DNA supercoiling occurs in all cells that undergo genetic processing. This event prevents the replication and transcriptional machinery from binding to the DNA helix, which proves harmful to the cell. However, current research is beginning to show that not all supercoiling effects produce negative results. These studies demonstrate that different coiling patterns increase the efficiency of epigenetic processes such as methylation and acetylation. Topoisomerase, a monomeric post-transcriptional enzyme, solves the double helix coiling problem by implementing transient cuts in the genome. As these cuts accumulate, the genome is essentially fragmented by the enzyme and the cell is unable to express essential genes; this genomic degradation by topoisomerase serves as a viable pathway in cancer research. This review article summarizes the numerous ideas surrounding cellular topological events and presents a new direction for research on chromatin modification in cancer cells. However, due to the time constraints of the project, this article will not discuss the mechanistic process of the replication pathway in depth. INTRODUCTION: A linear strand of DNA experiences enormous torsional forces when subjected to replication. The replication mechanism applies a force as it unwinds the double strand and divides the DNA to expose the genetic information. The helicase enzyme is responsible for putting this tension on the double helix and causing the event known as supercoiling (1). This event is problematic for the cell because it can make some regions of the genome inaccessible to replicative enzymes. As a result, the vital genetic information contained in these places is not read, leading to mutations in the middle of the paper...erosions, deletions and aberrations. The introduction of suitable inhibitory factors would force the topoisomerase to leave a partially degraded mutated genome, thus blocking the replication of cancer cells (3). Catalytic topoisomerase inhibitors are a diverse group of compounds that interfere with DNA and topoisomerase binding, stabilize noncovalent DNA-topoisomerase complexes, or inhibit ATP binding (9). Most catalytic inhibitors have additional targets and activities that likely contribute to their biological effects. Topoisomerase poisons can be used, along with inhibitors, to induce cellular tumor suppression. Poisons increase the steady-state concentration of their covalent DNA cleavage complexes; this action converts the topoisomerase into a physiological toxin that introduces high levels of protein-associated transient breaks into the genome of treated cells.