Abstract
Abstract Breast cancers evolve through interactions with the surrounding non-malignant tissue, with the non-malignant tissue providing a selective pressure during carcinogenesis. By conducting observational studies of non-malignant tissue, it is possible to identify pathways and phenotypes that contribute to cancer etiology and progression. Our gene expression profiling studies have demonstrated that cancer adjacent normal breast tissue is highly variable, with at least two distinct molecular subtypes. These subtypes are associated with histologic differences and distinct risk factor profiles, notably mammographic density. Given that mammographic density is the strongest, yet most poorly understood breast cancer risk factor, molecular studies to better understand this phenotype are important. We have also conducted studies of risk factor-associated gene expression in reduction mammoplasty tissue. Supervised analysis of gene expression in normal tissue is identifying novel biological phenotypes associated with established risk factors. For example, we have shown that aging is associated with specific gene expression changes in normal breast. Interestingly, the age-related pathways in non-diseased tissue are also dysregulated in the breast cancers that are more common in young women, providing a biological link between the aging process and tumor aggressiveness. Likewise, obesity causes alterations to the stromal milieu in normal breast tissue, with implications for the progression of basal-like breast cancers. Our results demonstrate that to study the evolution and outcome of breast cancers, it is important to consider the normal tissue microenvironment from which these cancers evolve. Citation Format: Melissa A. Troester. Insights on cancer risk from normal breast tissue gene expression. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr PL04-02.
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