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Dietary carotenoids have been hypothesized to protect against epithelial cancers. The authors analyzed the associations between intakes of specific carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein + zeaxanthin, and lycopene) and risk of colorectal cancer using the primary data from 11 cohort studies carried out in North America and Europe. Carotenoid intakes were estimated from food frequency questionnaires administered at baseline in each study. During 6–20 years of follow-up between 1980 and 2003, 7,885 incident cases of colorectal cancer were diagnosed among 702,647 participants. The authors calculated study-specific multivariate relative risks and then combined them using a random-effects model. In general, intakes of specific carotenoids were not associated with colorectal cancer risk. The pooled multivariate relative risks of colorectal cancer comparing the highest quintile of intake with the lowest ranged from 0.92 for lutein + zeaxanthin to 1.04 for lycopene; only for lutein + zeaxanthin intake was the result borderline statistically significant (95% confidence interval: 0.84, 1.00). The associations observed were generally similar across studies, for both sexes, and for colon cancer and rectal cancer. These pooled data did not suggest that carotenoids play an important role in the etiology of colorectal cancer. [ABSTRACT FROM AUTHOR]

Genetic polymorphism analysis for disease risk is widely used in epidemiology studies; blood or oral cavity cells are the most widely used source of DNA. However, these types of samples are not always available, particularly for studies that were conducted years ago. An alternative potential source of patient DNA exists in the form of paraffin-embedded normal tissue adjacent to tumor samples, which are collected and stored routinely for clinical use. The use of such samples can be conceptually problematic, however, due to the presence of field cancerization in the surrounding normal tissue, with the possible presence of chromosomal loss. Specifically, loss of heterozygosity (LOH) might bias the genotyping results and cause genotype misclassification. However, field cancerization and LOH might not be an issue because LOH is not easily found unless there is careful microdissection of only tumor cells (leaving stromal, inflammatory and fat cells), for example, laser-capture microdissection. In this study, we set out to determine the degree of genotype misclassification from normal tissues adjacent to tumors, if any, by comparing these results with blood genotyping. We examined samples from 106 subjects with breast cancer, analyzing five different genotypes selected from regions commonly known to have LOH in breast cancer. These genotypes were methylenetetrahydrofolate reductase (MTHFR), oxoguanosine glycosylase 1 (hOGG1), dopamine β-hydroxylase (DBH), dopamine receptor D2 (DRD2) and NAD(P)H dehydrogenase quinone 1 (NQO1), conducted by using real-time PCR and TaqMan genotyping analyses. We found that among these five genotypes and 106 comparisons, there was a 100% concordance for genotyping from normal tissue adjacent to tumor and from blood. Our findings indicate that the use of adjacent normal tissues provides accurate genotyping results with high specificity. Although this study only used breast tumor samples, and may be applicable only to breast cancer studies, we expect the results to be applicable to other types of cancers also. [ABSTRACT FROM AUTHOR]

Abstract Evidence is increasing that some early life exposures affect breast cancer risk. Exposure to secondhand smoke (SHS) during childhood may be one such exposure. As part of the WEB Study (Western New York Exposures and Breast Cancer Study), we conducted a population-based, case-control study with 1166 women aged 35 to 79 diagnosed with histologically confirmed, primary, incident breast cancer. Controls (n = 2105) were randomly selected from the Department of Motor Vehicles driver’s license list (≰age 65) and the Center for Medicare & Medicaid Services rolls (>age 65). Participants were queried regarding household and workplace SHS exposure. Person-years of lifetime cumulative SHS exposure were computed as well as cumulative exposure up to 21 years of age. Unconditional logistic regression adjusting for potential confounders was used to calculate odds ratios (OR) and 95% confidence intervals (95% CI). Lifetime cumulative exposure to household SHS was not associated with an increase in breast cancer risk for premenopausal (OR = 1.17, 95% CI  = 0.54–2.56) or postmenopausal (OR = 1.29; 95% CI  = 0.82–2.01) women. Neither was risk increased among women exposed to SHS before the age of 21 or at the time of birth, menarche, or a women’s first birth. In this study, exposure to SHS either in adult or early life does not appear to be associated with the risk of breast cancer. [ABSTRACT FROM AUTHOR]

ObjectiveThis study focused on geographic clustering of breast cancer based on residence in early life and identified spatio-temporal clustering of cases and controls. Methods: Data were drawn from the WEB study (Western New York Exposures and Breast Cancer Study), a population-based case–control study of incident, pathologically confirmed breast cancer (1996–2001) in Erie and Niagara counties. Controls were frequency-matched to cases on age, race, and county of residence. All cases and controls used in the study provided lifetime residential histories. The k-function difference between cases and controls was used to identify spatial clustering patterns of residence in early life. Results: We found that the evidence for clustered residences at birth and at menarche was stronger than that for first birth or other time periods in adult life. Residences for pre-menopausal cases were more clustered than for controls at the time of birth and menarche. We also identified the size and geographic location of birth and menarche clusters in the study area, and found increased breast cancer risk for pre-menopausal women whose residence was within the cluster compared to those living elsewhere at the time of birth. Conclusion: This study provides evidence that early environmental exposures may be related to breast cancer risk, especially for pre-menopausal women. [ABSTRACT FROM AUTHOR]

There is evidence linking alcohol consumption to p53 mutations in tumors, considerable evidence linking alcohol consumption with risk of breast cancer and some evidence that alcohol and folate consumption interact to affect risk. Further, while there is some indication that oxidation may play a role in breast cancer etiology, there has been little examination of an association of oxidative stress with p53 mutations. We examined several dietary components related to one-carbon metabolism and antioxidants to determine if these factors were related to the prevalence of p53 mutations in breast tumors. We conducted a case-control study of primary, histologically confirmed breast cancer in western New York. Controls <65 were selected from drivers license lists; those ≥65 were selected from Health Care Finance Administration lists. p53 mutations in archived tumor blocks were identified in exons 2–11 and flanking intron sequences. Usual dietary intake was assessed by interview regarding intake in the previous 2 years; alcohol consumption was queried for 2, 10 and 20 years in the past. Our data were consistent with increased likelihood of tumors with p53 mutations for premenopausal breast cancer with increased alcohol intake 10 or 20 years previous; for intake of 16 or more drinks per month in the period 20 years before the interview compared with non-drinkers, the OR was 5.25, 95% CI 1.48–18.58. For postmenopausal women, there was increased likelihood of tumors with p53 mutations among women with higher folate. Antioxidant nutrients were not differentially related to p53 mutations. These results indicate that there may be heterogeneity in breast tumors, as indicated by differences in associations for those with or without p53 mutations, and that causal pathways for these nutrients may vary for pre- and postmenopausal women. For premenopausal women, alcohol consumption in the past was associated with p53 mutations. [ABSTRACT FROM AUTHOR]

The relationship of glucose in the blood with colorectal adenoma or cancer is not clear. Fructosamine, equivalent to total serum glycated proteins, is a marker of blood glucose levels in the previous 3 weeks. We evaluated in a case–control study the association between fructosamine and colorectal adenoma, a precursor of colorectal cancer. Cases were subjects with the first occurrence of one or more histologically confirmed colorectal adenomatous polyps removed after a complete colonoscopy (153 cases), and controls were subjects with normal colonoscopy performed in the same endoscopy units during the same period (84 controls). Serum fructosamine was measured by a colorimetric method. Unconditional multiple logistic regression was used for statistical analysis. We found that in non-diabetic subjects the risk of colorectal adenoma increased with the level of fructosamine, and the odds ratio of colorectal adenoma in subjects with fructosamine levels higher than the median (270μg/100 ml), in comparison with subjects with fructosamine lower than the median, was 2.3 (95% CI: 1.1–4.8). The risk of colorectal adenoma increased also with increasing levels of serum triglycerides and cholesterol, and decreased with increasing levels of fasting serum insulin. The results of this study show that the risk of colorectal adenoma increases with the level of fructosamine, an indicator of the level of glucose in the blood more sensitive to foods with a high glycemic index. [ABSTRACT FROM AUTHOR]

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. © 2003 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]