subject:(estrogen receptor)

Georgia Tech

1. Walker, Christopher L. Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application.

Degree: PhD, Chemistry and Biochemistry, 2019, Georgia Tech

URL: http://hdl.handle.net/1853/61211

► Nuclear receptors are ligand activated transcription factors that are widely distributed throughout the mammalians. There are 48 known human nuclear receptors within the body located… (more)

▼ Nuclear receptors are ligand activated transcription factors that are widely distributed throughout the mammalians. There are 48 known human nuclear receptors within the body located in various systems. While some nuclear receptors can be located wholly within certain regions and tissues the clear majority are widely distributed, overlapping expression in the same locations. The role of nuclear receptors as transcription factors has caused them to be implicated in a vast number of diseases including metabolic, cardiovascular and neurological. The role of nuclear receptors in diseases and the potential to promote ligand activated transcription makes nuclear receptors of pharmaceutical significance. Currently it is estimated that 33% of nuclear receptors are targeted by the pharmaceutical industry resulting in ~20% of pharmaceutical development worldwide. The potential to control physiological responses via introduction of a ligand to nuclear receptors has continued the interest in development of new ligands to further the understanding of nuclear receptor behavior. The challenge nuclear receptors present is to develop ligands that are selective in targeting within families and among different classes of nuclear receptors. At the core, ligand activated nuclear receptor modulation is chiefly centered around the relationship between the ligand binding pocket of the receptor and the ligand. Composed primarily of non-polar amino acid residues the ligand binding pocket is the cavity by which small hydrophobic molecules bind. Demonstrating large variance across classes of nuclear receptor and little divergence within families the ligand binding pocket serves as the focal point for targeting selectivity. Successful binding and thus receptor response is contingent upon the ligand meeting criteria established by the ligand binding pocket such as satisfactory size/volume of the ligand and key ligand-receptor amino acid residue interaction. Research conducted by Katzenellenbogen was paramount in understanding the relationship between the estrogen receptors and its ligands. His established pharmacophore unraveled features for potential ligands that are exchangeable from those that are indispensable. The commercial success of estrogen receptor ligands has fueled the interest in not only understanding ligand-receptor binding interactions but its subcellular movement. The Green Fluorescent Protein completely revolutionized the way in which cellular probing is conducted. The chromophore internally synthesized by the protein through a series of folding of amino acid residues afforded the opportunity to monitor cellular movements with the aid of fluorescence. Commonly utilized in visualization as a fusion protein, the GFP chromophore provided the ideal tool for understanding protein cellular movement and interaction. Simply put due to the chromophore that resides at the center, GFP provides the perfect technique for cellular probing. Here in we report the use of GFP-chromophore inspired ligands for utility as estrogen receptor agonist.… Advisors/Committee Members: Williams, Loren (advisor), Liotta, Charles (committee member), Snell, Terry (committee member), Oyelere, Adegboyega (committee member), Azizi, Bahareh (committee member).

Subjects/Keywords: Estrogen receptor

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APA (6^th Edition):

Walker, C. L. (2019). Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/61211

Chicago Manual of Style (16^th Edition):

Walker, Christopher L. “Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application.” 2019. Doctoral Dissertation, Georgia Tech. Accessed January 24, 2021. http://hdl.handle.net/1853/61211.

MLA Handbook (7^th Edition):

Walker, Christopher L. “Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application.” 2019. Web. 24 Jan 2021.

Vancouver:

Walker CL. Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application. [Internet] [Doctoral dissertation]. Georgia Tech; 2019. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1853/61211.

Council of Science Editors:

Walker CL. Green fluorescent protein inspired chromophore as estrogen receptor agonist-synthesis, biological evaluations and cellular application. [Doctoral Dissertation]. Georgia Tech; 2019. Available from: http://hdl.handle.net/1853/61211

Rutgers University

2. Yasrebi, Ali, 1987-. ERE-independent ERα signalling in feeding and exploratory behaviors.

Degree: MS, Endocrinology and Animal Biosciences, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/62067/

► The reproductive steroid hormone, 17β-estradiol (E2), controls feeding and exploratory behaviors associated with mood disorders. The loss of circulating E2 puts menopausal women at an… (more)

▼ The reproductive steroid hormone, 17β-estradiol (E2), controls feeding and exploratory behaviors associated with mood disorders. The loss of circulating E2 puts menopausal women at an increased risk for developing obesity and mood disorders when compared to premenopausal women. Therefore, it is critically important to understand the role of sex steroids and their receptors in the neuroendocrine control of feeding and mood. The goal of this project is to understand the role of estrogen response Element (ERE)-dependent and ERE-independent ERα signaling on behavior by characterizing feeding patters and exploratory behaviors in male and female mice lacking either total ERα signaling or lacking ERE-dependent ERα signaling. We hypothesize that ERE-independent ERα is partially sufficient to restore feeding and exploratory behaviors that are lost in total ERα knockout mice. We tested three strains of mice: two ERα transgenic models, a total ERα knock out (ERKO) and a novel ERα knock in/knock out (KIKO) that lacks a functional DNA-binding domain) and their wild type (WT) C57 littermates using a real-time feeding behavior monitoring system and series of standard behavior tests (open field tests, elevated plus maze, forced swim test). To test our hypothesis FI and meal patterns were observed while the animals were given ad libitum access to a LFD (Experiment 1a) followed by HFD (Experiment 1b). A separate set of animals the response to fasting was monitored for 24 h after caloric restriction (Experiment 1c). Exploratory, depressive, and locomotor behavior testing was conducted on mice from Experiments 1a/b (open field, elevated plus maze, forced swim test). Each experiment was initially done with intact animals and then again repeated in ovariectomized (OVX) animals split into either an oil treated control group or an E2-treated group. We observed ERE-dependent mechanisms are the main modulator of homeostatic LFD feeding meal patterns while ERE- independent ERα signaling was involved in the control of palatable, high-fat diet food intake. During refeeding, ERE-independent mechanisms contribute to a decreased first meal food intake and slower rate of ingestion. When observed during a series of behavior tests, WT animals explored more, regardless of treatment (differences could be attributed to higher levels of locomotor activity in WT). However, similarities between WT and KIKO females in the EPM indicate that ERE-independent pathways may contribute towards reducing anxiety measures, independent of locomotor activity. WT females were shown to have a decreased free float time, indicating ERE dependent signaling may be influencing despair like tendencies. Collectively, these suggest that both ERE-dependent and -independent ERαsignaling are involved with both feeding and anxiety like homeostatic parameters. Advisors/Committee Members: Roepke, Troy A (chair), Bello, Nicholas T (internal member), Bagnell, Carol A (internal member), Samuels, Benjamin A (outside member), School of Graduate Studies.

Subjects/Keywords: Estrogen receptor alpha; Estrogen – Receptors

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APA (6^th Edition):

Yasrebi, Ali, 1. (2019). ERE-independent ERα signalling in feeding and exploratory behaviors. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/62067/

Chicago Manual of Style (16^th Edition):

Yasrebi, Ali, 1987-. “ERE-independent ERα signalling in feeding and exploratory behaviors.” 2019. Masters Thesis, Rutgers University. Accessed January 24, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/62067/.

MLA Handbook (7^th Edition):

Yasrebi, Ali, 1987-. “ERE-independent ERα signalling in feeding and exploratory behaviors.” 2019. Web. 24 Jan 2021.

Vancouver:

Yasrebi, Ali 1. ERE-independent ERα signalling in feeding and exploratory behaviors. [Internet] [Masters thesis]. Rutgers University; 2019. [cited 2021 Jan 24]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/62067/.

Council of Science Editors:

Yasrebi, Ali 1. ERE-independent ERα signalling in feeding and exploratory behaviors. [Masters Thesis]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/62067/

3. 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 January 24, 2021. 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. 24 Jan 2021.

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 2021 Jan 24]. 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

4. 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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Parent AA. Second-site inhibitors of the estrogen and androgen hormone receptors. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Jan 24]. 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

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

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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Koomson JN. The role of estrogen receptors alpha and beta in the development of uterine leiomyomas. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Jan 24]. 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

Cornell University

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

Degree: PhD, Biomedical Engineering, 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: van der Meulen, Marjolein (chair), Hernandez, Christopher J. (committee member), Schimenti, John C. (committee member).

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. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/38857

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. Doctoral Dissertation, Cornell University. Accessed January 24, 2021. http://hdl.handle.net/1813/38857.

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. 24 Jan 2021.

Vancouver:

Melville K. Estrogen Receptor Alpha In Osteoblasts Mediates Bone Mass And Bone’S Response To In Vivo Loading. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1813/38857.

Council of Science Editors:

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

University of Otago

7. 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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Tran KB. Synthetic Cannabinoids as a Novel Treatment for Triple Negative Breast Cancer . [Internet] [Masters thesis]. University of Otago; 2012. [cited 2021 Jan 24]. 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

Northeastern University

8. Gajadeera, Nisal. Design, Synthesis And In Vitro Investigations Of Novel Fluorescently Labeled Steroids.

Degree: MS, Department of Chemistry and Chemical Biology, 2018, Northeastern University

URL: http://hdl.handle.net/2047/D20316349

► Breast cancer is the most common cancer among women, accounting for nearly third of all the diagnosed cancers. According to the American cancer society, over… (more)

Subjects/Keywords: Estrogen receptor; Imaging agent; Chemistry

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APA (6^th Edition):

Gajadeera, N. (2018). Design, Synthesis And In Vitro Investigations Of Novel Fluorescently Labeled Steroids. (Masters Thesis). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20316349

Chicago Manual of Style (16^th Edition):

Gajadeera, Nisal. “Design, Synthesis And In Vitro Investigations Of Novel Fluorescently Labeled Steroids.” 2018. Masters Thesis, Northeastern University. Accessed January 24, 2021. http://hdl.handle.net/2047/D20316349.

MLA Handbook (7^th Edition):

Gajadeera, Nisal. “Design, Synthesis And In Vitro Investigations Of Novel Fluorescently Labeled Steroids.” 2018. Web. 24 Jan 2021.

Vancouver:

Gajadeera N. Design, Synthesis And In Vitro Investigations Of Novel Fluorescently Labeled Steroids. [Internet] [Masters thesis]. Northeastern University; 2018. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2047/D20316349.

Council of Science Editors:

Gajadeera N. Design, Synthesis And In Vitro Investigations Of Novel Fluorescently Labeled Steroids. [Masters Thesis]. Northeastern University; 2018. Available from: http://hdl.handle.net/2047/D20316349

University of Houston

9. Son, Jieun 1985-. Mechanism of Estrogen Receptor Alpha in Cervical Carcinogenesis.

Degree: PhD, Cell and Molecular Biology, 2017, University of Houston

URL: http://hdl.handle.net/10657/4602

► Most cervical cancers are associated with high-risk human papillomaviruses (HPVs). HPVs display tumorigenic functions in host cells mainly through viral oncogenes E6 and E7 that… (more)

▼ Most cervical cancers are associated with high-risk human papillomaviruses (HPVs). HPVs display tumorigenic functions in host cells mainly through viral oncogenes E6 and E7 that are best known to inhibit p53 and pRb tumor suppressor, respectively. However, HPV infection alone is not sufficient to induce cervical cancer. Other cofactors have been identified. Long-term use of oral contraceptives and multiple full-term pregnancies increase the risk of cervical cancer in women with HPV infection. Prolonged treatment of estrogen is required for initiation and maintenance of cervical cancer in HPV transgenic mice expressing E6 and E7. Genetic deletion of estrogen receptor alpha (ERα) inhibits the development of cervical cancer in the same mouse models. While these findings highlight the importance of estrogen and ERα in cervical carcinogenesis, there is little understanding of their mechanism of action. My dissertation seeks to explain how ERα contributes to cervical carcinogenesis. The main questions addressed in this dissertation are: (1) Is the DNA- binding domain (DBD) of ERα required for cervical carcinogenesis? (2) Is epithelial ERα required for cervical carcinogenesis? Genetically engineered mouse models expressing a DBD mutant or allowing a conditional deletion of ERα were used to answer these questions. The data in Chapter 1 demonstrate that point mutations within ERα DBD reduce estrogen-induced cell proliferation in the cervical epithelium. In HPV transgenic mice, ERα DBD is necessary for initiation of cervical cancer. In Chapter 2, I address the effect of specific deletion of ERα in the epithelial compartment on cervical carcinogenesis. Using epithelium-specific knockout mice, I conclude that epithelial ERα is not absolutely required for estrogen-induced cervical cancer in HPV transgenic mice. I should also note that, although almost all epithelial ERα-deficient HPV transgenic mice developed cervical neoplastic diseases, a smaller fraction of mice developed cervical cancer compared to epithelial ERα-sufficient control mice. These results are in accord with previous observations that stromal ERα signaling is required for progression of cervical neoplasia to cancer in the same mouse model. Lastly my dissertation gives a description on the establishment of a new orthotopic mouse model for human cervical cancer (Chapter 3). This novel preclinical model will be valuable in further studies to determine efficiency of drug candidates such as anti-estrogenic reagents in treating human cervical cancer. Advisors/Committee Members: Chung, Sang-Hyuk (advisor), Frigo, Daniel E. (committee member), Fuqua, Suzanne, A. W. (committee member), Lin, Chin-Yo (committee member).

Subjects/Keywords: Estrogen receptor alpha; Cervical cancer

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APA (6^th Edition):

Son, J. 1. (2017). Mechanism of Estrogen Receptor Alpha in Cervical Carcinogenesis. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/4602

Chicago Manual of Style (16^th Edition):

Son, Jieun 1985-. “Mechanism of Estrogen Receptor Alpha in Cervical Carcinogenesis.” 2017. Doctoral Dissertation, University of Houston. Accessed January 24, 2021. http://hdl.handle.net/10657/4602.

MLA Handbook (7^th Edition):

Son, Jieun 1985-. “Mechanism of Estrogen Receptor Alpha in Cervical Carcinogenesis.” 2017. Web. 24 Jan 2021.

Vancouver:

Son J1. Mechanism of Estrogen Receptor Alpha in Cervical Carcinogenesis. [Internet] [Doctoral dissertation]. University of Houston; 2017. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10657/4602.

Council of Science Editors:

Son J1. Mechanism of Estrogen Receptor Alpha in Cervical Carcinogenesis. [Doctoral Dissertation]. University of Houston; 2017. Available from: http://hdl.handle.net/10657/4602

University of Manitoba

10. Chooniedass, Shilpa. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.

Degree: Biochemistry and Medical Genetics, 2011, University of Manitoba

URL: http://hdl.handle.net/1993/4421

► In 1999, the discovery of the Steroid Receptor RNA Activator (SRA) was unprecedented in the field of steroid receptor co-regulator research. It was the first… (more)

▼ In 1999, the discovery of the Steroid Receptor RNA Activator (SRA) was unprecedented in the field of steroid receptor co-regulator research. It was the first time that an RNA molecule was demonstrated to function similarly to its protein counterpart and modulate the activity of steroid receptors. This peculiar steroid receptor co-activator thus attracted the attention of numerous research groups. Over the years, studies were reported deciphering SRA mechanisms of action, its role in co-regulating nuclear receptors and its possible implication in human diseases. While SRA was originally thought to exist solely as a non-coding RNA, our laboratory has identified longer SRA RNA isoforms with the theoretical capacity to encode for a protein. This discovery impelled us to investigate the existence of a Steroid Receptor RNA Activator Protein or SRAP. In this thesis, we first demonstrated the existence and function of endogenous evolutionary conserved SRA proteins. Based on these results we further explored SRAP expression in breast tumors. Interestingly, Western blot analysis of a small cohort of estrogen positive breast tumors suggested that SRAP expression correlates with a better overall survival in patients treated with tamoxifen. This observation prompted us to explore the biological role of SRAP. We found that MCF-7 cells stably expressing coding SRA isoforms had lower ligand dependent estrogen receptor alpha transcriptional activity. In order to dissect the function of the protein independently of its RNA counterpart, we separated the functions of the protein by introducing extensive silent mutations into the RNA sequence. Using this model, we established that SRAP, independent of its RNA counterpart, enhances estrogen receptor alpha activity in a ligand and response-element dependent manner. Furthermore, we showed for the first time that SRAP physically interacts with multiple transcription factors and is recruited to specific promoter regions. Moreover, by artificially recruiting SRAP to the promoter of a luciferase reporter gene under the control of the strong transcriptional activator VP16, we observed a decrease in transcription. These latter results suggest that SRA could function as a repressor through direct association with promoters. Overall, we believe that SRA is a very peculiar example of a bi-faceted system consisting of a functional RNA and its corresponding protein. Altogether our data suggest that SRAP, similarly to its RNA counterpart, is involved in many critical pathways that directly participate in gene expression regulation. Advisors/Committee Members: Leygue, Etienne (Biochemistry and Medical Genetics) (supervisor), Murphy, Leigh (Biochemistry and Medical Genetics) Davie, Jim (Biochemistry and Medical Genetics) Xie, Juiyong (Physiology) (examiningcommittee).

Subjects/Keywords: steoid receptor RNA activator; estrogen receptor

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APA (6^th Edition):

Chooniedass, S. (2011). The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/4421

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):

Chooniedass, Shilpa. “The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.” 2011. Thesis, University of Manitoba. Accessed January 24, 2021. http://hdl.handle.net/1993/4421.

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

MLA Handbook (7^th Edition):

Chooniedass, Shilpa. “The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer.” 2011. Web. 24 Jan 2021.

Vancouver:

Chooniedass S. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. [Internet] [Thesis]. University of Manitoba; 2011. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1993/4421.

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

Council of Science Editors:

Chooniedass S. The role of the newly discovered steroid receptor RNA activator protein (SRAP) in the estrogen signaling pathway and its implication in breast cancer. [Thesis]. University of Manitoba; 2011. Available from: http://hdl.handle.net/1993/4421

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

University of Rochester

11. 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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Hsu I. The Roles of Estrogen Receptors in the Bladder Cancer Development. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Jan 24]. 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

12. 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 January 24, 2021. 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. 24 Jan 2021.

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 2021 Jan 24]. 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

13. 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

►

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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Božović, Ana M. 1. Metilovanje promotora i ekspresija estrogenskog receptora beta (ERß) u invazivnim karcinomima dojke. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2021 Jan 24]. 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

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

Degree: MS, Department of Psychology, 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. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818

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. Masters Thesis, University of Guelph. Accessed January 24, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818.

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. 24 Jan 2021.

Vancouver:

Ervin K. The role of specific estrogen receptors in mediating rapid estrogenic improvements of social learning in female mice. [Internet] [Masters thesis]. University of Guelph; 2014. [cited 2021 Jan 24]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7818.

Council of Science Editors:

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

Cornell University

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

Degree: PhD, Biochemistry, 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: Kraus, William Lee (chair), Collins, Ruth N. (committee member), Lis, John T (committee member).

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. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/33589

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. Doctoral Dissertation, Cornell University. Accessed January 24, 2021. http://hdl.handle.net/1813/33589.

MLA Handbook (7^th Edition):

Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses.” 2011. Web. 24 Jan 2021.

Vancouver:

Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses. [Internet] [Doctoral dissertation]. Cornell University; 2011. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1813/33589.

Council of Science Editors:

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

Vanderbilt University

16. 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://hdl.handle.net/1803/12683

► 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), Barbara Fingleton (committee member), Fritz Parl (committee member), Robert Matusik (Committee Chair).

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

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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://hdl.handle.net/1803/12683

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 January 24, 2021. http://hdl.handle.net/1803/12683.

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. 24 Jan 2021.

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 2021 Jan 24]. Available from: http://hdl.handle.net/1803/12683.

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://hdl.handle.net/1803/12683

Vanderbilt University

17. Ludwik, Katarzyna Anna. RSKy Business in the Mammary Gland.

Degree: PhD, Pathology, 2018, Vanderbilt University

URL: http://hdl.handle.net/1803/11180

► The family of ribosomal S6 Ser/Thr protein kinases (RSK) controls proliferation, viability and motility and, therefore, contributes to the etiology of numerous cancers, including breast.… (more)

▼ The family of ribosomal S6 Ser/Thr protein kinases (RSK) controls proliferation, viability and motility and, therefore, contributes to the etiology of numerous cancers, including breast. We found that RSK2 is an obligate partner in estrogen receptor alpha (ER)-driven breast cancer by physically interacting with ER to activate a pro-neoplastic transcriptional network. ER sequesters RSK2 in the nucleus and ER+ tumor growth is dependent on nuclear RSK2. In a novel mouse model, mammary-specific expression of nuclear RSK2 drives development of high grade ER+ ductal carcinoma in situ. Besides being a driver in breast cancer, ER+ cells are indispensable for normal mammary gland function. Therefore, we investigated RSK2 contributions to mammary gland homeostasis. We discovered that activation of extracellular signal–regulated kinase 1/2 (ERK1/2) and subsequently RSK2 are necessary for maintenance of ER levels in the presence of estrogen. This protective mechanism is a part of a negative feedback loop, as estrogen positively regulates expression of growth factors that activate ERK1/2-RSK2 signaling. As ER degradation is intimately linked with its transcriptional activity, loss of RSK2 alters the transcriptome architecture in response to estrogen. Consequently, inappropriate hormonal responses cause increased DNA damage. Together, our findings indicate that RSK2 regulates ER-mediated processes in both breast cancer and in normal mammary epithelium. In addition to ER+ breast cancer, RSK contributes to triple negative breast cancer (TNBC). Levels of active RSK are increased in ~70% of TNBCs and RSK regulates migration in TNBC. As TNBC patients have increased probability of death due to metastasis, we described an in vivo study showing the efficacy of RSK-targeting in metastatic TNBC. We found that RSK1 and RSK2 regulate metastatic colonization and growth suggesting that targeting RSK is a potential therapeutic strategy for metastatic breast cancer. Development of targeted therapies for breast cancer is frequently hindered by the lack of in vitro models that recapitulate diverse tumor phenotypes. As tumor heterogeneity contributes to chemotherapy resistance and decreased patient survival, we developed an organoid culture system that recapitulates tumor heterogeneity. Our methodology focuses on quantifiable cellular phenotypes and provides a novel tool for drug-testing. Advisors/Committee Members: Thomas Stricker (committee member), Deborah Lannigan (committee member), Andries Zijlstra (committee member), Ian Macara (committee member), Christopher Wright (committee member), Alissa Weaver (Committee Chair).

Subjects/Keywords: breast cancer; mammary gland; RSK2; estrogen receptor

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

APA (6^th Edition):

Ludwik, K. A. (2018). RSKy Business in the Mammary Gland. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11180

Chicago Manual of Style (16^th Edition):

Ludwik, Katarzyna Anna. “RSKy Business in the Mammary Gland.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed January 24, 2021. http://hdl.handle.net/1803/11180.

MLA Handbook (7^th Edition):

Ludwik, Katarzyna Anna. “RSKy Business in the Mammary Gland.” 2018. Web. 24 Jan 2021.

Vancouver:

Ludwik KA. RSKy Business in the Mammary Gland. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1803/11180.

Council of Science Editors:

Ludwik KA. RSKy Business in the Mammary Gland. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://hdl.handle.net/1803/11180

Texas A&M University

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

Degree: PhD, Nutrition, 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) β knockout (ERβKO) 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 ERβ expression decreasing concomitantly with ERα expression increasing. Contrary to the protective effect of E2 on inflammation-associated colon tumor formation, which was dependent on ERβ, during acute inflammation in the colon E2 was protective against inflammation in both WT and ERβKO mice and injury in ERβKO 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 ERβKO mice. In vitro studies further elucidated the roles of ERα and ERβ in colonocytes. E2 and ERβ, but not ERα, specific agonists reduced cell number and induce apoptosis in nonmalignant colonocytes. This effect was lost in the presence of mutated p53. In ERα overexpressed nonmalignant colonocytes, E2 had no effect on cell number while ERβ agonist and ERα agonists decreased and increased cell number respectively. These studies suggest that E2 is protective in the colon and ERβ 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 (6^th Edition):

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

Chicago Manual of Style (16^th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Doctoral Dissertation, Texas A&M University. Accessed January 24, 2021. http://hdl.handle.net/1969.1/151883.

MLA Handbook (7^th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Web. 24 Jan 2021.

Vancouver:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1969.1/151883.

Council of Science Editors:

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

University of Ottawa

19. 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 (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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Boucher J. Perinatal Nicotine Exposure Upregulates ERα In the Dentate Gyrus of Adult Male Rat Offspring . [Internet] [Thesis]. University of Ottawa; 2015. [cited 2021 Jan 24]. 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

University of Houston

20. -8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells.

Degree: PhD, 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. (Doctoral Dissertation). 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

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. Doctoral Dissertation, University of Houston. Accessed January 24, 2021. http://hdl.handle.net/10657/2018.

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

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. 24 Jan 2021.

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] [Doctoral dissertation]. University of Houston; 2015. [cited 2021 Jan 24]. 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

Council of Science Editors:

-8465-3791. Defining Anti-Tumorigenic and Anti-Inflammatory Effects Mediated By Estrogen Receptor Beta In Colon Epithelial Cells. [Doctoral Dissertation]. 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

University of Houston

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

Degree: PhD, Biology, 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 receptors; Transcription factors

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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. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/956

Chicago Manual of Style (16^th Edition):

Butler, Ryan 1986-. “Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.” 2013. Doctoral Dissertation, University of Houston. Accessed January 24, 2021. http://hdl.handle.net/10657/956.

MLA Handbook (7^th Edition):

Butler, Ryan 1986-. “Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ.” 2013. Web. 24 Jan 2021.

Vancouver:

Butler R1. Physiological and pathological aspects of the ligand-activated transcription factors: AhR and ERβ. [Internet] [Doctoral dissertation]. University of Houston; 2013. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/10657/956.

Council of Science Editors:

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

University of Canterbury

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

Degree: PhD, Chemistry, 2012, University of Canterbury

URL: http://dx.doi.org/10.26021/8979

► 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. (Doctoral Dissertation). University of Canterbury. Retrieved from http://dx.doi.org/10.26021/8979

Chicago Manual of Style (16^th Edition):

Graham, Lisa Anne. “Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.” 2012. Doctoral Dissertation, University of Canterbury. Accessed January 24, 2021. http://dx.doi.org/10.26021/8979.

MLA Handbook (7^th Edition):

Graham, Lisa Anne. “Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor.” 2012. Web. 24 Jan 2021.

Vancouver:

Graham LA. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. [Internet] [Doctoral dissertation]. University of Canterbury; 2012. [cited 2021 Jan 24]. Available from: http://dx.doi.org/10.26021/8979.

Council of Science Editors:

Graham LA. Environmental Estrogens: Assessing Human Gestational Exposure and Interactions with the Estrogen Receptor. [Doctoral Dissertation]. University of Canterbury; 2012. Available from: http://dx.doi.org/10.26021/8979

Virginia Tech

23. 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. I. (committee member), Santos, Webster (committee member).

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

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

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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Rajalekshmi Devi S. Development of Novel anti-estrogens for endocrine resistant Breast Cancer. [Internet] [Masters thesis]. Virginia Tech; 2016. [cited 2021 Jan 24]. 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

24. 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

►

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 (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 January 24, 2021. 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. 24 Jan 2021.

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 2021 Jan 24]. 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

25. 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 (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 January 24, 2021. 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. 24 Jan 2021.

Vancouver:

Iorga A. Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta. [Internet] [Thesis]. UCLA; 2015. [cited 2021 Jan 24]. 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

Loyola University Chicago

26. Shults, Cody Lee. Mechanisms of Estrogen Receptor Alternative Splicing and the Consequences for Aging in the Female Brain.

Degree: PhD, Cell Biology, Neurobiology and Anatomy, 2015, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/1969

► The advances in healthcare and scientific knowledge have resulted in longer life expectancies in women. These advanced ages in women now means that they… (more)

▼ The advances in healthcare and scientific knowledge have resulted in longer life expectancies in women. These advanced ages in women now means that they are experiencing the effects of age-related changes in the body for much longer periods of time, mainly reproductive senescence, resulting in the loss of circulating ovarian hormones. The age at which menopause occurs has not changed, resulting in women now living over a third of their lives in a postmenopausal state. The major circulating estrogen produced by the ovaries, 17β-estradiol (E2), has many homeostatic effects in the body like neuroprotection and cardioprotection. Hormone replacement therapy (HT) was to become the standard in treating women undergoing reproductive senescence in order to abrogate the negative effects associated with the decline in circulating E2, however adverse effects of HT were observed mainly women who were at least 10 years removed from menopause. These findings led to the idea of a therapeutic window in which ET is beneficial, known as the “timing hypothesis”, pointing to age-related adjustments that occur during and after this critical period of declining E2 levels. E2 is known to regulate transcription through an important class of nuclear steroid receptors called estrogen receptors (ERs). ERβ mediate the actions of E2 upon binding through interactions within the promoter region of ER-regulated genes and is subject to alternative splicing. It is through this process that ERβ splice variants arise altering the receptor function and responsiveness to E2 in the brain. These observations led to the hypothesis that aging and diminished E2 levels affect the alternative splicing of ERβ in the aged female brain through altered expression of ER-regulated splicing factors. ERβ alternative splice variants were measured in the brain of young and aged female rats who were subjected to increasingly longer periods of hormone deprivation. In vitro data from brain-derived cell lines also provided mechanistic answers to how ERβ is alternatively spliced in the brain. This dissertation work contributes to our overall understanding of ERβ in the context of its expression and possible function in the aging female brain.

Subjects/Keywords: aging; alternative splicing; estrogen; estrogen receptor; menopause; Endocrinology

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APA (6^th Edition):

Shults, C. L. (2015). Mechanisms of Estrogen Receptor Alternative Splicing and the Consequences for Aging in the Female Brain. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/1969

Chicago Manual of Style (16^th Edition):

Shults, Cody Lee. “Mechanisms of Estrogen Receptor Alternative Splicing and the Consequences for Aging in the Female Brain.” 2015. Doctoral Dissertation, Loyola University Chicago. Accessed January 24, 2021. https://ecommons.luc.edu/luc_diss/1969.

MLA Handbook (7^th Edition):

Shults, Cody Lee. “Mechanisms of Estrogen Receptor Alternative Splicing and the Consequences for Aging in the Female Brain.” 2015. Web. 24 Jan 2021.

Vancouver:

Shults CL. Mechanisms of Estrogen Receptor Alternative Splicing and the Consequences for Aging in the Female Brain. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2015. [cited 2021 Jan 24]. Available from: https://ecommons.luc.edu/luc_diss/1969.

Council of Science Editors:

Shults CL. Mechanisms of Estrogen Receptor Alternative Splicing and the Consequences for Aging in the Female Brain. [Doctoral Dissertation]. Loyola University Chicago; 2015. Available from: https://ecommons.luc.edu/luc_diss/1969

Loyola University Chicago

27. Navarro Negredo, Flor Cecilia. Characterization of the Effects of Sex and Estrogen Receptor Signaling on Antigen-Specific T Cells for Immunotherapy.

Degree: PhD, Biological Science, 2019, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/3359

► Adoptive cell transfer (ACT) immunotherapy using antigen (Ag)-specific T cells is partially effective treating several malignancies but numerous challenges remain in order to improve its… (more)

▼ Adoptive cell transfer (ACT) immunotherapy using antigen (Ag)-specific T cells is partially effective treating several malignancies but numerous challenges remain in order to improve its therapeutic potential. The roles of host factors, such as sex hormone receptor signaling, that can affect the T cell anti-tumor function remain understudied. The work performed in this dissertation characterized the role of estrogen signaling on T cell function in vitro, and during ACT immunotherapy against hepatocellular carcinoma (HCC) in vivo. Estrogen signaling through ERa enhanced the expression and secretion of Type I effector cytokines including IFNg, TNFa, and Granzyme B in male and female Ag-specific T cells activated with their cognate Ag. Estrogen signaling through ERa enhanced the expression of the Type 2 cytokine IL-4 in male and female Ag-specific T cells. Estrogen signaling through ERb enhanced the polyfunctionality of male and female Ag-specific T cells activated with their cognate Ag. These results demonstrated for the first time that estrogen signaling through ERa and ERb can enhance the function of human Ag-specific T cells. Using an HCC mouse model treated with ACT immunotherapy, the effect of estrogen on the T cell anti-tumor immune response was measured. Estrogen presence resulted in reduced tumor burden and higher Ag-specific T cell tumor infiltration, survival, activation state, and cytokine expression. Removal of physiological estrogen reduced the survival and infiltration of CD4+ Ag-specific T cells. Lack of physiological estrogen during ACT also caused reduced cytokine production and polyfunctionality of CD4+ Ag-specific T cells. These results revealed for the first time that estrogen signaling can enhance the survival and function of CD4+ Ag-specific T cells in vivo which results in enhanced anti-tumor responses and reduced tumor burden. In summary, estrogen signaling enhances male and female Ag-specific T cell cytokine expression and secretion, and polyfunctionality which lead to enhanced tumor infiltration, survival, activation state, and function during ACT immunotherapy. This indicates that inducing estrogen signaling on Ag-specific T cells can enhance the efficacy and therapeutic outcome of ACT immunotherapy.

Subjects/Keywords: Estrogen; Estrogen Receptor; Hepatocellular Carcinoma; Immunotherapy; T cells; Tumor Immunology; Biochemistry

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APA (6^th Edition):

Navarro Negredo, F. C. (2019). Characterization of the Effects of Sex and Estrogen Receptor Signaling on Antigen-Specific T Cells for Immunotherapy. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/3359

Chicago Manual of Style (16^th Edition):

Navarro Negredo, Flor Cecilia. “Characterization of the Effects of Sex and Estrogen Receptor Signaling on Antigen-Specific T Cells for Immunotherapy.” 2019. Doctoral Dissertation, Loyola University Chicago. Accessed January 24, 2021. https://ecommons.luc.edu/luc_diss/3359.

MLA Handbook (7^th Edition):

Navarro Negredo, Flor Cecilia. “Characterization of the Effects of Sex and Estrogen Receptor Signaling on Antigen-Specific T Cells for Immunotherapy.” 2019. Web. 24 Jan 2021.

Vancouver:

Navarro Negredo FC. Characterization of the Effects of Sex and Estrogen Receptor Signaling on Antigen-Specific T Cells for Immunotherapy. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2019. [cited 2021 Jan 24]. Available from: https://ecommons.luc.edu/luc_diss/3359.

Council of Science Editors:

Navarro Negredo FC. Characterization of the Effects of Sex and Estrogen Receptor Signaling on Antigen-Specific T Cells for Immunotherapy. [Doctoral Dissertation]. Loyola University Chicago; 2019. Available from: https://ecommons.luc.edu/luc_diss/3359

Texas A&M University

28. Weige, Charles. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.

Degree: PhD, Genetics, 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838

► Hormone replacement therapy and estrogen replacement therapy have shown the ability to reduce risk of colon cancer development in clinical and animal studies, but in… (more)

▼ Hormone replacement therapy and estrogen replacement therapy have shown the ability to reduce risk of colon cancer development in clinical and animal studies, but in vitro research has been unable to reproduce an estradiol (E2) induced response in colon cancer cell lines. We demonstrated that young adult mouse colonocytes (YAMC, non-malignant colonocytes) exhibit an anti-proliferative response to E2 treatment. These cells demonstrate reduced cell culture growth and increased apoptosis in response to E2. YAMC cells containing an activated Ras mutation are considered to be malignantly transformed, and lose the ability to respond to E2 treatment. Fulvestrant (ICI) was used as an estrogen receptor antagonist to determine that these results were estrogen receptor mediated. Furthermore, this effect was demonstrated to require the presence of ER? through the use of a transgenic ERbeta knockout mouse. In these mice, the presence of E2 significantly reduced the formation of azoxymethane induced premalignant lesions. Since YAMC cells exhibit an anti-proliferative response to E2 treatment, we utilized isogenic YAMC cell lines with and without a dominant negative p53 mutation to demonstrate that this E2 induced action involves p53 activity. E2 treatment results in increased p53 transcriptional activity and a pro-apoptotic change in expression of p53 downstream targets. Presence of the dominant negative p53 mutant nullifies these effects of E2 treatment. The involvement of p53 in the previously described protection against AOM induced premalignant lesions, was investigated using wild type and heterozygous p53 knockout (Het p53KO) mice. The reduction in p53 protein corresponded to reduced effectiveness of E2 treatment on the prevention of premalignant lesion formation in Het p53KO mice. In summary, our data indicate that E2 treatment induces anti-proliferative responses in non-malignant colonocytes and protects against the formation of carcinogen-induced premalignant lesions. These effects require the presence of functional ER? and p53. Further studies are required to more thoroughly elucidate the specific interactions and downstream effects of ER? and p53 in response to E2 stimulation. Advisors/Committee Members: Allred, Clinton D. (advisor), Chapkin, Robert S. (committee member), Dabney, Alan R. (committee member), Lupton, Joanne R. (committee member).

Subjects/Keywords: Estrogen; estrogen receptor beta; colon cancer; p53; apoptosis; aberrant crypt foci

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

APA (6^th Edition):

Weige, C. (2012). Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838

Chicago Manual of Style (16^th Edition):

Weige, Charles. “Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.” 2012. Doctoral Dissertation, Texas A&M University. Accessed January 24, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838.

MLA Handbook (7^th Edition):

Weige, Charles. “Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development.” 2012. Web. 24 Jan 2021.

Vancouver:

Weige C. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. [Internet] [Doctoral dissertation]. Texas A&M University; 2012. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838.

Council of Science Editors:

Weige C. Estrogen Receptor Beta and p53 Play Integral Roles in Estradiol Mediated Protection against Colon Tumor Development. [Doctoral Dissertation]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11838

29. Gustafsson, Karin. Estrogen receptor α and Bone – Posttranslational modifications and cell-specific deletion.

Degree: 2019, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/60795

► Estrogen is involved in the regulation and development of reproductive organs. In addition, estrogen regulates several other organs including the skeleton, immune system, and adipose… (more)

▼ Estrogen is involved in the regulation and development of reproductive organs. In addition, estrogen regulates several other organs including the skeleton, immune system, and adipose tissue. Estrogen treatment protects against osteoporosis and some other hormone-related diseases, but this treatment is associated with an increased risk of cancer in reproductive organs and venous thrombosis. Because of these side effects it is important to elucidate the mechanisms behind estrogenic effects in different organs, to aid the development of tissue-specific estrogen treatments. The estrogenic effect in the skeleton and several other hormone-sensitive tissues, including adipose tissue, is mainly mediated by estrogen receptor alpha (ERα). ERα is subjected to posttranslational modifications (PTMs) that can affect receptor signaling in a tissue-specific manner. Therefore, the first aim of this thesis was to evaluate whether targeting of three different ERα PTMs –palmitoylation at site C451 – phosphorylation at site S122 – methylation at site R264 –, results in tissue-specific estrogenic effects. ERα is classically described as a transcription factor that affects the cell via nuclear (genomic) signaling. However, ERα can also be associated to the membrane and exert non-genomic signaling. To study the role of membrane-initiated ERα (mERα) signaling for the estrogenic response, we used mice lacking palmitoylation at site C451, which is crucial for membrane localization. Our study showed that the importance of mERα signaling is tissue-specific, with the trabecular bone in the axial skeleton being strongly dependent on functional mERα signaling, while adipose tissue is mainly mERα-independent. We also demonstrated that phosphorylation at site S122 in ERα has a tissue-dependent role with an impact specifically on fat mass in female mice. Finally, we found that methylation at site R264 in ERα has no effect on estrogenic regulation of the skeleton or other estrogen-sensitive tissues. ERα is expressed in several different cell types and ERα expression in bone cells has been shown to affect the skeleton. It is also known that T lymphocytes are involved in the regulation of bone mass. Therefore, the second aim of this thesis was to evaluate whether ERα expression in T lymphocytes is involved in the protective effect of estrogen in the skeleton. We identified that ERα expression in T lymphocytes is dispensable for normal estrogenic regulation of bone mass. In conclusion, this thesis has increased our knowledge of estrogen signaling mechanisms. Specifically, this thesis shows that mERα is important for estrogen signaling and has a tissue-specific role. In addition, phosphorylation at site S122 modulates the activity of ERα in a tissue-dependent manner. This thesis also shows that methylation at site R264 is dispensable for estrogenic regulation of the skeleton and other estrogen-responsive tissues and that T lymphocytes are not direct target cells for ERα-mediated estrogenic skeletal effects.

Subjects/Keywords: estrogen receptor α; bone; osteoporosis; adipose tissue; estrogen; posttranslational modifications

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

APA (6^th Edition):

Gustafsson, K. (2019). Estrogen receptor α and Bone – Posttranslational modifications and cell-specific deletion. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/60795

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):

Gustafsson, Karin. “Estrogen receptor α and Bone – Posttranslational modifications and cell-specific deletion.” 2019. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 24, 2021. http://hdl.handle.net/2077/60795.

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

MLA Handbook (7^th Edition):

Gustafsson, Karin. “Estrogen receptor α and Bone – Posttranslational modifications and cell-specific deletion.” 2019. Web. 24 Jan 2021.

Vancouver:

Gustafsson K. Estrogen receptor α and Bone – Posttranslational modifications and cell-specific deletion. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2019. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2077/60795.

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

Council of Science Editors:

Gustafsson K. Estrogen receptor α and Bone – Posttranslational modifications and cell-specific deletion. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2019. Available from: http://hdl.handle.net/2077/60795

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

University of Illinois – Urbana-Champaign

30. Carroll, Vincent. I. Development of novel silicon precursors for rapid and efficient radiofluorination reactions: synthesis and biological evaluation of a 18f-labelled estrogen dendrimer conjugate II. Other studies on 18f-labelled estrogens.

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

URL: http://hdl.handle.net/2142/95662

► Molecular imaging (MI) has revolutionized the visualization of complex biochemical processes in normal physiology and diseased states. Although still in its infancy, the data generated… (more)

▼ Molecular imaging (MI) has revolutionized the visualization of complex biochemical processes in normal physiology and diseased states. Although still in its infancy, the data generated from MI studies aids in identifying sites of pathological involvement and provides key insight into the mechanisms that lead to the onset and progression of disease. Consequently, these techniques hold tremendous potential in the areas of diagnostics, therapy assessment, and drug development in the coming years. Amongst MI techniques, Positron Emission Tomography (PET) separates itself from the rest of the field with its exceptional sensitivity, near limitless depth of penetration and its ability to quantify metabolic processes in living patients. With the ability to visualize and quantify on an individualized basis, PET imaging has received considerable attention recently because of its potential for contributing to personalized medicine. Through better diagnosis, rational selection of targeted therapies, and individualization of therapy regimens for each patient, personalized medicine holds the promise of greatly improving patient outcomes as well as safeguarding against the use of unnecessary, harmful medical procedures. Given the current status of the PET field and the impact it has on many fields, significant effort is being made to expand the existing repertoire of imaging agents capable of further detailing pathophysiological processes beyond the most commonly used PET tracer, [18F]fluorodeoxyglucose, including the use of large, sensitive biomolecules such as peptides and antibodies, which may be of considerable clinical importance. However, the available methodology associated with PET isotope incorporation, specifically fluorine-18, involves rather harsh conditions that are incompatible with sensitive substrates, which restricts the availability of these agents and their subsequent clinical evaluation. Thus, there remains a tremendous need for rapid, mild and efficient methodology that can be used to label these previously inaccessible substrates in a direct, late-stage fashion. Chapter 1 presents a brief introduction into molecular imaging and the techniques available for use in the preclinical and clinical setting as well as in drug development. Additionally, the basics of PET principles and radiochemistry are introduced, with a significant focus on the synthetic difficulties involved in working with the most commonly used PET isotope, fluorine-18, and why there is a need for improved methodology for its incorporation into new radiopharmaceutical agents, especially sensitive ones. Chapter 2 details the development of methodology that targets the shortcomings of C-18F strategies through Si-18F bond formation approaches. We have developed a simple and straightforward strategy in radiofluorinating complex substrates at a late stage, at room temperature, or in an aqueous environment in high radiochemical yields and specific activities through a reactive silyl acetate moiety. The utility and versatility of the approach is… Advisors/Committee Members: Katzenellenbogen, John A (advisor), Katzenellenbogen, John A (Committee Chair), Katzenellenbogen, Benita S (committee member), Silverman, Scott K (committee member), Hergenrother, Paul J (committee member).

Subjects/Keywords: 2-fluoroestradiol; estrogen dendrimer conjugate; estrogen receptor; fluorine-18

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

APA (6^th Edition):

Carroll, V. (2012). I. Development of novel silicon precursors for rapid and efficient radiofluorination reactions: synthesis and biological evaluation of a 18f-labelled estrogen dendrimer conjugate II. Other studies on 18f-labelled estrogens. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/95662

Chicago Manual of Style (16^th Edition):

Carroll, Vincent. “I. Development of novel silicon precursors for rapid and efficient radiofluorination reactions: synthesis and biological evaluation of a 18f-labelled estrogen dendrimer conjugate II. Other studies on 18f-labelled estrogens.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 24, 2021. http://hdl.handle.net/2142/95662.

MLA Handbook (7^th Edition):

Carroll, Vincent. “I. Development of novel silicon precursors for rapid and efficient radiofluorination reactions: synthesis and biological evaluation of a 18f-labelled estrogen dendrimer conjugate II. Other studies on 18f-labelled estrogens.” 2012. Web. 24 Jan 2021.

Vancouver:

Carroll V. I. Development of novel silicon precursors for rapid and efficient radiofluorination reactions: synthesis and biological evaluation of a 18f-labelled estrogen dendrimer conjugate II. Other studies on 18f-labelled estrogens. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/2142/95662.

Council of Science Editors:

Carroll V. I. Development of novel silicon precursors for rapid and efficient radiofluorination reactions: synthesis and biological evaluation of a 18f-labelled estrogen dendrimer conjugate II. Other studies on 18f-labelled estrogens. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/95662

Open Access Theses and Dissertations