ABSTRACT
Cancer is a leading cause of death in the United States. “Cancer” is a general term that represents more than 100 diseases, each with its own etiology. Cancer risk is in•uenced by both genetic and environmental factors, including dietary habits. While each type of cancer has unique characteristics, they share one common feature: unregulated cell division. All cancers begin when a single cell acquires multiple genetic changes and loses control of its normal growth and replication processes (Hanahan and Weinberg 2000). The cancer process, which can occur over decades, includes fundamental yet diverse, wide-ranging cellular processes that can be in•uenced by diet, such as carcinogen bioactivation, cellular differentiation, DNA repair, cellular proliferation/signaling, and apoptosis (Davis and Milner 2007). These cellular processes are altered via deregulation of key genes, resulting in an altered cellular phenotype (Wiseman 2008). Such anomalous gene expression may result from genetic disruption, i.e., mutation, or from epigenetic modulation by silencing genes that should be active or activating genes that should be silent. Diet and bioactive food factors may directly in•uence both processes.
