Objective Because of local infiltrated growth and spread,the operative resection of hilar (cholangiocacinoma) is very difficult. Recently,combined extended hepatectomy and vascular resection had been performed for treatment of hilar cholangiocarcinoma and has greatly increased the resection rate and survival rate.However, it is associated with high operative morbidity and mortality. The aim of this study is to explore a reasonable hepatic resection strategy, that is safe and beneficial for the patient. Method Sixteen (consecutive) cases of hilar cholangiocarcinoma with involvement of hilar vessels have been treated in our hospital since 1977. En bloc resection of the hilar tumor that included hepatic segment I,IV and involved blood (vessel), as well as hepato-duodenal ligament skeletonization was performed in 15 patients. Results All 15 cases were successfully operated on with a resection rate of 93.8%, and 12 cases with R_0 resection. The operative mortality and in-hospital mortality rate were 0. Temporary bile leak and abdominal infection (respectively) developed in 1 patienteach,with an overall morbidity of 13.3%,and both were cured by non-(operative) therapy. No case of liver failure occurred. Follow up showed the median survival was 22 months and 7 are still alive. Conclusions (1)The resection rate and survival rate for hilar cholangiocarcinoma could be improved by combination of liver and hilar vascular resection.(2)Hilar cholangiocarcinoma mainly spreads to the medial segment(S4) and caudate(S1), and these segments need to be resected in the combined (operation).(3)Although resection of the middle part of liver takes little more time than hemi-hepatectomy and trisegmentectomy, it could preserve more liver parenchyma and reduce postoperative morbidity (such as liver failure) and mortality rates.(4)The resection of the hilar blood vessel involved by tumor was necessary to improve the resection rate and cure rate. Reconstruction of the blood vessel was made selectively by taking the circumstances into consideration.

OBJECTIVETo evaluate the oncologic safety and short-term outcomes of laparoscopic surgery in early and advanced rectal cancers.

METHODSClinical and follow-up data of 186 cases with rectal cancer undergoing laparoscopic radical resection from June 2009 to December 2013 were analyzed retrospectively, including 48 early rectal cancer (stage 0-I) and 138 advanced cancer (stage II-III). Thirty-seven cases with early rectal cancer and 275 with advanced cancer undergoing open radical surgery were selected as control group. Surgical safety, oncologic safety and short-term outcomes were compared between two groups.

RESULTSAs for either early or advanced rectal cancer, there were no significant differences in the number of harvested lymph nodes, length of distal resection margin, complication morbidity, rate of local recurrence, distant metastasis, and 3-year survival rate between the two groups (all P>0.05). Although the operation time was longer in laparoscopic group, the laparoscopic group presented less intra-operative blood loss, faster recovery of bowel function, and shorter postoperative hospital stay (all P<0.05). As for advanced rectal cancer, laparoscopic radical surgery tended to achieve less lymph nodes dissected (mean, 13.5 vs. 15.0) and develop more anastomotic leakage (8.0% vs. 5.5%) compared to open surgery, although neither reached statistical significance (P=0.112, P=0.221). Moreover, the conversion rate in patients with advanced rectal cancer was significantly higher than that in those with early cancer (10.9% vs 2.1%, P=0.048).

CONCLUSIONSLaparoscopic surgery can obtain the same oncologic and surgical safety for early rectal cancer as compared to open surgery. However, due to higher conversion rate, potential risk of decreased number of harvested lymph nodes and increased anastomotic leakage, laparoscopic surgery for advanced rectal cancer should be carried out prudently, especially in some hospitals with less laparoscopic experience.

Digestive System Surgical Procedures ; Humans ; Laparoscopy ; Lymph Nodes ; Neoplasm Staging ; Operative Time ; Rectal Neoplasms ; Retrospective Studies ; Safety ; Survival Rate

OBJECTIVETo investigate the effect of ASCT2 gene (glutamine transporter) knock-down by shRNA on biological behaviors of colorectal cancer cells.

METHODSshRNA was transfected into colorectal cancer cells Lovo and SW480 to knockdown ASCT2 mediated by Lipofectamine 2000. Reverse transcription-PCR and Western blot were used to examine the mRNA and protein expression of ASCT2. MTT and transwell assay were used to determine the proliferation and invasiveness of Lovo and SW480 cells. Radioactive-tracer was used to detect the uptake of glutamine.

RESULTSASCT2 mRNA and protein levels were significantly down-regulated by shRNA in Lovo and SW480 cells(P<0.01). MTT and transwell assays showed that ASCT2 knock-down could significantly inhibit the proliferation of Lovo and SW480 cells (A490) and decrease the number of invasive Lovo and SW480 cells from the membrane (both P<0.01). The number of membrane Lovo cells in shASCT group and control group was 46.3±5.9 and 197.7±9.1, respectively while the number of membrane SW480 cells in shASCT group and control group was 29.7±3.8 and 139.0±9.5, respectively. Radioactive-tracer showed that shASCT2 transfection could significantly reduce the uptake of glutamine, with an inhibition rate of 79.15% in Lovo and 67.22% in SW480 cells (both P<0.01).

CONCLUSIONSASCT2 plays an oncogenic role in colonic cancer, and its promotion mechanism may be associated with glutamine metabolism. ASCT2 may be a novel therapeutic target of colonic cancer.

Amino Acid Transport System ASC ; drug effects ; genetics ; physiology ; Cell Line, Tumor ; physiology ; Cell Proliferation ; genetics ; Colorectal Neoplasms ; genetics ; physiopathology ; Down-Regulation ; drug effects ; Gene Knockdown Techniques ; methods ; Glutamine ; drug effects ; genetics ; physiology ; Humans ; Minor Histocompatibility Antigens ; drug effects ; genetics ; physiology ; Neoplasm Invasiveness ; genetics ; physiopathology ; Oncogenes ; drug effects ; genetics ; RNA, Messenger ; physiology ; RNA, Small Interfering ; pharmacology ; Transfection