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dc.contributor.authorDiss, Eric
dc.date.accessioned2012-02-10T21:02:25Z
dc.date.available2012-02-10T21:02:25Z
dc.date.issued2010
dc.identifier.urihttp://hdl.handle.net/10713/917
dc.descriptionUniversity of Maryland in Baltimore. Molecular Medicine. M.S. 2010en_US
dc.description.abstractGlioblastoma is an aggressive form of brain cancer that limits patients to an average survival of 12 months after diagnosis [9]. Long term survival is limited by an inability to completely eradicate glioblastomas even with high dose radiation. Glioblastoma's aggressiveness allows it to regenerate rapidly if even trace amounts of the cancerous cells are alive [9]. Even when combined with drugs such as temozolomide current standards of care call for partial brain radiation of 60 Gy [10]. Such high doses have detrimental effects on patients to include extreme nausea, skin damage, hair loss, general malaise, and links have been found to reduction in life expectancy [9]. In order to reduce these adverse effects, drugs that induce radiosensitization such as Vorinostat (SAHA), are key to furthering cancer research. By inducing a conformational change to a more open form in chromatin structure, HDAC inhibitors could sensitize cancer cells to radiation treatments that are harmful to the brain.en_US
dc.language.isoen_USen_US
dc.subjectHDACIen_US
dc.subjectp53en_US
dc.subjectPTENen_US
dc.subjectradiosensitivityen_US
dc.subjectvorinostaten_US
dc.subject.meshGlioblastomaen_US
dc.subject.meshRadiation-Sensitizing Agentsen_US
dc.titleHyper-radiosensitization Induced by the Histone Deacetylase Inhibitor Vorinostat, in glioblastomaen_US
dc.typedissertationen_US
dc.contributor.advisorCarrier, France
dc.identifier.ispublishedYesen_US
dc.description.urinameFull Text
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