Annual Meeting

November 13-16, 2012
Hilton San Francisco Financial District, San Francisco, CA

sponsored by
AVON Foundation
Speaker Abstracts

Pregnancy, Obesity, and Basal-like Microenvironments.

Melissa Troester, PhD, MPH, Department of Epidemiology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC

Epidemiologic and experimental data show that a full term pregnancy reduces breast cancer risk. However, recent studies have suggested that while full term pregnancy does reduce risk for estrogen receptor and luminal breast cancers, pregnancy may actually increase risk of more aggressive basal-like breast cancers. There are complex relationships between age, race, parity, and obesity in observational human datasets making it difficult to translate these findings into public health. Further understanding of the molecular and biological mechanisms underlying the effects of pregnancy and obesity are important for disentangling these factors. For example, to identify biological underpinnings of obesity, parity and age, we are conducting histology and gene expression studies using normal breast tissue. Comparisons of these observational results with studies in vitro and in vivo and across species are helping to identify important pathways in basal-like cancer etiology.  Using mouse models of basal-like breast cancer, our data show that pregnancy and high fat diet decrease latency for basal-like breast tumors. Coculture model systems have helped us to identify stromal-epithelial interactions that promote basal-like breast cancer progression. Together, molecular epidemiology studies of normal breast tissue and experimental studies of stromal-epithelial interactions are yielding interesting insights regarding basal-like breast cancer progression.

(Supported by the Avon Foundation for Women Breast Cancer Research Program and the National Institutes of Environmental Health Sciences Breast Cancer and the Environment Research Program U01-019472)

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