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"October 2003" / Bibliography: leaves 223-271. / xiii, 271 leaves : ill. (some col.), plates (col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / 1. Hormonal control of human breast cancer -- 2. General materials and methods -- 3. Proliferative effects of androgens -- 4. Cross-talk between androgen and estrogen signalling pathways -- 5. Androgen receptor function in the MDA-MB-453 cell line -- 6. Gene expression profiles in breast cancer cells: identification of androgen regulated genes -- 7. Regulation of BRCA1 expression -- 8. Regulation of prostate specific antigen expression -- 9. General discussion. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 2004

Thesis (Ph. D.)--University of Texas at Austin, 2002. / Vita. Includes bibliographical references (leaves 125-138). Available also in a digital version from Dissertation Abstracts.

Thesis (M.S.)--Boise State University, 2009. / Title from t.p. of PDF file (viewed Feb. 23, 2010). Includes abstract. Includes bibliographical references.

Thesis (Ph. D.)--University of Texas at Austin, 2002. / Vita. Includes bibliographical references. Available also from UMI Company.

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The human androgen receptor (hAR) is a ligand-activated, DNA-binding nuclear transcription factor. Mutations in the hAR result in varying degrees of androgen insensitivity (AI); they may play a predisposing or pathogenetic role in both prostate and breast cancer. Expansion of the hAR's N-terminal polymorphic Glutamine (Gln) repeat causes a late-onset progressive motoneuronopathy which is associated with mild androgen insensitivity: spinal and bulbar muscular atrophy (SBMA). SBMA belongs to a group of translated CAG trinucleotide repeat expansion neuronopathies that includes Huntington disease, dentatorubral-pallidoluysian atrophy and five distinct spinocerebellar ataxias. The fact that this group of disorders is caused by polyGln expansions in totally unrelated proteins, is one of the main reasons for postulating that a common gain-of-function mechanism must underlie their communal pathogenesis. This common pathogenetic mechanism is postulated to occur via aberrant protein interactions. / I undertook a search for hAR-interacting proteins using a yeast two-hybrid system. A human testes cDNA library was screened several times with two forms of an N-terminal fragment of the hAR: a normal (20 Gin) hAR and an expanded (50 Gin) hAR. A few candidate hAR-interacting proteins were isolated during the library screenings and I tested them for physiological relevance. / A second aspect of my project included the analysis of an aberrant 75-kD protein fragment generated in COS-1 cells transfected with a polyCAG-expanded (n = 44) hAR cDNA. Recent work in Huntington disease and spinocerebellar ataxia type 3 shows the accumulation of insoluble protein aggregates primarily in the nucleus of certain brain cells (Davies et al., 1997; Scherzinger et al., 1997; Paulson et al., 1997). I confirmed the presence of the aberrant hAR-fragment in the nucleus through western analysis of protein samples extracted from the nucleus.