The functions of, and interactions between, the innate and adaptive immune systems are vital for anticancer immunity. Cytotoxic T cells expressing cell-surface CD8 are the most powerful effectors in the anticancer immune response and form the backbone of current successful cancer immunotherapies. Immune-checkpoint inhibitors are designed to target immune-inhibitory receptors that function to regulate the immune response, whereas adoptive cell-transfer therapies use CD8+ T cells with genetically modified receptors—chimaeric antigen receptors—to specify and enhance CD8+ T-cell functionality. New generations of cytotoxic T cells with genetically modified or synthetic receptors are being developed and evaluated in clinical trials. Furthermore, combinatory regimens might optimise treatment effects and reduce adverse events. This review summarises advances in research on the most prominent immune effectors in cancer and cancer immunotherapy, cytotoxic T cells, and discusses possible implications for future cancer treatment.

Multimodal rehabilitation prevents reduction in lean body mass, pulmonary function, oxygenation and cardiovascular response to exercise after colonic surgery.

Irritable bowel syndrome is a common functional gastrointestinal disorder and it is now evident that irritable bowel syndrome is a multi-factorial complex of changes in microbiota and immunology. The bidirectional neurohumoral integrated communication between the microbiota and the autonomous nervous system is called the gut-brain-axis, which integrates brain and GI functions, such as gut motility, appetite and weight. The gut-brain-axis has a central function in the perpetuation of irritable bowel syndrome and the microbiota plays a critical role. The purpose of this article is to review recent research concerning the epidemiology of irritable bowel syndrome, influence of microbiota, probiota, gut-brainaxis, and possible treatment modalities on irritable bowel syndrome. The integrated actions and communication between the microbiota and the autonomous nervous system are central players in the perpetuation of IBS symptoms. This signaling pathway is called the GutBrain Axis (GBA). The GBA is a bidirectional neurohumoral communication system that integrates brain and GI functions, such as gut motility, appetite and weightand here the microbiota plays a critical role. 2Changes in gastrointestinal or central nervous system physiology may result in an altered habitat, which again may cause changes in the composition of the microbiota.Disruption of the physiologic symbiotic relationship (eubiosis) between the human host and the microbiota is called dysbiosis and is regarded a basic factor for initiating and maintaining IBS in the majority of patients. Current evidence has suggested that the dysbiosis observed in IBS and the resulting immunological response may drive and perpetuate gastrointestinal symptoms of IBS suggesting that IBS is in fact a disorder of the microbiota and the GBA. It is unclear whether the initiating factor is brain abnormalities that drive the gut changes or if changes in the gut alter brain function through vagal and sympathetic pathways.3,4 The purpose of this article is to review recent research concerning the influence of microbiota and gut-brain-axis on IBS. IBSIt is estimated that approximately 10% of the World population and 15% of the population in the Western World suffer from IBS characterized by a mixture of recurrent abdominal pain, bloating, changing stool consistency such as diarrhea (IBS-D), constipation (IBS-C), or interchanging diarrhea and constipation (mixed-type or IBS-M), mucus secretion, and nausea. 5,6 Community-based data indicate that IBS-M is the most prevalent type followed by IBS-D and IBS-C and that switching among subtypes occurs. Bloating is the most prevalent symptom reported by 96% of patients with IBS of whatever subgroup. 7 In addition to abdominal symptoms, poor sleep, headache, CONTACT Hans Raskov raskov@mail.dk Lundevangsvej 23, DK-2900 Hellerup, Denmark. Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/kgmi.

Colorectal cancer (CRC) is a very common malignancy in the Western World and despite advances in surgery, chemotherapy and screening, it is still the second leading cause of cancer deaths in this part of the world. Numerous factors are found important in the development of CRC including colonocyte metabolism, high risk luminal environment, inflammation, as well as lifestyle factors such as diet, tobacco, and alcohol consumption. In recent years focus has turned towards the genetics and molecular biology of CRC and several interesting and promising correlations and pathways have been discovered. The major genetic pathways of CRC are the Chromosome Instability Pathway representing the pathway of sporadic CRC through the K-ras, APC, and P53 mutations, and the Microsatellite Instability Pathway representing the pathway of hereditary non-polyposis colon cancer through mutations in mismatch repair genes. To identify early cancers, screening programs have been initiated, and the leading strategy has been the use of faecal occult blood testing followed by colonoscopy in positive cases. Regarding the treatment of colorectal cancer, significant advances have been made in the recent decade. The molecular targets of CRC include at least two important cell surface receptors: the epidermal growth factor receptor and the vascular endothelial growth factor receptor. The genetic and molecular knowledge of CRC has widen the scientific and clinical perspectives of diagnosing and treatment. However, despite significant advances in the understanding and treatment of CRC, results from targeted therapy are still not convincing. Future studies will determine the role for this new treatment modality.

Background: Molecular markers for localized colon tumours and for prognosis following therapy are needed. Proteomics research is currently producing numerous biomarker studies with clinical potential. We investigate the protein composition of plasma and of tumour extracts with the aim of identifying biomarkers for colon cancer.