Clinical Review ABC of colorectal cancer

Innovative treatment for colon cancer

BMJ 2000; 321 doi: https://doi.org/10.1136/bmj.321.7273.1397 (Published 02 December 2000) Cite this as: BMJ 2000;321:1397
  1. G A Chung Faye,
  2. D J Kerr

    Despite advances in treatment for colon cancer, the five year survival has not significantly altered over the past decade. Survival could improve in several key areas:

    Dietary modifications to reduce the incidence of colon cancer may be difficult to implement (dietary interventional studies have shown this to be the case for cardiovascular disease); the roles of screening, chemotherapy, and radiotherapy have been covered earlier in this series

    Use of non-steroidal anti-inflammatory drugs (NSAID) and relative risk of colorectal cancer

    • Preventive measures—such as diet and chemoprevention with agents such as non-steroidal anti-inflammatory drugs

    • Screening strategies—such as faecal occult blood testing and flexible sigmoidoscopy

    • Optimisation of current chemotherapy and radiotherapy regimens and the development of more effective antineoplastic agents

    • New therapeutic approaches—such as immunotherapy and gene therapy.

    This article will focus on prevention with non-steroidal anti-inflammatory drugs and on new strategies for treating colon cancer.

    Non-steroidal anti-inflammatory drugs

    Evidence strongly suggests a protective effect of non-steroidal anti-inflammatory drugs in colon cancer. Several cohort and case-control studies have consistently shown dose related reductions of colorectal cancer in regular users of these drugs. Furthermore, patients with familial adenomatous polyposis who took the non-steroidal anti-inflammatory sulindac had reductions in the number and size of their polyps. Gene knockout studies in mice suggest that inhibition of the cyclo-oxygenase type 2 pathway by non-steroidal anti-inflammatory drugs may be important in the mechanism of action.

    Cell mediated immunity against tumours. Tumour antigens are taken up and processed by antigen presenting cells (APC) and re-presented to class II receptors on T helper cells. This requires a costimulatory signal, B7, which binds to the CD28 ligand, causing T helper cell activation. This leads to secretion of cytokines, which in turn activates cytotoxic lymphocytes to bind to tumour cells via class I receptors and causes tumour lysis

    The only randomised controlled trial examining the …

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