Conclusion
This review highlights the many mechanisms whereby colorectal cancer induces immune suppression and how this relates to clinical prognosis (see Figure 2). Suppression begins at a molecular and cellular level and can result in a fundamental shift in immune function detectable in the systemic circulation. It is apparent that tumours use many different strategies to escape host immune responses and create an environment in which tumour cells can survive and proliferate. Here, we argue that the many mechanisms deployed strongly suggest that the immune system is capable of being very effective in containing colorectal tumours. Moreover, randomized-clinical trials have reported significant clinical benefits for an autologous cell-based vaccine[19,20] and preoperative cytokine protocols have also been reported to make a significant difference.[28,29] We therefore propose that the case for further studies with cancer vaccine and other immunotherapy candidates is overwhelming for Dukes' B disease and should be incorporated with standard adjuvant therapies for more advanced disease. Of note is the fact that current adjuvant regimens are remarkably non-immunosuppressive and would therefore be ideal for combination studies.[214]
Potential changes to host immunity caused by colorectal cancer that result in poor prognosis. DC, dendritic cell; NK, natural killer; TGF, transforming growth factor; IL, interleukin; VEGF, vascular endothelial growth factor; COX, cyclo-oxygenase.
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This review has been supported by Cancer Vaccine Institute, Celgene and Fischer Family Trust.
Prof. D. Kumar, Colorectal Surgery Unit, St James Wing (Level III), St George's Hospital, Blackshaw Road, London SW17 0QT, UK. E-mail: dkumar@sgul.ac.uk
Aliment Pharmacol Ther. 2006;24(8):1163-1177. © 2006 Blackwell Publishing
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