Laparoscopic ventral rectopexy is a safe operation. Mesh erosion rates are 2% and occasionally require resectional surgery that might be reduced by the use of biological graft. An international ventral mesh registry is recommended to monitor mesh problems and to assess whether type of mesh has any impact on functional outcomes or the need for revisional surgery for nonerosion problems.

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Summary Background Advances in immunology and molecular biology have shown that colorectal cancer is potentially immunogenic and that host immune responses influence survival. However, immune surveillance and activation is frequently ineffective in preventing and/or controlling tumour growth. Aim To discuss potential ways in which colorectal cancer induces immune suppression, its effect upon prognosis and avenues for therapeutic development. Method A literature review was undertaken for evidence of colorectal cancer‐induced immune suppression using PubMed and Medline searches. Further studies were identified from the reference lists of identified papers. Results Immune suppression occurs at a molecular and cellular level and can result in a shift from cellular to humoral immunity. Several mechanisms for immune suppression have been described affecting innate and adaptive immunity with suppression linked to poorer clinical outcome. Conclusions Colorectal cancer causes direct inhibition of the host's immune response with a detrimental effect upon prognosis. Immunotherapy offers a therapeutic strategy to counteract these effects with promising results seen particularly in precancerous conditions and early tumours. This review strongly suggests that immunotherapy should be incorporated into adjuvant therapeutic trials for stage 2 tumours and be considered as adjuvant treatment in conjunction with standard chemotherapy regimes for advanced disease.

Colorectal cancer development is associated with a shift in host immunity with suppression of the cell-mediated immune system (CMI) and a predominance of humoral immunity (HI). Tumour progression is also associated with increased rates of cell proliferation and apoptosis. The aim of this study was to investigate whether these factors correlate and have an influence upon prognosis. Longterm follow-up was performed on 40 patients with colorectal cancer who had levels of tumour necrosis factor (TNF)-a, interferon (IFN)-g and interleukin (IL)-10 measured from stimulated blood cultures before surgery. Their archived tumour specimens were analysed to determine a Ki-67-derived proliferation index (PI) and a M30-derived apoptosis index (AI). Tumour necrosis factor-a levels negatively correlated to tumour proliferation (r ¼ À0.697, P ¼ 0.01). Interleukin-10 levels had a positive correlation with tumour proliferation (r ¼ 0.452, P ¼ 0.05) and apoptosis (r ¼ 0.587, P ¼ 0.01). Patient survival correlates to tumour pathological stage (P ¼ 0.0038) and vascular invasion (P ¼ 0.0014). An AIp0.6% and TNF-a levels X8148 pg ml À1 correlate to improved survival (P ¼ 0.032, P ¼ 0.021). Tumour proliferation and apoptosis correlate to progressive suppression of the CMI-associated cytokine TNFa and to and higher levels of IL-10. Survival is dependent upon the histological stage of the tumour, vascular invasion, rates of apoptosis and proliferation and systemic immunity which are all interconnected.