Randomized trial of umbilical incisional hernia in high-risk patients: extraction of gallbladder through subxiphoid port vs. umbilical port after laparoscopic cholecystectomy.

INTRODUCTION: Trocar site incisional hernia (TSIH) is one of the most common complications of laparoscopic surgery. Using the umbilical port as a common hole for removing the gallbladder in laparoscopic cholecystectomy is more likely to lead to TSIH than other ports. Thus, extracting the gallbladder through other ports may reduce the incidence of TSIH. AIM: To ascertain whether extraction of the gallbladder through the subxiphoid port is more beneficial for reducing umbilical incisional hernia than the umbilical port. MATERIAL AND METHODS: From April 2014 to March 2017, a randomized clinical trial was conducted among patients with high risk of incisional hernia and accepted for three-port laparoscopic cholecystectomy (TLC) in our department. 182 patients with indications of cholecystectomy were allocated randomly to group A (subxiphoid port) and group B (umbilical port). Data collection was carried out on operative time, postoperative pain, hospital stay, wound infection and TSIH in the early postoperative course, and at 1, 10, and 24 months after surgery. RESULTS: The incidence of TSIH in group A was lower than that in group B (4.9% vs. 14.6%; odds ratio = 8.02; 95% CI: 2.15-47.6; p < 0.001). The mean operative time of group A was significantly shorter than that of group B (35 ±15.16 min vs. 42 ±14.58 min, p < 0.01). There was no significant difference in wound infection rate between group A and group B (p = 0.068). The data of hospital stay (p = 0.428) and postoperative pain (p = 0.349) of all analyzed patients were similar in the two groups. CONCLUSIONS: Extraction of the gallbladder through the subxiphoid port can reduce umbilical incisional hernia in high-risk patients effectively.

MEK1 expression and its relationship with clinical pathological features in hepatocellular carcinoma.

BACKGROUND: MEK1 is overexpressed in various human carcinomas, but the role of MEK1 is not well unknown in hepatocellular carcinoma (HCC). In the present study, we aimed to explore MEK1 expression of in HCC tissues, and to evaluate its relationship with clinical pathological features. METHODS: Expressions of MEK1 were detected by western blot assay, real-time quantitative PCR and immunohistochemical (IHC) staining in 30 HCC tissues and their adjacent normal tissues. Pearson Chi-square test was used to analyze the relationship between MEK1 expression and clinical pathological features. The survival curve was drawn by Kaplan-Meier method, and survival was analyzed by Lon-rank test. RESULTS: The expression of MEK1 mRNA in HCC tissues was significantly higher than that in adjacent normal tissues and so was the expression of MEK1 protein. In the 30 specimens, 70% was with Tumor/Normal ratio > 2, 10% with Tumor/Normal ratio < 1 and 20% with 1 < Tumor/Normal ratio < 2. The mean survival time in high MEK1 expression group was significantly lower than that in low MEK1 expression group (Log-rank value = 11.946, P < 0.01). CONCLUSION: MEK1 expressions in HCC tissues were significantly higher than that in adjacent normal tissues, which indicated that MEK1 was involved in the genesis and development of HCC. Moreover, it was closely related to the postoperative survival time of patients with HCC.

MicroRNA-29a inhibits cell migration and invasion via targeting Roundabout homolog 1 in gastric cancer cells.

Deregulation of Roundabout homolog 1 (Robo1) has been demonstrated to be associated with several types of human cancer, including gastric cancer. However, the detailed role of Robo1 and its regulatory mechanism in gastric cancer remain largely unclear. In the current study, it was demonstrated that the expression of microRNA (miR)­29a was frequently reduced in gastric cancer tissues, compared with their matched normal adjacent tissues. Similar results were additionally observed in AGS and SGC­7901 human gastric cancer cells. Overexpression of miR­29a led to reduced migration and invasion of AGS cells. To explore the targets of miR­29a in gastric cancer, bioinformatics analysis was conducted and Robo1 was identified as a putative target of miR­29a. Further western blotting and luciferase activity assay data confirmed that miR­29a was able to negatively regulate the protein expression of Robo1, through directly binding to the 3'­untranslated region of Robo1 mRNA in gastric cancer cells. In addition, it was demonstrated that Robo1 was frequently upregulated in gastric cancer tissues compared with their matched adjacent normal tissues, and a significant inverse correlation was identified between miR­29a and Robo1 expression. In addition, knockdown of Robo1 by small interfering RNA markedly inhibited the migratory and invasive capabilities of AGS cells, which the results obtained with overexpression of miR­29a. In conclusion, to the best of our knowledge the current study suggested for the first time, that miR­29a inhibits migration and invasion in part via direct inhibition of Robo1 in gastric cancer cells. Therefore, Robo1 and miR­29a may serve as diagnostic or therapeutic targets for gastric cancer.

Do patients with pN0 gastric cancer benefit from prophylactic extended lymphadenectomy?

PURPOSE: To investigate the impact of prophylactic extended lymphadenectomy on survival for patients with node-negative (pN0) advanced gastric cancer according to the extent of lymph node dissection. METHODS: This study retrospectively investigated the clinicopathological characteristics and prognostic outcomes of 458 patients who had pN0 advanced gastric cancer between 1995 and 2001. Postoperative survival was compared in patients who underwent different extents of prophylactic lymphadenectomy. RESULTS: The overall 5-year and 10-year survival rates were 62.01% (284/458) and 40.83% (187/458), respectively. The survival rates differed significantly in patients who underwent a different extent of prophylactic lymphadenectomy (≤D1+ versus D2 versus D3 versus ≥D3) (X(2) = 8.59, P = 0.035). Survival in patients who received less than D1+ dissection, however, were not significantly better than patients who received D2 dissection (X(2) = 0.907, P = 0.341). Survival in patients who received D2 dissection was significantly better than survival in patients who received D3 dissection (X(2) = 5.685, P = 0.017). No differences in postoperative survival rates were observed between patients who received D3 dissection and those received more than D3 dissection (X(2) = 2.468, P = 0.116). Patients who were older than 60 years and receive more than D2 dissection experienced significantly worse postoperative survival than those who received less than D2 dissection (X(2) = 14.885, P = 0.001). The extent of prophylactic lymphadenectomy did not significantly affect local tumor recurrence in patients with node-negative advanced gastric cancer (X(2) = 0.458, P = 0.928). CONCLUSIONS: D2 prophylactic lymphadenectomy is appropriate for pN0 patients who were less than 60 years old, and less than D2 dissection was suitable for the older cases.

Comparison of the multi-drug resistant human hepatocellular carcinoma cell line Bel-7402/ADM model established by three methods.

BACKGROUND: To compare the biological characteristics of three types of human hepatocellular carcinoma multi-drug resistant cell sub-lines Bel-7402/ADM models established by three methods. METHODS: Established human hepatocellular carcinoma adriamycin (ADM) multi-drug resistant cell sub-lines models Bel-7402/ADMV, Bel-7402/ADML and Bel-7402/ADMS by three methods of in vitro concentration gradient increased induction, nude mice liver-implanted induction and subcutaneous-implanted induction respectively. Phase contrast microscopy was used to observe the cells and the MTT (methyl thiazolyl tetrazolium) method was used to detect drug resistance of the three different sub-lines of cells. RESULTS: The three groups of drug resistant cells, Bel-7402/ADMV, Bel-7402/ADML and Bel-7402/ADMS generated cross-resistance to ADM and CDDP (cis-Diaminedichloroplatinum), but showed a significant difference in resistance to Bel-7402 IC50 value (P < 0.01). The doubling times were significantly extended compared to the parent cell line (39 h) and were 65 h (Bel-7402/ADMV), 46 h (Bel-7402/ADML), and 45 h (Bel-7402/ADMS). The excretion rates of ADM were significantly increased compared with the parent cell (34.14%) line and were 81.06% (Bel-7402/ADMV), 66.56% (Bel-7402/ADML) and 61.56% (Bel-7402/ADMS). Expression of P-gp and MRP in the three groups of resistant cells was significantly enhanced (P < 0.01). There was no significant variation in the expression of GSH/GST (P > 0.05). CONCLUSIONS: Stable resistance was involved in the resistant cell line model established by the above three methods. Liver implantation was a good simulation of human hepatocellular and proved to be an ideal model with characteristics similar to human hepatocellular biology and the pharmacokinetics of anticancer drugs.