two types of anastomosis techniques have been applied during LTG: the reverse puncture device (RPD) (28 patients) and overlap (35 patients). RESULTS: A total of 63 patients (51 males and 12 females: mean age = 58 years and mean body mass index [BMI] = 26.3 kg/m2) were enrolled in this study. There were no significant difference in age, BMI, duration of surgery, duration of anastomosis, blood loss, post-operative hospital stay, tumour location, tumour size, degree of tumour differentiation, Borrmann type, total number of lymph nodes, number of positive lymph nodes, hospital stay, hospitalisation costs, intra-operative complications, post-operative complications and prognosis between the RPD group and the overlap group. RPD group showed a significant advantage in terms of the distance between the top border of tumours and the top resection margin (P < 0.001). We further found that the oesophageal lateral negative surgical margin distance of the upper gastric cancer in the RPD group was significantly longer than that in the overlap group (P < 0.001). CONCLUSIONS: Both the RPD and overlap techniques are safe and applicable in LTG. However, RPD has the advantage of obtaining an adequate safe margin compared with that of overlap technique, especially in patients with gastro-oesophageal junction carcinoma.

PRMT3 promotes tumorigenesis by methylating and stabilizing HIF1α in colorectal cancer.

Abnormal angiogenesis occurs during the growth of solid tumors resulting in increased vascular permeability to fluids and metastatic cancer cells. Anti-angiogenesis therapy for solid tumors is effective in the treatment of cancer patients. However, the efficacy of anti-angiogenesis therapy is limited by drug resistance. The findings of the current study showed that HIF1α R282 is methylated by PRMT3, which is necessary for its stabilization and oncogene function. Analysis showed that PRMT3-mediated tumorigenesis is HIF1α methylation-dependent. A novel therapeutic molecule (MPG-peptide) was used to inhibit HIF1α expression. These findings provided information on PRMT3 signaling pathway and HIF1/VEGFA signaling pathway and offer a novel therapeutic strategy for colorectal cancer, mainly for treatment of anti-angiogenesis resistance patients.

Plumbagin inhibits tumor angiogenesis of gastric carcinoma in mice by modulating nuclear factor-kappa B pathway.

BACKGROUND: We aimed to determine the mechanism of plumbagin on tumor growth of gastric carcinoma. METHODS: Sixty BALB/c mice were treated with 200 µL SGC-7901 cells to establish gastric carcinoma xenograft and randomly divided into four groups: model group, low dose of plumbagin group (2 mg/kg), medium dose of plumbagin group (4 mg/kg) and high dose of plumbagin group (6 mg/kg). The tumor volume and weight were measured every week, and the ratio of anti-tumor was analyzed. The contents of vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR2) in serum and tumor tissues were tested by enzyme linked immunosorbent assay (ELISA), immunohistochemistry and Western blot, respectively. The microvessel density (MVD) in tumor tissues was evaluated by immunohistochemistry and Western blot. The levels of nuclear factor-kappa B (NF-κB) p-p65/NF-κB p65, p-inhibitor of NF-κB (IκB)α/IKBα, p-IκB kinase (IKK)/IKK in tumor tissues were also analyzed by Western blot. RESULTS: Compared with model group, plumbagin treatment significantly suppressed the growth of tumor (P<0.05). The inhibition rate was 50.32% in high dose group (6 mg/kg). Furthermore, we found that the expressions of VEGF, VEGRF2 and MVD were obviously decreased in plumbagin treatment groups when compared to model group (P<0.05). Importantly, plumbagin treatment could down-regulate the levels of NF-κB p-p65/NF-κB p65, p-IKK/IKK and p-IKBα/IKBα in tumor tissues. CONCLUSIONS: Our study indicated that plumbagin might be an effective drug in inhibiting the tumor angiogenesis of gastric cancer and the mechanism of anti-tumor may be associated with NF-κB pathway.