Biomedical subjects

R Alexandra Goldbohm

Publications and source records attributed to R Alexandra Goldbohm.

At least 37 records · Page 2Linked to original sources

PubMed2005

Dietary patterns and breast cancer risk: results from three cohort studies in the DIETSCAN project.

OBJECTIVE: Only a few consistent findings on individual foods or nutrients that influence breast cancer risk have emerged thus far. Since people do not consume individual foods but certain combinations of them, the analysis of dietary patterns may offer an additional aspect for assessing associations between diet and diseases such as breast cancer. It is also important to examine whether the relationships between dietary patterns and breast cancer risk are consistent across populations. METHODS: We examined the risk of breast cancer with two dietary patterns, identified as "Vegetables" (VEG) and "Pork, Processed Meat, Potatoes" (PPP), common to all cohorts of the DIETSCAN project. During 7 to 13 years of follow-up, three of the cohorts--the Netherlands Cohort Study on diet and cancer (NLCS), the Swedish Mammography Cohort (SMC), and the Ormoni e Dieta nella Eziologia dei Tumori (Italy-ORDET)--provided data on 3271 breast cancer cases with complete information on their baseline diet measured by a validated food frequency questionnaire. RESULTS: After adjustment for potential confounders, VEG was not associated with the risk of breast cancer across all cohorts. PPP was also not associated with the risk of breast cancer in SMC and ORDET, but a high PPP score tended to be inversely associated with breast cancer in the NLCS study (RR = 0.69; 95% CI, 0.52-0.92, highest versus lowest quartile). PPP differed in one aspect between the cohorts: butter loaded positively on the pattern in all cohorts except NLCS, in which butter loaded negatively and appeared to be substituted by low-fat margarine loading positively. CONCLUSION: In general, the dietary patterns showed consistent results across the three cohorts except for the possible protective effect of PPP in the NLCS cohort, which could be explained by a difference in that pattern for NLCS. The results supported the suggestion derived from traditional epidemiology that relatively recent diet may not have an important role in the etiology of breast cancer.

Adult↗

PubMed2005

Alcohol consumption and risk of lung cancer: a pooled analysis of cohort studies.

BACKGROUND: Although smoking is the primary cause of lung cancer, much is unknown about lung cancer etiology, including risk determinants for nonsmokers and modifying factors for smokers. OBJECTIVE: We hypothesized that alcohol consumption contributes to lung cancer risk. DESIGN: We conducted a pooled analysis using standardized exposure and covariate data from 7 prospective studies with 399,767 participants and 3137 lung cancer cases. Study-specific relative risks (RRs) and CIs were estimated and then combined to calculate pooled multivariate RRs by using a random-effects model. RESULTS: We found a slightly greater risk for the consumption of > or = 30 g alcohol/d than for that of 0 g alcohol/d in men (RR: 1.21; 95% CI: 0.91, 1.61; P for trend = 0.03) and in women (RR: 1.16; 95% CI: 0.94, 1.43; P for trend = 0.03). In male never smokers, the RR for consumption of > or = 15 g alcohol/d rather than 0 g alcohol/d was 6.38 (95% CI: 2.74, 14.9; P for trend < 0.001). In women, there were few never-smoking cases and no evidence of greater risk (RR: 1.35; 95% CI: 0.64, 2.87). Because of possible residual confounding by smoking, we performed sensitivity analyses by reclassifying the never smokers in the highest drinking category as former smokers. Resulting associations for alcohol consumption were somewhat attenuated, but P for trend = 0.05 for men, which was near the original P = 0.03. CONCLUSIONS: A slightly greater risk of lung cancer was associated with the consumption of > or = 30 g alcohol/d than with no alcohol consumption. Alcohol consumption was strongly associated with greater risk in male never smokers. Residual confounding by smoking may explain part of the observed relation.

Alcohol Drinking↗

PubMed2005

Hypertension, antihypertensives and mutations in the Von Hippel-Lindau gene in renal cell carcinoma: results from the Netherlands Cohort Study.

OBJECTIVES: Hypertension and/or antihypertensive medication are reported to be risk factors of renal cell carcinoma (RCC). We investigated whether these risk factors are associated with von Hippel-Lindau gene (VHL) mutations in RCC. METHODS: The Netherlands Cohort Study on Diet and Cancer (NLCS) started in 1986 (n = 120 852 men and women) and uses the case-cohort methodology. After 11.3 years of follow-up, 337 RCC cases and 4774 subcohort members were available for analysis. DNA was isolated from paraffin-embedded tumour tissue for VHL analysis. RESULTS: Cohort members who reported hypertension or use of antihypertensive medication had a slightly (non-significant) increased risk of RCC: rate ratios (RR) 1.22 [95% confidence interval (CI), 0.94-1.58] and 1.14 (95% CI, 0.85-1.52), respectively. RRs were adjusted for sex, age, body mass index (BMI) and cigarette smoking. Of the 235 patients for whom tumour tissue specimens were collected, 187 had a clear-cell RCC, of whom 114 had a VHL mutation. History of hypertension was associated with a non-significantly increased risk of clear-cell RCC with VHL mutations: RR = 1.34 (95% CI, 0.87-2.07), and was not associated with the risk of clear-cell RCC without VHL mutations; RR = 0.88 (95% CI, 0.51-1.53). Use of diuretics was associated with clear-cell RCC without VHL mutations; RR = 2.11 (95% CI, 1.16-3.83). CONCLUSIONS: In this study non-significantly increased risks for history of hypertension and use of antihypertensive medication with RCC were observed. The association with hypertension was stronger in RCC patients with VHL mutations, while there was a positive association of diuretics use and risk of RCC without VHL mutations.

Aged↗

PubMed2005

Dietary patterns associated with male lung cancer risk in the Netherlands Cohort Study.

The objective of this article was to study the association between dietary patterns and lung cancer incidence in the Netherlands Cohort Study on Diet and Cancer. The baseline measurement of this prospective case cohort study that was completed by 58,279 men in 1986 included a self-administered questionnaire on dietary intake, smoking habits, and other covariates. Follow-up was established by computerized record linkage to cancer registries and a pathology register. After 9.3 years of follow-up, 1,426 confirmed cases of incident male lung cancer were detected. Five dietary patterns were identified by exploratory factor analysis in a randomly sampled subcohort (n = 2,190). The dietary pattern labeled "salad vegetables" was associated with decreased risk of lung cancer [rate ratios (RR)(Q5), 0.75; 95% confidence interval (CI), 0.55-1.01], after multivariate adjustment. This inverse association was most evident among current and former smokers. A dietary pattern labeled "sweet foods" was also inversely associated with lung cancer risk (RR(Q5), 0.62; 95% CI, 0.43-0.89). However, the higher intake of monosaccharides and disaccharides, fruits, and lower consumption of alcohol associated with this pattern could not account for its full protective effect. The "pork, processed meat, and potatoes" pattern was nonsignificantly associated with increased risk (RR(Q5), 1.44; 95% CI, 0.99-2.09), and this positive association was most evident among current smokers. The other dietary patterns characterized by brown/white bread substitution and by consumption of cooked vegetables were not associated with lung cancer risk. These results show how studying both single factors and dietary patterns gives more insight into the complex, and often seemingly inconsistent, associations between diet and cancer.

Aged↗

PubMed2005

Fruits, vegetables, and hMLH1 protein-deficient and -proficient colon cancer: The Netherlands cohort study.

BACKGROUND: Clinical and pathologic differences exist between colon carcinomas deficient and proficient in the mismatch repair protein hMLH1. Animal and in vitro studies suggest that fruits, vegetables, folate, and antioxidants are associated with colonic expression of mismatch repair genes. METHODS: Associations between consumption of fruits and vegetables and hMLH1 protein-deficient and -proficient colon cancer were evaluated in the Netherlands Cohort Study on diet and cancer using a case-cohort approach. A self-administered food frequency questionnaire was completed, in 1986, by 120,852 individuals ages 55 to 69 years. Using immunohistochemistry, hMLH1 protein expression was assessed in colon cancer tissue obtained from 441 patients who were identified over 7.3 years of follow-up excluding the initial 2.3 years. Incidence rate ratios (RR) were estimated for hMLH1 protein-deficient and -proficient colon cancer. RESULTS: hMLH1 protein expression was absent in 54 tumors (12.2%) and present in 387 tumors. Fruit consumption was associated with hMLH1 protein-deficient colon cancer [highest versus lowest tertile, RR, 0.46; 95% confidence interval (95% CI), 0.23-0.90; P(trend) = 0.029] but not with hMLH1 protein-proficient tumors (highest versus lowest tertile, RR, 1.03; 95% CI, 0.78-1.35; P(trend) = 0.81). Total consumption of vegetables was not associated with either type of tumor (hMLH1 protein deficient: RR, 0.86; 95% CI, 0.45-1.65; P(trend) = 0.67; hMLH1 protein proficient: RR, 0.94; 95% CI, 0.72-1.23; P(trend) = 0.72). No associations were observed for folate, fiber, antioxidants, or subgroups of vegetables. CONCLUSION: These analyses indicate that an inverse association between consumption of fruits and colon cancer may be confined to the subgroup of tumors with a deficient mismatch repair system.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Fruits and vegetables and ovarian cancer risk in a pooled analysis of 12 cohort studies.

Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food-frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer risk-the pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21; P value, test for trend = 0.73; P value, test for between-studies heterogeneity = 0.74]. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90; 95% CI, 0.78-1.04, for the highest versus the lowest quartile; P value, test for trend = 0.06; P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and individual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.

Adult↗

PubMed2004

Relation of height, body mass, energy intake, and physical activity to risk of renal cell carcinoma: results from the Netherlands Cohort Study.

Data from the Netherlands Cohort Study on Diet and Cancer were used to investigate the association between anthropometry, energy intake, and physical activity and risk of renal cell carcinoma (RCC). The Netherlands Cohort Study on Diet and Cancer consists of 120,852 men and women aged 55-69 years who completed a self-administered questionnaire at baseline (1986). A case-cohort approach was used. After 9.3 years of follow-up, 275 microscopically confirmed incident cases were available for analysis. Incidence rate ratios for RCC were estimated using Cox proportional hazards models. Height was associated with RCC risk only in women (per 5-cm increment, rate ratio (RR) = 1.23, 95% confidence interval (CI): 1.03, 1.46). Body mass index (weight (kg)/height (m)(2)) was associated with increased risk of RCC (per 1-kg/m(2 )increment, RR = 1.07, 95% CI: 1.02, 1.12) for men and women, as was gain in body mass index from age 20 years to baseline (per 1-kg/m(2 )increment, RR = 1.06, 95% CI: 1.01, 1.10). Energy intake was not related to RCC risk, while a possible protective effect was observed for physical activity in men. These results suggest that body mass index and gain in body mass index since age 20 are associated with increased risk of RCC.

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PubMed2004

Anthropometry, physical activity, and endometrial cancer risk: results from the Netherlands Cohort Study.

Although obesity is an established risk factor for endometrial cancer, evidence linking risk to height, weight change since age 20, and physical activity is limited. In this case-cohort study, 62 573 women from The Netherlands Cohort Study on Diet and Cancer were followed up from 1986 to 1995, and 226 endometrial cancer case patients were identified. In Cox proportional hazards analyses, women 175 cm or taller had an increased risk of endometrial cancer compared with those less than 160 cm (rate ratio [RR] = 2.57, 95% confidence interval [CI] = 1.32 to 4.99). Compared with women with a body mass index (BMI; kg/m2) between 20 and 22.9, women with a BMI of 30 or greater had a higher risk (RR = 4.50, 95% CI = 2.62 to 7.72; P(trend)<.001). Moreover, BMI at age 20 and BMI gain since age 20 were positively associated with endometrial cancer risk (P(trend) = .02 and <.001, respectively). Women who spent 90 minutes per day or more doing nonoccupational physical activities had a lower risk (RR = 0.54, 95% CI = 0.34 to 0.85; P(trend) = .002) compared with those who spent less than 30 minutes per day. High BMI and low physical activity were strong and independent risk factors for endometrial cancer.

Adult↗

PubMed2004

Dairy foods, calcium, and colorectal cancer: a pooled analysis of 10 cohort studies.

BACKGROUND: Studies in animals have suggested that calcium may reduce the risk of colorectal cancer. However, results from epidemiologic studies of intake of calcium or dairy foods and colorectal cancer risk have been inconclusive. METHODS: We pooled the primary data from 10 cohort studies in five countries that assessed usual dietary intake by using a validated food frequency questionnaire at baseline. For most studies, follow-up was extended beyond that in the original publication. The studies included 534 536 individuals, among whom 4992 incident cases of colorectal cancer were diagnosed between 6 and 16 years of follow-up. Pooled multivariable relative risks for categories of milk intake and quintiles of calcium intake and 95% confidence intervals (CIs) were calculated. All statistical tests were two-sided. RESULTS: Milk intake was related to a reduced risk of colorectal cancer. Compared with the lowest category of intake (<70 g/day), relative risks of colorectal cancer for increasing categories (70-174, 175-249, and > or =250 g/day) of milk intake were 0.94 (95% CI = 0.86 to 1.02), 0.88 (95% CI = 0.81 to 0.96), and 0.85 (95% CI = 0.78 to 0.94), respectively (P(trend)<.001). Calcium intake was also inversely related to the risk of colorectal cancer. The relative risk for the highest versus the lowest quintile of intake was 0.86 (95% CI = 0.78 to 0.95; P(trend) =.02) for dietary calcium and 0.78 (95% CI = 0.69 to 0.88; P(trend)<.001) for total calcium (combining dietary and supplemental sources). These results were consistent across studies and sex. The inverse association for milk was limited to cancers of the distal colon (P(trend)<.001) and rectum (P(trend) =.02). CONCLUSION: Higher consumption of milk and calcium is associated with a lower risk of colorectal cancer.

Adenoma↗

PubMed2004

Fat and K-ras mutations in sporadic colorectal cancer in The Netherlands Cohort Study.

Associations between dietary intake of various fats and specific K-ras mutations in colorectal cancer (CRC) were investigated within the framework of The Netherlands Cohort Study on diet and cancer (NLCS). After 7.3 years of follow-up and with exclusion of the first 2.3 years, 448 colon and 160 rectal cancer patients and 2948 subcohort members (55-69 years at baseline) were available for data-analyses. Mutation analysis of the K-ras gene was performed on all archival colon and rectal adenocarcinoma specimens. Case-cohort analyses were used to compute adjusted incidence rate ratios (RR) and 95% confidence intervals (CI) for colon and rectal cancer cases and for K-ras mutation subgroups. The intake of total, saturated and monounsaturated fat was not significantly associated with colon or rectal cancer. High intake of dietary polyunsaturated fat and, specifically, linoleic acid is associated with an increased risk of mutated K-ras colon tumours. The RRs for 1 SD of increase of polyunsaturated fat and linoleic acid were 1.21 (95% CI 1.05-1.41) and 1.22 (95% CI 1.05-1.42), respectively, and similar associations were observed for both G > A transitions and G > T or G > C transversions in the colon. In contrast, no significant associations were observed with rectal cancer risk, overall nor with specific K-ras mutation status. A high intake of polyunsaturated fat, in particular linoleic acid, may be an important dietary risk factor for K-ras mutated colon tumours, possibly by generating G > A transitions or G > T or G > C transversions in the K-ras oncogene.

Aged↗

PubMed2004

Alcohol intake and colorectal cancer: a pooled analysis of 8 cohort studies.

BACKGROUND: Epidemiologic studies have generally reported positive associations between alcohol consumption and risk for colorectal cancer. However, findings related to specific alcoholic beverages or different anatomic sites in the large bowel have been inconsistent. OBJECTIVE: To examine the relationship of total alcohol intake and intake from specific beverages to the incidence of colorectal cancer and to evaluate whether other potential risk factors modify the association. DESIGN: Pooled analysis of primary data from 8 cohort studies in 5 countries. SETTING: North America and Europe. PARTICIPANTS: 489,979 women and men with no history of cancer other than nonmelanoma skin cancer at baseline. MEASUREMENTS: Alcohol intake was assessed in each study at baseline by using a validated food-frequency questionnaire. RESULTS: During a maximum of 6 to 16 years of follow-up across the studies, 4687 cases of colorectal cancer were documented. In categorical analyses, increased risk for colorectal cancer was limited to persons with an alcohol intake of 30 g/d or greater (approximately > or =2 drinks/d), a consumption level reported by 4% of women and 13% of men. Compared with nondrinkers, the pooled multivariate relative risks were 1.16 (95% CI, 0.99 to 1.36) for persons who consumed 30 to less than 45 g/d and 1.41 (CI, 1.16 to 1.72) for those who consumed 45 g/d or greater. No significant heterogeneity by study or sex was observed. The association was evident for cancer of the proximal colon, distal colon, and rectum. No clear difference in relative risks was found among specific alcoholic beverages. LIMITATIONS: The study included only one measure of alcohol consumption at baseline and could not investigate lifetime alcohol consumption, alcohol consumption at younger ages, or changes in alcohol consumption during follow-up. It also could not examine drinking patterns or duration of alcohol use. CONCLUSIONS: A single determination of alcohol intake correlated with a modest relative elevation in colorectal cancer rate, mainly at the highest levels of alcohol intake.

Adult↗

PubMed2004

APC mutations in sporadic colorectal carcinomas from The Netherlands Cohort Study.

The adenomatous polyposis coli (APC) gene is considered to be a gatekeeper in colorectal tumourigenesis. Inactivating mutations in APC have been reported in 34-70% of sporadic colorectal cancer patients, the majority of which occur in the mutation cluster region (MCR). In this study, tumour tissue from 665 incident colorectal cancer patients, who originate from 120 852 men and women (55-69 years of age at baseline) participating in The Netherlands Cohort Study, was evaluated for the occurrence and type of APC mutations with regard to age at diagnosis, gender, family history of colorectal cancer, Dukes' stage, tumour differentiation and sub-localization. Mutation analysis of the MCR, which spans codons 1286-1513, was performed on archival adenocarcinoma samples using macrodissection, nested PCR and direct sequencing of purified PCR fragments. A large number of genetic aberrations (n = 978), including point mutations (n = 833), deletions (n = 126) and insertions (n = 19) was detected in the MCR in 72% of patients (479/665). In particular, we observed a large number of missense mutations, more than reported previously. This may indicate involvement in colorectal carcinogenesis, although their significance for APC functions is unclear. Truncating mutations were found in 37% of patients (248/665). Patients with rectosigmoid and rectum tumours relatively more frequently harboured C > T nonsense mutations and truncating frameshift mutations as compared with patients with proximal and distal colon tumours (P = 0.009 and P = 0.045, respectively). Differences in occurrence of truncating mutations with regard to tumour sub-localization suggest a different aetiology of tumourigenesis in colon and rectum.

Adenomatous Polyposis Coli Protein↗

PubMed2004

Alcohol and ovarian cancer risk: results from the Netherlands Cohort Study.

OBJECTIVE: To study alcohol consumption in relation to ovarian cancer risk in a prospective cohort study. METHODS: The Netherlands Cohort Study on diet and cancer was initiated in 1986. A self-administered questionnaire on dietary habits and other risk factors for cancer was completed by 62,573 postmenopausal women. Follow-up for cancer was established by annual record linkages with the Netherlands Cancer Registry. After 9.3 years of follow-up, 214 incident invasive epithelial ovarian cancer cases and 2211 subcohort members with complete data on alcohol intake were available for analysis. All incidence rate ratios (RRs) were corrected for age, use of oral contraceptives, parity, height, body mass index, energy intake and current cigarette smoking. RESULTS: The RRs of ovarian cancer for women who consumed up to 5, 15 and >15 g of alcohol per day were 1.13 (95% confidence interval, 95% CI = 0.79-1.63), 0.85 (95% CI = 0.53-1.37) and 0.92 (95% CI = 0.55-1.54), respectively, compared to non-drinkers. Alcohol consumption in the form of wine, beer or liquor was not associated with ovarian cancer risk. CONCLUSION: These data do not suggest a major association between alcohol intake and ovarian cancer risk in this population.

Aged↗

PubMed2004

Dietary patterns associated with colon and rectal cancer: results from the Dietary Patterns and Cancer (DIETSCAN) Project.

BACKGROUND: An analysis of dietary patterns or combinations of foods may provide insight regarding the influence of diet on the risk of colon and rectal cancer. OBJECTIVE: A primary aim of the Dietary Patterns and Cancer (DIETSCAN) Project was to develop and apply a common methodologic approach to study dietary patterns and cancer in 4 European cohorts: the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study (Finland-ATBC), the Netherlands Cohort Study (NLCS) on Diet and Cancer, the Swedish Mammography Cohort (SMC), and the Ormoni e Dieta nella Eziologia dei Tumori (Italy-ORDET). Three cohorts (ATBC, NLCS, and SMC) provided data on colon and rectal cancer for the present study. DESIGN: The cohorts were established between 1985 and 1992; follow-up data were obtained from national cancer registries. The participants completed validated semiquantitative food-frequency questionnaires at baseline. RESULTS: Exploratory factor analysis, conducted within each cohort, identified 3-5 stable dietary patterns. Two dietary patterns-Vegetables and Pork, Processed Meats, Potatoes (PPP)-were common across all cohorts. After adjustment for potential confounders, PPP was associated with an increased risk of colon cancer in the SMC women (quintile 4(multivariate) relative risk: 1.62; 95% CI: 1.12, 2.34; P for trend = 0.01). PPP was also associated with an increased risk of rectal cancer in the ATBC men (quintile 4(multivariate) relative risk: 2.21; 95% CI: 1.07, 4.57; P for trend = 0.05). Neither pattern was associated with the risk of colon or rectal cancer in the NLCS women and men. CONCLUSION: Although certain dietary patterns may be consistent across European countries, associations between these dietary patterns and the risk of colon and rectal cancer are not conclusive.

Adult↗

PubMed2004

A prospective study of occupation and prostate cancer risk.

A wide variety of occupations has been associated with prostate cancer in previous retrospective studies. Most attention has been paid to farming, metal working, and the rubber industry. Today, these results cannot be affirmed with confidence, because many associations could be influenced by recall bias, have been inconsistent, or have not been confirmed satisfactory in subsequent studies. This study was conducted to investigate and confirm these important associations in a large prospective cohort study. The authors conducted a prospective cohort study among 58,279 men. In September 1986, the cohort members (55-69 years) completed a self-administered questionnaire on potential cancer risk factors, including job history. Related job codes were clustered in professional groups. These predefined clusters were investigated in 3 time windows: 1) profession ever performed, 2) longest profession ever held, and 3) last profession held at baseline. Follow up for incident prostate cancer was established by linkage to cancer registries until December 1993. A case-cohort approach was used based on 830 cases and 1525 subcohort members. To minimize false-positive results, 99% confidence intervals (99% CI) were calculated. Although moderately decreased prostate cancer risks were found for electricians, farmers, firefighters, woodworkers, textile workers, butchers, salesmen, teachers, and clerical workers, none of the relative risks (RR) were found to be statistically significant. For road transporters, metal workers, and managers, no association with prostate cancer risk was found. Although the RR for railway workers, mechanics, welders, chemists, painters, and cooks was moderately increased, these estimates were not statistically significant. For men who reported to have ever worked in the rubber industry, we found a substantially increased prostate cancer risk, but not statistically significant (RR, 4.18; 99% CI = 0.22-80.45). For policemen, we found a substantial and marginally statistically significant increased prostate cancer risk, especially for those who reported working as a policeman for most of their occupational life (RR, 3.91; 99% CI = 1.14-13.42) or as the last profession held at baseline (RR, 4.00; 99% CI = 1.19-13.37). Most of the previously investigated associations between occupation and prostate cancer risk could not be confirmed with confidence in this prospective study. The lack of statistical significance for rubber workers could be caused by the scarcity of rubber workers in this cohort and subsequent lack of power. The results for policemen were substantial and statistically significant, although a conservative value for significance level was used.

Aged↗

PubMed2004

Dietary carotenoids and risk of lung cancer in a pooled analysis of seven cohort studies.

Intervention trials with supplemental beta-carotene have observed either no effect or a harmful effect on lung cancer risk. Because food composition databases for specific carotenoids have only become available recently, epidemiological evidence relating usual dietary levels of these carotenoids with lung cancer risk is limited. We analyzed the association between lung cancer risk and intakes of specific carotenoids using the primary data from seven cohort studies in North America and Europe. Carotenoid intakes were estimated from dietary questionnaires administered at baseline in each study. We calculated study-specific multivariate relative risks (RRs) and combined these using a random-effects model. The multivariate models included smoking history and other potential risk factors. During follow-up of up to 7-16 years across studies, 3,155 incident lung cancer cases were diagnosed among 399,765 participants. beta-Carotene intake was not associated with lung cancer risk (pooled multivariate RR = 0.98; 95% confidence interval, 0.87-1.11; highest versus lowest quintile). The RRs for alpha-carotene, lutein/zeaxanthin, and lycopene were also close to unity. beta-Cryptoxanthin intake was inversely associated with lung cancer risk (RR = 0.76; 95% confidence interval, 0.67-0.86; highest versus lowest quintile). These results did not change after adjustment for intakes of vitamin C (with or without supplements), folate (with or without supplements), and other carotenoids and multivitamin use. The associations generally were similar among never, past, or current smokers and by histological type. Although smoking is the strongest risk factor for lung cancer, greater intake of foods high in beta-cryptoxanthin, such as citrus fruit, may modestly lower the risk.

Carotenoids↗

PubMed2003

Fruits, vegetables and lung cancer: a pooled analysis of cohort studies.

Inverse associations between fruit and vegetable consumption and lung cancer risk have been consistently reported. However, identifying the specific fruits and vegetables associated with lung cancer is difficult because the food groups and foods evaluated have varied across studies. We analyzed fruit and vegetable groups using standardized exposure and covariate definitions in 8 prospective studies. We combined study-specific relative risks (RRs) using a random effects model. In the pooled database, 3,206 incident lung cancer cases occurred among 430,281 women and men followed for up to 6-16 years across studies. Controlling for smoking habits and other lung cancer risk factors, a 16-23% reduction in lung cancer risk was observed for quintiles 2 through 5 vs. the lowest quintile of consumption for total fruits (RR = 0.77; 95% CI = 0.67-0.87 for quintile 5; p-value, test for trend < 0.001) and for total fruits and vegetables (RR = 0.79; 95% CI = 0.69-0.90; p-value, test for trend = 0.001). For the same comparison, the association was weaker for total vegetable consumption (RR = 0.88; 95% CI = 0.78-1.00; p-value, test for trend = 0.12). Associations were similar between never, past, and current smokers. These results suggest that elevated fruit and vegetable consumption is associated with a modest reduction in lung cancer risk, which is mostly attributable to fruit, not vegetable, intake. However, we cannot rule out the possibility that our results are due to residual confounding by smoking. The primary focus for reducing lung cancer incidence should continue to be smoking prevention and cessation.

Analysis of Variance↗

PubMed2003

Effects of dietary folate and alcohol intake on promoter methylation in sporadic colorectal cancer: the Netherlands cohort study on diet and cancer.

Sporadic colorectal cancer (CRC) is characterized by genetic and epigenetic changes such as regional DNA hypermethylation and global DNA hypomethylation. Epidemiological and animal studies suggest that aberrant DNA methylation is associated with low dietary folate intake, which is aggravated by high alcohol intake. The relationship between promoter methylation of genes involved in CRC carcinogenesis and folate and alcohol intake was investigated. Methylation of the APC-1A, p14(ARF), p16(INK4A), hMLH1, O(6)-MGMT, and RASSF1A promoters was studied using methylation-specific PCR in 122 sporadic CRCs, derived from patients with folate and alcohol intake at either the lower or the higher quintiles of the distribution. Overall, promoter hypermethylation frequencies observed were: 39% for APC; 33% for p14(ARF); 31% for p16(INK4A); 29% for hMLH1; 41% for O(6)-MGMT; and 20% for RASSF1A. For each of the tested genes, the prevalence of promoter hypermethylation was higher in CRCs derived from patients with low folate/high alcohol intake (n = 61) when compared with CRCs from patients with high folate/low alcohol intake (n = 61), but the differences were not statistically significant. The number of CRCs with at least one gene methylated was higher (84%) in the low folate intake/high alcohol intake group when compared with the high folate intake/low alcohol intake group (70%; P = 0.085). Despite the size limitations of this study, these data suggest that folate and alcohol intake may be associated with changes in promoter hypermethylation in CRC.

Aged↗