Monday, May 13, 2019
DNA repair mechanisms role in survival to nucleoside analogues Thesis
desoxyribonucleic acid redress mechanisms role in survival to nucleoside analogues treatment in S.pombe - Thesis ExampleTwo methods of treatment where this is especially important to interpret are topoisomerase inhibitors and nucleoside analogues. In both of these cases, DNA repair systems involve the use of the Mre11/Rad50/NBS1 complex. This project aims to examine how DNA repair mechanisms of Schizosaccharomyces pombe contribute to resistance to treatment with nucleoside analogues. This information should help to domiciliate further cleverness into the delegacy in which human jail cells are able to develop resistance to this form of treatment, and possibly provide some indication of a method to prevent this.In everyday life, cells are exposed to outer and internal agents that cause thousands of DNA mutations per day. These mutations range from being small, such as affecting a case-by-case nucleotide, to large mutations where accurate repair can be difficult. For the accura te propagation of the genetic information at bottom cells, it is essential that the body has mechanisms of repairing damage in a reliable manner. However, while many methods for DNA repair exist, these are not always successful and mutations can accumulate, resulting in the development of cancer (Helleday et al., 2007). Understanding these processes, wherefore they occur the way that they do and what can be done to influence these is crucial for knowing the way that cancer occurs, and determining methods of treating it effectively.In our modern society, cancer has remained one of the most well studied diseases and perhaps one of the least understood. The fundamental aspects of cancer are damage in the DNA of a cell that results in a lack of control over cell growth and replication, as well diminution the likelihood that cells will enter apoptosis. These cells are able to proliferate well beyond the normal constraints of the tissue that they are in (Loeb et al., 2003). With high levels of replication and low cell death, abnormal cells build up
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