DNA provides the instructions and regulation of cell growth and survival. Mutations in DNA can cause uncontrolled and unregulated cell proliferation, resulting in cancer. Treatment of cancer involves physical removal of these cells through surgery or inducing cell death by causing irreversible damage to DNA through chemotherapy and radiotherapy. However, natural DNA repair mechanisms may interfere with therapy and may even be increased in cases of therapy resistant cancer. The use of chemotherapy and radiotherapy leads to increased recruitment of DNA repair proteins while aggressive, therapy resistant cancers show overexpression of DNA repair proteins. Rad51 is a protein involved in the homologous recombination (HR) DNA repair process. Rad51 is recruited to sites of DNA damage caused by double stranded breaks, often generated by chemotherapy and radiotherapy. It is expected that inhibition of Rad51 will impair the HR repair process while enhancing the effectiveness of chemotherapy and radiotherapy compared to conventional means. As a result, this literature review aims to identify and examine the drug inhibitors of Rad51 in order to demonstrate the potential viability of this novel treatment in a variety of cancers.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/15618 |
| Date | 12 March 2016 |
| Creators | Le, Douglas |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
| Rights | Attribution 4.0 International, http://creativecommons.org/licenses/by/4.0/ |
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