Reversal of the p53 gene from oncogenic to a normal functioning gene

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dc.contributor.advisor Olesen, James B.
dc.contributor.author Follis, Nathan K.
dc.date.accessioned 2016-01-06T15:10:08Z
dc.date.available 2016-01-06T15:10:08Z
dc.date.issued 2015-12-19
dc.identifier.uri http://cardinalscholar.bsu.edu/handle/123456789/200095
dc.description.abstract This paper will examine P53, a gene that can be mutated into an oncogenic form that can cause extensive cellular damage. Such mutations can induce a loss of cell cycle control and promote abnormal cellular growth resulting in tumor formation. The feasibility of mutating P53 back into its original non-oncogenic form will be examined and discussed. Thus, by mutating the oncogenic P53 gene, it could allow the cell to regain cell cycle control and inhibit further cancerous growth. Genes P16 and P21 will also be included in the discussion because of their immense implication in aberrant growth control. P53, if mutated from the cancerous form into the original form, could reverse multiple types of cancer and activate various tumor suppressor genes that have altered function due to a P53 mutation. en_US
dc.description.sponsorship Department of Biology
dc.subject.lcsh p53 antioncogene.
dc.subject.lcsh p53 protein.
dc.title Reversal of the p53 gene from oncogenic to a normal functioning gene en_US
dc.type Research paper (M.A.), 3 hours.
dc.description.degree Thesis (M.A.) en_US
dc.identifier.cardcat-url http://liblink.bsu.edu/catkey/1811063


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  • Research Papers [5068]
    Research papers submitted to the Graduate School by Ball State University master's degree candidates in partial fulfillment of degree requirements.

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