Abstract
Prevention of breast cancer, first and foremost, requires an understanding of the etiology of the disease. Although epidemiological studies have identified a number of risk factors for breast cancer over the last several decades, there is still a sizeable proportion of variability in disease incidence that is unexplained. It is likely that heterogeneity, both in tumor biology and in inherent genomic make up, may blur potential associations. If we accept that breast cancer is more than one disease, as increasingly demonstrated by better understanding of breast tumor subtypes, then it stands to reason that risk factors may differ in etiologic pathways. For example, parity has long been considered to reduce risk of breast cancer. However, there is a growing body of evidence suggesting that having children does reduce risk of estrogen receptor (ER) positive or luminal A breast cancer, but actually increases risk of ER negative and/or basal-like breast cancer, which occurs more often in women of African ancestry. Further examination of risk factors by breast cancer subtypes may clarify some of the uncertainty regarding associations between other exposures and breast cancer risk.
In addition to tumor heterogeneity, the genetic make-up of at-risk populations is known to vary substantially. Common differences in genomic DNA, such as single nucleotide polymorphisms (SNPs), occur in genes that are involved in numerous pathways that could be related to breast cancer risk, including hormone metabolism, carcinogen activation and detoxification, DNA repair, and cell cycle control. Although there has been focused attention on the potential role of gene/environment interactions in breast cancer risk over the last decades, with some persuasive findings, the majority of these studies have not examined such associations in relation to breast tumor subtypes. In this presentation, the role of tumor and genomic heterogeneity in breast cancer risk will be presented, particularly in relation to breast cancer in African American women, and potential preventive strategies will be discussed.
Citation Information: Cancer Prev Res 2011;4(10 Suppl):CN04-02.
RSS Feeds