LIBCSPLong Island Breast Cancer Study Project (Connecticut and New York study; National Cancer Institute)
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Fruit/vegetable intake was dichotomized based on previously reported associations with breast cancer incidence in the LIBCSP (Gaudet et al.
The number of LIBCSP respondents for whom traffic B[a]P estimates were available (520-1,274 case participants; 566-1,334 control participants) varied according to the exposure definition and the imputed data set (some women exceeded the limit on imputation percentage in certain imputation draws), and the participants showed a wide range of exposure levels (Table 1).
The proposed project was unlike the LIBCSP in several ways.
Although projects such as the LIBCSP and the BCERCs have general guidelines and requirements for advocate participation in the research process, other factors may inhibit advocate-scientist collaboration.
Distribution of p53 mutations by PAH-related exposures among LIBCSP case participants [n(%)].
Associations between PAH-related exposures and the risk of breast cancer subtype as defined by p53 mutation type in the LIBCSP.
The goal of our present analysis was to investigate whether multiple GST polymorphisms modified the relationship between PAH exposure and breast cancer, using the lymphocyte PAH-DNA adduct biomarker as our primary exposure measure of interest using a large, population-based sample of cases and controls from the LIBCSP.
The population-based sample of cases and controls from the LIBCSP has been described previously (Gammon et al.
In addition to the samples collected as part of the LIBCSP, data collected by the U.
cooking), and/or dust track-in, we expect that the ambient signal should be detectable in the carpet PAH measurements that were collected as part of the LIBCSP to provide an exposure marker inclusive of indoor-generated PAHs.
The Breast Cancer and the Environment on Long Island case--control study, the centerpiece of the LIBCSP, applied a typical hypothesis-testing framework to investigate whether an association exists between breast cancer risk and organochlorine compounds [dichlorodiphenyltrichloroethane (DDT)/dichlorodiphenyldichloroethylene (DDE), chlordane, dieldrin, and polychlorinated biphenyl], which are EDCs, and polycyclic aromatic hydrocarbons (PAHs), which are mammary carcinogens (Gammon et al.
Several factors favored the potential in the LIBCSP to produce persuasive evidence that organochlorines increase breast cancer risk: the biologically plausible hypothesis that EDCs affect breast cancer, several earlier studies showing an association between breast cancer and serum organochlorines, a large sample size (providing good statistical power to detect an effect), rapid case ascertainment (so serum measures could not be affected by breast cancer treatment), extensive interviews about established and hypothesized breast cancer risk factors (to control for confounding and investigate effect modification), and individual-level biologic markers of exposure.