Background. Robotic surgery has been recently used as a novel tool for rectal surgery. This study assessed the current evidence regarding the efficiency, safety, and potential advantages of robotic rectal surgery (RRS) compared with laparoscopic rectal surgery (LRS). Methods. We comprehensively searched PubMed, Embase, and the Cochrane Library databases and performed a systematic review and cumulative meta-analysis of all randomized controlled trials (RCTs) assessing the 2 approaches. Results. Seven RCTs including a total of 1022 cases were identified. The conversion rate is significantly lower for RRS (odds ratio: 0.29; 95% confidence interval: 0.09 to 0.96; P = .04). The length of the distal margin was significantly shorter in the LRS group than in the RRS group (weighted mean difference: 0.60; 95% confidence interval: 0.09 to 1.10; P = .02). Perioperative complication rates, harvested lymph nodes, positive circumferential resection margins, complete total mesorectal excision, first flatus, and length of stay did not differ significantly between approaches ( P > .05). Conclusions. This meta-analysis indicates that RRS is a safe and effective approach. It is not inferior to LRS in terms of oncologic outcomes and postoperative complications. Future large-volume, well-designed RCTs with extensive follow-up are awaited to confirm and update the findings of this analysis.

The serine threonine kinase Akt1 has been implicated in the control of cellular metabolism, survival and growth. Herein, disruption of the ubiquitously expressed member of the Akt family of genes, Akt1, in the mouse, demonstrates a requirement for Akt1 in miRNA-mediated cellular apoptosis. The miR-17/20 cluster is known to inhibit breast cancer cellular proliferation through G1/S cell cycle arrest via binding to the cyclin D1 3'UTR. Here we show that miR-17/20 overexpression sensitizes cells to apoptosis induced by either Doxorubicin or UV irradiation in MCF-7 cells via Akt1. miR-17/20 mediates apoptosis via increased p53 expression which promotes Akt degradation. Akt1 −/− mammary epithelial cells which express Akt2 and Akt3 demonstrated increased apoptosis to DNA damaging agents. Akt1 deficiency abolished the miR-17/20-mediated apoptosis. These results demonstrated a novel pathway through which miR17/20 regulate p53 and Akt controlling breast cancer cell apoptosis.

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Genome-wide association studies (GWAS) have reported a number of loci harboring common variants that influence risk of colorectal cancer (CRC) in European descent. But all the SNPs identified explained a small fraction of total heritability. To identify more genetic factors that modify the risk of CRC, especially Chinese Han specific, we conducted a three-stage GWAS including a screening stage (932 CRC cases and 966 controls) and two independent validations (Stage 2: 1,759 CRC cases and 1,875 controls; Stage 3: 943 CRC cases and 1,838 controls). In the combined analyses, we discovered two novel loci associated with CRC: rs12522693 at 5q23.3 (CDC42SE2-CHSY3, OR = 1.31, P = 2.08 × 10−8) and rs17836917 at 17q12 (ASIC2-CCL2, OR = 0.75, P = 4.55 × 10−8). Additionally, we confirmed two previously reported risk loci, rs6983267 at 8q24.21 (OR = 1.17, P = 7.17 × 10−7) and rs10795668 at 10p14 (OR = 0.86, P = 2.96 × 10−6) in our cohorts. These results bring further insights into the CRC susceptibility and advance our understanding on etiology of CRC.