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DNA repair mechanisms role in survival to nucleoside analogues treatment in S.pombe - Thesis Example

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Edgar Hartsuiker for his support and Andrea for her invaluable advice and supervision. I am grateful to the Government of the Kingdom of Saudi Arabia for support me to finished this course.
The human is exposed to a large number of agents each day that…
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DNA repair mechanisms role in survival to nucleoside analogues treatment in S.pombe
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Two methods of treatment where this is especially important to consider 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 provide further insight into the way in which human cells are able to develop resistance to this form of treatment, and perhaps provide some indication of a method to prevent this.

In everyday life, cells are exposed to external and internal agents that cause thousands of DNA mutations per day. These mutations range from being small, such as affecting a single nucleotide, to large mutations where accurate repair can be difficult. For the accurate propagation of the genetic information within 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, why 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 reducing 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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