Objective To investigate the role of PPAR? in the pathogenesis of colorectal cancer. Methods Literatures about PPAR? and the pathogenesis of colorectal cancer were reviewed and analyzed.Results PPAR? is expressed in the nucleuses of glandular epithelia lining colon and rectum. It is normally suppressed by wild-type adenomatous polyposis coli (APC) but is up-regulated by enhanced ?-catenin/T cell factor-4 (TCF-4) binding to TCF-4-responsive elements in the PPAR promoter when an inactivating APC mutation occurs, which indicates PPAR is a potential downstream target of the APC/?-catenin/TCF-4 signaling pathway in colorectal cancer. Consistent with PPAR’s role as an APC/?-catenin/TCF-4 target, some studies reported that PPAR mRNA is frequently overexpressed in colorectal cancers of both humans and rodent animals, which indicates that PPAR is relevant to the tumorigenesis of colorectal cancer. Conclusion PPAR? is closely related with the pathogenesis of colorectal cancer.

The incidence of esophagogastric junction cancer (EGJC) is rising dramatically both in western countries and in China.For type Ⅱ EGJC,controversies over the optimal surgical approach still remain.More and more studies support the abdominal transhiatial extended gastrectomy to be superior to the abdominothoracic combined approach.The aim of this report is to evaluate the feasibility and safety of laparoscopic transabdominal hiatal extended gastrectomy for surgical treatment of type Ⅱ and Ⅲ esophagogastric junction cancer.Based on clinical experience of 95 patients who underwent laparoscopic tansabdominal hiatal extended gastrectomy,we conclude that laparoscopic transabdominal hiatal extended gastrectomy is feasible and safe,offering a safer and simpler way of intramediastinal dissection and digestive tract reconstruction at experienced hands as compared with open surgery.This procedure also offers the merit of longer esophageal resection length without entering the pleural cavity.

OBJECTIVETo assess the feasibility of laparoscopic total mesorectal excision (TME) for low or ultralow anterior resection of rectal cancer.

METHODSExcision of the mesorectum and low (ultralow) colo-anal anastomoses were performed laparoscopically in 62 patients with low rectal cancer based on the concept of TME and double stapling technique (DST).

RESULTSSixty-two operations with TME and DST were performed in a totally laparoscopic manner, and only one was converted to open procedures because of dysfunction of coagulation. The operative time was 125 min (110-210 min) and the operative blood loss 20 ml (5-80 ml). The time for bowel function recovery and post-operatively dietary intake was 1-2 days. Twenty-eight patients received postoperative analgesics. Average hospital stay was 8 days (5-14 days). Complications were observed in only 2 of the 62 patients, one had suffered from urinary retention and the other, anastomotic leakage.

CONCLUSIONSTotally laparoscopic excision of the mesorectum for low or ultralow anterior resection of rectal cancer is a minimally invasive technique with sphincter preservation, less postoperative pain, and rapid recovery.

Adult ; Aged ; Aged, 80 and over ; Anal Canal ; surgery ; Anastomosis, Surgical ; methods ; Colon ; surgery ; Female ; Humans ; Laparoscopy ; Male ; Middle Aged ; Rectal Neoplasms ; surgery ; Treatment Outcome

OBJECTIVETo observe the effect of activation of Notch1 signaling pathway by Notch intracellular domain (NICD) plasmid transfection on pancreatic cancer cell proliferation and explore the underlying mechanism.

METHODSThe transfection rates were observed under microscope with fluorescence stimulation, and mRNA expression levels of Hes1 were detected by real-time PCR. Cell proliferation changes were evaluated by CCK-8 after NICD and control plasmid transfection in pancreatic cancer cells. Caspase 3 activity was examined using a caspase 3 detection kit.

RESULTSThe transfection rates of NICD plasmid were up to 80% by fluorescence stimulation observation. Hes1 expression was significantly increased after NICD plasmid transfection, suggesting the activation of Notch1 signaling pathway. NICD plasmid transfection significantly promoted cancer cell proliferation compared to control plasmid transfeciton. The activities of caspase 3 were obviously decreased after NICD plasmid transfection in 3 pancreatic cancer cell lines.

CONCLUSIONActivation of Notch1 signaling pathway by NICD plasmid transfection can promote the proliferation of pancreatic cancer cells by inhibiting the apoptosis pathway.

Apoptosis ; Basic Helix-Loop-Helix Transcription Factors ; metabolism ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Homeodomain Proteins ; metabolism ; Humans ; Pancreatic Neoplasms ; metabolism ; pathology ; Plasmids ; Receptor, Notch1 ; genetics ; metabolism ; Signal Transduction ; Transcription Factor HES-1 ; Transfection

Objective To observe the effect of activation of Notch1 signaling pathway by Notch intracellular domain (NICD) plasmid transfection on pancreatic cancer cell proliferation and explore the underlying mechanism. Methods The transfection rates were observed under microscope with fluorescence stimulation, and mRNA expression levels of Hes1 were detected by real-time PCR. Cell proliferation changes were evaluated by CCK-8 after NICD and control plasmid transfection in pancreatic cancer cells. Caspase 3 activity was examined using a caspase 3 detection kit. Results The transfection rates of NICD plasmid were up to 80% by fluorescence stimulation observation. Hes1 expression was significantly increased after NICD plasmid transfection, suggesting the activation of Notch1 signaling pathway. NICD plasmid transfection significantly promoted cancer cell proliferation compared to control plasmid transfeciton. The activities of caspase 3 were obviously decreased after NICD plasmid transfection in 3 pancreatic cancer cell lines. Conclusions Activation of Notch1 signaling pathway by NICD plasmid transfection can promote the proliferation of pancreatic cancer cells by inhibiting the apoptosis pathway.

Objective To observe the effect of activation of Notch1 signaling pathway by Notch intracellular domain (NICD) plasmid transfection on pancreatic cancer cell proliferation and explore the underlying mechanism. Methods The transfection rates were observed under microscope with fluorescence stimulation, and mRNA expression levels of Hes1 were detected by real-time PCR. Cell proliferation changes were evaluated by CCK-8 after NICD and control plasmid transfection in pancreatic cancer cells. Caspase 3 activity was examined using a caspase 3 detection kit. Results The transfection rates of NICD plasmid were up to 80% by fluorescence stimulation observation. Hes1 expression was significantly increased after NICD plasmid transfection, suggesting the activation of Notch1 signaling pathway. NICD plasmid transfection significantly promoted cancer cell proliferation compared to control plasmid transfeciton. The activities of caspase 3 were obviously decreased after NICD plasmid transfection in 3 pancreatic cancer cell lines. Conclusions Activation of Notch1 signaling pathway by NICD plasmid transfection can promote the proliferation of pancreatic cancer cells by inhibiting the apoptosis pathway.