The Columbia, Missouri serum bank was established as part of the National Cancer Institute’s Biological Markers Project to identify serum markers for breast cancer. A total of 7,224 women living in and around Columbia, MO who were free of cancer other than non-melanoma skin cancer, donated blood to the serum bank on one or more occasions between 1977 and 1987. Approximately 25% of the women were premenopausal. At the time of each blood collection, interview information was obtained from participants on the major known breast cancer risk factors including age, height, weight, reproductive and menstrual histories, family history of breast cancer, medical conditions, and drug use, including oral contraceptives and menopausal hormone therapy. Date of last menstrual period was obtained for women who were premenopausal at the time of each blood collection. Approximately 30% of the women donated multiple samples over the first 10 years of the study, including 20% who had 3 or more samples, with collections occurring on average one year apart. In 1989, the first follow-up ascertained 107 breast cancers among women who were cancer-free at blood collection. A subset of these breast cancers was included in a number of biomarker studies, including the measurement of sex steroid hormones, carotenoids, alpha-tocopherol, selenium, organochlorine pesticides and PCBs. A more recent follow-up was completed in 2002, at which time an additional 279 breast cancers were identified.
Using the expanded group of breast cancer cases in the Columbia, MO Serum Bank Follow-up Study, additional biomarker studies have been conducted, including how adipokines relate to breast cancer risk factors. These analyses showed lower levels of adiponectin and higher levels of absolute plasminogen activator inhibitor (aPAI-1) were associated with increasing body mass index, but not with breast cancer risk. In more recently completed analyses, a newly developed tandem mass spectrometry assay was used to measure a panel of 15 estrogens and estrogen metabolites in relation to postmenopausal breast cancer risk. This showed that both a higher ratio of the 2/16 hydroxylation pathway and of the ratios of 2- or 4- hydroxylation were associated with reduced breast cancer risk. These findings support that analyses of metabolic pathways may help elucidate the role of estrogen metabolism in breast carcinogenesis.
For more information, contact Louise Brinton.