Show simple item record

dc.contributor.advisorFutscher, Bernard W.en_US
dc.contributor.authorRice, Judd Christopher*
dc.creatorRice, Judd Christopheren_US
dc.date.accessioned2013-05-09T09:35:24Z
dc.date.available2013-05-09T09:35:24Z
dc.date.issued2000en_US
dc.identifier.urihttp://hdl.handle.net/10150/289142
dc.description.abstractThe RNA expression of the tumor suppressor genes BRCA1 and maspin are frequently decreased or lost in sporadic breast cancer. We hypothesized that inactivation of these genes was due to aberrant epigenetic silencing at the level of gene transcription. In this study we show that aberrant cytosine methylation of the BRCA1 and maspin CpG island promoters is a common event in the inactivation of these genes in sporadic breast cancer cell lines. Furthermore, we show that the methylation-associated inactivation of BRCA1 occurs in 15-30% of sporadic breast cancer patient specimens and our data suggests that the methylation-associated inactivation of maspin occurs in ∼70% of advanced sporadic breast cancers. Additional studies indicate that the methylation associated inactivation of these genes is coincident with the repressive epigenetic events of histone hypoacetylation and chromatin condensation. These data suggest that aberrant cytosine methylation, histone hypoacetylation and chromatin condensation act together in the BRCA1 and maspin promoters to inactivate their transcription, thereby, contributing to the progression of sporadic breast cancer.
dc.language.isoen_USen_US
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.subjectBiology, Molecular.en_US
dc.subjectBiology, Genetics.en_US
dc.subjectHealth Sciences, Oncology.en_US
dc.titleEpigenetic silencing of BRCA1 and maspin in sporadic breast canceren_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.identifier.proquest9972095en_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplinePharmacology and Toxicologyen_US
thesis.degree.namePh.D.en_US
dc.identifier.bibrecord.b40639502en_US
refterms.dateFOA2018-06-16T11:02:10Z
html.description.abstractThe RNA expression of the tumor suppressor genes BRCA1 and maspin are frequently decreased or lost in sporadic breast cancer. We hypothesized that inactivation of these genes was due to aberrant epigenetic silencing at the level of gene transcription. In this study we show that aberrant cytosine methylation of the BRCA1 and maspin CpG island promoters is a common event in the inactivation of these genes in sporadic breast cancer cell lines. Furthermore, we show that the methylation-associated inactivation of BRCA1 occurs in 15-30% of sporadic breast cancer patient specimens and our data suggests that the methylation-associated inactivation of maspin occurs in ∼70% of advanced sporadic breast cancers. Additional studies indicate that the methylation associated inactivation of these genes is coincident with the repressive epigenetic events of histone hypoacetylation and chromatin condensation. These data suggest that aberrant cytosine methylation, histone hypoacetylation and chromatin condensation act together in the BRCA1 and maspin promoters to inactivate their transcription, thereby, contributing to the progression of sporadic breast cancer.


Files in this item

Thumbnail
Name:
azu_td_9972095_sip1_m.pdf
Size:
4.495Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record