ABSTRACT
Our genome contains information related to gene structure and function but when and how long that information is utilized is determined by our epigenome. Epigenetics includes alterations in gene expression that do not include a change in DNA sequence during growth, development, and disease states (Ballestar and Esteller 2008). For normal function of a cell or organ, epigenetic regulation is needed; however, this regulation is disturbed during disease initiation and progression. Thus our genome is the “hardware” and our epigenome is the “software” of the body. Genetic information is static whereas epigenetic information is dynamic and transient. In the body, all the cells have the same genome but each cell has a different epigenome. The phenotype of a cell is determined by its epigenome (Murrell et al. 2005). Environmental factors (e.g., exposure to radiation, infectious agents), nutrients, toxins, and disease states affect the epigenome resulting in altered gene expression (Verma 2003; Kumar and Verma 2009) (Figure 1.1). Epigenetic changes can be measured quantitatively and followed during the progression/regression and recurrence of a disease (Ganesan et al. 2009; Feinberg 2010; Verma et al., 2004; 2006). This chapter compiles existing knowledge regarding the application of epigenetics toward understanding the dynamic interrelationship between bioactive food components (and/or a combination thereof) and cancer prevention.
