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dc.contributor.authorGrecu, Iulius
dc.date.accessioned2018-02-26T23:22:35Z
dc.date.available2018-02-26T23:22:35Z
dc.date.issued2018-02-26
dc.identifier.urihttp://hdl.handle.net/10150/626852
dc.descriptionA Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.en
dc.description.abstractGlioblastoma multiforme (GBM) is among the most aggressive and lethal of all human cancers. Characteristically, GBM is genetically heterogenous with different tumors portions exhibiting vastly different genetic profiles. Due to this, GBM patients are plagued with poor prognosis and high recurrence rates. Within the last decade there has been an increase in knowledge of the molecular finger print of GBM but improvement in patient outcome has been slow as personalized treatment regimens have not been linked to significant improvement. However, there is hope with feasible multiagent personalized regimens as well as expanding the amount of treatment options with repurposed agents and immunologic modulators improving patient outcomes. One hypothesized gene of interest in tumor development and progression is PTEN. In this study we investigate two repurpose agents Metformin and Chlorpromazine which are thought to depress downstream oncogenic proteins specific to the PTEN pathway using a cell culture model. For this study four Xenograft cell lines with differing PTEN status were treated with titrated concentrations of Metformin and Chlorpromazine. After treatment, results were quantified by SiRNA function using cell-titer glo assay a marker for cell viability.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the College of Medicine - Phoenix, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subject.meshMetforminen
dc.subject.meshChlorpromazineen
dc.titleTargeted Treatment on PTEN Mutated GBM Cell Lines using Metformin and Chlorpromazineen_US
dc.typetext; Electronic Thesisen
dc.contributor.departmentThe University of Arizona College of Medicine - Phoenixen
dc.description.collectioninformationThis item is part of the College of Medicine - Phoenix Scholarly Projects 2018 collection. For more information, contact the Phoenix Biomedical Campus Library at pbc-library@email.arizona.edu.en_US
dc.contributor.mentorTran, Nhanen
refterms.dateFOA2018-08-18T22:44:16Z
html.description.abstractGlioblastoma multiforme (GBM) is among the most aggressive and lethal of all human cancers. Characteristically, GBM is genetically heterogenous with different tumors portions exhibiting vastly different genetic profiles. Due to this, GBM patients are plagued with poor prognosis and high recurrence rates. Within the last decade there has been an increase in knowledge of the molecular finger print of GBM but improvement in patient outcome has been slow as personalized treatment regimens have not been linked to significant improvement. However, there is hope with feasible multiagent personalized regimens as well as expanding the amount of treatment options with repurposed agents and immunologic modulators improving patient outcomes. One hypothesized gene of interest in tumor development and progression is PTEN. In this study we investigate two repurpose agents Metformin and Chlorpromazine which are thought to depress downstream oncogenic proteins specific to the PTEN pathway using a cell culture model. For this study four Xenograft cell lines with differing PTEN status were treated with titrated concentrations of Metformin and Chlorpromazine. After treatment, results were quantified by SiRNA function using cell-titer glo assay a marker for cell viability.


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