The Effect of the Histone Deacetylase Inhibitor PXD101 on the Transcriptional Regulation of Diffuse Large B-Cell Lymphona

Persistent Link:
http://hdl.handle.net/10150/244400
Title:
The Effect of the Histone Deacetylase Inhibitor PXD101 on the Transcriptional Regulation of Diffuse Large B-Cell Lymphona
Author:
Klein, Mary Elizabeth
Issue Date:
May-2012
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, 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.
Abstract:
Diffuse Large B-cell Lymphoma (DLBCL) is the most common type of adult lymphoma. With current treatments this disease is curable, but remains fatal for 30-40% of patients. DLBCL is an extremely heterogeneous disease, and the lack of understanding about its variations makes it difficult to determine a second line of treatment for patients who do not respond to standard chemotherapy. Histone deacetylase inhibitors (HDACI) have been shown to be effective against blood cancers. HDACIs are known to have transcriptional and non-transcriptional effects; however, little is understood about their complex functions. Some DLBCL cell lines have been shown to be growth sensitive, while others are resistant, to the HDACI PXD101. In order to better understand both DLBCL and the mechanisms of PXD101 action, transcription factor binding site overrepresentation analysis of gene expression profiling data was used to identify signaling pathways modulated by drug treatment. Cells resistant to PXD101 were transfected with reporter vectors designed to measure the activity of specific transcription factors. Studying the transcription factor NF-κB has proven that this technique is sufficient to detect changes in activity upon drug treatment, and that the transcription factors identified can be linked to biological pathways that help explain the phenotypic response observed.
Type:
text; Electronic Thesis
Degree Name:
B.S.
Degree Level:
bachelors
Degree Program:
Honors College; Biochemistry and Molecular Biophysics
Degree Grantor:
University of Arizona

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleThe Effect of the Histone Deacetylase Inhibitor PXD101 on the Transcriptional Regulation of Diffuse Large B-Cell Lymphonaen_US
dc.creatorKlein, Mary Elizabethen_US
dc.contributor.authorKlein, Mary Elizabethen_US
dc.date.issued2012-05-
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, 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.description.abstractDiffuse Large B-cell Lymphoma (DLBCL) is the most common type of adult lymphoma. With current treatments this disease is curable, but remains fatal for 30-40% of patients. DLBCL is an extremely heterogeneous disease, and the lack of understanding about its variations makes it difficult to determine a second line of treatment for patients who do not respond to standard chemotherapy. Histone deacetylase inhibitors (HDACI) have been shown to be effective against blood cancers. HDACIs are known to have transcriptional and non-transcriptional effects; however, little is understood about their complex functions. Some DLBCL cell lines have been shown to be growth sensitive, while others are resistant, to the HDACI PXD101. In order to better understand both DLBCL and the mechanisms of PXD101 action, transcription factor binding site overrepresentation analysis of gene expression profiling data was used to identify signaling pathways modulated by drug treatment. Cells resistant to PXD101 were transfected with reporter vectors designed to measure the activity of specific transcription factors. Studying the transcription factor NF-κB has proven that this technique is sufficient to detect changes in activity upon drug treatment, and that the transcription factors identified can be linked to biological pathways that help explain the phenotypic response observed.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.nameB.S.en_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplineBiochemistry and Molecular Biophysicsen_US
thesis.degree.grantorUniversity of Arizonaen_US
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