Objective: The majority of patients with colorectal cancer are diagnosed with locally advanced and/or disseminated disease, and treatment options include surgery in combination with cytotoxic chemotherapy regimens, biologics, and/or radiotherapy. Thus, colorectal cancer remains a heavy burden on society and health care systems. Mounting evidence show that driver gene mutations play only part of the role in carcinogenesis. Epigenetics are strongly implicated in initiation and progression of colorectal cancer along with major players such as intestinal microbiotic dysbiosis and chronic mucosal inflammation. To assess phenotypic changes in proteins and gene expression, multigene expression signatures based on sequencing techniques have been developed to hopefully improve predictors of the tumor profile, immune response, and therapeutic outcomes. Our objective was to review current advances in the field and to update surgeons and academics on driver gene mutations and epigenetics in colorectal cancer. Background and methods: This is a narrative review studying relevant research published in the PUBMED database from 2012–2018. Results and conclusion: Increased understanding of the molecular biology will improve options to characterize colorectal cancer with regard to mutations and molecular pathways, including microsatellite instability, epigenetics, microbiota, and microenvironment. Research will inevitably improve risk group stratification and targeted treatment approaches. Epigenetic profiling and epigenetic modulating drugs will increase risk stratification, increase accessibility for DNA targeting chemotherapeutics and reduce cytotoxic drug resistance. New generation antibiotics such as biofilm inhibitors and quorum sensing inhibitors are being developed to target the carcinogenetic impact of colonic dysbiosis and inflammation.

Background: Mechanisms contributing to the perioperative stress response remain poorly understood. This study investigated changes in the amount of bacterial DNA in blood and the diversity of blood microbiota in the perioperative period in patients undergoing minimally invasive surgery for colonic cancer in an enhanced recovery after surgery setting. Methods: DNA encoding the bacterial 16S ribosomal RNA gene (16S rDNA) in whole blood obtained the day before surgery, and on postoperative day (POD) 1 and POD 10-14 was amplified and quantified by PCR before sequencing for taxonomic assignment. Richness, evenness and similarity measures were calculated to compare microbiota between days. Differences in relative abundance were analysed using the linear discriminant analysis effect size (LEfSe) algorithm. Results: Thirty patients were included between January and July 2016. The concentration of bacterial 16S rDNA in blood increased between the day before surgery and POD 1 (P = 0.025). Bacterial richness was lower on POD 10-14 than on the day before surgery and POD 1 (both P < 0⋅001). LEfSe analysis comparing the day before surgery and POD 10-14 identified changes in the abundance of several bacteria, including Fusobacterium nucleatum, which was relatively enriched on POD 10-14. Conclusion: These findings suggest that the blood of patients with colonic cancer harbours bacterial 16S rDNA, which increases in concentration after surgery.

BackgroundSeveral studies have shown a possible causal relationship between the occurrence of systemic in ammation in patients with malignant disease and increased risk of cardiovascular events. Our objective was to estimate the association between malignant disease and postoperative cardiovascular complications. Secondarily, we aimed to identify risk factors for postoperative cardiovascular complications. MethodsWe conducted a retrospective cohort study of all patients ≥ 18 years undergoing emergency laparotomy