ABSTRACT
A frequently observed feature of many cancer cells is a decrease in their capacity to repair damaged DNA, which leads in turn to an enhanced mutation rate. The preference for clustered genomic loci means that cancer-associated DNA hypomethylation frequently involves repeated DNA elements, such as long interspersed nuclear elements, whereas cancer-associated hypermethylation seems to occur predominantly in the nonrepeated regions of the genome. The consequences of DNA hypomethylation that can lead to cancer formation depend for the most part on the genomic loci that are affected by this aberration. In many types of cancer cells, genes encoding histone acetyltransferase enzymes are known to undergo translocations that could change their expression levels, which could in turn alter the ability of the cell to maintain an appropriate level of acetylation at tumor suppressor loci. The leukemias as a group are probably the twelfth most common form of neoplastic disease and the eleventh most common cause of cancer-related death.
