subject:(estrogen receptor)

1. Magruder, Hilary. Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression.

Degree: PhD, Pathobiology, 2014, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:386260/

► Stimulation of estrogen receptor (ER)-negative human breast cancer cells with 17β-estradiol (E2β) results in fibronectin (FN) matrix assembly and transactivation of the epidermal growth factor… (more)

▼ Stimulation of estrogen receptor (ER)-negative human breast cancer cells with 17β-estradiol (E2β) results in fibronectin (FN) matrix assembly and transactivation of the epidermal growth factor receptor (EGFR) via the G protein-coupled estrogen receptor (GPER). This mechanism of action results in the recruitment of FN-engaged integrin α5β1 to fibrillar adhesions and the formation of integrin α5β1-Shc adaptor protein complexes. Here, we show that GPER stimulation of murine 4T1 or human SKBR3 breast cancer cells promotes the formation of focal adhesions, actin stress fibers, and results in increased cellular adhesion and haptotaxis on FN, but not collagen. These actions are also induced by the xenoestrogen, bisphenol A, and the ER antagonist, ICI 182, 780, but not the inactive stereoisomer, 17α-estradiol (E2α). In addition, we show that GPER stimulation of breast cancer cells allows for FN-dependent, anchorage-independent growth and FN fibril formation in hanging drop assays, indicating that these GPER-mediated actions occur independently of adhesion to solid substrata. Furthermore, stable expression of Shc mutant Y317F lacking its primary tyrosyl phosphorylation site disrupts E2β-induced focal adhesion and actin stress fiber formation, and abolishes E2β-enhanced haptotaxis on FN and anchorage-dependent growth. We also show that overexpression of a phosphatase, PTPN12, known to interact with Shc inhibits focal adhesion and FN fibril formation, adhesion and haptotaxis on FN, and anchorage independent growth. Moreover, PTPN12 knockdown positively influences these events associated with cellular survival. Collectively, these data demonstrate that E2β action via GPER enhances cellular adhesivity and FN matrix assembly and allows for anchorage-independent growth, cellular events that may allow for cellular survival and tumor progression. Advisors/Committee Members: Filardo, Edward (Director), Reichner, Jonathan (Reader), Freiman, Richard (Reader), Yang, Wentian (Reader), Prossnitz, Eric (Reader).

Subjects/Keywords: estrogen receptor (ER)

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APA (6^th Edition):

Magruder, H. (2014). Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:386260/

Chicago Manual of Style (16^th Edition):

Magruder, Hilary. “Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression.” 2014. Doctoral Dissertation, Brown University. Accessed June 18, 2018. https://repository.library.brown.edu/studio/item/bdr:386260/.

MLA Handbook (7^th Edition):

Magruder, Hilary. “Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression.” 2014. Web. 18 Jun 2018.

Vancouver:

Magruder H. Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression. [Internet] [Doctoral dissertation]. Brown University; 2014. [cited 2018 Jun 18]. Available from: https://repository.library.brown.edu/studio/item/bdr:386260/.

Council of Science Editors:

Magruder H. Signaling Effectors Required for G Protein-Coupled Estrogen Receptor-, GPER, Induced Events Associated with Breast Cancer Progression. [Doctoral Dissertation]. Brown University; 2014. Available from: https://repository.library.brown.edu/studio/item/bdr:386260/

University of Illinois – Urbana-Champaign

2. Parent, Alexander A. Second-site inhibitors of the estrogen and androgen hormone receptors.

Degree: PhD, 0335, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/29523

► The estrogen and androgen receptors are members of the nuclear hormone receptor protein superfamily and play an important role in the development of primary and… (more)

Subjects/Keywords: estrogen receptor; androgen receptor; inhibitor; nuclear receptor

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APA (6^th Edition):

Parent, A. A. (2012). Second-site inhibitors of the estrogen and androgen hormone receptors. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29523

Chicago Manual of Style (16^th Edition):

Parent, Alexander A. “Second-site inhibitors of the estrogen and androgen hormone receptors.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed June 18, 2018. http://hdl.handle.net/2142/29523.

MLA Handbook (7^th Edition):

Parent, Alexander A. “Second-site inhibitors of the estrogen and androgen hormone receptors.” 2012. Web. 18 Jun 2018.

Vancouver:

Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/2142/29523.

Council of Science Editors:

Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29523

Boston University

3. Koomson, Jacqueline Nyarkoa. The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.

Degree: MS, Medical Sciences, 2017, Boston University

URL: http://hdl.handle.net/2144/23835

► Uterine leiomyomas are benign tumors within the uterus, where patients present with symptoms such as abnormal bleeding, urinary retention, and pelvic pressure. The exact etiology… (more)

▼ Uterine leiomyomas are benign tumors within the uterus, where patients present with symptoms such as abnormal bleeding, urinary retention, and pelvic pressure. The exact etiology of uterine leiomyomas is unknown, but numerous theories have been proposed, indicating a multifactorial mechanism, including lifestyle and steroid hormones. Uterine leiomyomas have become a public health concern due to the high cost of treatment as well as the high prevalence within African American communities. Currently, many treatment options exist, ranging from conservative treatments that address symptoms, to surgical intervention to remove the uterus. Research efforts thus far have determined the relationship between the role of estrogen in the growth of uterine leiomyomas (which has led to development of medications that target different approaches to estrogen synthesis) and its effects in the pathogenesis. Studies have shown that estrogen acts on estrogen receptor subtypes, ER and ER. This study examines the role of these two receptors in estrogenic effects, and how these effects relate to the development of uterine leiomyomas. Available research has shown that each receptor has its unique functions and impacts the growth of tumors differently. There is conflicting evidence in how the number of receptors and surrounding environment modulate leiomyomas, with some studies reporting that it is the corepressors and/or coactivators that ultimately determine the influence of estrogenic effects. However, the general consensus of such studies suggests that estrogen receptor-specific therapeutic intervention is a novel area with great potential. The primary benefit of estrogen receptor-specific treatment, such as selective estrogen receptor modulators, is the ability to regulate physiological processes that contribute to the growth of uterine leiomyomas. Future directions of research include confirming the exact roles of ER and ER and harnessing the effects of their differing functions to manage uterine leiomyomas.

Subjects/Keywords: Medicine; Estrogen; Estrogen receptor alpha; Estrogen receptor beta; Receptor-mediated therapies; Uterine fibroids; Uterine leiomyoma

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APA (6^th Edition):

Koomson, J. N. (2017). The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23835

Chicago Manual of Style (16^th Edition):

Koomson, Jacqueline Nyarkoa. “The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.” 2017. Masters Thesis, Boston University. Accessed June 18, 2018. http://hdl.handle.net/2144/23835.

MLA Handbook (7^th Edition):

Koomson, Jacqueline Nyarkoa. “The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.” 2017. Web. 18 Jun 2018.

Vancouver:

Koomson JN. The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. [Internet] [Masters thesis]. Boston University; 2017. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/2144/23835.

Council of Science Editors:

Koomson JN. The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23835

University of Otago

4. Tran, Khanh Bao. Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer .

Degree: 2012, University of Otago

URL: http://hdl.handle.net/10523/2292

► Approximately one in five breast cancer patients exhibits triple negative tumors that are characterized by the lack of estrogen receptor (ER), progesterone receptor and HER2.… (more)

▼ Approximately one in five breast cancer patients exhibits triple negative tumors that are characterized by the lack of estrogen receptor (ER), progesterone receptor and HER2. While ER and HER2 positive tumors are responsive respectively to ER antagonists and anti-HER2 antibodies, triple negative breast cancer (TNBC) tumors do not benefit from any of these therapies. As a result, it is imperative to search for alternative treatments for this subtype. Since synthetic cannbinoids has been shown to possess anticancer effects in a number of other cancer types, we therefore hypothesize that synthetic cannabinoids also have anticancer effects against TNBC tumors. The current study focused on the anticancer potential against TNBC of two synthetic cannabinoids, WIN55,212-2 and JWH-133. In vitro cytotoxicity assessment demonstrated that WIN55,212-2 inhibited the proliferation in vitro of MDA-MB-231 and MDA-MB-468 TNBC cells in a dose-dependent and time-dependent manner; whereas JWH-133 showed no significant cytotoxicity up to 30 µM in MDA-MB-231 and 10 µM in MDA-MB-468 cells. Flow cytometry experiments demonstrated that treatment with WIN55,212-2 (6 µM) for 24 h, 36 h and 48 h significantly increased the proportion of MDA-MB-231 and MDA-MB-468 cells in G1 phase. In vivo, mice bearing MDA-MB-468 xenografts and treated with WIN55,212-2 (25 µg/day i.p. for 10 weeks) showed a significant 76% reduction in tumour volume compared to vehicle treated mice, and this effect was reversed by 60% by co-treatment with CB2 antagonist AM630. In contrast, JWH-133 (25 µg/day i.p. for 10 weeks) increased tumor volume by 166% compared to vehicle treated mice and this acceleration effect was abolished by co-treatment of AM630. Toxicity profiling studies showed that mice remained healthy after long-term treatment with either WIN55,212-2 or JWH-133 confirmed by no significant change in body weight or major organ weight, and normal plasma ALT levels for each treatment group. Assessment of receptor expression status demonstrated the presence of both CB1 and CB2 cannabinoid receptors in MDA-MB-468 xenografts. Importantly, WIN55,212-2 treatment significantly downregulated the expression of both CB1 and CB2 receptors while tended to downregulate EGFR expression. JWH-133 treatment on the other hand was associated with a tendency to activate EGFR. Furthermore, the current study demonstrated for the first time that WIN55,212-2 treatment activated p38 MAPK and inhibited NF-κB expression in the TNBC tumors; whereas JWH-133 treatment tended to activate the survival Akt and β-catenin pathways and the inhibition of p27. The results strongly suggest the diversity in biological effects and complexity in molecular mechanisms of different cannabinnoids, and that a re-consideration on the use of cannabinoids in cancer patients might be needed. Advisors/Committee Members: Rosengren, Rhonda (advisor).

Subjects/Keywords: cannabinoids; breast cancer; estrogen receptor

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APA (6^th Edition):

Tran, K. B. (2012). Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer . (Masters Thesis). University of Otago. Retrieved from http://hdl.handle.net/10523/2292

Chicago Manual of Style (16^th Edition):

Tran, Khanh Bao. “Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer .” 2012. Masters Thesis, University of Otago. Accessed June 18, 2018. http://hdl.handle.net/10523/2292.

MLA Handbook (7^th Edition):

Tran, Khanh Bao. “Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer .” 2012. Web. 18 Jun 2018.

Vancouver:

Tran KB. Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer . [Internet] [Masters thesis]. University of Otago; 2012. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10523/2292.

Council of Science Editors:

Tran KB. Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer . [Masters Thesis]. University of Otago; 2012. Available from: http://hdl.handle.net/10523/2292

Cornell University

5. Melville, Katherine. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading .

Degree: 2014, Cornell University

URL: http://hdl.handle.net/1813/38857

► Decreased bioavailable estrogen levels are a major cause of bone loss in postmenopausal women, but sex hormones are important regulators of bone mass in both… (more)

▼ Decreased bioavailable estrogen levels are a major cause of bone loss in postmenopausal women, but sex hormones are important regulators of bone mass in both sexes. Estrogen signaling in bone occurs mainly through estrogen receptors ER[alpha] and ER[beta]. ER[alpha] in particular is important in regulating bone mass and bone's response to mechanical loading, but its particular role in each bone cell type and its cross-talk with BMP signaling are not well studied. ` Osteoblast-specific ER[alpha] knockout (pOC-ER[alpha]KO) and littermate control (LC) were bred by crossing Osteocalcin-Cre and ER[alpha]fl/fl mice. The effects of removing ER[alpha] in osteoblasts and osteocytes on bone mass, bone strength, and bone's response to mechanical loading were studied in 10-week-old animals. In general, cancellous and cortical bone mass were both reduced in pOC-ER[alpha]KO female mice, while bone mass was increased in pOC-ER[alpha]KO male mice compared to their sex-matched LC, measured by microCT in the proximal and midshaft tibia, femur, and L5 vertebra. These bone mass changes correlated with decreased vertebral compressive strength in female knockout mice and increased femoral bending strength in male knockout mice. After two weeks of in vivo tibial compression, female pOC-ER[alpha]KO mice showed a greater increase in bone mass in the proximal tibia, where baseline bone mass was decreased, and at the tibial midshaft, where baseline bone mass was similar to LC. Male pOC-ER[alpha]KO mice exhibited a normal response to mechanical loading. Next, 10-week-old female pOC-ER[alpha]KO and LC mice were administered either RAP-661, a BMPR1a inhibitor, or placebo, and all mice were subjected to daily in vivo tibial compression for two weeks. RAP-661 markedly increased bone mass in the L5 vertebra and cancellous tibial metaphysis of both genotypes, but not at the femoral midshaft, tibial midshaft, or tibial metaphyseal cortex. In the vertebra, the drug-induced increase in bone mass was less in pOC-ER[alpha]KO mice than LC. Animals treated with RAP-661 responded less to mechanical loading in the tibial metaphysis than placebo animals, but similarly at the tibial midshaft. This is the first evidence to indicate that BMPR1a may mediate bone's response to mechanical loading and interact with ER[alpha] in osteoblasts in vivo. Advisors/Committee Members: Hernandez, Christopher J. (committeeMember), Schimenti, John C. (committeeMember).

Subjects/Keywords: estrogen receptor alpha; bone; loading

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APA (6^th Edition):

Melville, K. (2014). Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/38857

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Melville, Katherine. “Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading .” 2014. Thesis, Cornell University. Accessed June 18, 2018. http://hdl.handle.net/1813/38857.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Melville, Katherine. “Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading .” 2014. Web. 18 Jun 2018.

Vancouver:

Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading . [Internet] [Thesis]. Cornell University; 2014. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1813/38857.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading . [Thesis]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/38857

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

6. Lee, Wan-Ru. Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3).

Degree: 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-1207

► The estrogen receptor (ER) is a ligand-activated transcription factor that regulates gene expression. The classical mechanisms of nuclear ER action include ligand-induced dimerization of ER… (more)

▼ The estrogen receptor (ER) is a ligand-activated transcription factor that regulates gene expression. The classical mechanisms of nuclear ER action include ligand-induced dimerization of ER which binds estrogen responsive elements (EREs) in promoters of target genes. In addition, non-genomic pathways of ER action have also been identified in breast cancer cells. Cdc25A is a tyrosine phosphatase that catalyzes dephosphorylation of cyclin/cyclin-dependent kinase complexes to regulate G1- to S-phase cell cycle progression. Cdc25A mRNA levels are induced by 17?-estradiol (E2) in ZR-75 breast cancer cells, and deletion analysis of the Cdc25A promoter identified the -151 to -12 region as the minimal E2-responsive sequence. Subsequent mutation/deletion analysis showed that at least three different cis-elements were involved in activation of Cdc25A by E2, namely, GC-rich Sp1 binding sites, CCAAT motifs, and E2F sites. Studies with inhibitors and dominant negative expression plasmids show that E2 activates Cdc25A expression through activation of genomic ER?/Sp1 and E2F1 and cAMP-dependent activation of NF-YA. Thus, both genomic and non-genomic pathways of estrogen action are involved in induction of Cdc25A in breast cancer cells. The PIAS family was initially identified as cytokine-induced inhibitors of STATs which contain several conserved domains involved in binding to other nuclear coactivators. In this study we have investigated coactivation of ER? by PIAS3 in breast cancer cell lines transiently cotransfected with the pERE3 constructs which contain three tandem EREs linked to a luciferase reporter gene. PIAS3 coactivated ER?-mediated transactivation in cells cotransfected with pERE3 and wild-type ER?. In contrast to many other coactivators, PIAS3 also enhanced transactivation of ER? when cells were cotransfected with the TAF1 ER? mutant. In addition, PIAS3 does not interact with activation function 2 (AF2) domain of ER? in a mammalian two-hybrid assay. These data indicate that coactivation of ER? by PIAS3 was AF2-domain independent. Analysis of several PIAS3 deletion mutants showed that the region containing amino acids 274 to 416 of PIAS3 are required for coactivation suggesting that the RING finger domain and acidic region of PIAS3 are important for interactions with wild-type ER?. These results demonstrate that PIAS3 coactivated ER? and this represents a non-classical LXXLL-independent coactivation pathway. Advisors/Committee Members: Safe, Stephen H. (advisor), Burghardt, Robert C. (committee member), Phillips, Timothy D. (committee member), Porter, Weston W. (committee member).

Subjects/Keywords: Estrogen receptor; Cdc25A; PIAS3

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APA (6^th Edition):

Lee, W. (2009). Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3). (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-1207

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lee, Wan-Ru. “Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3).” 2009. Thesis, Texas A&M University. Accessed June 18, 2018. http://hdl.handle.net/1969.1/ETD-TAMU-1207.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lee, Wan-Ru. “Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3).” 2009. Web. 18 Jun 2018.

Vancouver:

Lee W. Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3). [Internet] [Thesis]. Texas A&M University; 2009. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1207.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lee W. Mechanisms of hormonal activation of Cdc25A and coactivation of estrogen receptor alpha by protein inhibitor of activated STAT3 (PIAS3). [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1207

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. Butler, Ryan 1986-. Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.

Degree: Biology and Biochemistry, 2013, University of Houston

URL: http://hdl.handle.net/10657/956

► Ligand-activated transcription factors are a diverse group of proteins that are involved a variety of physiological processes. The purpose of these studies was to investigate… (more)

▼ Ligand-activated transcription factors are a diverse group of proteins that are involved a variety of physiological processes. The purpose of these studies was to investigate the aryl hydrocarbon receptor (AhR) knockout mouse and the effects of hormone replacement therapy on the postmenopausal breast in order to better understand the functions of the ligand-activated transcription factors AhR and estrogen receptor β (ERβ). In the first part of these studies, we investigated the AhR knockout mouse in order to further elucidate the physiological functions of AhR. These mice developed stones in their urinary bladders composed of 100% uric acid while the serum uric acid levels remained normal. We determined these stones were formed by the breakdown of DNA into uric acid from a large number of dying cells. These mice also develop fibrosis of their ventral prostates and a phenotype in the immune system similar to chronic myeloid leukemia. The second part of these studies was to investigate the effects of hormone replacement therapy on the histology and expression of various ligand-activated transcription factors in the postmenopausal breast. We treated postmenopausal women with estrogen or estrogen-progesterone therapy for 3 months and took biopsies of the breasts before and after treatment. Expression of several proteins including AhR, ERα, and ERβ were unchanged after treatment while expression of progesterone receptors was increased. Proliferation and breast density were unchanged by treatment in these breasts; however, we show possible mechanisms leading to proliferation and development of density in non-cancerous breast tissue. In conclusion, these studies revealed a role for AhR in prostatic development, uric acid formation, and leukemia, and have provided new information on the safety of short-term use of HRT. Advisors/Committee Members: Gustafsson, Jan-Åke (advisor), Warner, Margaret (committee member), Ziburkus, Jokubas (committee member), Webb, Paul (committee member).

Subjects/Keywords: aryl hydrocarbon receptor; estrogen receptor; transcription factor

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APA (6^th Edition):

Butler, R. 1. (2013). Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. (Thesis). University of Houston. Retrieved from http://hdl.handle.net/10657/956

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Butler, Ryan 1986-. “Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.” 2013. Thesis, University of Houston. Accessed June 18, 2018. http://hdl.handle.net/10657/956.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Butler, Ryan 1986-. “Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.” 2013. Web. 18 Jun 2018.

Vancouver:

Butler R1. Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. [Internet] [Thesis]. University of Houston; 2013. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10657/956.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Butler R1. Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. [Thesis]. University of Houston; 2013. Available from: http://hdl.handle.net/10657/956

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

8. Hsu, Iawen. The Roles of Estrogen Receptors in the Bladder Cancer Development.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27302

► Early studies documented the existence of sexual dimorphism in bladder cancer occurrence and progression with higher bladder cancer incidence in males than females. However, the… (more)

Subjects/Keywords: Estrogen Receptor Alpha; Estrogen Receptor Beta; MCM5; Bladder Cancer BBN; Inpp4β

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APA (6^th Edition):

Hsu, I. (2013). The Roles of Estrogen Receptors in the Bladder Cancer Development. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27302

Chicago Manual of Style (16^th Edition):

Hsu, Iawen. “The Roles of Estrogen Receptors in the Bladder Cancer Development.” 2013. Doctoral Dissertation, University of Rochester. Accessed June 18, 2018. http://hdl.handle.net/1802/27302.

MLA Handbook (7^th Edition):

Hsu, Iawen. “The Roles of Estrogen Receptors in the Bladder Cancer Development.” 2013. Web. 18 Jun 2018.

Vancouver:

Hsu I. The Roles of Estrogen Receptors in the Bladder Cancer Development. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1802/27302.

Council of Science Editors:

Hsu I. The Roles of Estrogen Receptors in the Bladder Cancer Development. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27302

University of Toronto

9. Tan, Susanna Shu Xian. Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/76045

►

Estrogens exert their effects by activating estrogen receptor alpha (ERα) and beta (ERβ). A number of different co-regulator proteins regulate the activities of both receptors.… (more)

Subjects/Keywords: Estrogen; Estrogen Receptor; Nuclear transcription factors; Receptor Signalling; TIPARP; 0307

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APA (6^th Edition):

Tan, S. S. X. (2016). Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/76045

Chicago Manual of Style (16^th Edition):

Tan, Susanna Shu Xian. “Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling.” 2016. Masters Thesis, University of Toronto. Accessed June 18, 2018. http://hdl.handle.net/1807/76045.

MLA Handbook (7^th Edition):

Tan, Susanna Shu Xian. “Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling.” 2016. Web. 18 Jun 2018.

Vancouver:

Tan SSX. Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1807/76045.

Council of Science Editors:

Tan SSX. Characterizing the Role of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly-ADP-ribose Polymerase (TIPARP) in Estrogen Receptor Signalling. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/76045

Univerzitet u Beogradu

10. Božović, Ana M., 1977-. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke.

Degree: Biološki fakultet, 2014, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get

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Biologija - Molekularna genetika kancera / Biology - Molecular genetics of cancer

Invazivni karcinom dojke je najčešći kancer kod žena. Pored genetičkih i epigenetički faktori… (more)

Subjects/Keywords: Breast cancer; estrogen receptor alpha; estrogen receptor beta; progesterone receptor; methylation; quantitative PCR

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APA (6^th Edition):

Božović, Ana M., 1. (2014). Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Božović, Ana M., 1977-. “Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke.” 2014. Thesis, Univerzitet u Beogradu. Accessed June 18, 2018. https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Božović, Ana M., 1977-. “Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke.” 2014. Web. 18 Jun 2018.

Vancouver:

Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2018 Jun 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. [Thesis]. Univerzitet u Beogradu; 2014. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Guelph

11. Ervin, Kelsy. The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice .

Degree: 2014, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818

► Social learning is a process by which an animal gains information from another; however much of the research on estrogens effects on learning focuses on… (more)

Subjects/Keywords: estradiol; social transmission of food preference; estrogen receptor alpha; estrogen receptor beta; G protein-coupled estrogen receptor; GPER; GPR30

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APA (6^th Edition):

Ervin, K. (2014). The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice . (Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ervin, Kelsy. “The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice .” 2014. Thesis, University of Guelph. Accessed June 18, 2018. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ervin, Kelsy. “The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice .” 2014. Web. 18 Jun 2018.

Vancouver:

Ervin K. The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice . [Internet] [Thesis]. University of Guelph; 2014. [cited 2018 Jun 18]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ervin K. The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice . [Thesis]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Cornell University

12. Hah, Nasun. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses .

Degree: 2011, Cornell University

URL: http://hdl.handle.net/1813/33589

► Estrogens play crucial roles in regulating gene expression in physiological and disease states. Estrogens acts through estrogen receptors (ERs) and their binding sites in genomic… (more)

▼ Estrogens play crucial roles in regulating gene expression in physiological and disease states. Estrogens acts through estrogen receptors (ERs) and their binding sites in genomic DNA to modulate transcription by RNA polymerase II. Although recent gene-specific and genomic analyses have provided considerable information about of estrogen-dependent transcription, many aspects of the estrogen signaling network have not yet been elucidated. The goal of my studies was to uncover new information about the immediate and direct effects of estrogen signaling at the cell membrane, in the cytoplasm, and in the nucleus to elucidate the underlying regulatory networks. First, I investigated an ER transcriptional coregulators, SWI/SNF, an ATPdependent chromatin remodeling complex. I explored the molecular functions of the BAF57 and BAF180 subunits of SWI/SNF using a quantitative proteomic approach called SILAC (Stable Isotope Labeling by Amino Acids in Cell Culture). I found that depletion of BAF57 results in a significant depletion of BAF180 from the SWI/SNF complex without decreasing the total cellular BAF180 levels, resulting in an accumulation of cells in the G2/M phase. Knockdown of BAF57 also causes transcriptional misregulation of cell cycle-related genes involved in the late G2 checkpoint. Collectively, these studies have elucidated the role of BAF57 and BAF180 in the transcriptional control of cell proliferation. Second, I have used GRO-Seq (Global Nuclear Run-On and Massively Parallel Sequencing) to explore the immediate effects of estrogen signaling on the transcriptome of breast cancer cells. I found that estrogen directly regulates a strikingly large fraction of the transcriptome in a rapid, robust, and unexpectedly transient manner. In addition to protein coding genes, estrogen regulates the distribution and activity of all three RNA polymerases, and virtually every class of non-coding RNA that has been described to date. I also identified a large number of previously undetected estrogen-regulated intergenic transcripts, many of which are found proximal to ER[alpha] binding sites. These results provide the most comprehensive measurement of the primary and immediate estrogen effects to date. I expect that genome-wide inferences based on the direct estrogen-regulated transcriptome in combination with estrogen-regulated signaling pathway will be useful for understanding estrogen biology. Advisors/Committee Members: Collins, Ruth N. (committeeMember), Lis, John T (committeeMember).

Subjects/Keywords: estrogen; estrogen receptor; GRO-seq; swi/snf; baf57; baf180; silac; proteomic; enhancer; edc; estrogen signaling

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APA (6^th Edition):

Hah, N. (2011). Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/33589

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses .” 2011. Thesis, Cornell University. Accessed June 18, 2018. http://hdl.handle.net/1813/33589.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses .” 2011. Web. 18 Jun 2018.

Vancouver:

Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses . [Internet] [Thesis]. Cornell University; 2011. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1813/33589.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses . [Thesis]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/33589

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Georgia State University

13. Russell, Nancy. Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen.

Degree: MS, Biology, 2010, Georgia State University

URL: https://scholarworks.gsu.edu/biology_theses/25

► Male rat sexual behavior requires aromatization of testosterone (T) to estradiol (E2) in the medial preoptic area (MPO) where estrogen receptors (ER) exist in… (more)

Subjects/Keywords: Medial preoptic area; Estrogen receptor; Estradiol

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APA (6^th Edition):

Russell, N. (2010). Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/biology_theses/25

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Russell, Nancy. “Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen.” 2010. Thesis, Georgia State University. Accessed June 18, 2018. https://scholarworks.gsu.edu/biology_theses/25.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Russell, Nancy. “Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen.” 2010. Web. 18 Jun 2018.

Vancouver:

Russell N. Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen. [Internet] [Thesis]. Georgia State University; 2010. [cited 2018 Jun 18]. Available from: https://scholarworks.gsu.edu/biology_theses/25.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Russell N. Estrogen Receptor Alpha in the Medial Preopic Area Mediates Male Rat Sexual Responses to Estrogen. [Thesis]. Georgia State University; 2010. Available from: https://scholarworks.gsu.edu/biology_theses/25

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

14. -8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.

Degree: Biology and Biochemistry, 2015, University of Houston

URL: http://hdl.handle.net/10657/2018

► Despite its slow development and our capacity for early detection using endoscopy, colorectal cancer remains the second leading cause of cancer death in the United… (more)

▼ Despite its slow development and our capacity for early detection using endoscopy, colorectal cancer remains the second leading cause of cancer death in the United States. Epidemiological studies indicate a role for estrogen in protecting against colorectal cancer. Estrogen receptor β (ERβ) has been found to be the main ER in the colon. Cell line studies have implicated that ERβ has anti-tumorigenic and anti-proliferative effects on colon cancer cells lines while human epidemiological data suggest that polymorphisms in the ERβ gene are associated with greater cancer risk and lower survival. Overexpression of ERβ changes the miRnome. Here we show that ERβ can alleviate the progression of colon cancer by inhibiting proliferation through decreasing MYC transcription and therefore decreasing levels of miR-17-92 (OncomiR-1). This is reflected in a decrease in cell number, decrease in migration, and increase in apoptosis. Furthermore, addition of miR-17 using miRNA mimics reverses the effects of ERβ. This demonstrates that ERβ influences not only the transcriptome, but also the miRnome and that the miRnome can be potential targets for novel treatment approaches. ERβ upregulates miR-205 and downregulates PROX1. This study uncovers the pathway in which ERβ downregulates the transcription factor PROX1 by upregulating miR-205 directly. MiR-205 then targets PROX1 mRNA for degradation. This results in the cells adopting a more adhesive phenotype and reduces the metastatic potential. This study uncovers the potential for ERβ to be anti-metastatic in addition to being anti-proliferative and anti-inflammatory. ERβ modulates the NFkB inflammatory cascade. One of ERβ’s attributes is that it has anti-inflammatory capabilities. Using a whole genome approach, this study reveals that ERβ can modulate the NFkB inflammatory network. In SW480 cells, ERβ downregulates NFkB transcription factors and induces apoptosis. In HT29 cells, ERβ prevents p65 subunit of NFkB from translocating to the nucleus. Overall, ERβ attenuates the NFkB signaling cascade by attenuating genes related to inflammation while enhancing genes related to apoptosis and cellular defenses. This makes ERβ a useful target for anti-inflammatory drug treatments for patients suffering from chronic inflammatory diseases. Advisors/Committee Members: Williams, Cecilia M. (advisor), Lin, Chin-Yo (committee member), Gunaratne, Preethi H. (committee member), Lee, Mong-Hong (committee member).

Subjects/Keywords: Estrogen receptor beta; colon cancer epithelial cells

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APA (6^th Edition):

-8465-3791. (2015). Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. (Thesis). University of Houston. Retrieved from http://hdl.handle.net/10657/2018

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

-8465-3791. “Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.” 2015. Thesis, University of Houston. Accessed June 18, 2018. http://hdl.handle.net/10657/2018.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

-8465-3791. “Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.” 2015. Web. 18 Jun 2018.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. [Internet] [Thesis]. University of Houston; 2015. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10657/2018.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

-8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. [Thesis]. University of Houston; 2015. Available from: http://hdl.handle.net/10657/2018

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Tech

15. Rajalekshmi Devi, Sarika. Development of Novel anti-estrogens for endocrine resistant Breast Cancer.

Degree: MS, Chemistry, 2016, Virginia Tech

URL: http://hdl.handle.net/10919/81275

► ER+ breast cancer raises a significant diagnostic challenge since resistance invariably develops to the current endocrine therapies. 70% of breast cancers are ER+, which results… (more)

▼ ER+ breast cancer raises a significant diagnostic challenge since resistance invariably develops to the current endocrine therapies. 70% of breast cancers are ER+, which results from the overexpression of estrogen receptor. ER mediates strong anti-inflammatory signaling in ER+ tissues. Once activated with estradiol (E2), ER inhibits inflammatory gene expression via protein-protein interactions that block NF-kappa B transcriptional activity. Importantly, NF-kappa B is a primary mediator of resistance in many cancers, including breast cancer. All current endocrine suppressive treatments block this palliative signaling pathway, along with the desired proliferative pathway. Thus, there is a significant unmet clinical need for novel endocrine treatments for breast cancer that can ameliorate patient outcome in resistant populations, be less prone to resistance development, retain anti-inflammatory action, and cause fewer side effects. Following the hypothesis driven approach, the work described here introduces structural analogs of an innovative ligand scaffold, 5,6-bis-(4-hydroxyphenyl)-7-oxabicyclo[2.2.1]hept-5-ene-2-sulfonic acid phenyl ester, termed OBHS, which reduces gene activation through ligand-induced shifts in helices 8 and 11, thereby indirectly modulating helix 12 of ER (hence, indirect antagonists). This new class of ligands with a bicyclic hydrophobic core retains strong anti-inflammatory effects while dialing out the proliferative effects of E2 (similar to Selective Estrogen Receptor Modulators, SERMS), and could potentially replace the current endocrine therapies of breast cancer. In this work, we carried out rational design and syntheses of two series of OBHS analogs, namely OBHS-A (for acetamido derivatives), and OBHS-P (for propargyl derivatives), while we explored a synthetic methodology for a third series of OBHS compounds. Many analogs from the OBHS-A series exhibited high binding affinity. For example, the exo diastereomer of 2.11a, 2.11b, 2.11c, 2.11d, and 2.11e exhibited Relative Binding Affinities (RBAs) of 22.6%, 10.5%, 19.5%, 12.1%, and 14.4%, respectively. As observed before, endo OBHS compounds exhibited lower binding affinities than exo compounds. The RBA values with acetamide, and isobutyramide (i.e. short hydrophobic chains) were very comparable to each other. However, unexpectedly the propionamide compound showed lower binding affinity than butyramide. Nevertheless, we consider OBHS analogs with RBA values greater than 1% (Kd = 20 nM) to be very potent. This data is only the first step in a battery of assays that will be conducted eventually on these compounds. In particular, our emphasis is in ascertaining and improving the NF-kappa B mediated anti-inflammatory property, where these compounds have shown promising activity in conjunction with their anti-proliferative activity. Advisors/Committee Members: Josan, Jatinder (committeechair), Kingston, David G (committee member), Santos, Webster (committee member).

Subjects/Keywords: Chemistry; organic; breast cancer; estrogen receptor; OBHS

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APA (6^th Edition):

Rajalekshmi Devi, S. (2016). Development of Novel anti-estrogens for endocrine resistant Breast Cancer. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/81275

Chicago Manual of Style (16^th Edition):

Rajalekshmi Devi, Sarika. “Development of Novel anti-estrogens for endocrine resistant Breast Cancer.” 2016. Masters Thesis, Virginia Tech. Accessed June 18, 2018. http://hdl.handle.net/10919/81275.

MLA Handbook (7^th Edition):

Rajalekshmi Devi, Sarika. “Development of Novel anti-estrogens for endocrine resistant Breast Cancer.” 2016. Web. 18 Jun 2018.

Vancouver:

Rajalekshmi Devi S. Development of Novel anti-estrogens for endocrine resistant Breast Cancer. [Internet] [Masters thesis]. Virginia Tech; 2016. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10919/81275.

Council of Science Editors:

Rajalekshmi Devi S. Development of Novel anti-estrogens for endocrine resistant Breast Cancer. [Masters Thesis]. Virginia Tech; 2016. Available from: http://hdl.handle.net/10919/81275

University of Canterbury

16. Graham, Lisa Anne. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.

Degree: Chemistry, 2012, University of Canterbury

URL: http://hdl.handle.net/10092/7173

► Environmental xenoestrogens (EEs) are chemicals that when they enter the body, the body responds to them as it would to endogenous estrogens. Humans are exposed… (more)

▼ Environmental xenoestrogens (EEs) are chemicals that when they enter the body, the body responds to them as it would to endogenous estrogens. Humans are exposed to these chemicals on a daily basis via natural components, additives and contaminants in food and water, through the use of pharmaceuticals and personal care products such as sunscreens, lotions and toothpaste. Exposure to EEs is thought to result in adverse effects on humans such as decreased fertility, increased susceptibility to hormone-sensitive cancers, deformities of the male genitalia and precocious puberty in females. The critical window of exposure is thought to be early fetal development, when tissues are rapidly differentiating under the control of endogenous estrogens. However, there is limited data in the literature on human fetal exposure to EEs. The first objective of this study was to assess human fetal exposure to a suite of 35 EEs by analysis of paired samples of amniotic fluid and maternal urine were collected from 32 New Zealand women between 14 and 20 weeks gestation. The analytical chemistry methods required for this study were developed and validated. The results demonstrate that fetal exposure is highly correlated with maternal exposure. This study is the first to report maternal urine levels of two UV filters and amniotic fluid levels of parabens, UV filters and triclosan. A model based on simple additivity of effect was developed that combined the measured concentrations with literature data on relative estrogenic potency to assess the magnitude of the estrogen signal that may be attributed to the EEs. This model suggests that the fetus may experience an estrogen signal due to the measured EEs that could be as large as the endogenous estrogen signal. A second objective was to use computational docking to study the interactions of the EEs with the human estrogen receptor (hER) protein. The docking studies show that the rigid endogenous ligand, 17β-estradiol (E2) interacts with the hER to produce a single, well-defined complex with the receptor and the flexible EEs produce multiple, distinct energy-equivalent complexes. EEs are not able to interact with the binding cavity to stabilise the rigid hER-E2-like topology of the complex. As a result, the hER-EE complexes can be thought of as more pliable or ‘floppy’ and thus able to respond to the cell context in multiple ways, leading to variations in gene expression in different target tissues. These multiple pathways may explain the range of physiological responses attributed to exposure that depend on the timing of exposure and the sex of the individual exposed.

Subjects/Keywords: Estradiol; human effects; gestational exposure; estrogen receptor

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APA (6^th Edition):

Graham, L. A. (2012). Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. (Thesis). University of Canterbury. Retrieved from http://hdl.handle.net/10092/7173

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Graham, Lisa Anne. “Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.” 2012. Thesis, University of Canterbury. Accessed June 18, 2018. http://hdl.handle.net/10092/7173.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Graham, Lisa Anne. “Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.” 2012. Web. 18 Jun 2018.

Vancouver:

Graham LA. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. [Internet] [Thesis]. University of Canterbury; 2012. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10092/7173.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Graham LA. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. [Thesis]. University of Canterbury; 2012. Available from: http://hdl.handle.net/10092/7173

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Van der Plas, Steven. Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors.

Degree: 2009, Ghent University

URL: http://hdl.handle.net/1854/LU-505579

► Worldwide concern has been growing on the increasing distribution of endocrine disrupting chemicals (EDCs) during the last decade. The overall anxiety is caused by their… (more)

Subjects/Keywords: Chemistry; EDC; solid phase; estrogen receptor

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APA (6^th Edition):

Van der Plas, S. (2009). Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors. (Thesis). Ghent University. Retrieved from http://hdl.handle.net/1854/LU-505579

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Van der Plas, Steven. “Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors.” 2009. Thesis, Ghent University. Accessed June 18, 2018. http://hdl.handle.net/1854/LU-505579.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Van der Plas, Steven. “Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors.” 2009. Web. 18 Jun 2018.

Vancouver:

Van der Plas S. Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors. [Internet] [Thesis]. Ghent University; 2009. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1854/LU-505579.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Van der Plas S. Development of chemosensors for endocrine disrupting chemicals (EDCs): synthesis and evaluation of solid-phase bound receptors. [Thesis]. Ghent University; 2009. Available from: http://hdl.handle.net/1854/LU-505579

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Duquesne University

18. Kirker, Mary Rachel. The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development.

Degree: PhD, Pharmacology-Toxicology, 2009, Duquesne University

URL: https://dsc.duq.edu/etd/750

► The increased risk of age-related cataracts in postmenopausal women and studies in animal models suggest that estrogen may have a protective role in the lens.… (more)

▼ The increased risk of age-related cataracts in postmenopausal women and studies in animal models suggest that estrogen may have a protective role in the lens. However, very little is known regarding the role of estrogen and its receptors in the lens. To begin unraveling the estrogen signaling mechanism in the lens, the following aims were investigated: 1) to determine if estrogen receptors are expressed in the lens, [125I]-17beta-estradiol binding and mRNA expression of ERalpha, ERbeta, and GPR30 were examined in the mouse and human lens; 2) to determine if the loss of ERalpha and/or ERbeta receptors will induce spontaneous development of cataracts and to examine their role in an inducible cataract model; and 3) to identify estrogen-regulated genes in the lens that influence cataract development in the ERdelta3-induced cataract model. High-affinity, saturable binding sites for 17beta-estradiol were identified in the nuclear, cytosolic, and membrane fractions of the mouse and human lens. Additionally, detectable binding in the membrane fraction and expression of GPR30 mRNA in the mouse and human lens are the first evidence of this novel transmembrane estrogen receptor in the lens of any species. Transcripts for ERalpha, ERbeta, and GPR30 were expressed in the mouse lens which suggests that one or more of these estrogen receptor subtypes are responsible for the binding detected. With the loss of nuclear ER in the lens, spontaneous cataracts did not occur; however, diminished levels or loss of ERalpha in ERdelta3 female mice increased the severity of cortical cataracts with age. These results suggest that ERalpha in the lens may provide protection against the progression of cataracts in the ERdelta3 model. Together with the cataract induction and gene expression studies, six genes were identified to be differentially expressed with estrogen versus vehicle treatment in the lenses of ERdelta3 mice. The pax6, tcfap2a, tgfbeta2, six3, sox2, and pdgfalpha genes are known to have a critical role in lens development, proliferation, differentiation and maintenance of lens homeostasis. Therefore, future examination of these genes and their pathways in the lens may contribute to the understanding of the mechanisms of estrogen-mediated protection of lens transparency. Knowledge of pathways that function to maintain lens transparency and how estrogen regulated these pathways will assist in the development of estrogen therapies that can be clinically used to delay the onset and/or progression of cataracts. Advisors/Committee Members: Vicki Davis, Jane Cavanaugh, Carmen Colitz, Kyle Selcer, Paula Witt-Enderby.

Subjects/Keywords: Cataract; Estrogen Receptor; Human; Lens; Mouse

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APA (6^th Edition):

Kirker, M. R. (2009). The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development. (Doctoral Dissertation). Duquesne University. Retrieved from https://dsc.duq.edu/etd/750

Chicago Manual of Style (16^th Edition):

Kirker, Mary Rachel. “The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development.” 2009. Doctoral Dissertation, Duquesne University. Accessed June 18, 2018. https://dsc.duq.edu/etd/750.

MLA Handbook (7^th Edition):

Kirker, Mary Rachel. “The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development.” 2009. Web. 18 Jun 2018.

Vancouver:

Kirker MR. The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development. [Internet] [Doctoral dissertation]. Duquesne University; 2009. [cited 2018 Jun 18]. Available from: https://dsc.duq.edu/etd/750.

Council of Science Editors:

Kirker MR. The Identification and Characterization of Estrogen Receptors in the Mouse and Human Lens and Their Role in Cataract Development. [Doctoral Dissertation]. Duquesne University; 2009. Available from: https://dsc.duq.edu/etd/750

University of Florida

19. Weil, Roxana F. Activation of the Largemouth Bass Estrogen Receptors by Model Environmental Estrogenic Compounds.

Degree: Medical Sciences
Physiology and Pharmacology (IDP), 2011, University of Florida

URL: http://ufdc.ufl.edu/UFE0043634

► Endocrine disrupting chemicals are ubiquitous in the aquatic environment and have been found to interact with sex-hormone receptors of aquatic organisms, thus altering their interactions… (more)

▼ Endocrine disrupting chemicals are ubiquitous in the aquatic environment and have been found to interact with sex-hormone receptors of aquatic organisms, thus altering their interactions with the endogenous ligand. In largemouth bass, estrogen is involved in a wide array of physiological processes during development as well as adult life, and its action is predominantly mediated via three known estrogen receptors (ERalpha, ERbeta-b and ERbeta-a). The mRNA expression levels of these receptors are tissue dependent and vary throughout the reproductive stages, thus allowing for fine control of downstream gene regulation. Although gene expression of the three ER isoforms has been extensively studied in response to estradiol and xenoestrogens, little is known about the regulation of these receptors at the protein level, due to the lack of specific antibodies. In this study recombinant proteins and polypeptides synthesized based on the hinge region of the ERs were used as antigens in order to obtain isoform-specific antibodies. The antibodies were found to recognize their recombinant hinge-regions, without cross-reactivity between ERs. Steady state mRNA and protein levels of ERalpha were measured in the liver whereas ERbeta-a and ERbeta-b mRNA and protein were measured in the ovaries of LMB females at three distinct stages of reproduction. ERalpha transcript levels in the liver parallel plasma estradiol, but the ER protein was decreased in the final stage of reproduction, even though ERalpha mRNA was still up-regulated, suggesting an increase in protein degradation. In the ovaries, ERalpha mRNA levels showed only a slight increase at later stages of oocyte maturation. In contrast, in the ovaries, both the mRNA and protein levels of the LMB ERbetas were highest during the earliest stage of gonadal development, and significantly decreased afterwards, however, the cell types expressing these are not known, so the transcript changes in a particular cell type is not known. The ERbeta-a antibody recognized only one band in the female ovaries in the cortical alveoli stage, whereas up to three splice variants of ERbeta-b may be present in the ovaries during this stage. Advisors/Committee Members: Denslow, Nancy D (committee chair), Shiverick, Kathleen A (committee member), Harrison, Jeffrey K (committee member), Chegini, Nasser (committee member).

Subjects/Keywords: endocrine – estrogen – receptor; Physiology and Pharmacology (IDP)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Weil, R. F. (2011). Activation of the Largemouth Bass Estrogen Receptors by Model Environmental Estrogenic Compounds. (Doctoral Dissertation). University of Florida. Retrieved from http://ufdc.ufl.edu/UFE0043634

Chicago Manual of Style (16^th Edition):

Weil, Roxana F. “Activation of the Largemouth Bass Estrogen Receptors by Model Environmental Estrogenic Compounds.” 2011. Doctoral Dissertation, University of Florida. Accessed June 18, 2018. http://ufdc.ufl.edu/UFE0043634.

MLA Handbook (7^th Edition):

Weil, Roxana F. “Activation of the Largemouth Bass Estrogen Receptors by Model Environmental Estrogenic Compounds.” 2011. Web. 18 Jun 2018.

Vancouver:

Weil RF. Activation of the Largemouth Bass Estrogen Receptors by Model Environmental Estrogenic Compounds. [Internet] [Doctoral dissertation]. University of Florida; 2011. [cited 2018 Jun 18]. Available from: http://ufdc.ufl.edu/UFE0043634.

Council of Science Editors:

Weil RF. Activation of the Largemouth Bass Estrogen Receptors by Model Environmental Estrogenic Compounds. [Doctoral Dissertation]. University of Florida; 2011. Available from: http://ufdc.ufl.edu/UFE0043634

Texas A&M University

20. Wu, Fei. Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors.

Degree: 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2433

► Estrogen receptor ? (ER?) is a ligand activated transcription factor. Many widely used synthetic compounds and natural chemicals can activate ER?. The compounds investigated in… (more)

▼ Estrogen receptor ? (ER?) is a ligand activated transcription factor. Many widely used synthetic compounds and natural chemicals can activate ER?. The compounds investigated in this study include 17?-estradiol (E2), diethylstilbestrol (DES), antiestrogens ICI 182,780, 4-hydroxytamoxifen, the phytoestrogen resveratrol, and the xenoestrogens bisphenol A (BPA), nonylphenol (NP), octylphenol (OP), endosulfan, kepone, 2,2-bis(p-hydroxyphenyl)-1,1,1- trichloroethane (HPTE) and 2,3,4,5-tetrachlorobiphenylol-4-ol (HO-PCB-Cl4). With the exception of the antiestrogens, all the compounds induced transactivation in MCF-7 or MDA-MB-231 cells transfected with wild-type ER? and a construct (pERE3) containing three tandem estrogen responsive elements (EREs) linked to a luciferase gene. However, these compounds differentially activated C-terminal deletion mutants of ER?. For example, neither E2 nor DES induced transactivation in MCF-7 transfected with ER?(1-537) due to partial deletion of helix 12 of ER?; however, OP, NP, resveratrol, kepone and HPTE induced this ER? mutant, demonstrating that the estrogenic activity of these synthetic compounds do not require activation function 2 (AF-2) of ER?. This study also investigated the effects of xenoestrogens on activation of reporter gene activity in MCF-7 and MDA-MB-231 cells transfected with a construct (pSp13) containing three tandem GC-rich Sp binding sites linked to the luciferase gene. In MCF-7 cells, antiestrogen-induced activation of ER?/Sp1 required the zinc finger motifs of ER?, whereas activation by estrogen and some xenoestrogens activation, such as endosulfan, NP and OP required the H12 of ER?. In contrast, xenoestrogens, such as HPTE, BPA, kepone and HO-PCBCl4, significantly induced transactivation of all four ER? deletion mutants tested in this study. Moreover, RNA interference assays demonstrated structuredependent differences in activation of ER?/Sp1, ER?/Sp3 and ER?/Sp4. The in vivo activities of E2, ICI 182,780, BPA and NP were further investigated in a transgenic mouse model containing pSp13 transgene. All the compounds induced luciferase activity in the mouse uterus; however activities observed in the penis and testis of male and stomach of both male and female mice were structure-dependent,. These results demonstrate that various ER ligands differentially activate ER? in breast cancer cells and transgenic mice, and their activities are dependent on ER? variants, promoter-, cell-context and selective use of different Sp proteins, suggesting these structurally diverse compounds are selective ER modulators (SERMs). Advisors/Committee Members: Safe, Stephen (advisor), Burghardt, Robert (committee member), Kunkel, Gary (committee member), Sacchettini, James (committee member).

Subjects/Keywords: estrogen receptor; endocrine disruptors; breast cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wu, F. (2009). Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2433

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wu, Fei. “Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors.” 2009. Thesis, Texas A&M University. Accessed June 18, 2018. http://hdl.handle.net/1969.1/ETD-TAMU-2433.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wu, Fei. “Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors.” 2009. Web. 18 Jun 2018.

Vancouver:

Wu F. Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors. [Internet] [Thesis]. Texas A&M University; 2009. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2433.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wu F. Comparative activation of estrogen receptor alpha (er alpha) by endocrine disruptors. [Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2433

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

21. Armstrong, Cameron Michelle. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.

Degree: 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151883

► Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein… (more)

▼ Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein aim to determine the protective mechanisms of estradiol (E2) during sporadic and inflammation-associated colonic carcinogenesis. When investigating the role of E2 and fish oil at the earliest stage of sporadic colon cancer development, E2 had no effect on DNA adduct formation while dietary fish oil significantly reduced DNA adduct formation. Contrarily, E2 significantly induced apoptosis of damaged colonocytes while fish oil was not protective. In an in vivo model of inflammation-associated colon carcinogenesis with E2 administered following induction of DNA damage and initiation of inflammation, E2 treatment was associated with decreased colon tumor size and number in wild type (WT) but not estrogen receptor (ER) ? knockout (ER?KO) mice. Interestingly, apoptosis was reduced and proliferation increased by E2 in these tumors in WT mice. This may be due to the altered ER expression in these tissues as the tumors developed, with ER??expression decreasing concomitantly with ER? expression increasing. Contrary to the protective effect of E2 on inflammation-associated colon tumor formation, which was dependent on ER?, during acute inflammation in the colon E2 was protective against inflammation in both WT and ER?KO mice and injury in ER?KO mice. The protection against inflammation is likely due to the reduction of pro-inflammatory cytokine expression by E2. Apoptosis and proliferation were decreased and increased in the proximal and distal colon respectively in ER?KO mice. In vitro studies further elucidated the roles of ER? and ER? in colonocytes. E2 and ER?, but not ER?, specific agonists reduced cell number and induce apoptosis in nonmalignant colonocytes. This effect was lost in the presence of mutated p53. In ER? overexpressed nonmalignant colonocytes, E2 had no effect on cell number while ER? agonist and ER? agonists decreased and increased cell number respectively. These studies suggest that E2 is protective in the colon and ER? is required for protection against carcinogenesis but not protection against inflammation. Additionally, the protection against colon carcinogenesis is likely p53 mediated. Advisors/Committee Members: Allred, Clinton D (advisor), Turner, Nancy D (committee member), Villalobos, Alice R (committee member), Weeks, Brad R (committee member).

Subjects/Keywords: colon cancer; estradiol; estrogen receptor; inflammation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Armstrong, C. M. (2013). The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151883

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Thesis, Texas A&M University. Accessed June 18, 2018. http://hdl.handle.net/1969.1/151883.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Web. 18 Jun 2018.

Vancouver:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Internet] [Thesis]. Texas A&M University; 2013. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1969.1/151883.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Thesis]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151883

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Ottawa

22. Boucher, Julie. Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring .

Degree: 2015, University of Ottawa

URL: http://hdl.handle.net/10393/32957

► Cigarette smoking during pregnancy contributes to the development of neurological health problems in offspring. As a result, public health organizations are recommending NRT to pregnant… (more)

▼ Cigarette smoking during pregnancy contributes to the development of neurological health problems in offspring. As a result, public health organizations are recommending NRT to pregnant women to wean them off tobacco. If nicotine itself is injurious to the developing brain, then nicotine substitution may not eliminate the deleterious health outcomes of maternal smoking. In studies of cognitive decline, estradiol elicits a neuroprotective effect through ER activation. However, the underlying mechanism remains unclear. Evidence suggests that estrogen-mediated neuroprotection is activated through glial cell interaction, mitigating inflammation and protecting neurons critical for learning and memory. If NRT antagonizes these cellular targets, it may put individuals at risk for future cognitive impairments. Randomly assigned nulliparous female Wistar rats were injected subcutaneously with 1 mg/kg/day of nicotine bitartrate or saline for 2 weeks before mating until weaning (PND 21). Pups (saline n=6 and nicotine, n=6) were sacrificed at 26 weeks of age and the hippocampal formation was processed for Nissl and immunohistochemical staining for GFAP and ERα. Gestational exposure to nicotine only produced a significant increase in the expression of ERα in the DG of the hippocampus. While additional research is needed, these findings suggest that NRT might indeed interfere with proper brain development, making offspring increasingly susceptible to long-term adverse health effects. Le tabac fumé pendant la grossesse affecte de manière importante le développement neurologique de la progéniture, y compris à long terme. C’est pourquoi, les autorités de la santé publique recommandent les substituts nicotiniques comme soutien au sevrage tabagique chez les femmes enceintes. Si le danger se situe dans la nicotine de la cigarette, alors les produits de substitution nicotiniques risquent également d’interférer avec le développement cérébral. De nombreuses données expérimentales convergent pour attribuer un rôle protecteur à l’oestradiol sur le fonctionnement cognitif. Par contre, le mécanisme sous-jacent est inconnu. Il se peut que l’oestradiol arrive à neutraliser la réaction inflammatoire provoquée par les cellules gliales, amoindrissant la détérioration des neurones impliqués au niveau de la mémoire. Ainsi, une perturbation de ce mécanisme par la nicotine pourrait engendrer une détérioration progressive des fonctions cognitives. Des rats femelles Wistars nullipares assignées de façon alléatoire à un groupe ont reçu soit une injection sous-cutanée de 1mg/kg/jour de nicotine bitartrate ou de saline, 2 semaines avant l’accouplement jusqu'au sevrage au jour 21 postnatal. A 26 semaines, les ratons furent sacrifiés (saline n=6 et nicotine, n=6) et une analyse du Nissl et immunohistochimique de GFAP et ERα furent réalisées sur les formations hippocampiques. L’exposition prénatale à la nicotine a…

Subjects/Keywords: nicotine; estrogen receptor; immunohistochemistry; astrocyte; neuron

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Boucher, J. (2015). Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/32957

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Boucher, Julie. “Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring .” 2015. Thesis, University of Ottawa. Accessed June 18, 2018. http://hdl.handle.net/10393/32957.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Boucher, Julie. “Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring .” 2015. Web. 18 Jun 2018.

Vancouver:

Boucher J. Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring . [Internet] [Thesis]. University of Ottawa; 2015. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10393/32957.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Boucher J. Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring . [Thesis]. University of Ottawa; 2015. Available from: http://hdl.handle.net/10393/32957

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Vanderbilt University

23. Pruitt, Freddie Lee. A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis.

Degree: PhD, Cancer Biology, 2013, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;

► Stromal-epithelial interactions are important in both prostate development and cancer. Stromal changes have been shown to be powerful prognostic indicators of prostate cancer progression and… (more)

▼ Stromal-epithelial interactions are important in both prostate development and cancer. Stromal changes have been shown to be powerful prognostic indicators of prostate cancer progression and of patient death helping to define lethal versus indolent phenotypes. The specific molecular underpinnings of these interactions are incompletely understood. Several molecules found to be aberrantly expressed in cancer associated fibroblasts (CAFs) (including cyclin D1 [CD1], stromal derived factor 1 [SDF-1]) contribute to tumorigenesis and malignant transformation in xenograft experiments. These molecules can be regulated by a number of different factors, but are both putative estrogen regulated genes. In this study, we show that dysregulation of ERα expression in cancer associated stroma results in the differential regulation of estrogen responsive genes that are key factors in enhancing the invasive potential of the epithelial tumor. The cell cycle regulator CD1 and the estrogen receptor are known to interact and can induce estrogenic gene transcription. Cathepsin D (CathD) is an estrogen regulated aspartic endopeptidase, known to be involved in a number of physiological processes as well as in the regulation of apoptosis. In this study, we highlight CathD as a mediator of cancer associated stromal promotion of prostate tumorigenesis. An examination of human prostate tissue revealed significantly increased stromal staining of CathD in malignant prostate tissue in comparison to benign prostate tissue. Stromal specific overexpression of CathD in benign prostate stromal cells induced malignancy in adjacent epithelium through increased TGFβ signaling and responsive gene expression. The proteolytic function of stromally-derived CathD is dependent on the activity of hydrogen-proton pump activity on the surface of prostate epithelial cell lines. The study presented here indicates that CathD is not only an important mediator of stroma-epithelial cross talk, but also an essential component in promotion of tumorigenesis in vivo, and Inhibition of ER signaling in the cancer associated stroma inhibits malignant transformation in the adjacent epithelium. Advisors/Committee Members: Simon W. Hayward (committee member), Robert Matusik (chair), Barbara Fingleton (committee member), Fritz Parl (committee member).

Subjects/Keywords: Stroma; microenvironment; estrogen receptor; cathepsin D

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pruitt, F. L. (2013). A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;

Chicago Manual of Style (16^th Edition):

Pruitt, Freddie Lee. “A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed June 18, 2018. http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;.

MLA Handbook (7^th Edition):

Pruitt, Freddie Lee. “A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis.” 2013. Web. 18 Jun 2018.

Vancouver:

Pruitt FL. A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2018 Jun 18]. Available from: http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;.

Council of Science Editors:

Pruitt FL. A role for estrogen receptor and the estrogen-regulated protease cathepsin D in stromally-driven prostatic carcinogenesis. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-06242013-125056/ ;

University of North Carolina – Wilmington

24. Perry, Heather N. Synthesis of compounds capable of producing cytotoxic N3-methyladenine DNA adducts in estrogen receptor positive cells.

Degree: 2009, University of North Carolina – Wilmington

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760

► This project describes the design and synthesis of new compounds that are capable of targeting cells that express the estrogen receptor and producing cytotoxic N3-methyladenine… (more)

Subjects/Keywords: Cell receptors; DNA adducts – Synthesis; Estrogen – Receptors; Selective estrogen receptor modulators

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APA (6^th Edition):

Perry, H. N. (2009). Synthesis of compounds capable of producing cytotoxic N3-methyladenine DNA adducts in estrogen receptor positive cells. (Masters Thesis). University of North Carolina – Wilmington. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760

Chicago Manual of Style (16^th Edition):

Perry, Heather N. “Synthesis of compounds capable of producing cytotoxic N3-methyladenine DNA adducts in estrogen receptor positive cells.” 2009. Masters Thesis, University of North Carolina – Wilmington. Accessed June 18, 2018. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760.

MLA Handbook (7^th Edition):

Perry, Heather N. “Synthesis of compounds capable of producing cytotoxic N3-methyladenine DNA adducts in estrogen receptor positive cells.” 2009. Web. 18 Jun 2018.

Vancouver:

Perry HN. Synthesis of compounds capable of producing cytotoxic N3-methyladenine DNA adducts in estrogen receptor positive cells. [Internet] [Masters thesis]. University of North Carolina – Wilmington; 2009. [cited 2018 Jun 18]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760.

Council of Science Editors:

Perry HN. Synthesis of compounds capable of producing cytotoxic N3-methyladenine DNA adducts in estrogen receptor positive cells. [Masters Thesis]. University of North Carolina – Wilmington; 2009. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=1760

University of Kansas

25. Wang, Pan. Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp.

Degree: PhD, Pharmacology, Toxicology & Therapeutics, 2010, University of Kansas

URL: http://hdl.handle.net/1808/7432

► The endogenous estrogens are vitally-important female sex hormones with diverse biological functions. Disruption of their actions contributes to the pathogenesis of a number of disease… (more)

Subjects/Keywords: Pharmacology; Antiestrogen; Estrogen; Estrogen receptor; Molecular docking; Molecular modeling; Pdip

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, P. (2010). Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/7432

Chicago Manual of Style (16^th Edition):

Wang, Pan. “Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp.” 2010. Doctoral Dissertation, University of Kansas. Accessed June 18, 2018. http://hdl.handle.net/1808/7432.

MLA Handbook (7^th Edition):

Wang, Pan. “Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp.” 2010. Web. 18 Jun 2018.

Vancouver:

Wang P. Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp. [Internet] [Doctoral dissertation]. University of Kansas; 2010. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/1808/7432.

Council of Science Editors:

Wang P. Computational Molecular Modeling Studies of the Interactions of Estrogens with Their Receptors and Intracellular Estrogen Binding Protein PDIp. [Doctoral Dissertation]. University of Kansas; 2010. Available from: http://hdl.handle.net/1808/7432

University of Cincinnati

26. Minges, Cheryl. Targeted Deletion of Estrogen Receptor Alpha in Mouse Pituitary Lactotrophs.

Degree: MS, Pharmacy: Pharmaceutical Sciences, 2011, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494

► Prolactin (PRL) is a major anterior pituitary (AP) hormone that is necessary for mammary gland development, lactation, and female fertility. The synthesis and release… (more)

▼ Prolactin (PRL) is a major anterior pituitary (AP) hormone that is necessary for mammary gland development, lactation, and female fertility. The synthesis and release of PRL from specialized pituitary cells (lactotrophs) is tightly regulated and primarily under tonic inhibition by dopamine (DA), produced by the tuberoinfundibular dopaminergic neurons (TIDA) of the hypothalamus. In turn, PRL regulates its own release by acting on the TIDA neurons in a short feedback loop to increase inhibition by DA and maintain homeostasis. Superimposed on this negative regulation are the stimulatory effects of estrogen. Estrogen (E2) stimulates PRL synthesis, secretion, and lactotroph proliferation by direct action at the level of the AP. E2 also stimulates PRL indirectly at the level of the hypothalamus by inhibiting TIDA activity. Finally, E2 can also modify lactotroph response to DA and other PRL-regulatory factors. The normal growth and function of lactotrophs depends on an interactive balance between DA and E2. However, the relative contribution of E2 regulation directly on the pituitary lactotrophs versus hypothalamic DA, particularly during various physiological states in the female, is not well defined and current animal models are unable to distinguish this. Thus, there is a need for a new model with which to study the regulatory role of E2 action at the level of the pituitary versus the hypothalamus. Through transgenic Cre/loxP technology and homologous recombination, we have generated a selective knockout mouse model in which the primary mediator of E2 action in the lactotroph, estrogen receptor alpha (ERa), is deleted only in pituitary lactotrophs, while conserving E2 action at the TIDA neurons. Herein is the generation of this animal model and its characterization. Results show the successful generation of mice with the ERa knockout targeted to lactotrophs but not in other ERa expressing tissues of these animals. Estrogen responsiveness of the selective knockout mouse was evaluated. In vivo studies, utilizing a model of spontaneous prolactinoma formation, showed no significant differences in AP growth between mice with the selective deletion of ERa and those without. DA levels in the AP were low in both groups, suggesting that loss of dopaminergic inhibition contributes more to lactotroph proliferation than does a direct action of E2 however further investigation is required to support this conclusion. In vitro studies demonstrated that lactotrophs with ERa deletion did not respond to E2 or E2 antagonist with regard to cell content of PRL, highlighting the direct action of E2 on the lactotroph in modulating PRL synthesis. Our mouse model, with selective loss of ERa in pituitary lactotrophs, and E2 action at the level of the hypothalamus maintained, will provide an effective tool in elucidating the primary effects of estrogen, as well as other factors, on PRL regulation. Advisors/Committee Members: Gregerson, Karen (Committee Chair).

Subjects/Keywords: Pharmaceuticals; Lactotrophs; Anterior Pituitary; Estrogen; Prolactin; Dopamine; Estrogen Receptor

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APA (6^th Edition):

Minges, C. (2011). Targeted Deletion of Estrogen Receptor Alpha in Mouse Pituitary Lactotrophs. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494

Chicago Manual of Style (16^th Edition):

Minges, Cheryl. “Targeted Deletion of Estrogen Receptor Alpha in Mouse Pituitary Lactotrophs.” 2011. Masters Thesis, University of Cincinnati. Accessed June 18, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494.

MLA Handbook (7^th Edition):

Minges, Cheryl. “Targeted Deletion of Estrogen Receptor Alpha in Mouse Pituitary Lactotrophs.” 2011. Web. 18 Jun 2018.

Vancouver:

Minges C. Targeted Deletion of Estrogen Receptor Alpha in Mouse Pituitary Lactotrophs. [Internet] [Masters thesis]. University of Cincinnati; 2011. [cited 2018 Jun 18]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494.

Council of Science Editors:

Minges C. Targeted Deletion of Estrogen Receptor Alpha in Mouse Pituitary Lactotrophs. [Masters Thesis]. University of Cincinnati; 2011. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307441494

University of Western Australia

27. Dennis, Maxine Elizabeth. Oestrogen and atherosclerosis.

Degree: PhD, 2008, University of Western Australia

URL: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01

►

[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a… (more)

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[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative effect of hormone replacement therapy (HRT) on cardiovascular disease (CVD) risk amongst postmenopausal women. It is important to determine how a hormone with numerous positive effects on intermediate pathways of atherosclerosis fails to offer cardioprotection. Further investigation into the actions of oestrogen in the vasculature may add to our current understanding of the pathogenesis of atherosclerosis and oestrogen biology. The primary aim of this thesis was to investigate involvement of the oestrogen receptors (ERs) in atherosclerotic CVD and to provide further insight into the actions of oestrogen on the vasculature by studying the actions of oestrogen on the regulation of an oestrogen-responsive gene within human vascular cells. Following confirmation of ERα and ERβ expression at the RNA and protein level in human aorta sections, correlations of receptor expression with age and atherosclerosis were examined. Significantly strong negative relationships of ERα, androgen receptor (AR), and progesterone receptor (PR) with age in both males and females were detected. No trend was detected between ERβ expression and age. These findings suggest that the receptor-mediated actions of hormones in the vasculature may change with age. Further, this thesis compared for the first time sex hormone receptor expression in normal and adjacent atherosclerotic aortic tissue providing a critical assessment of receptor differences due to atherosclerosis. Results revealed reductions of all hormone receptors in early atherosclerotic versus normal aorta tissue. ... These results suggest that the 3'-UTR SNPS may have more of an influence on carotid thickening when oestrogen levels are lower, suggesting the importance of both genetic variation of the ERβ gene and oestrogen status on carotid thickening. Finally, this was the first study to investigate oestrogen-induced regulation of angiotensinogen (AGT), a candidate gene for CVD, in human vascular cells. Oestrogen influenced AGT transcription in a cell specific manner. The overall influence of oestrogen on AGT transcription in the vasculature is unknown. This thesis adds to the knowledge of oestrogen and atherosclerosis by suggesting the involvement of the sex hormone receptors (ERα, ERβ, PR and AR) in atherosclerosis, presenting ERβ as a potentially important candidate gene for atherosclerosis, revealing interactions between estrogen status and associations of ERβ SNPs with carotid thickening, and demonstrating vascular cell-specific actions of oestrogen on the regulation of a candidate gene for CVD. These factors may have contributed to the lack of cardio-protection following HRT, as revealed by large clinical trials.

[Truncated abstract] Our understanding of the actions of oestrogen on the vasculature has recently been questioned following the results of large clinical trials revealing a negative…

Subjects/Keywords: Angiotensins; Atherosclerosis; Estrogen; Estrogen; Atherosclerosis; Oestrogen receptor; Angiotensinogen

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dennis, M. E. (2008). Oestrogen and atherosclerosis. (Doctoral Dissertation). University of Western Australia. Retrieved from http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01

Chicago Manual of Style (16^th Edition):

Dennis, Maxine Elizabeth. “Oestrogen and atherosclerosis.” 2008. Doctoral Dissertation, University of Western Australia. Accessed June 18, 2018. http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01.

MLA Handbook (7^th Edition):

Dennis, Maxine Elizabeth. “Oestrogen and atherosclerosis.” 2008. Web. 18 Jun 2018.

Vancouver:

Dennis ME. Oestrogen and atherosclerosis. [Internet] [Doctoral dissertation]. University of Western Australia; 2008. [cited 2018 Jun 18]. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01.

Council of Science Editors:

Dennis ME. Oestrogen and atherosclerosis. [Doctoral Dissertation]. University of Western Australia; 2008. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=3846&local_base=GEN01-INS01

University of Saskatchewan

28. -6560-0432. HERG and STAT1 Interactions in Estrogen Receptor Positive and Estrogen Receptor Negative Human Breast Cancers.

Degree: 2016, University of Saskatchewan

URL: http://hdl.handle.net/10388/7660

► The human ether-a-go-go-related gene (HERG) potassium channel, a known regulator of cell proliferation, is overexpressed in several cancer cell lines. Despite its importance, there have… (more)

▼ The human ether-a-go-go-related gene (HERG) potassium channel, a known regulator of cell proliferation, is overexpressed in several cancer cell lines. Despite its importance, there have not been many studies regarding the mechanism by which it contributes to aberrant proliferation of cancer cells. In this study, we identified a novel estrogen signalling pathway that plays a role in regulating cell proliferation in estrogen receptor positive breast cancer cells. We provide the initial characterization of this signal transduction pathway which results in up-regulation of HERG channels and increased proliferation of estrogen receptor positive breast cancer cell lines. Using biochemical and confocal microscopy imaging, we revealed that there is a protein-protein interaction between HERG and Signal Transducers and Activators of Transcription 1 (STAT1) in breast cancer cell lines that express estrogen receptors (ER+) (MCF-7, T47D) and in those that lack ERs (ER-) (MDA-MB-231, BT-20). After estrogen treatment (E2, 10µM), only the ER+ human breast cancer cell lines showed increased co-precipitation of HERG and STAT1 and higher levels of subcellular colocalization, and these effects were prevented by pharmacological blockers of ERs (ICI 182 780, 5nM) or STAT1 (fludarabine, 50µM). Furthermore, we demonstrated that the enhanced STAT1 and HERG interaction induced by estrogen is important for upregulation of the HERG channel surface expression. Consistent with our prediction that HERG surface expression plays a critical role in cancer cell proliferation, proliferation assays revealed a marked upregulation of ER+ cancer cell proliferation after E2 stimulation, and this was prevented by ICI, fludarabine and the HERG blocker E4031 (10µM). Together, these results suggest that there is an estrogen receptor mediated signalling pathway involving a physical complex between STAT1 and HERG channels, and this proposed pathway may be an attractive strategy for anti-cancer therapeutic targeting of ER+ human breast tumors. Next, since it is known that HERG contains multiple tyrosine residues whose phosphorylation could be increased after estrogen receptor stimulation, we hypothesized that these phosphorylated tyrosine residues could serve as binding sites of the SH2 domain of STAT1. We have used FR-peptide, a 28 amino acid peptide mimetic of STAT1 SH2 domain, to disrupt interaction between HERG and STAT1. Our biochemistry and imaging data demonstrated that FR-peptide did disrupt the HERG-STAT1 interaction, and this cell-permeable peptide did prevent the estrogen-induced upregulation of HERG channel and cancer cell proliferation of ER+ breast cancer cells. Finally, we also demonstrated that the HERG-STAT1 interaction was specific to breast cancer cells, as similar biochemical studies failed to show physical interactions in normal brain and cardiac tissue. Together, this study reveals a novel estrogen receptor signalling pathway which enhances the HERG channel surface expression and its contribution to cancer cell proliferation in ER+… Advisors/Committee Members: Cayabyab, Francisco (advisor), Campanucci, Veronica (committee member), Taghibiglou, Changiz (committee member), Fisher, Thomas (committee member), Vizeacoumar, Franco (committee member).

Subjects/Keywords: HERG; STAT1; Estrogen; Estrogen Receptor; Breast Cancer; Cell Proliferation; Signaling Pathway

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

-6560-0432. (2016). HERG and STAT1 Interactions in Estrogen Receptor Positive and Estrogen Receptor Negative Human Breast Cancers. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/7660

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

-6560-0432. “HERG and STAT1 Interactions in Estrogen Receptor Positive and Estrogen Receptor Negative Human Breast Cancers.” 2016. Thesis, University of Saskatchewan. Accessed June 18, 2018. http://hdl.handle.net/10388/7660.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

-6560-0432. “HERG and STAT1 Interactions in Estrogen Receptor Positive and Estrogen Receptor Negative Human Breast Cancers.” 2016. Web. 18 Jun 2018.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-6560-0432. HERG and STAT1 Interactions in Estrogen Receptor Positive and Estrogen Receptor Negative Human Breast Cancers. [Internet] [Thesis]. University of Saskatchewan; 2016. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10388/7660.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

-6560-0432. HERG and STAT1 Interactions in Estrogen Receptor Positive and Estrogen Receptor Negative Human Breast Cancers. [Thesis]. University of Saskatchewan; 2016. Available from: http://hdl.handle.net/10388/7660

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

29. Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Yuya. Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy.

Degree: 博士(医学), 2017, University of Miyazaki / 宮崎大学

URL: http://hdl.handle.net/10458/5983

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学位論文の一部を構成しているため、http://hdl.handle.net/10458/5984 に本文を掲載。

Although estrogen is implicated in the regulation of cell growth and differentiation in many organs, the exact mechanism for liver regeneration is not… (more)

Subjects/Keywords: estrogen; estrogen receptor α; liver regeneration; partial hepatectomy; cell proliferation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Y. (2017). Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy. (Thesis). University of Miyazaki / 宮崎大学. Retrieved from http://hdl.handle.net/10458/5983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Yuya. “Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy.” 2017. Thesis, University of Miyazaki / 宮崎大学. Accessed June 18, 2018. http://hdl.handle.net/10458/5983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi, Yuya. “Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy.” 2017. Web. 18 Jun 2018.

Vancouver:

Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi Y. Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy. [Internet] [Thesis]. University of Miyazaki / 宮崎大学; 2017. [cited 2018 Jun 18]. Available from: http://hdl.handle.net/10458/5983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Baatarsuren, Batmunkh; Narantsog, Choijookhuu; Naparee, Srisowanna; Uugantsetseg, Byambatsogt; Phyu Synn, Oo; Mohmand Noor, Ali; Yamaguchi Y. Estrogen Accelerates Cell Proliferation through Estrogen Receptor α during Rat Liver Regeneration after Partial Hepatectomy. [Thesis]. University of Miyazaki / 宮崎大学; 2017. Available from: http://hdl.handle.net/10458/5983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

UCLA

30. Iorga, Andrea. Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.

Degree: Molec, Cell, & Integ Physiology, 2015, UCLA

URL: http://www.escholarship.org/uc/item/9f1833b6

► Cardiac hypertrophy, defined as an enlargement of the ventricles, is often triggered when the heart is subjected to hemodynamic stress from physiological stimuli such as… (more)

Subjects/Keywords: Physiology; Angiogenesis; Aromatase; Estrogen; Estrogen Receptor Beta; Fibrosis; Heart Failure

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Iorga, A. (2015). Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/9f1833b6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Iorga, Andrea. “Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.” 2015. Thesis, UCLA. Accessed June 18, 2018. http://www.escholarship.org/uc/item/9f1833b6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Iorga, Andrea. “Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta.” 2015. Web. 18 Jun 2018.

Vancouver:

Iorga A. Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta. [Internet] [Thesis]. UCLA; 2015. [cited 2018 Jun 18]. Available from: http://www.escholarship.org/uc/item/9f1833b6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Iorga A. Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta. [Thesis]. UCLA; 2015. Available from: http://www.escholarship.org/uc/item/9f1833b6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Open Access Theses and Dissertations