Role of Gut Microbiota in the Development and Treatment of Colorectal Cancer.

Human guts harbor abundant microbes that regulate many aspects of host physiology. However, bacterial imbalance or dysbiosis in the gut due to the dietary or environmental changes may cause colorectal cancer (CRC). Increasing studies show that gut microbiota plays an important role in the occurrence and development of CRC, as a result of virulence factors, bacterial metabolites, or inflammatory pathways. In the future, probiotics or targeting the microbiota will probably be a powerful weapon in the battle against CRC. This review seeks to outline the relationship between gut microbiota and the development of CRC as well as the potential mechanisms of microbiota involved in treatment of CRC, so as to provide some references for research on the development, prevention, and treatment of this disease.

Defunctioning cannula ileostomy after lower anterior resection of rectal cancer.

BACKGROUND AND OBJECTIVE: Most surgeons suggest the use of fecal diversion in patients undergoing low anterior resections of rectal tumors at high risk for anastomotic leakage. We describe an exploratory study to evaluate the efficacy and safety of a new diversion method called a spontaneously closing cannula ileostomy, which was designed to protect rectal anastomoses in patients at high risk for anastomotic leakage. The outcomes of patients treated with cannula ileostomy were compared to those of patients treated with loop ileostomy. MAIN OUTCOME MEASURES: Outcomes included the rates of anastomotic leakage, reoperation and other complications, as well as length of hospital stay and cost. DESIGN AND PATIENTS: From January 2011 to December 2012, 294 patients undergoing low colorectal or coloanal anastomosis were treated with ileum diversion using cannula ileostomy or traditional loop ileostomy. Demographics, clinical features, and operational data were recorded. RESULTS: The anastomotic leakage rates were 8.1% (12/149) in the cannula ileostomy group and 8.3% (12/145) in the loop ileostomy group (p = 1.0). The reoperation rate was 3% (4/149) in patients treated with a cannula ileostomy and 3.4% (5/145) in those who underwent a loop ileostomy (p = 0.75). The median length of the hospital stay was 8.6 days in the cannula ileostomy group and 17.1 days (p < 0.01) in the loop ileostomy group, including time for the initial and reversal operations. In the cannula ileostomy group, the median time to defecation from the anus was 16.5 days after the operation. During the follow-up period, 13 patients in the loop ileostomy group retained their stoma, as compared to 2 in the cannula ileostomy group (p < 0.01). LIMITATIONS: This study was a nonrandomized design and lacked contrast enema data to identify anastomotic leaks. CONCLUSIONS: Cannula ileostomy is a safe and effective diverting technique that protects low colorectal and coloanal anastomoses. Patients receiving a cannula ileostomy had shorter hospital stays and lower rates of permanent stoma than those receiving a loop ileostomy.

Honokiol augments the anti-cancer effects of oxaliplatin in colon cancer cells.

Oxaliplatin is an important drug in the chemotherapy of colorectal carcinoma, but its toxicity, especially dose-related neurosensory toxicity, is not well tolerated. In this study, we investigated whether honokiol could augment the anti-tumor effect of oxaliplatin in colon cancer HT-29 cells in vitro and whether honokiol could be used with oxaliplatin to decrease oxaliplatin dose. We used the normal colon cells, human colonic epithelial cells (HCoEpiCs) as control cells. Cell proliferation, apoptosis, prostaglandin E2 (PGE2) and vascular endothelial growth factor (VEGF) levels were also investigated. Expression levels of cyclo-oxygenase 2 (COX-2), VEGF, AKT/p-AKT, extracellular signal-related kinase (ERK)1/2/p-ERK1/2, nuclear factor kappa B (NF-κB) P65/p-P65, and caspase-3 were measured. Honokiol or oxaliplatin suppressed the proliferation of HT-29 cells in a concentration-dependent manner, but only high concentrations of honokiol would suppress the proliferation of HCoEpiCs. HT-29 cells were more sensitive to oxaliplatin treatment in the presence of honokiol. Oxaliplatin combined with honokiol improved the apoptosis rate of HT-29 cell and reduced PGE2 and VEGF secretion levels. Expression levels of COX-2 and VEGF protein and phosphorylation of AKT, ERK1/2, and NF-κB P65 were also inhibited. Caspase-3 levels were upregulated after honokiol treatment. Therefore, honokiol can be used in combination with oxaliplatin in the chemotherapy of colon cancer. This combination allows a reduction in oxaliplatin dose, and thereby reduces its adverse effects. It may also enhance the chemotherapeutic effect of oxaliplatin for this disease.