REDUCING RISK OF COLORECTAL CANCER

Prospects for preventing death from colorectal cancer are now more promising than even 10 years ago. To achieve this goal public health decisions have to be taken, and part of this decision process involves deciding at which point enough epidemiological evidence is available to change focus comfortably from information generation to health actions.
To turn research findings into public health strategies for controlling the incidence of and mortality from colorectal cancer requires a profound change of mentality in the epidemiological community. It is easy to say that more studies are needed, but they would be unlikely to alter existing conclusions. Moreover, the implementation of strategies to control cancer must be considered separately from research into the control of cancer.
One consequence of epidemiological research into the contribution of lifestyle factors to cancer risk has been to blame the individual who develops cancer. Smoking, alcohol, dietary imprudence, and exposure to sunlight tend to assign responsibility to the individual. The individual is often not principally responsible for decisions about factors that influence his or her risk of cancer, and society-including government

Cancers arising in colitis versus those in adenomas Important clinical and biological differences exist between the adenoma carcinoma sequence and ulcerative colitis associated neoplasia. Firstly, cancer in ulcerative colitis probably evolves from microscopic dysplasia with or without a mass lesion rather than from adenomas. Secondly, the time interval from the presence of adenoma to progression to carcinoma probably exceeds the interval separating ulcerative colitis associated dysplasia from ulcerative colitis associated neoplasia. Thirdly, patients with a family history of colorectal cancer (but not ulcerative colitis associated neoplasia) and who also have ulcerative colitis are at further increased risk, suggesting additive factors.

DNA and is often seen in many human primary tumours and premalignant conditions. It has been shown that aneuploid "fields" tend to populate the epithelium of patients with ulcerative colitis even in histologically benign colitis. These changes may occur initially in some cases by loss of one allele at a chromosomal locus (loss of heterozygosity) and may imply the presence of a tumour suppressor gene at that site. Loss of both alleles at a given locus (homozygous deletion) is an even stronger indicator of the existence of a tumour suppressor gene. Loss of heterozygosity occurs clonally in both the adenoma carcinoma sequence and ulcerative colitis associated neoplasia. Many of these loci are already associated with one or more known candidate tumour suppressor genes