Cancer genetics and epigenetics: theranostic targets and mechanisms

Cancer poses a threat to global health and is among the leading causes of mortality worldwide. Hence, a mechanistic understanding of cancer aimed toward developing successful interventions mandates particular focus. Being a multifactorial disease, the development and progress of cancer intercepts genetic alterations, epigenetic dysregulation, and environmental influences. These research topics highlight the growing knowledge of the genetic and epigenetic mechanisms of cancer, and how it can be harnessed for successful therapeutic interventions. Cancer initiates and progresses through genetic and epigenetic alterations fostered by environmental and genetic interactions. Most cancer-causing mutations damage the DNA sequence, i.e., genetic mutations, while others are dynamic and heritable but independent of the DNA sequence, i.e., epigenetic mutations. DNA mutations may be irreversible point mutations, chromosomal rearrangement, deletion, duplication, etc., or reversible epigenetic changes like alterations in methylation patterns and histone posttranslational modifications. Epigenetic mutations can disrupt methylation patterns and modify histones and nucleosome positioning to alter gene expression. Also, inactivating genetic mutations within the epigenome alters the epigenomic machinery. Therefore, an interplay of genomic and epigenomic circuits is the basis of cancer development and progression.