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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.

OBJECTIVE: To investigate the association of prediagnostic circulating levels of C-peptide, as a marker of pancreatic insulin secretion, and IGF binding proteins -1 and -2, as indicators of the bio ...

Objective: Body size is an important modifiable risk factor for breast cancer. Although obesity has generally been found to be associated with increased risk for postmenopausal breast cancer, there remain questions concerning the role of body fat distribution, lifetime weight history, and effects within specific subgroups of women. Methods: We assessed the relationship of several anthropometric measures and risk of postmenopausal breast cancer in 85,917 women aged 50-79 at entry in the Women's Health Initiative Observational Study. Women were enrolled during 1993-1998 at 40 clinics in the US and 1030 developed invasive breast cancer by April 2000. Upon entry, trained clinical center staff measured each woman's height, weight, and waist and hip circumference. Results: Anthropometric factors were not associated with breast cancer among women who had ever used hormone replacement therapy (HRT). Among HRT non-users, heavier women (baseline body mass index (BMI) >31.1) had an elevated risk of postmenopausal breast cancer (relative risk (RR) = 2.52; 95% confidence interval (CI) = 1.62-3.93), compared to slimmer women (baseline BMI < 22.6). The elevation in risk associated with increasing BMI appeared to be most pronounced among younger postmenopausal women. Change in BMI since age 18, maximum BMI, and weight were also associated with breast cancer in HRT non-users. While both waist and hip circumference were associated with breast cancer risk, their ratio, a measure of fat distribution, was not (RR = 1.33; 95% CI = 0.88-2.01). Conclusions: Our study confirms previously reported findings that generalized obesity is an important risk factor for postmenopausal breast cancer, but only among women who have never taken HRT. Lifetime weight gain is also a strong predictor of breast cancer. Waist to hip ratio, a measure of weight distribution, does not appear to be related to postmenopausal breast cancer risk.

Objective: To analyze the association of prostate cancer risk with estrogen metabolism, expressed as the ratio of 2-hydroxyestrone (2-OHE1) to 16α-hydroxyestrone (16α-OHE1), in a case–control study conducted in Buffalo, NY, between 1998 and 2001. Methods: One hundred and thirteen men, aged 45–85 years, with incident, primary pathologically confirmed prostate cancer were enrolled in the study; 317 residence-matched controls were also enrolled. Cases were enrolled and the specimens collected before starting any therapy. To exclude latent prostate carcinomas, the present study included only patients with clinically apparent disease (stage B and higher). Prostate cancer cases and control subjects were excluded if on hormonal treatment, or affected with metabolic or endocrine diseases. Control subjects with a prostate-specific antigen (PSA) value higher than 4ng/ml were excluded from the control group. Urine was used for the determinations of 2-OHE1 and 16α-OHE1. Age, race, body weight, waist-to-hip ratio, and smoking were analyzed as possible confounders. Results: Although the results were not statistically significant, elevated 2-OHE1 urinary levels suggested a reduced prostate cancer risk: men in the highest tertile had an adjusted odds ratio (OR) for prostate cancer of 0.83 (95% confidence interval (CI) 0.43–1.44). Conversely, elevated 16α-OHE1 urinary levels were associated with an increased risk of prostate cancer: the highest tertile had an adjusted OR for prostate cancer of 1.69 (95% CI 0.93–3.06, p for linear trend = 0.02). Finally, the 2-OHE1 to 16α-OHE1 ratio was associated with a reduced risk of prostate cancer with an OR of 0.61 (95% CI 0.33–1.15, p for linear trend = 0.04). Conclusion: Results of this case–control study suggest that the estrogen metabolic pathway favoring 2-hydroxylation over 16α-hydroxylation may reduce risk of clinically evident prostate cancer.

Objectives: Because alcohol dehydrogenase 3 (ADH3) is rate-limiting in alcohol oxidation and is polymorphic, we examined ADH3 genotype in relation to alcohol intake and breast cancer risk.