Publications
103 results found
Wark PA, Peto J, 2008, Cancer Epidemiology, International Encyclopedia of Public Health, Editors: Heggenhougen, Quah, San Diego, Publisher: Academic Press, Pages: 416-424, ISBN: 9780122272257
Wark PA, Van der Kuil W, Ploemacher J, et al., 2006, Diet, lifestyle and risk of K-<i>ras</i> mutation-positive and -negative colorectal adenomas, INTERNATIONAL JOURNAL OF CANCER, Vol: 119, Pages: 398-405, ISSN: 0020-7136
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- Citations: 43
Lüchtenborg M, Weijenberg MP, Wark PA, et al., 2005, Mutations in <i>APC</i>, <i>CTNNBI</i> and <i>K-ras</i> genes and expression of <i>hMLHI</i> in sporadic colorectal carcinomas from the Netherlands Cohort Study -: art. no. 160, BMC CANCER, Vol: 5, ISSN: 1471-2407
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- Citations: 54
Tijhuis MJ, Wark PA, Aarts JM, et al., 2005, Cruciferous vegetable consumption, glutathione-s-transferase polymorphisms, and colorectal adenoma risk in a dutch case-control study., International Research Conference on Diet, Nutrition and Cancer, Publisher: AMER SOC NUTRITIONAL SCIENCE, Pages: 3044S-3044S, ISSN: 0022-3166
Tijhuis MJ, Wark PA, Aarts JMMJG, et al., 2005, GSTP1 and GSTA1 polymorphisms interact with cruciferous vegetable intake in colorectal adenoma risk., Cancer Epidemiol Biomarkers Prev, Vol: 14, Pages: 2943-2951, ISSN: 1055-9965
The possible interplay between cruciferous vegetable consumption, functional genetic variations in glutathione S-transferases (GST) M1, T1, P1, and A1, and colorectal adenomas, was investigated in a Dutch case-control study. The GSTM1 and GSTT1 deletion polymorphisms, and the single nucleotide polymorphisms in GSTP1 (A313G) and in GSTA1 (C-69T) were assessed among 746 cases who developed colorectal adenomas and 698 endoscopy-based controls without any type of colorectal polyps. High and low cruciferous vegetable consumption was defined based on a median split in the control group. High consumption was slightly positively associated with colorectal adenomas [odds ratio (OR) 1.15; 95% confidence interval, 0.92-1.44]. For GSTP1, a positive association with higher cruciferous vegetable intake was only apparent in individuals with the low-activity GSTP1 genotype (GG genotype, OR 1.94; 95% confidence interval, 1.02-3.69). This interaction was more pronounced in men, with higher age and with higher meat intake. The GSTA1 polymorphism may have a modifying role as well: the OR for higher intake compared with lower intake was 1.57 (0.93-2.65) for individuals homozygous for the low expression variant (TT genotype). This seemed to be stronger with younger age and higher red meat intake. Cruciferous vegetable consumption and the combined GSTA1 and GSTP1 genotypes showed a statistically significant interaction (P = 0.034). The GSTM1 and GSTT1 genotypes did not seem to modify the association between cruciferous vegetable intake and colorectal adenomas. In conclusion, GSTP1 and GSTA1 genotypes might modulate the association between cruciferous vegetable intake and colorectal adenomas.
Lüchtenborg M, Weijenberg MP, de Goeij AFPM, et al., 2005, Meat and fish consumption, APC gene mutations and hMLH1 expression in colon and rectal cancer: a prospective cohort study (The Netherlands)., Cancer Causes Control, Vol: 16, Pages: 1041-1054, ISSN: 0957-5243
OBJECTIVE: The aim of this study was to investigate the associations between meat and fish consumption and APC mutation status and hMLH1 expression in colon and rectal cancer. METHODS: The associations were investigated in the Netherlands Cohort Study, and included 434 colon and 154 rectal cancer patients on whom case-cohort analyses (subcohort n = 2948) were performed. RESULTS: Total meat consumption was not associated with the endpoints studied. Meat product (i.e. processed meat) consumption showed a positive association with colon tumours harbouring a truncating APC mutation, whereas beef consumption was associated with an increased risk of colon tumours without a truncating APC mutation (incidence rate ratio (RR) highest versus lowest quartile of intake 1.61, 95% confidence interval (CI) 0.96-2.71, p-trend = 0.04 and 1.58, 95% CI 1.10-2.25, p-trend = 0.01, respectively). Consumption of other meat (horsemeat, lamb, mutton, frankfurters and deep-fried meat rolls) was associated with an increased risk of rectal cancer without a truncating APC mutation (RR intake versus no intake 1.79, 95% CI 1.10-2.90). No associations were observed for meat consumption and tumours lacking hMLH1 expression. CONCLUSIONS: Our data indicate that several types of meat may contribute differently to the aetiology of colon and rectal cancer, depending on APC mutation status but not hMLH1 expression of the tumour.
Wark PA, Weijenberg MP, van 't Veer P, et al., 2005, Fruits, vegetables, and hMLH1 protein-deficient and -proficient colon cancer:: The Netherlands Cohort Study, CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION, Vol: 14, Pages: 1619-1625, ISSN: 1055-9965
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- Citations: 13
Wark PA, Wu K, Van't Veer P, et al., 2004, Diet, lifestyle, and advanced and non-advanced colorectal adenomas in men., 3rd Annual AACR International Conference, Publisher: AMER ASSOC CANCER RESEARCH, Pages: 1891S-1891S, ISSN: 1055-9965
Wark PA, Grubben MJAL, Peters WHM, et al., 2004, Habitual consumption of fruits and vegetables:: associations with human rectal glutathione <i>S</i>-transferase, CARCINOGENESIS, Vol: 25, Pages: 2135-2142, ISSN: 0143-3334
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- Citations: 27
Wark PA, Weijenberg MP, Van 't Veer P, et al., 2004, Consumption of fruits and vegetables, and expression of the mismatch repair gene hMLH1 in human colorectal cancer:: A prospective study., 3rd Annual AACR International Conference, Publisher: AMER ASSOC CANCER RESEARCH, Pages: 1853S-1853S, ISSN: 1055-9965
Tiemersma EW, Wark PA, Ocké MC, et al., 2003, Alcohol consumption, alcohol dehydrogenase 3 polymorphism, and colorectal adenomas., Cancer Epidemiol Biomarkers Prev, Vol: 12, Pages: 419-425, ISSN: 1055-9965
Alcohol is a probable risk factor with regard to colorectal neoplasm and is metabolized to the carcinogen acetaldehyde by the genetically polymorphic alcohol dehydrogenase 3 (ADH3) enzyme. We evaluated whether the association between alcohol and colorectal adenomas is modified by ADH3 polymorphism. We recruited 433 cases with adenomatous polyps and 436 polyp-free controls among Caucasians undergoing endoscopy between 1995 and 2000. Frequency and amount of habitual alcohol consumption were assessed by beverage type, using a validated self-administered food frequency questionnaire. All participants provided blood for genotyping of ADH3. Multivariate analyses adjusting for gender, age, and indication for endoscopy showed that alcohol increased the risk of colorectal adenomas among women [odds ratio (OR), 1.8; 95% confidence interval (CI), 1.0-3.2, >/=10 versus <1 drink/week]. Among men, the risk of adenomas was increased only for those consuming > 21 drinks/week (OR, 1.8; 95% CI, 0.9-3.8, compared with men drinking < 1 drink/week). Among subjects in the highest tertile of alcohol consumption, those with the ADH3*1/*1 genotype were at higher risk (OR, 1.8; 95% CI, 1.0-3.1) than those with other ADH3 genotypes (OR, 1.2; 95% CI, 0.7-1.9) when compared with those in the lowest tertile with ADH3*1/*2 or ADH3*2/*2 genotypes. In conclusion, our findings are consistent with results of other studies, suggesting that alcohol consumption elevates the risk of adenomatous colorectal polyps. ADH3 polymorphism may modify the association between alcohol consumption and colorectal adenomas.
Weijenberg MP, Brink M, Lüchtenborg M, et al., 2002, Dietary factors, genetic susceptibility and somatic mutations in colorectal cancer: a prospective study., IARC Sci Publ, Vol: 156, Pages: 503-504, ISSN: 0300-5038
, 2000, Precancerous lesions of the digestive tract. The 18th Annual Symposium of the European Cancer Prevention Organization. Maastricht, The Netherlands. 12-14 October 2000. Abstracts., Pages: 443-463, ISSN: 0959-8278
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