The Generation, Detection, and Prevention of Genomic Instability During Cancer Progression and Metastasis

© Springer International Publishing Switzerland 2015 C. Maxwell, C. Roskelley (eds.), Genomic Instability and Cancer Metastasis, Cancer Metastasis Biology and Treatment 20, DOI 10.1007/978-3-319-12136-9_2 C. Maxwell () · H. Chen · M. Connell Department of Pediatrics, Child & Family Research Institute, University of British Columbia, Room 3086, 950 W 28th Ave., Vancouver, BC V5Z 4H4, Canada e-mail: [email protected] Abstract Genome stability is tightly regulated through the cell cycle. Aberrations in genome structure and sequence are a hallmark of malignancy and these changes can allow abnormal cells to escape the regulatory mechanisms that would otherwise direct these cells into apoptosis or senescence. When genome instability occurs, it can happen as large or small structural changes in the genome, changes in gene expression, or even changes at the epigenetic level. There are many environmental factors that can induce DNA damage and strain the machinery that is responsible for maintaining genome stability. In some cases, such as UV light or chemical carcinogens, it is possible to avoid these factors and thus reduce the risk of cancer. But, in other instances, hereditary mutations impair the function of genes and their products, which normally protect the stability of the genome. While genomic instability offers selective advantages to the tumor, the tumor-specific loss of these pathways may provide therapeutic opportunities, which could be personalized through knowledge of the specific types of genomic instability that characterize an individual’s tumor.