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Chapter 3: Epigenetics of Cancer Epigenetics of Cancer: Introduction Cancer is a disease involving the failure of function of regulatory genes that control normal cellular homeostasis. The key roles of mutational processes in the generation of human cancer have been identified in the past decades. More recently the potential for epigenetic processes to complement genetic changes has been realized. In addition to multiple mutations, almost all human cancers contain substantial epigenetic abnormalities that cooperate with genetic lesions to generate the cancer phenotype. Epigenetic aberrations arise early in carcinogenesis preceding gene mutations and therefore provide targets for early detection. Epimutations may be reversed by drug treatments, providing the opportunity to design epigenetic therapies. This chapter will describe t he role of epigenetic processes in cancer etiology and discuss their potential as biomarkers for early detection of cancer and precancerous lesions and their promise for drug development. Epigenetic Processes Epigenetic processes are essential to ensure the appropriate packaging of the genome to fit within the confines of the mammalian nucleus, while maintaining its functionality. DNA is not found as a naked molecule in the nucleus but is wrapped up in nucleosomes composed of histone octamers and 146 base pairs (bp) of DNA, which are the fundamental building blocks of chromatin. Epigenetics is fundamental to organismal development: pluripoten t cells arising at fertilization progressively lose their plasticity as they move through the consecutive differentiation steps necessary for embryogenesis. The recent development of whole epigenome approaches allows for the appreciation of the plethora of epigenomic processes that occur during development and the understanding of their role in activation and silencing of regulatory pathways. The development of “next generation” sequencing approaches coupled with chromatin immunoprecip itation permits assessment of the distribution of the chemical “marks” imparted on the chromatin proteins and DNA. These epigenetic marks include DNA methylation and histone modifications (Table 3.1) and allow the orchestration of activation and silencing pathways. The marks or chemical modifications are placed on the chromatin components by enzymes such as methyltransferases and some of them can be r emoved by other enzymes (Table 3.1). While we are just beginning to understand the potential roles of specific chemical marks in ensuring the mitotically heritable variation in cell metabolism, which does not involve direct changes in the DNA sequence itself, the key role of a subset of these marks in controlling the potential for gene expression is becoming apparent (Table 3.1).

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