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The Ulster medical journal 06/2003; 72(1):50-1.
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ABSTRACT: Intracellular folate deficiency has been implicated in colonic carcinogenesis in epidemiological studies and animal and human cancer models. Our aim was to determine the effect of folate supplementation on patients with recurrent adenomatous polyps using rectal mucosal cell proliferation as a biomarker.
Eleven patients with recurrent adenomatous polyps of the colon were randomised into a treatment group (n=6) receiving a dietary supplement of 2 mg folic acid per day for three months and a control group (n=5) receiving a placebo. Rectal biopsies where taken at 10 cm from the anal verge prior to supplementation and repeated at four, 12, and 18 weeks from the start of the supplementation. Each biopsy was immediately incubated in culture medium enriched with bromodeoxyuridine (BrdU). The S phase cells which incorporated BrdU into their DNA were identified following immunohistochemical staining. Twenty five orientated crypts were identified for each time point and the number and position of BrdU positive and BrdU negative cells were counted. BrdU labelling indices (LIs) were calculated for the entire crypt and for each of five equal compartments running consequently from the base to the luminal surface.
The LI of the treatment group (9.1 (6.7, 12.3)) and the control group (9.3 (7.8, 10.3)) were comparable at the start. Over the duration of the supplementation period, LI in the control group did not alter significantly (9.3 (7.8, 10.3) v 9.6 (8.9, 10.4)). However, LI of the folate treated group was lowered after 12 weeks of supplementation (9.1 (6.7, 12.3) v 7.4 (5.3, 9.6)). Analysis of the LI for compartments within the crypt showed that the most significant drop in number of proliferating cells was in the upper most regions of the crypt.
These data indicate that (a) folate supplementation decreases colonic mucosal cell proliferation in a high risk group for colon cancer and (b) the most significant reduction takes place at the luminal aspect of the crypt.
Gut 09/2002; 51(2):195-9. · 10.11 Impact Factor
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ABSTRACT: To describe the variation in the incidence of colorectal cancer across Northern Ireland and relate it to factors associated with community deprivation.
This was a cross sectional descriptive study.
Incidence data were obtained from a population based register for the period 1990-91. Small areas were characterised by their "affluence", or lack of it, by deriving a Townsend deprivation score for each electoral ward, using information from the 1991 census. PARTICIPANTS, MAIN OUTCOME MEASURES, AND STATISTICAL METHODS: The age standardised incidence was calculated for all colorectal cancer cases diagnosed histologically in 1990-91. Electoral wards were grouped into quintiles of the population after ranking of their Townsend scores and the association with incidence was studied using Poisson regression.
The age standardised colorectal cancer incidence ranged from 22.5 (for quintile 1) to 29.9/100,000 (quintile 5) for men but the trend for women was less regular and rates were 18.4, 23.8, 27.3, 26.5, and 23.9/100,000 for quintiles 1-5 respectively (that is, from the most "affluent" to the most "deprived" fifths of the population). After adjusting for age and sex in Poisson regression, there was a significant association between the total colorectal cancer incidence and levels of community deprivation. The rate ratio for the most deprived quintile of the population (compared with the least) was 1.28 (95% CI 1.06,1.53). The effect was stronger for rectal cancer than for colonic cancer. There was no association between community deprivation and the cancer stage at diagnosis.
In this population, the colorectal cancer incidence is associated with the level of material deprivation. The disease stages at the time of diagnosis in patients from more deprived areas seem to be comparable with those of patients from affluent areas. As others have shown, associations such as these are not explicable entirely on the basis of the distribution of known risk factors. Further research is needed to determine plausible mechanisms for the association.
Journal of Epidemiology & Community Health 01/1997; 50(6):640-4. · 3.19 Impact Factor
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The European Journal of Surgery 05/1994; 160(4):243-6.
