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Sun J.,Shanghai JiaoTong University | Sun J.,Shanghai Minimally Invasive Surgery Center | Jiang T.,Shanghai JiaoTong University | Qiu Z.,Shanghai JiaoTong University | And 7 more authors.
BMC Gastroenterology | Year: 2011

Background: Laparoscopic procedure is a rapid developed technique in colorectal surgery. In this investigation we aim at assessing the diversities of short-term and medium-term clinical outcomes of laparoscopic-assisted versus open surgery for colorectal cancer.Methods: A total number of 519 patients with non-metastatic colorectal cancer were enrolled for this study. The patients underwent either laparoscopic-assisted surgery (LAP) (n = 254) or open surgery (OP) (n = 265). Surgical techniques, perioperative managements and clinical follow-ups were standardized. Short-term perioperative data and medium-term recurrence and survival were compared and analyzed between the two groups.Results: There were no differences in perioperative parameters between the two groups except in regards to a trend of faster recovery in laparoscopic procedures. There was no statistically significant difference in postoperative complications, reoperation rate, or perioperative mortality. Statistically significant differences in a faster return of gastrointestinal function and shorter hospital stay were identified in favor of laparoscopic-assisted resection. In colon and rectal cancer cases separately, the overall survival, cancer-free survival and recurrence rate were similar in two groups. There was also no tendency of significant differences in overall survival, cancer-free survival and recurrence in stage I-II and stage III patients in two cancer categories between the two groups, respectively. pT, lymph node metastasis, and clinical stage were independent predictors of overall death risk, while pT, pN, lymph node metastasis and clinical stage were found to be the independent predictors of recurrence risk in enrolled patients database.Conclusions: Laparoscopic-assisted procedure has more benefits on postoperative recovery, while has the same effects on medium-term recurrence and survival compared with open surgery in the treatment of non-metastatic colorectal cancer. © 2011 Sun et al; licensee BioMed Central Ltd. Source


Qiu Z.,Shanghai JiaoTong University | Sun J.,Shanghai JiaoTong University | Sun J.,Shanghai Minimally Invasive Surgery Center | Pu Y.,Shanghai JiaoTong University | And 3 more authors.
World Journal of Surgery | Year: 2011

Background: Transumbilical single incision laparoscopic surgery (SILS) is a new laparoscopic procedure in which only one transumbilical incision is made, demonstrated as a scarless procedure. Here we report a single-center preliminary experience of transumbilical single incision laparoscopic cholecystectomy (SILC) in the treatment of benign gallbladder diseases, defining a single surgeon's learning curve. Methods: A total of 80 patients underwent SILC successfully by a single experienced laparoscopic surgeon. The operation was performed following the routine LC procedure. Then the perioperative demographics were recorded and the operative time was used to define the learning curve. Results: The study group included 27 male and 53 female patients with gallstones (56 cases), cholesterol polyps (16 cases), an adenomatous polyp (3 cases), adenomyomatosis (1 case), or complex diseases (4 cases), and all consented to undergo SILC. No patient was converted to normal LC or open surgery. There were no perioperative port-related or surgical complications. The average operative time was 46.9 ± 14.6 min. The average postoperative hospital stay was 1.8 ± 1.3 days. The learning curve of the SILC procedures for this series of selected patients confirmed that SILC is a feasible, safe, and effective approach to the treatment of benign gallbladder diseases. Conclusions: For experienced laparoscopic surgeons, SILC is an easy and safe procedure. Patients benefit from milder pain, a lower incidence of port-related complications, better cosmesis, and fast recovery. The SILC procedure may become another option for the treatment of benign gallbladder diseases for selected patients. © 2011 Société Internationale de Chirurgie. Source


Li L.-H.,Xiamen University | Luo Q.,Xiamen University | Zheng M.-H.,Shanghai JiaoTong University | Zheng M.-H.,Shanghai Institute of Digestive Surgery | And 10 more authors.
Oncology Reports | Year: 2012

P21-activated protein kinase (Pak1), a main downstream effector of small Rho GTPases, plays an important role in the regulation of cell morphogenesis, motility, mitosis and angiogenesis. However, the role of Pak1 in gastric cancer metastasis remains unclear. Here, we showed that Pak1 is overexpressed in gastric cancer tissues from 74 patients by immunohistochemistry. Overexpression of Pak1 was associated with metastasis and prognosis of gastric cancer. In addition, overexpression of Pak1 increased gastric cancer cell motility and invasion, whereas downregulation of Pak1 expression reduced gastric cancer cell migration and invasion. In further study, data showed that activated Pak1 inhibited stress fiber and focal adhesion complex formation in gastric cancer cells and led to the formation of motile phenotypes. Importantly, activated Pak1 elicited phosphorylation of the ERK and JNK-dependent pathway in gastric cancer cell lines. In conclusion, our results suggest that Pak1 is overexpressed in gastric cancer and plays an important role in the metastasis of gastric cancer. The mechanism by which Pak1 induces cancer metastasis may involve activation of ERK and JNK. Source


Feng B.,Shanghai JiaoTong University | Feng B.,Shanghai Institute of Digestive Surgery | Feng B.,Shanghai Minimally Invasive Surgery Center | Dong T.T.,Shandong University | And 11 more authors.
PLoS ONE | Year: 2012

MicroRNAs have been implicated in the regulation of several cellular signaling pathways of colorectal cancer (CRC) cells. Although emerging evidence proves that microRNA (miR)-106a is expressed highly in primary tumor and stool samples of CRC patients; whether or not miR-106a mediates cancer metastasis is unknown. We show here that miR-106a is highly expressed in metastatic CRC cells, and regulates cancer cell migration and invasion positively in vitro and in vivo. These phenotypes do not involve confounding influences on cancer cell proliferation. MiR-106a inhibits the expression of transforming growth factor-β receptor 2 (TGFBR2), leading to increased CRC cell migration and invasion. Importantly, miR-106a expression levels in primary CRCs are correlated with clinical cancer progression. These observations indicate that miR-106a inhibits the anti-metastatic target directly and results in CRC cell migration and invasion. © 2012 Feng et al. Source


Sun J.,Shanghai JiaoTong University | Sun J.,University of New South Wales | Sun J.,Shanghai Minimally Invasive Surgery Center | Zhang D.,University of New South Wales | And 11 more authors.
Carcinogenesis | Year: 2013

The metastasis suppressor, N-myc downstream regulated gene 1 (NDRG1), is negatively correlated with tumor progression in multiple neoplasms, being a promising new target for cancer treatment. However, the precise molecular effects of NDRG1 remain unclear. Herein, we summarize recent advances in understanding the impact of NDRG1 on cancer metastasis with emphasis on its interactions with the key oncogenic nuclear factor-kappaB, phosphatidylinositol-3 kinase/phosphorylated AKT/mammalian target of rapamycin and Ras/Raf/mitogenactivated protein kinase kinase/extracellular signal-regulated kinase signaling pathways. Recent studies demonstrating the inhibitory effects of NDRG1 on the epithelial-mesenchymal transition, a key initial step in metastasis, TGF-β pathway and the Wnt/β-catenin pathway are also described. Furthermore, NDRG1 was also demonstrated to regulate molecular motors in cancer cells, leading to inhibition of F-actin polymerization, stress fiber formation and subsequent reduction of cancer cell migration. Collectively, this review summarizes the underlying molecular mechanisms of the antimetastatic effects of NDRG1 in cancer cells. © The Author 2013. Published by Oxford University Press. All rights reserved. Source

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