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dc.contributor.advisorThatcher, Gregory
dc.creatorLu, Yunlong
dc.date.accessioned2019-08-06T14:17:52Z
dc.date.available2019-08-06T14:17:52Z
dc.date.created2019-05
dc.date.issued2019-04-18
dc.date.submittedMay 2019
dc.identifier.urihttp://hdl.handle.net/10027/23690
dc.description.abstractEstrogen receptors (ERs) are nuclear hormone receptors and regulate many target genes associated with cell survival, growth and development. ERs act as transcription factors and bind to estrogen and initiate gene expression that regulates biological activities, such as bone remodeling, cardiovascular system functioning, reproductive organ development, metabolism and behavior. In ER+ breast cancer, ER plays a significant role in emergence, progression and metastasis of disease pathogenesis. Multiple therapeutic approaches have been directly or indirectly targeted at the ER signaling pathway to disturb its function. Selective estrogen receptor modulators (SERMs), i.e. tamoxifen, aromatase inhibitors (AIs) i.e. anatrozole, and selective estrogen receptor degraders (SERDs) i.e. fulvestrant are developed to restrict the bioactivity of ER and serve as endocrine therapy for treatment resistant ER+ breast cancer.
dc.format.mimetypeapplication/pdf
dc.subjectBreast cancer
dc.subjectER+
dc.subjectbasic-amino selective estrogen receptor degraders (B-SERDs)
dc.subjectSelective mixed-function estrogen receptor degraders (SMERDs)
dc.titleNovel Treatment for ER+ Treatment Resistant Breast Cancer
dc.typeThesis
thesis.degree.departmentMedicinal Chemistry and Pharmacognosy
thesis.degree.grantorUniversity of Illinois at Chicago
thesis.degree.levelDoctoral
thesis.degree.namePhD, Doctor of Philosophy
dc.contributor.committeeMemberDiMagno, Steven
dc.contributor.committeeMemberJohnson, Jeremy
dc.contributor.committeeMemberHickok, Jason
dc.contributor.committeeMemberMoore, Terry
dc.contributor.committeeMemberBolton, Judy
dc.type.materialtext
dc.contributor.chairThatcher, Gregory


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