BackgroundThe impact of obesity on surgical outcomes after laparoscopic colorectal cancer resection in Chinese patients is still unclear.MethodsWe retrospectively reviewed the prospectively collected data from 527 consecutive colorectal cancer patients who under went laparoscopic resection from January 2008 to September 2013. Patients were categorized into three groups: nonobese (body mass index (BMI) <25.0 kg/m2), obese I (BMI 25.0 = to 29.9 kg/m2) and obese II (BMI ≥30.0 kg/m2). Clinical characteristics, surgical outcomes and postoperative complications were compared between nonobese, obese I and obese II patients.ResultsFrom among the 527 patients, there were 371 patients with in the nonobese group, 142 patients in the obese I group and 14 patients in the obese II group. The patients were well-matched for age, sex and American Society of Anesthesiologists class, except for BMI (P = 0.001). The median operative time correlated highly significantly with increasing weight (median: nonobese = 135 minutes, obese I = 145 minutes, obese II = 162.5 minutes; P = 0.001). There appeared to be a slight tendency toward grade III complications (rated according to the Clavien-Dindo Classification of Surgical Complications) in the obese II group, but this difference was not significant (nonobese = 5.1%, obese I = 3.5% and obese II = 14.3%; P = 0.178). None of the grade III complications which occurred in the obese II group were wound dehiscences that required a stitch. Other aspects, such as estimated blood loss, harvested lymph nodes, operation type, pathological results, conversion rate and overall postoperative complications, were not statistically significant.ConclusionWith sufficient experience, laparoscopic colorectal cancer surgery is feasible and safe in obese Chinese patients.

Transforming growth factor-β (TGF-β) regulates cell functions and has key roles in pancreatic cancer development. SMAD4, as one of the Smads family of signal transducer from TGF-β, mediates pancreatic cell proliferation and apoptosis and is specifically inactivated in half of advanced pancreatic cancers. In recent years, many advances concerning SMAD4 had tried to unravel the complex signaling mechanisms of TGF-β and its dual role of tumor-suppressive and tumor-promoting efforts in pancreatic cancer initiation and progression through SMAD4-dependent TGF-β signaling and SMAD4-independent TGF-β signaling pathways. Meanwhile, its potential prognostic value based on immunohistochemical expression in surgical sample was variably reported by several studies and short of a systematic analysis. This review aimed to discuss the structure, functions, and regulation of this principal protein and its effects in determining the progression and prognosis of pancreatic cancer.

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BackgroundAim to determine the clinicopathological and prognostic role of miR-301a-3p in pancreatic ductal adenocarcinoma(PDAC), to investigate the biological mechanism of miR-301a-3p in vitro and in vivo.MethodsBy tissue microarray analysis, we studied miR-301a-3p expression in PDAC patients and its clinicopathological correlations as well as prognostic significance. qRT-PCR was used to test miR-301a-3p expression in PDAC tissues and cell lines. Functional experiments including in vitro and in vivo were performed.ResultsSignificantly higher expression of miR-301a-3p were found in PDAC patients with lymph node metastasis and advanced pathological stages and identified as an independent prognostic factor for worse survival. In PDAC samples and cell lines, miR-301a-3p was significantly up-regulated compared with matched non-tumor tissues and normal pancreatic ductal cells, respectively. Overexpression of miR-301a-3p enhanced PDAC cells colony, invasion and migration abilities in vitro as well as tumorigenicity in vivo. Furthermore, SMAD4 was identified as a target gene of miR-301a-3p by cell as well as mice xenograft experiments. In PDAC tissue microarray, a significantly inverse correlation between miR-301a-3p ISH scores and SMAD4 IHC scores were observed in both tumor and corresponding non-tumor tissues.ConclusionMiR-301a-3p functions as a novel oncogene in PDAC and the oncogenic activity may involve its inhibition of the target gene SMAD4.