subject:(Estrogen receptor beta)

Boston University

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

Degree: MS, Medical Sciences, 2017, Boston University

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

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

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

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

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APA (6^th Edition):

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

Chicago Manual of Style (16^th Edition):

Koomson, Jacqueline Nyarkoa. “The role of estrogen receptors alpha and beta in the development of uterine leiomyomas.” 2017. Masters Thesis, Boston University. Accessed January 22, 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. 22 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 22]. Available from: http://hdl.handle.net/2144/23835.

Council of Science Editors:

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

University of Rochester

2. 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 22, 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. 22 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 22]. 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 Houston

3. -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 22, 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. 22 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 22]. 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

Univerzitet u Beogradu

4. 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 22, 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. 22 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 22]. 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

UCLA

5. 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 22, 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. 22 Jan 2021.

Vancouver:

Iorga A. Estrogen Therapy Rescues Advanced Heart Failure via Estrogen Receptor Beta. [Internet] [Thesis]. UCLA; 2015. [cited 2021 Jan 22]. 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

Texas A&M University

6. 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 (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 22, 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. 22 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 22]. 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

University of Guelph

7. 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 22, 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. 22 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 22]. 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

University of Southern California

8. Cho, Tae Hoon. The role of estrogen receptors and nociceptive signaling pathway of primary sensory neurons.

Degree: PhD, Chemical Engineering, 2012, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/42498/rec/7220

► Clinical studies suggest the comorbidity of functional pain syndromes such as irritable bowel syndrome (IBS), chronic pelvic pain (CPP), fibromyalgia, and somatoform disorders approaches 40%… (more)

▼ Clinical studies suggest the comorbidity of functional pain syndromes such as irritable bowel syndrome (IBS), chronic pelvic pain (CPP), fibromyalgia, and somatoform disorders approaches 40% to 60%. The incidence of episodic or persistent visceral pain associated with these functional disorders is two to three times higher women than in men. One of the possible explanations for this phenomenon is the estrogen modulation of pain transmission. While a central site of this modulation has been shown previously, here we proposed to study a peripheral site, the dorsal root ganglion (DRG). In DRG neurons, 17β-estradiol (E2) rapidly inhibits intracellular calcium ([Ca²⁺]i) flux induced by ATP, a putative nociceptive signal. This proposal, ""Estrogen Receptors mediate Nociceptive Signaling in Primary Sensory Neurons in Female Mice"" will test a general hypothesis that E2 acting on primary afferent nociceptors has both pro-nociceptive and anti-nociceptive effects depending on which signals converge upon DRG. First, the role of different estrogen receptors (ERs) in E2 activation of purinergic (P2X3) and vanilloid (TRPV1) receptors will be studied in wild type, estrogen receptor-α, and estrogen receptor-β knock-out mice. Second, since we hypothesize that E2 may act differently on visceral then on cutaneous nociceptors, we will compare the [Ca²⁺]i response to activation of P2X3 and TRPV1 receptors in retrogradely-labeled visceral and cutaneous DRG neurons from knock-out and wild type mice. Third, E2 may negatively modulate opioid analgesia by interfering with μ-opioid receptor (MOR). Pharmacological manipulations will be used to determine how ER activation modulates Ca2+ channel and MOR functions. Receptor binding will determine if E2 alters the number and affinity of MOR in the DRG and the site-specific regulation of MOR coupling to G-proteins. Together these experiments will define a new site(s) and mechanism of E2 modulation of nociceptive signaling. Furthermore, they will provide important information about the action of E2 on primary sensory neurons for a better understanding of sex-differences observed in the clinical presentation of functional pain-associated syndromes. Nociceptive systems implicated in the etiology of functional disorders, which often are complicated by comorbid depression will have a major impact on health-related quality of life in patients with functional pain disorders, significantly reducing therapeutic interventions. Advisors/Committee Members: Wang, Pin (Committee Chair), Shing, Katherine (Committee Member), Zhang, Li I. (Committee Member).

Subjects/Keywords: 17beta-estradiol; DRG; ATP; Capsaicin; calcium; estrogen receptor alpha; estrogen receptor beta

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APA (6^th Edition):

Cho, T. H. (2012). The role of estrogen receptors and nociceptive signaling pathway of primary sensory neurons. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/42498/rec/7220

Chicago Manual of Style (16^th Edition):

Cho, Tae Hoon. “The role of estrogen receptors and nociceptive signaling pathway of primary sensory neurons.” 2012. Doctoral Dissertation, University of Southern California. Accessed January 22, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/42498/rec/7220.

MLA Handbook (7^th Edition):

Cho, Tae Hoon. “The role of estrogen receptors and nociceptive signaling pathway of primary sensory neurons.” 2012. Web. 22 Jan 2021.

Vancouver:

Cho TH. The role of estrogen receptors and nociceptive signaling pathway of primary sensory neurons. [Internet] [Doctoral dissertation]. University of Southern California; 2012. [cited 2021 Jan 22]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/42498/rec/7220.

Council of Science Editors:

Cho TH. The role of estrogen receptors and nociceptive signaling pathway of primary sensory neurons. [Doctoral Dissertation]. University of Southern California; 2012. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/42498/rec/7220

Brigham Young University

9. Watson, Kristin Dawn. The Molecular Mechanism of Migraine.

Degree: MS, 2011, Brigham Young University

URL: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4047&context=etd

► Migraine is a common, episodic neurological disorder that includes headache, nausea and hypersensitivity to sensory stimuli. During the headache phase of migraine, migraine patients… (more)

▼ Migraine is a common, episodic neurological disorder that includes headache, nausea and hypersensitivity to sensory stimuli. During the headache phase of migraine, migraine patients can be especially hypersensitive to thermal stimuli. The unpredictable and episodic nature of migraine makes it difficult to treat and much of the mechanism of migraine has yet to be elucidated. A T44A substitution in casein kinase 1δ is inherited with migraine with aura. A transgenic mouse model suggests that animals with this mutation exhibit increased sensitivity to thermal stimuli after injection with nitroglycerin (NTG). We performed behavior assays that measure animal responses to thermal stimuli, after injection with NTG, a known migraine-inducer in human migraine patients. Female animals with the CK1δ-T44A mutation are more sensitive than wildtype littermates, suggesting a sex difference emerges in pain sensitivity in animals that express the CK1δ-T44A but not in wildtype siblings. Female CK1δ-T44A animals are more sensitive to the effects of NTG on pain than male CK1δ-T44A mice. This indicates a potential sex hormone related pain response. Since estrogen is implicated in both migraine and pain response, we test the thermal sensitivity of heterozygous ERβKO/+ and CK1δ-T44A; ERβKO/+ mice compared to wildtype and CK1δ-T44A mice. Overall thermal sensitivity is decreased before stress of injection in both male and female ERβKO/+ and CK1δ-T44A: ERβKO/+ mice. This demonstrates that ERβ is necessary for thermal nociception in untreated mice. However, after injection with saline or NTG, animals of all genotypes responded to thermal stimuli similarly. This suggests that estrogen signaling through ERβ is likely not part of the pathway of NTG-induced thermal sensitivity or that one copy of ERβ is sufficient for NTG-induced thermal sensitivity. Since ERβ is fully functional in CK1δ-T44A mice and CK1δ-T44A mice have wildtype thermal sensitivity at baseline, we can conclude that CK1δ-T44A does not modulate ERβ to affect thermal sensitivity in untreated animals.

Subjects/Keywords: migraine; casein kinase 1 alpha; estrogen; estrogen receptor β; pain; sex difference; Biochemistry; Chemistry

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APA (6^th Edition):

Watson, K. D. (2011). The Molecular Mechanism of Migraine. (Masters Thesis). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4047&context=etd

Chicago Manual of Style (16^th Edition):

Watson, Kristin Dawn. “The Molecular Mechanism of Migraine.” 2011. Masters Thesis, Brigham Young University. Accessed January 22, 2021. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4047&context=etd.

MLA Handbook (7^th Edition):

Watson, Kristin Dawn. “The Molecular Mechanism of Migraine.” 2011. Web. 22 Jan 2021.

Vancouver:

Watson KD. The Molecular Mechanism of Migraine. [Internet] [Masters thesis]. Brigham Young University; 2011. [cited 2021 Jan 22]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4047&context=etd.

Council of Science Editors:

Watson KD. The Molecular Mechanism of Migraine. [Masters Thesis]. Brigham Young University; 2011. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4047&context=etd

Freie Universität Berlin

10. Schwanstecher, Annekatrin. Regulation of Adipose Tiglycerid Lipase (ATGL) expression by nuclear estrogen receptors.

Degree: 2015, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-9781

► Estrogen Receptors (ERs) are known to play an important role in the metabolic functions of adipose tissue (AT). Gender specific differences concerning lipolysis have been… (more)

▼ Estrogen Receptors (ERs) are known to play an important role in the metabolic functions of adipose tissue (AT). Gender specific differences concerning lipolysis have been reported. For instance, female mice are known to mobilize energy from fat more efficiently than male littermates under exercise conditions. Also, changes in fat distribution and metabolic activity of adipose tissue during menopause are associated with an increasing risk for metabolic and cardiovascular complications in humans. The characterization of molecular mechanisms of estrogen-action in AT might help understand and treat metabolic disorders in the future. This study investigates the impact of nuclear ERs (alpha and beta on the expression of the Adipose Triglycerid Lipase (ATGL), the rate-limiting lipolytic enzyme in the process of triglyceride-degradation. Methods and Results: The regulatory impact of ERalpha and ERbeta on the expression of ATGL was investigated in 3T3L1-preadipocytes on promoter-, and mRNA level. Cells were transiently transfected with ERalpha/ERbeta or PSG5 and stimulated with vehicle vs. selective ERalpha/ERbeta agonists PPT/DPN (c=100nM) for 24h. Promoter-activity of the sequence 3000bp upstream of the first exon of the ATGL-gene was assessed by performing luciferase assay. Transcription increased both ligand- independently under the overexpression of ERalpha/ERbeta (1.6-/2.5-fold, p<0.05 vs. PSG5-control), as well as under receptor-overexpression and stimulation with the respective ER-agonist (2.7-/3.3-fold, p<0.05 vs. vehicle). In accordance, bioinformatical promoter analysis performed on the murine sequence revealed 7 putative ERbeta- and only 1 putative ERalpha- binding site. qRT-PCR-analysis demonstrated a significant increase in the amount of ATGL-mRNA by factor 1.3 under vehicle- and factor 1.5 under PPT- stimulation for cells overexpressing ERalpha vs. PSG5-control (both p<0.05). Similar experiments for the overexpression of ERbetashowed a significant increase in ATGL-mRNA-amount by factor 3.5 in DPN-stimulated cells vs. PSG5-control (p<0.05). Additionally, in cells overexpressing ERbeta a significant increase by factor 2.3 could be observed between vehicle- and DPN- stimulation (p<0.05). Most likely attributable to endogenous ERbeta a significant 2-fold increase of ATGL-mRNA could be observed under DPN- stimulation in PSG5-control-cells (p<0.05). Western Blot showed an increase in the amount of ATGL for both control-cells, as well as cells overexpressing ERbeta when stimulated with DPN. PPT stimulation did not show conclusive corresponding effects in control-cells or cells overexpressing ERalpha Conclusions: The present study demonstrates that both ERs exert positive regulatory actions on the expression of ATGL. The impact of ERbeta on ATGL promoter-activity, mRNA-expression and protein amount appears to be stronger when compared to ERalpha Further experiments will be required to determine the importance of these finding for an ER isoform-specific regulation of lipolysis. Advisors/Committee Members: [email protected] (contact), w (gender), N.N. (firstReferee), N.N. (furtherReferee).

Subjects/Keywords: estrogen; estrogen receptor alpha; estrogen receptor beta, ATGL; Adipocyte Triglyceride Lipase; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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

APA (6^th Edition):

Schwanstecher, A. (2015). Regulation of Adipose Tiglycerid Lipase (ATGL) expression by nuclear estrogen receptors. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-9781

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):

Schwanstecher, Annekatrin. “Regulation of Adipose Tiglycerid Lipase (ATGL) expression by nuclear estrogen receptors.” 2015. Thesis, Freie Universität Berlin. Accessed January 22, 2021. http://dx.doi.org/10.17169/refubium-9781.

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

MLA Handbook (7^th Edition):

Schwanstecher, Annekatrin. “Regulation of Adipose Tiglycerid Lipase (ATGL) expression by nuclear estrogen receptors.” 2015. Web. 22 Jan 2021.

Vancouver:

Schwanstecher A. Regulation of Adipose Tiglycerid Lipase (ATGL) expression by nuclear estrogen receptors. [Internet] [Thesis]. Freie Universität Berlin; 2015. [cited 2021 Jan 22]. Available from: http://dx.doi.org/10.17169/refubium-9781.

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

Council of Science Editors:

Schwanstecher A. Regulation of Adipose Tiglycerid Lipase (ATGL) expression by nuclear estrogen receptors. [Thesis]. Freie Universität Berlin; 2015. Available from: http://dx.doi.org/10.17169/refubium-9781

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

11. Božović Ana. Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers.

Degree: PhD, Biology, 2013, University of Belgrade

URL: http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927

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Breast cancer is the most common invasive cancer in women. Beside genetic, epigenetic factors influence its initiation and progression. The purpose of this study was… (more)

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Breast cancer is the most common invasive cancer in women. Beside genetic, epigenetic factors influence its initiation and progression. The purpose of this study was to test whether methylation of the promoter ON of the gene for ERβ protein (ESR2) influences its expression (on mRNA and protein level) and to correlate the methylation index of the ON promoter, ERβ1-mRNA and ERβ1 protein levels with clinicopathological parameters. In this study, 131 archival samples of breast cancer tissue were used. Custom designed two step PCR method, was done for amplification and relative quantification of the specific region of the ON promoter of the ESR2 gene. Measuring of ERβ1-mRNA was done by quantitative real time RT-PCR, and relative quantification of ERβ1 protein isoform was done by Western blot. Statistical analysis was performed and results for methylation index of ON promoter, mRNA and ERβ1 protein levels were correlated with clinicopathological parameters. The methylation index of ERβ-ON promoter was significantly higher in a group of patients with positive axillary lymph node status, than in a group with negative one. A significant positive correlation between methylation index of ON promoter and ERα protein levels was obtained. It can be concluded that methylation index of the ERβ-ON promoter could be more confident parameter for prediction and/or prognosis of breast cancer, than measuring of ERβ1-mRNA or ERβ1 protein levels.

Invazivni karcinom dojke je najčešći kancer kod žena. Pored genetičkih i epigenetički faktori imaju važnu ulogu u njegovoj inicijaciji i progresiji. Cilj ove studije bio je ispitati da li metilacija promotora ON, gena za ERβ protein (ESR2) utiče na njegovu ekspresiju (na nivou iRNK i proteina) i utvrditi povezanost metilacionog indeksa promotora ON sa nivoima ERβ1-iRNK i ERβ1 proteina, kao i sa kliničkim i patohistološkim parametrima. U ovoj studiji analiziran je 131 arhivski uzorak kancera dojke. Pomoću posebno dizajniranog PCR testa iz dva koraka, amplifikovan je i kvantifikovan specifični region promotora ON ESR2 gena. Za kvantifikaciju ERβ1-iRNK korišćena je metoda kvantitativnog RT-PCR u realnom vremenu. Metoda „Western Blot“ je korišćena za relativnu kvantifikaciju ERβ1 proteinske izoforme. Dobijeni podaci, metilacioni indeks promotora ON, nivoi iRNK i ERβ1 proteina, analizirani su i korelisani sa kliničkopatološkim parametrima neparametrijskim statističkim testovima. Nađeno je da je metilacioni indeks promotora ON ERβ gena značajno veći u grupi pacijentkinja sa pozitivnim, u odnosu na grupu sa negativnim statusom aksilarnih limfnih čvorova. Takođe, pronađena je značajna pozitivna korelacija metilacionog indeksa promotora ON ERβ gena sa nivoom estrogenskog receptora α. Na osnovu dobijenih rezultata pokazano je da metilacioni indeks promotora ON, ERβ gena može biti pouzdaniji marker prognoze kancera dojke nego ekspresija ERβ1-iRNK ili proteina ERβ1.

Subjects/Keywords: Breast cancer; estrogen receptor alpha; estrogen receptor beta; progesterone receptor; methylation; quantitative PCR; Kancer dojke; estrogenski receptor alfa; estrogenski receptor beta; progesteronski receptor; metilacija; kvantitativni PCR

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

APA (6^th Edition):

Ana, B. (2013). Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers. (Doctoral Dissertation). University of Belgrade. Retrieved from http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927

Chicago Manual of Style (16^th Edition):

Ana, Božović. “Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers.” 2013. Doctoral Dissertation, University of Belgrade. Accessed January 22, 2021. http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927.

MLA Handbook (7^th Edition):

Ana, Božović. “Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers.” 2013. Web. 22 Jan 2021.

Vancouver:

Ana B. Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers. [Internet] [Doctoral dissertation]. University of Belgrade; 2013. [cited 2021 Jan 22]. Available from: http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927.

Council of Science Editors:

Ana B. Estrogen receptor beta (ERß) promoter methylation and expression in invasive breast cancers. [Doctoral Dissertation]. University of Belgrade; 2013. Available from: http://dx.doi.org/10.2298/BG20130703BOZOVIC ; http://eteze.bg.ac.rs/application/showtheses?thesesId=799 ; https://fedorabg.bg.ac.rs/fedora/get/o:7126/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=44646927

University of Cincinnati

12. Cookman, Clifford. Characterization of 17ß-Estradiol Survival Signaling in Medulloblastoma: Relation to Tumor Growth and IGF1 Signaling.

Degree: PhD, Medicine: Molecular, Cellular and Biochemical Pharmacology, 2015, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447158097

► Medulloblastoma has been identified as an estrogen-responsive tumor that expresses estrogen receptor ß and whose growth is regulated by 17ß-estradiol both in vitro and in… (more)

Subjects/Keywords: Biology; Medulloblastoma; estrogen; estrogen receptor beta; insulin-like growth factor; brain tumor

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

APA (6^th Edition):

Cookman, C. (2015). Characterization of 17ß-Estradiol Survival Signaling in Medulloblastoma: Relation to Tumor Growth and IGF1 Signaling. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447158097

Chicago Manual of Style (16^th Edition):

Cookman, Clifford. “Characterization of 17ß-Estradiol Survival Signaling in Medulloblastoma: Relation to Tumor Growth and IGF1 Signaling.” 2015. Doctoral Dissertation, University of Cincinnati. Accessed January 22, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447158097.

MLA Handbook (7^th Edition):

Cookman, Clifford. “Characterization of 17ß-Estradiol Survival Signaling in Medulloblastoma: Relation to Tumor Growth and IGF1 Signaling.” 2015. Web. 22 Jan 2021.

Vancouver:

Cookman C. Characterization of 17ß-Estradiol Survival Signaling in Medulloblastoma: Relation to Tumor Growth and IGF1 Signaling. [Internet] [Doctoral dissertation]. University of Cincinnati; 2015. [cited 2021 Jan 22]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447158097.

Council of Science Editors:

Cookman C. Characterization of 17ß-Estradiol Survival Signaling in Medulloblastoma: Relation to Tumor Growth and IGF1 Signaling. [Doctoral Dissertation]. University of Cincinnati; 2015. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447158097

13. Megas, Georgios. Η μελέτη της έκφρασης των οιστρογονικών υποδοχέων ER(α) και ER(β) σε συνάρτηση με τους ανδρογονικούς υποδοχείς στον τοπικά προχωρημένο καρκίνο του προστάτη ως προγνωστικό παράγοντα στην βιοχημική υποτροπή και την πρόοδο της νόσου.

Degree: 2014, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/41641

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The objective of this study was to evaluate the expression of estrogen receptors (ER(α) and ER(β)) and androgen receptors (ARs) as prognostic factors for biochemical… (more)

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The objective of this study was to evaluate the expression of estrogen receptors (ER(α) and ER(β)) and androgen receptors (ARs) as prognostic factors for biochemical recurrence, disease progression and survival in patients with locally advanced prostate cancer. Protein expression of receptors was determined by immunostainning in prostate tissue, and the prognostic value of the ER(α), ER(β) and AR was assessed in terms of recurrence, progression, and survival. ER(b) had significant predictive value for biochemical relapse, disease progression and overall survival. Patients with positive ER(a) expression were 3.55 times at higher risk of relapse compared with patients with negative ER (a) expression and 4 times higher risk of disease progression. Also, with increasing values of ER (β) the lower the risk of relapse. The AR was not associated significantly with the risk of relapse. Finally, patients who had a positive ER (α) and ER (β) <1.7 units was at 18.60 times higher risk of relapse in comparison with patients with normal ER(a) and ER(β). Regarding overall survival, patients with positive ER(α) were at 3.41 times higher risk compared with

Σκοπός της παρούσας έρευνας είναι να μελετήσει την έκφραση των οιστρογονικών υποδοχέων ER(α) και ER(β), σε σχέση με την έκφραση των ανδρογονικών υποδοχέων AR στον προστατικό ιστό των ασθενών με τοπικά προχωρημένο καρκίνο του προστάτη, και την συσχέτιση τους με την επιβίωση και την βιοχημική υποτροπή. Με τη μέθοδο της ανοσοϊστοχημείας, καθορίσθηκε η πρωτεϊνική έκφραση των υποδοχέων αυτών στα κύτταρα του προστατικού ιστού και η διαφοροποίηση της έκφρασης των υποδοχέων αυτών μεταξύ φυσιολογικού και καρκινικού ιστού. Ο δείκτης ER(β) είχε σημαντική προγνωστική αξία για την υποτροπή, την πρόοδο νόσου και τη συνολική επιβίωση. Οι ασθενείς με θετικό ER(α) είχαν 3,55 φορές υψηλότερο κίνδυνο υποτροπής σε σύγκριση με τους ασθενείς με μηδενικό ER(α) και 4 φορές υψηλότερο κίνδυνο προόδου της νόσου. Επίσης, όσο αυξάνονται οι τιμές του ER(β) τόσο μικρότερος είναι ο κίνδυνος υποτροπής. Το AR δεν σχετιζόταν σε σημαντικό βαθμό με τον κίνδυνο υποτροπής. Τέλος, οι ασθενείς που είχαν θετικό ER(α) και ER(β) <1,7 μονάδων είχαν 18,60 φορές υψηλότερο κίνδυνο υποτροπής σε σύγκριση με τους ασθενείς με φυσιολογικά ER(α) και ER(β). Όσον αφορά την συνολική επιβίωση, οι ασθενείς με θετικό ER(α) είχαν 3,41 φορές υψηλότερο κίνδυνο σε σύγκριση με τους ασθενείς με μηδενικό ER(α), ενώ όσο αυξάνονται οι τιμές του ER(β) τόσο μικρότερος είναι ο κίνδυνος

Subjects/Keywords: Ανδρογονικός υποδοχέας; Οιστρογονικός υποδοχέας (α); Οιστρογονικός υποδοχέας (β); Τοπικά προχωρημένος καρκίνος του προστάτη; Ριζική προστατεκτομή; Androgen receptor; Estrogen receptor (α); Estrogen receptor (β); Locally advanced prostate cancer; Radical prostatectomy

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

APA (6^th Edition):

Megas, G. (2014). Η μελέτη της έκφρασης των οιστρογονικών υποδοχέων ER(α) και ER(β) σε συνάρτηση με τους ανδρογονικούς υποδοχείς στον τοπικά προχωρημένο καρκίνο του προστάτη ως προγνωστικό παράγοντα στην βιοχημική υποτροπή και την πρόοδο της νόσου. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/41641

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):

Megas, Georgios. “Η μελέτη της έκφρασης των οιστρογονικών υποδοχέων ER(α) και ER(β) σε συνάρτηση με τους ανδρογονικούς υποδοχείς στον τοπικά προχωρημένο καρκίνο του προστάτη ως προγνωστικό παράγοντα στην βιοχημική υποτροπή και την πρόοδο της νόσου.” 2014. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 22, 2021. http://hdl.handle.net/10442/hedi/41641.

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

MLA Handbook (7^th Edition):

Megas, Georgios. “Η μελέτη της έκφρασης των οιστρογονικών υποδοχέων ER(α) και ER(β) σε συνάρτηση με τους ανδρογονικούς υποδοχείς στον τοπικά προχωρημένο καρκίνο του προστάτη ως προγνωστικό παράγοντα στην βιοχημική υποτροπή και την πρόοδο της νόσου.” 2014. Web. 22 Jan 2021.

Vancouver:

Megas G. Η μελέτη της έκφρασης των οιστρογονικών υποδοχέων ER(α) και ER(β) σε συνάρτηση με τους ανδρογονικούς υποδοχείς στον τοπικά προχωρημένο καρκίνο του προστάτη ως προγνωστικό παράγοντα στην βιοχημική υποτροπή και την πρόοδο της νόσου. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10442/hedi/41641.

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

Council of Science Editors:

Megas G. Η μελέτη της έκφρασης των οιστρογονικών υποδοχέων ER(α) και ER(β) σε συνάρτηση με τους ανδρογονικούς υποδοχείς στον τοπικά προχωρημένο καρκίνο του προστάτη ως προγνωστικό παράγοντα στην βιοχημική υποτροπή και την πρόοδο της νόσου. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2014. Available from: http://hdl.handle.net/10442/hedi/41641

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

Colorado State University

14. Osterlund, Kristen Leanne. Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation.

Degree: PhD, Biomedical Sciences, 2011, Colorado State University

URL: http://hdl.handle.net/10217/48162

► Vascular inflammation plays a key role in the etiology of cardiovascular disease, particularly stoke. Vascular inflammation is under the control of several transcription factors, including… (more)

▼ Vascular inflammation plays a key role in the etiology of cardiovascular disease, particularly stoke. Vascular inflammation is under the control of several transcription factors, including nuclear factor kappa B and hypoxia inducible factor-1 alpha (HIF-1α). Activation of these transcription factors can lead to the production of inflammatory mediators such as cyclooxygenase-2 (COX-2). COX-2 plays a role in vascular inflammation, cerebral ischemia-induced injury, and has been implicated as a source of reactive oxygen species (ROS). Inflammatory mediators, such as endotoxin or cellular breakdown products released following injury, are known to signal through the Toll-like receptor 4 (TLR4). TLR4 activation leads to NFκB activation and subsequent production of COX-2. Like COX-2, TLR4 has also been implicated in injury-induced oxidative stress and cerebral ischemia damage. Previous studies have demonstrated that gonadal steroid hormones can also modulate vascular inflammation. Both protective and detrimental effects of androgens on the cardiovascular system have been reported. Since the potent androgen receptor (AR) agonist dihydrotestosterone (DHT) can be converted to 3β-diol, an estrogen receptor (ER) β-selective agonist, I hypothesized that ERβ may mediate some of the protective effects of androgens, while the AR may mediate some of the detrimental effects. The overall goal of this dissertation was to determine the mechanisms by which androgens can influence the vascular inflammatory response under both physiological and pathophysiological conditions. The hypothesis to be tested was that DHT influences vascular inflammation under both physiological and pathophysiological conditions. In my first set of experiments, using Western blot, I found that DHT increases expression of the vascular inflammatory mediator COX-2 under physiological conditions in human coronary artery vascular smooth muscle (VSM) cells and human brain VSM cells. This effect of DHT was attenuated in the presence of the AR antagonist bicalutamide. This data indicates that the pro-inflammatory effect of DHT under normal physiological conditions is AR mediated. In my second set of experiments, I examined the effects of DHT on vascular inflammation under a variety of pathophysiological conditions. Surprisingly, I found that DHT decreased cytokine-induced COX-2 expression and oxidative stress, endotoxin-induced COX-2 and TLR4 expression in human VSM cells. Furthermore, DHT also decreased hypoxia induced HIF-1α and COX-2 expression in human brain VSM cells and rat pial arteries. Finally, I found that DHT decreased hypoxia with glucose deprivation (HGD)-induced HIF-1α, COX-2 and TLR4 expression in human brain VSM cells. DHT`s anti-inflammatory effects during cytokine or HGD-induced inflammation in human brain VSM cells were not blocked by the AR antagonist bicalutamide, indicating that they were not AR mediated. These results led me to my second hypothesis, that DHT's anti-inflammatory effects are ERβ-mediated. In my third set of… Advisors/Committee Members: Handa, Robert (advisor), Gonzales, Rayna (committee member), Amberg, Gregory (committee member), Garrity, Deborah (committee member), Tobet, Stuart (committee member).

Subjects/Keywords: vascular smooth muscle; inflammation; ischemia; androgen; estrogen receptor beta

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

APA (6^th Edition):

Osterlund, K. L. (2011). Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/48162

Chicago Manual of Style (16^th Edition):

Osterlund, Kristen Leanne. “Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation.” 2011. Doctoral Dissertation, Colorado State University. Accessed January 22, 2021. http://hdl.handle.net/10217/48162.

MLA Handbook (7^th Edition):

Osterlund, Kristen Leanne. “Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation.” 2011. Web. 22 Jan 2021.

Vancouver:

Osterlund KL. Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation. [Internet] [Doctoral dissertation]. Colorado State University; 2011. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10217/48162.

Council of Science Editors:

Osterlund KL. Dihydrotestosterone attenuates endotoxin, cytokine, and hypoxia-induced vascular inflammation. [Doctoral Dissertation]. Colorado State University; 2011. Available from: http://hdl.handle.net/10217/48162

15. Fejsa Levakov Aleksandra. Ekspresija estrogenog receptora β u prekanceroznim lezijama i adenokarcinomu prostate.

Degree: 2016, University of Novi Sad

URL: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija145510527202039.pdf?controlNumber=(BISIS)99993&fileName=145510527202039.pdf&id=4922&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=99993&source=OATD&language=en

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Adenokarcinom prostate (PCa) je najčešći karcinom u muškaraca. Intraepitelne prostatične neoplazme visokog gradusa (HGPIN) su lezije koje prethode nastanku invazivnog karcinoma i podrazumevaju kompletno… (more)

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Adenokarcinom prostate (PCa) je najčešći karcinom u muškaraca. Intraepitelne prostatične neoplazme visokog gradusa (HGPIN) su lezije koje prethode nastanku invazivnog karcinoma i podrazumevaju kompletno odsustvo bazalnih ćelija i invaziju strome malignim acinusima. Estrogeni receptor &beta; (ER&beta;) se nalazi u jedrima bazalnih i sekretornih ćelija acinusa i delimično u stromalnim ćelijama. Cilj istraživanja je da prikaže i lokalizuje ER&beta; u različitim morfološkim lezijama prostate: hiperplaziji (BHP), PINu i u PCa sa različitim Gleason scorom. Pretpostavlja se da prekancerozne lezije u svojim različitim fazama evolucije ne koreliraju u potpunosti sa ekspresijom ER&beta;. LGPIN pokazuje ekspresiju, dok u HGPINu nema ekspresije. Takođe je pretpostavka da ekspresija ER&beta; postoji u većine srednje diferentovanih PCa, te da se ekspresija posmatranog receptora gubi sa porastom Gleason scora. Ispitivano je pet grupa bolesnika: kontrolna grupa sa BHP i četiri eksperimentalne grupe (PIN i 3 različite grupe PCa). Studija je sprovedena na muškarcima različite starosti u periodu 2010–2012. Nijedan pacijent nije prethodno primio hormonsku terapiju. Sekstant biopsije prostate su bojene na ER&beta; (Novocastra). Lokalizacija i intenzitet ER&beta; ekspresije prikazani su kroz skor: 0 = nula; 1 = <1%; 2 = 1–10%; 3 = 11–33%; 4 = 34–66%; 5 = > 66%. Pozitivni fibroblasti i endotelne ćelije su korišćene za poređenje. Smanjena ekspresija ER&beta; primećena je kod malignih i premalignih lezija prostate naspram BHP. Ekspresija ER&beta; u epitelnim ćelijama acinusa bila je najslabija u dobro diferentovanim PCa. Kod BHP i dobro diferentovanih PCa bila je veća ekspresija ER&beta; u bazalnim ćelijama nego u sekretornim. Loše diferentovani PCa prikazali su smanjenje ekspresije ER&beta; u bazalnim ćelijama. Ukupna ćelijska ekspresija ER&beta; predstavlja složen i ponekad moguće paradoksalan nalaz, na osnovu čega primarni PCa zadržava ekspresiju ovog receptora, ali ipak značajno nižu u poređenju sa benignim epitelom i premalignim lezijama. Ovaj nalaz podupire stanovište o antiproliferativnoj ulozi ER&beta; u tkivu prostate.

Adenocarcinoma of the prostate (PCa) is the most common cancer in men. High-grade prostatic intraepithelial neoplasia (HGPIN) are lesions that precede to invasive carcinomas and include complete absence of basal cells and stromal invasion by malignant acini. Estrogen receptor ß(ERß) is located in the nuclei of basal and secretory cells and partly in stromal ones.The aim of the research is to describe and localize ERß in different morphological lesions: prostate hyperplasia (BPH), PIN and PCa with different Gleason score. It is assumed that pre-cancerous lesions in different stages of their evolution not correlate completely with the expression ERß. LGPIN shows expression, while there is no expression in HGPIN. It is also an assumption that the expression ERß exists in most medium…

Advisors/Committee Members: Đolai Matilda, Vučković Nada, Sekulić Vuk, Ćebović Tatjana, Matavulj Milica, Lalošević Dušan.

Subjects/Keywords: neoplazme prostate; adenokarcinom; prekancerozna stanja; estrogeni receptor beta; dijagnoza; Prostatic Neoplasms; Adenocarcinoma; Precancerous Conditions; Estrogen Receptor beta; Diagnosis

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

APA (6^th Edition):

Aleksandra, F. L. (2016). Ekspresija estrogenog receptora β u prekanceroznim lezijama i adenokarcinomu prostate. (Thesis). University of Novi Sad. Retrieved from https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija145510527202039.pdf?controlNumber=(BISIS)99993&fileName=145510527202039.pdf&id=4922&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=99993&source=OATD&language=en

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):

Aleksandra, Fejsa Levakov. “Ekspresija estrogenog receptora β u prekanceroznim lezijama i adenokarcinomu prostate.” 2016. Thesis, University of Novi Sad. Accessed January 22, 2021. https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija145510527202039.pdf?controlNumber=(BISIS)99993&fileName=145510527202039.pdf&id=4922&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=99993&source=OATD&language=en.

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

MLA Handbook (7^th Edition):

Aleksandra, Fejsa Levakov. “Ekspresija estrogenog receptora β u prekanceroznim lezijama i adenokarcinomu prostate.” 2016. Web. 22 Jan 2021.

Vancouver:

Aleksandra FL. Ekspresija estrogenog receptora β u prekanceroznim lezijama i adenokarcinomu prostate. [Internet] [Thesis]. University of Novi Sad; 2016. [cited 2021 Jan 22]. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija145510527202039.pdf?controlNumber=(BISIS)99993&fileName=145510527202039.pdf&id=4922&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=99993&source=OATD&language=en.

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

Council of Science Editors:

Aleksandra FL. Ekspresija estrogenog receptora β u prekanceroznim lezijama i adenokarcinomu prostate. [Thesis]. University of Novi Sad; 2016. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija145510527202039.pdf?controlNumber=(BISIS)99993&fileName=145510527202039.pdf&id=4922&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=99993&source=OATD&language=en

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

16. Γουλιούμης, Αναστάσιος. Επιθηλιακή προς μεσεγχυματική μετατροπή και καρκίνωμα του λάρυγγος : ο ρόλος του μοριακού μονοπατιού μεταγωγής σήματος της ILK και των υποδοχέων ανδρογόνων και οιστρογόνων.

Degree: 2008, University of Patras

URL: http://nemertes.lis.upatras.gr/jspui/handle/10889/1548

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Η επιθηλιακή προς μεσεγχυματική μετατροπή είναι ένα φαινόμενο που πιθανότατα εμπλέκεται στην παθογένεια του καρκίνου του λάρυγγα. Η ΕΜΤ εξελισσόμενη μέσα από δαιδαλώδη μονοπάτια μεταγωγής… (more)

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Η επιθηλιακή προς μεσεγχυματική μετατροπή είναι ένα φαινόμενο που πιθανότατα εμπλέκεται στην παθογένεια του καρκίνου του λάρυγγα. Η ΕΜΤ εξελισσόμενη μέσα από δαιδαλώδη μονοπάτια μεταγωγής σήματος καταλήγει να προσδώσει στο καρκινικό κύτταρο δομικά και λειτουργικά χαρακτηριστικά που το καθιστούν ικανό να μπορεί να διεισδύει στους ιστούς και να μεθίσταται. Κεντρικό μόριο στα μοριακά μονοπάτια που διαμεσολαβούν την ΕΜΤ στον καρκίνο του λάρυγγα είναι μια κινάση, η ILK, που δέχεται σήματα από τις ιντεγκρίνες και τους υποδοχείς αυξητικών παραγόντων. Στους επιθηλιακούς καρκίνους αναφέρεται η εμπλοκή της σε λειτουργίες όπως ρύθμιση του κυτταρικού κύκλου, αποφυγή της απόπτωσης, νεοαγγειογένεση, απώλεια των δομών συνοχής του κυττάρου, έκφραση μεταλλοπρωτεασών και αναδιαμόρφωση του κυτταροσκελετού. Στο λαρυγγικό καρκίνο όμως κρίσιμα φαινόμενα για τον μεταστατικό-επιθετικό χαρακτήρα των κυττάρων, όπως, η εξαφάνιση των E-cadherin, η μετακίνηση των β-catenin στον πυρήνα και η συσχέτιση μεταξύ τους, που διαπιστώθηκαν, δεν βρέθηκε να συνδέονται με την υπερέκφραση της ILK καθιστώντας προφανώς άλλους μηχανισμούς υπεύθυνους για την επιτέλεση αυτών των λειτουργιών. Ιδιαίτερα ενδιαφέρουσα όμως ήταν και η εντόπιση της ILK στον πυρήνα των κυττάρων του καρκίνου του λάρυγγα δίνοντας μια νέα προοπτική στην έρευνα για τον ρόλο της ILK στον καρκίνο. Στο μονοπάτι μεταγωγής σήματος της ILK στο λαρυγγικό καρκίνο βρέθηκε πως συμμετέχει και η ενεργοποιημένη Akt με την οποία επίσης σχετίζονται πολλές κρίσιμες λειτουργίες για το καρκινικό κύτταρο. Ωστόσο η p-Akt στο λαρυγγικό καρκίνο φαίνεται πως έχει κάποιο ρόλο αντίθετο με την λειτουργία του καρκινικού κυττάρου καθώς χαρακτηρίζει όγκους καλύτερης διαφοροποίησης. Ο λαρυγγικός καρκίνος τέλος διαπιστώθηκε πως χαρακτηρίζεται από την έκφραση υποδοχέων ανδρογόνων και οιστρογόνων καθιστώντας πολύ πιθανό το ρόλο αυτών των μορίων στην παθογένεια της νόσου. Ενδιαφέρουσα για την πιθανότητα εμπλοκής των υποδοχέων στερεοειδών ορμονών του φύλου στην ΕΜΤ ίσως να είναι η συσχέτιση των υποδοχέων ανδρογόνων και οιστρογόνων με την ILK και p-Akt αντίστοιχα. Οι υποδοχείς οιστρογόνων μάλιστα χαρακτηρίζοντας όγκους λάρυγγα αρχικών σταδίων ίσως θα μπορούσε να αποδειχτεί μόριο με προγνωστική αξία αλλά και θεραπευτικός στόχος. Τέλος η μελέτη της έκφρασης της ILK, της p-Akt και των υποδοχέων στεροειδών ορμονών του φύλου δεν ανέδειξε μια διαφορετική έκφραση μεταξύ υπεργλωττιδικών και γλωττιδικών καρκίνων του λάρυγγος ώστε να υποστηρίξει την ύπαρξη ενός μοριακού υποβάθρου στην παρατήρηση της ανόμοιας κλινικής συμπεριφοράς μεταξύ όγκων από τις δύο αυτές ανατομικά διακριτές περιοχές.

Epithelial to mesenchymal transition (EMT) is a process possibly implicated in the pathogenesis of laryngeal cancer. EMT is a type of epithelial cell plasticity which is characterized by long lasting phenotypic and molecular modifications of the epithelial cell as a result of a transforming procedure leading to a cell of mesenchymal type. This molecular procedure seems to be pivotal for the metastasis of epithelial cancers and its…

Advisors/Committee Members: Πέτρου-Παπαδάκη, Ελένη, Goulioumis, Anastasios, Βαράκης, Ιωάννης, Γκούμας, Παναγιώτης, Παπαβασιλείου, Αθανάσιος, Ναξάκης, Στέφανος, Παπαδάς, Θεόδωρος, Ασημακοπούλου, Μάρθα, Πέτρου-Παπαδάκη, Ελένη.

Subjects/Keywords: Επιθηλιακή προς μεσεγχυματική μετατροπή; Λαρυγγικός καρκίνος; Υποδοχέας ανδρογόνων; Υποδοχέας οιστρογόνων-β; 616.994 22; Epithelial to mesenchymal transition (EMT); Laryngeal carcinoma; Androgen receptor (AR); Estrogen receptor-β (ER-β)

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

APA (6^th Edition):

Γουλιούμης, �. (2008). Επιθηλιακή προς μεσεγχυματική μετατροπή και καρκίνωμα του λάρυγγος : ο ρόλος του μοριακού μονοπατιού μεταγωγής σήματος της ILK και των υποδοχέων ανδρογόνων και οιστρογόνων. (Doctoral Dissertation). University of Patras. Retrieved from http://nemertes.lis.upatras.gr/jspui/handle/10889/1548

Chicago Manual of Style (16^th Edition):

Γουλιούμης, Αναστάσιος. “Επιθηλιακή προς μεσεγχυματική μετατροπή και καρκίνωμα του λάρυγγος : ο ρόλος του μοριακού μονοπατιού μεταγωγής σήματος της ILK και των υποδοχέων ανδρογόνων και οιστρογόνων.” 2008. Doctoral Dissertation, University of Patras. Accessed January 22, 2021. http://nemertes.lis.upatras.gr/jspui/handle/10889/1548.

MLA Handbook (7^th Edition):

Γουλιούμης, Αναστάσιος. “Επιθηλιακή προς μεσεγχυματική μετατροπή και καρκίνωμα του λάρυγγος : ο ρόλος του μοριακού μονοπατιού μεταγωγής σήματος της ILK και των υποδοχέων ανδρογόνων και οιστρογόνων.” 2008. Web. 22 Jan 2021.

Vancouver:

Γουλιούμης �. Επιθηλιακή προς μεσεγχυματική μετατροπή και καρκίνωμα του λάρυγγος : ο ρόλος του μοριακού μονοπατιού μεταγωγής σήματος της ILK και των υποδοχέων ανδρογόνων και οιστρογόνων. [Internet] [Doctoral dissertation]. University of Patras; 2008. [cited 2021 Jan 22]. Available from: http://nemertes.lis.upatras.gr/jspui/handle/10889/1548.

Council of Science Editors:

Γουλιούμης �. Επιθηλιακή προς μεσεγχυματική μετατροπή και καρκίνωμα του λάρυγγος : ο ρόλος του μοριακού μονοπατιού μεταγωγής σήματος της ILK και των υποδοχέων ανδρογόνων και οιστρογόνων. [Doctoral Dissertation]. University of Patras; 2008. Available from: http://nemertes.lis.upatras.gr/jspui/handle/10889/1548

17. Zanatta, Alysson. Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide.

Degree: PhD, Obstetrícia e Ginecologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;

► INTRODUÇÃO: Apesar de a endometriose profunda (EPF) ser a forma da doença de maior repercussão clínica, os estudos sobre a doença costumam ser baseados em… (more)

▼ INTRODUÇÃO: Apesar de a endometriose profunda (EPF) ser a forma da doença de maior repercussão clínica, os estudos sobre a doença costumam ser baseados em lesões de endometriose ovariana (EOV) e peritoneal (EPT). A patogênese da EPF ainda é objeto de amplo debate, pois há poucos estudos feitos exclusivamente com lesões de EPF. O fator de transcrição codificado pelo gene homeobox A10 (HOXA10) regula a conferência de identidade tecidual de útero ao ducto paramesonéfrico indiferenciado durante o período embrionário. O gene mantém um padrão de expressão temporal e espacial bem definido e, durante a fase adulta, continua expresso no miométrio e endométrio. Sugere-se que HOXA10 esteja implicado na patogênese da endometriose, pois é expresso em EOV, EPT, endometriose pulmonar e endometriose retovaginal, um tipo de EPF. Possivelmente, o gene HOXA10 seja necessário para conferir identidade de endometriose a um tecido indiferenciado. O estradiol e a progesterona ativam a transcrição do gene HOXA10 e regulam diretamente sua ação. Esses hormônios estão envolvidos na patogênese da EPF, e suas atividades podem ser inferidas pelo estudo da expressão tecidual de seus receptores. A endometriose de reto-sigmoide (ERS) é um modelo representativo para o estudo da EPF. Neste estudo, avaliamos a expressão proteica do fator de transcrição HOXA10, das isoformas ? (ER-alfa) e beta (ER-beta) dos receptores de estrogênio, e do receptor de progesterona AB (PR-AB) e sua isoforma B (PR-B) na lesão (LES) e no tecido muscular liso perilesional (TMLP) de ERS de pacientes inférteis, durante as fases proliferativa e secretora do ciclo menstrual. MÉTODOS: amostras de LES e TMLP de ERS de 18 pacientes (9 operadas em cada fase do ciclo menstrual) foram agrupadas em blocos de microarranjos de tecidos (tissue microarray). As amostras foram coradas com anticorpos específicos para análise imunoistoquímica de cada uma das proteínas. Foram então avaliadas por microscopia ótica (MO) e pela análise das imagens digitalizadas das lâminas com por um software específico, a análise morfométrica (AM). RESULTADOS: HOXA10 foi expresso no estroma de LES de ERS durante a fase secretora, de acordo com a MO. ER-alfa e ER-betaforam expressos em glândulas e estroma de LES e TMLP de ERS durante ambas as fases do ciclo, de acordo com a MO e a AM. PR-AB e PR-B foram expressos em glândulas e estroma de LES de ERS durante ambas as fases do ciclo, de acordo com a MO. PR-B foi mais expresso durante a fase secretora, independentemente do local de expressão, segundo a AM. A expressão de HOXA10 correlacionou-se diretamente com PR-AB e PR-B na ERS, segundo a AM. Não houve correlação entre ER-alfa e ER-beta com HOXA10, PR-AB ou PR-B em nenhuma fase do ciclo ou local de expressão de ERS. CONCLUSÕES: HOXA10 é expresso em ERS, um local fora do seu eixo espacial de expressão. A presença de HOXA10 pode ser necessária para conferir a identidade \"de novon̈a EPF, incluindo ERS. A progesterona pode ativar o gene HOXA10 e regular esta ação, possivelmente mediada por PR-B. O estradiol exerce sua… Advisors/Committee Members: Serafini, Paulo Cesar.

Subjects/Keywords: Deep endometriosis; Endometriose de retosigmoide; Endometriose profunda; Estrogen receptor-alfa; Estrogen receptor-beta; Gene HOXA10; HOXA gene; Progesterone receptor-B; Progesterone receptor; Receptor de estrogênio alfa; Receptor de estrogênio beta; Receptor de progesterona; Receptor de progesterona B; Rectosigmoid endometriosis

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

APA (6^th Edition):

Zanatta, A. (2013). Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;

Chicago Manual of Style (16^th Edition):

Zanatta, Alysson. “Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide.” 2013. Doctoral Dissertation, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;.

MLA Handbook (7^th Edition):

Zanatta, Alysson. “Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide.” 2013. Web. 22 Jan 2021.

Vancouver:

Zanatta A. Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide. [Internet] [Doctoral dissertation]. University of São Paulo; 2013. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;.

Council of Science Editors:

Zanatta A. Expressão proteíca do gene HOXA10 e dos receptores de estrogênio e progesterona no epitélio, estroma e tecido muscular liso perilesional de endometriose e do reto-sigmoide. [Doctoral Dissertation]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-06112013-085759/ ;

UCLA

18. Kim, Youn-Jung Roy. Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands.

Degree: Molec, Cell, & Integ Physiology, 2018, UCLA

URL: http://www.escholarship.org/uc/item/09j2798f

► Currently, available drugs for multiple sclerosis (MS) are predominantly immune-modulatory. They are effective in reducing relapses, but not in slowing down or stopping progressive disease… (more)

▼ Currently, available drugs for multiple sclerosis (MS) are predominantly immune-modulatory. They are effective in reducing relapses, but not in slowing down or stopping progressive disease course. Therefore, there is a need to develop treatment strategies that will provide neuroprotection and halt disability progression. Pregnancy is neuroprotective in patients with MS. A pregnancy hormone and a moderate estrogen receptor beta (ERβ)-ligand, estriol, has been reported to have beneficial effects on reducing relapses and improving cognition when treated in MS patients. Although, the mechanisms of ERβ-ligand mediated treatment effects on neuroprotection remains poorly understood. Here I hypothesized that ERβ signaling on CD11c+ immune cells and Olig1+ oligodendrocytes plays an essential role in providing neuroprotection and enhancing remyelination. To test the hypothesis, I created conditional knockout mice (CKO) with ERβ deleted from each cell type using the Cre-LoxP recombinase system and investigated neuroprotective effects of ERβ-ligand treatment in experimental autoimmune encephalomyelitis (EAE) and cuprizone diet-induced demyelinating disease models. Also, I used RiboTag mice to determine oligodendrocyte specific gene expression to understand the molecular mechanisms of remyelination. Subsequently, I studied the mechanisms of ERβ-ligand treatment effects in oligodendrocytes during remyelination. The results revealed that ERβ-ligand treatment reduced pro-inflammatory responses through ERβ on CD11c+ myeloid DC/MΦ and increased oligodendrocyte maturation through ERβ on Olig1+ oligodendrocytes during EAE. The use of CKO mice proved that both were necessary as one without the other was not sufficient. Mechanistic insights on remyelination using the RiboTag mice revealed that oligodendrocytes upregulate de novo cholesterol biosynthesis during remyelination after chronic demyelination. Furthermore, when compared to vehicle treated naturally remyelinating mice, ERβ-ligand treated mice showed enhanced remyelination by increasing oligodendrocyte maturation, increasing cholesterol synthesis pathway genes, increasing oligodendrocyte progenitor cells (OPCs), and increasing Sox2 expression in OPCs during remyelination. I extended our investigation of ERβ-ligand treatment in the cuprizone model to the EAE model, to discover that ERβ-ligand treated mice showed neuroprotection by increasing oligodendrocyte maturation, and increasing cholesterol synthesis pathway genes, but not by increasing OPC Sox2 expression. This comprehensive approach using two different demyelinating disease models of MS and two transgenic mouse models provided critical insights regarding treatment effects of ERβ-ligand on neuroprotection and remyelination in vivo.

Subjects/Keywords: Neurosciences; Physiology; Cuprizone; Estrogen Receptor Beta Ligand; Experimental Autoimmune Encephalomyelitis; Multiple Sclerosis; Myeloid cells; Oligodendrocytes

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

APA (6^th Edition):

Kim, Y. R. (2018). Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/09j2798f

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):

Kim, Youn-Jung Roy. “Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands.” 2018. Thesis, UCLA. Accessed January 22, 2021. http://www.escholarship.org/uc/item/09j2798f.

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

MLA Handbook (7^th Edition):

Kim, Youn-Jung Roy. “Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands.” 2018. Web. 22 Jan 2021.

Vancouver:

Kim YR. Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands. [Internet] [Thesis]. UCLA; 2018. [cited 2021 Jan 22]. Available from: http://www.escholarship.org/uc/item/09j2798f.

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

Council of Science Editors:

Kim YR. Mechanisms of Neuroprotection and Remyelination in Demyelinating Disease Models of Multiple Sclerosis: A Lesson From Estrogen Receptor Specific Ligands. [Thesis]. UCLA; 2018. Available from: http://www.escholarship.org/uc/item/09j2798f

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

University of Houston

19. Dey, Prasenjit 1978-. Antiproliferative and pro-apoptotic actions of Estrogen receptor β in prostate cancer.

Degree: PhD, Biochemistry, 2013, University of Houston

URL: http://hdl.handle.net/10657/955

► High Gleason grade prostate cancers are aggressive. Currently, the major target for treatment is the androgen receptor. Recent literature points towards a tumor suppressive role… (more)

▼ High Gleason grade prostate cancers are aggressive. Currently, the major target for treatment is the androgen receptor. Recent literature points towards a tumor suppressive role of estrogen receptor β (ERβ), which has a potential to be exploited as a target for novel therapeutics used for treatment of prostate cancer. In Chapter 2 of the thesis, we showed that ERβ-selective agonists elicited an increase in apoptosis and this was accompanied by an increase in expression of the pro-apoptotic factor PUMA. Induction of PUMA was dependent on the presence of the transcription factor FOXO3 but was independent of p53. In the ventral prostates of ERβ-/- mice, expression of FOXO3a is lower than that in WT littermates demonstrating a relationship between ERβ and FOXO3a expression found in PC3 and LNCaP cells. Furthermore, in prostate cancers of Gleason grade 4 or higher there was a marked reduction of both ERβ and FOXO3a, while both genes were well expressed in BPH sections. In Chapter 3 of the thesis, we investigated whether the loss of ERβ (also called as ERβ1) and/or expression of its splice variant ERβ2 affected signaling pathways involved in proliferation and bone metastasis of prostate cancer. We found repressed expression of the bone metastasis regulator Runx2 and its target gene, Slug by ERβ1. In addition, the expression of Twist1, a factor whose expression strongly correlates with high Gleason grade prostate cancer, was increased by ERβ2. In terms of cell cycle modification, of the two receptors, ERβ1, but not ERβ2, inhibited proliferation and expression of the proliferation markers Cyclin E, c-Myc, and p45Skp2. Xenograft studies using athymic nude mice confirmed the proliferative effect of ERβ2, as tumors in mice bearing PC3-ERβ2 cells were substantially larger than tumors in mice bearing PC3-control and PC3-ERβ1 cells. Advisors/Committee Members: Gustafsson, Jan-Åke (advisor), Ström, Anders M. (committee member), Schwartz, Robert J. (committee member), Webb, Paul (committee member), Wang, Yuhong (committee member).

Subjects/Keywords: Prostate cancer; Estrogen receptor beta; Apoptosis; Proliferation; FOXO3a; PUMA; Bone metastasis; Biochemistry

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

APA (6^th Edition):

Dey, P. 1. (2013). Antiproliferative and pro-apoptotic actions of Estrogen receptor β in prostate cancer. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/955

Chicago Manual of Style (16^th Edition):

Dey, Prasenjit 1978-. “Antiproliferative and pro-apoptotic actions of Estrogen receptor β in prostate cancer.” 2013. Doctoral Dissertation, University of Houston. Accessed January 22, 2021. http://hdl.handle.net/10657/955.

MLA Handbook (7^th Edition):

Dey, Prasenjit 1978-. “Antiproliferative and pro-apoptotic actions of Estrogen receptor β in prostate cancer.” 2013. Web. 22 Jan 2021.

Vancouver:

Dey P1. Antiproliferative and pro-apoptotic actions of Estrogen receptor β in prostate cancer. [Internet] [Doctoral dissertation]. University of Houston; 2013. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10657/955.

Council of Science Editors:

Dey P1. Antiproliferative and pro-apoptotic actions of Estrogen receptor β in prostate cancer. [Doctoral Dissertation]. University of Houston; 2013. Available from: http://hdl.handle.net/10657/955

20. Κεφαλοπούλου, Ζηνοβία - Μαρία. Μορφολογική μελέτη της έκφρασης του οιστρογονικού υποδοχέα β (ERβ), συν-ρυθμιστών της μεταγραφής και πιθανών δεικτών καρκινικών stem κυττάρων σε αστροκυτταρικούς όγκους εγκεφάλου. Μια συστημική προσέγγιση.

Degree: 2011, University of Patras

URL: http://hdl.handle.net/10889/5570

► Τα αστροκυττώματα αποτελούν το συχνότερο τύπο πρωτοπαθών όγκων του κεντρικού νευρικού συστήματος (ΚΝΣ) και παραδοσιακά θεωρούνται ότι σχετίζονται με ιδιαίτερα δυσμενή πρόγνωση. Η Συστημική προσέγγιση… (more)

▼ Τα αστροκυττώματα αποτελούν το συχνότερο τύπο πρωτοπαθών όγκων του κεντρικού νευρικού συστήματος (ΚΝΣ) και παραδοσιακά θεωρούνται ότι σχετίζονται με ιδιαίτερα δυσμενή πρόγνωση. Η Συστημική προσέγγιση της καρκινογένεσης, εστιάζοντας στην αποκρυπτογράφηση του τρόπου λειτουργίας και δυναμικής αλληλεπίδρασης πολύπλοκων παθοβιολογικών δικτύων, προσφέρει σήμερα καινούριες ερευνητικές προοπτικές και πιθανές εναλλακτικές, περισσότερο αποτελεσματικές θεραπευτικές στρατηγικές. Οι οιστρογονικοί υποδοχείς και οι συν – ρυθμιστές της μεταγραφής συνιστούν κομβικά σημεία “συνομιλίας” (cross – talk) πολύπλοκων μοριακών οδών του κυττάρου, διαμεσολαβώντας πλήθος κυτταρικών λειτουργιών φυσιολογικά αλλά και σε παθολογικές καταστάσεις, ανάμεσα στις οποίες και ο καρκίνος. Οι παράγοντες EZH2 και SOX2 θεωρούνται μόρια κλειδιά του ρυθμιστικού μεταγραφικού κυκλώματος που χαρακτηρίζει το stemness. Η αποσαφήνιση της συμπεριφοράς του συγκεκριμένου αυτού δικτύου στα διάφορα νεοπλάσματα και ρόλος του σε σχέση με την απόκτηση ιδιότητας καρκινικού stem κυττάρου, θεωρείται καθοριστικής σημασίας στην προσπάθεια ερμηνείας του φαινομένου του καρκίνου ως πολύπλοκο προσαρμόσιμο σύστημα, που θα αναδείξει εναλλακτικούς θεραπευτικούς στόχους και θα επιτρέψει περισσότερο αποτελεσματικές σε σχέση με τις υπάρχουσες παρεμβάσεις. Σκοπός. Υπό το πρίσμα της Συστημικής προσέγγισης της κατανόησης της κακοήθους ανάπτυξης και εξέλιξης των αστροκυτταρικών όγκων, η παρούσα μελέτη διερεύνησε τα επίπεδα έκφρασης του Οιστρογονικού υποδοχέα β (ERβ), και των συν – ρυθμιστών AIB1, TIF2 and PELP1, όπως και την έκφραση των παραγόντων EZH2 και SOX2 σε αστροκυττώματα grade II ως IV και τη συσχέτιση μεταξύ του προφίλ έκφρασης των συγκεκριμένων παραγόντων, με κλινικοπαθολογικά δεδομένα. Υλικό και μέθοδος. Η έκφραση των πρωτεϊνών ERβ, AIB1, TIF2, PELP1, EZH2 και SOX2 εκτιμήθηκε σε 86 περιπτώσεις αστροκυτταρικών όγκων χρησιμοποιώντας τη μέθοδο της ανοσοϊστοχημείας. Είκοσι grade II αστροκυττώματα, 22 grade III αναπλαστικά αστροκυττώματα και 46 grade IV πλειόμορφα γλοιοβλαστώματα (GBM) συμπεριλήφθησαν στη συγκεκριμένη μελέτη. Η μέθοδος με χρήση συστήματος ανίχνευσης EnVision (Envision, Dako, CA, USA) ή MACH4 Universal HRP-Polymer Detection (Biocare Medical, CA, USA) και πρωτογενή αντισώματα έναντι των ERβ (Biogenex, CA, USA), AIB1 (BD Biosciences, Ca, USA), TIF2 (BD Biosciences, Ca, USA), PELP-1/MNAR (Novus Biologicals, CO, USA) EZH2 (Novocastra, UK) και SOX2 (R&D Systems, Inc.) χρησιμοποιήθηκαν στην παρούσα μελέτη. Σε κάθε περιστατικό και για κάθε δείκτη εκτιμήθηκε το ποσοστό των καρκινικών κυττάρων που εμφάνιζαν θετική ανοσοχρώση. Αντιπροσωπευτικές περιοχές επιλέχθηκαν κατόπιν σάρωσης του πλακιδίου σε οπτικό πεδίο μικρής μεγέθυνσης (Χ100), ενώ η καταμέτρηση των θετικών κυττάρων πραγματοποιήθηκε σε μεγάλης μεγέθυνσης πεδίο (400X). Η στατιστική ανάλυση έγινε με τη χρήση του SPSS στατιστικού πακέτου (SPSS©, Release 17.0, Chicago, IL, USA). Τιμές p<0.05 θεωρήθηκαν ως στατιστικά σημαντικές. Αποτελέσματα. Σημαντική μείωση των επιπέδων του ERβ παρατηρήθηκε παράλληλα με την αύξηση του… Advisors/Committee Members: Σωτηροπούλου - Μπονίκου, Γεωργία, Kefalopoulou, Zinovia - Maria, Ζολώτα, Βασιλική, Μαραζιώτης, Θεόδωρος, Καλόφωνος, Χαράλαμπος, Καρδαμάκης, Δημήτριος, Κωστόπουλος, Γεώργιος, Παπαθανασόπουλος, Παναγιώτης, Σωτηροπούλου - Μπονίκου, Γεωργία.

Subjects/Keywords: Αστροκυτταρικοί όγκοι εγκεφάλου; Οιστρογονικός υποδοχέας β; Συνρυθμιστές της μεταγραφής; Καρκινικά stem κύτταρα; Συστημική προσέγγιση; 616.994 81; Astrocytic brain tumors; Estrogen receptor beta; Coregulators of transcription; Cancer stem cells; Systems approach

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

APA (6^th Edition):

Κεφαλοπούλου, �. -. �. (2011). Μορφολογική μελέτη της έκφρασης του οιστρογονικού υποδοχέα β (ERβ), συν-ρυθμιστών της μεταγραφής και πιθανών δεικτών καρκινικών stem κυττάρων σε αστροκυτταρικούς όγκους εγκεφάλου. Μια συστημική προσέγγιση. (Doctoral Dissertation). University of Patras. Retrieved from http://hdl.handle.net/10889/5570

Chicago Manual of Style (16^th Edition):

Κεφαλοπούλου, Ζηνοβία - Μαρία. “Μορφολογική μελέτη της έκφρασης του οιστρογονικού υποδοχέα β (ERβ), συν-ρυθμιστών της μεταγραφής και πιθανών δεικτών καρκινικών stem κυττάρων σε αστροκυτταρικούς όγκους εγκεφάλου. Μια συστημική προσέγγιση.” 2011. Doctoral Dissertation, University of Patras. Accessed January 22, 2021. http://hdl.handle.net/10889/5570.

MLA Handbook (7^th Edition):

Κεφαλοπούλου, Ζηνοβία - Μαρία. “Μορφολογική μελέτη της έκφρασης του οιστρογονικού υποδοχέα β (ERβ), συν-ρυθμιστών της μεταγραφής και πιθανών δεικτών καρκινικών stem κυττάρων σε αστροκυτταρικούς όγκους εγκεφάλου. Μια συστημική προσέγγιση.” 2011. Web. 22 Jan 2021.

Vancouver:

Κεφαλοπούλου �-�. Μορφολογική μελέτη της έκφρασης του οιστρογονικού υποδοχέα β (ERβ), συν-ρυθμιστών της μεταγραφής και πιθανών δεικτών καρκινικών stem κυττάρων σε αστροκυτταρικούς όγκους εγκεφάλου. Μια συστημική προσέγγιση. [Internet] [Doctoral dissertation]. University of Patras; 2011. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10889/5570.

Council of Science Editors:

Κεφαλοπούλου �-�. Μορφολογική μελέτη της έκφρασης του οιστρογονικού υποδοχέα β (ERβ), συν-ρυθμιστών της μεταγραφής και πιθανών δεικτών καρκινικών stem κυττάρων σε αστροκυτταρικούς όγκους εγκεφάλου. Μια συστημική προσέγγιση. [Doctoral Dissertation]. University of Patras; 2011. Available from: http://hdl.handle.net/10889/5570

Universidade do Rio Grande do Sul

21. Lichtenfels, Martina. Estudo sobre o tamoxifeno : papel dos receptores de estrogênio na resposta terapêutica e efeitos cognitivos do tratamento.

Degree: 2016, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/150703

►

Introdução: Estimativas mostram que mais de dois terços das mulheres com câncer de mama possuem receptores hormonais positivos, e recebem terapia endócrina como tratamento, sendo… (more)

▼

Introdução: Estimativas mostram que mais de dois terços das mulheres com câncer de mama possuem receptores hormonais positivos, e recebem terapia endócrina como tratamento, sendo tamoxifeno (TAM) o tratamento padrão (EBCTCG 2005; Davies et al., 2012). Porém, muitas pacientes se tornam resistentes com o passar do tempo. Estudos prévios mostraram que a expressão do receptor de estrogênio β (REβ) aumenta a resposta ao tratamento com TAM em células de câncer de mama, assim como a coexpressão de REα e REβ esta associada com maior ação proliferativa de TAM (Treeck et al., 2010; Sun et al., 2014). Também foi observada a existência de “cross-talk” entre os RE e a família do receptor do fator de crescimento epidérmico (HER) na resposta ao tratamento com TAM (Lindberg et al., 2011; Blows et al., 2010). Objetivo: Verificar a expressão do REβ, e suas interações com REα e receptores HER, durante o tratamento com TAM e em células resistentes ao TAM. Métodos: A expressão do REβ foi analisada em dois bancos de dados contendo informações de pacientes com câncer de mama. A expressão de RNAm dos RE, receptores HER e vias de sinalização PTEN, Akt e MAPK foram avaliadas após tratamento com TAM, em células resistentes ao TAM e em células silenciadas para os genes dos RE. Também foi avaliada a viabilidade celular após tratamento com TAM e nas células silenciadas para os genes dos RE. Resultados: Pacientes com câncer de mama apresentaram expressão reduzida do REβ, e os subtipos de câncer de mama REα positivos apresentaram baixa expressão do REβ quando comparados aos subtipos REα negativos. Células expressando níveis moderados de REβ apresentaram melhor resposta ao tratamento com TAM. Diminuição nos níveis dos RE é acompanhada por aumento nos níveis dos receptores ErbB2 e ErbB3, aumento de PTEN e diminuição de Akt e MAPK3 após tratamento com TAM. ERβ modula a ação antiproliferativa do TAM através da via de MAPK3. Células resistentes ao TAM apresentaram baixos níveis dos RE e altos níveis dos receptores EGFR, ErbB3 e ErbB4. Conclusão: Estes resultados demonstram que o REβ, e suas interações com REα e receptores HER, possuem papel importante na resposta ao tratamento com TAM.

Introduction: Approximately two-thirds of all breast cancer patients overexpress hormonal receptors, and are treated with endocrine therapy, being tamoxifen (TAM) the standard treatment. However many of initial responders to TAM as first-line experience relapse. Several mechanisms have been proposed to explain the occurrence of acquired TAM resistance. Previous studies showed that estrogen receptor β (ERβ) expression is associated with better response to tamoxifen treatment, as the co-expression of ERα and ERβ is associated with TAM antiproliferative effects. Moreover, there is growing interest about the cross-talk between ERs and ErbB family in response to endocrine therapy. Suggesting that TAM can acts through ERβ and/or ErbB family as compensatory pathways. Objective: To evaluate the expression of ERβ and the relation of ERβ with ERα and ErbB family in response to…

Advisors/Committee Members: Schwartsmann, Gilberto.

Subjects/Keywords: Resistência a medicamentos; Breast cancer; Neoplasias da mama; Estrogen receptor alpha; Tamoxifeno; Estrogen receptor beta; ErbB receptors; Moduladores seletivos de receptor estrogênico; Tamoxifen; Drug resistance

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

APA (6^th Edition):

Lichtenfels, M. (2016). Estudo sobre o tamoxifeno : papel dos receptores de estrogênio na resposta terapêutica e efeitos cognitivos do tratamento. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/150703

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):

Lichtenfels, Martina. “Estudo sobre o tamoxifeno : papel dos receptores de estrogênio na resposta terapêutica e efeitos cognitivos do tratamento.” 2016. Thesis, Universidade do Rio Grande do Sul. Accessed January 22, 2021. http://hdl.handle.net/10183/150703.

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

MLA Handbook (7^th Edition):

Lichtenfels, Martina. “Estudo sobre o tamoxifeno : papel dos receptores de estrogênio na resposta terapêutica e efeitos cognitivos do tratamento.” 2016. Web. 22 Jan 2021.

Vancouver:

Lichtenfels M. Estudo sobre o tamoxifeno : papel dos receptores de estrogênio na resposta terapêutica e efeitos cognitivos do tratamento. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2016. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10183/150703.

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

Council of Science Editors:

Lichtenfels M. Estudo sobre o tamoxifeno : papel dos receptores de estrogênio na resposta terapêutica e efeitos cognitivos do tratamento. [Thesis]. Universidade do Rio Grande do Sul; 2016. Available from: http://hdl.handle.net/10183/150703

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

University of Bath

22. Mottinelli, Marco. Targeting estrogen biosynthesis and hormone receptor pathways for the treatment of cancer.

Degree: PhD, 2014, University of Bath

URL: https://researchportal.bath.ac.uk/en/studentthesis/targeting-estrogen-biosynthesis-and-hormone-receptor-pathways-for-the-treatment-of-cancer(0d0587d8-61c3-4d06-8ae2-77d3d9be1a78).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.642016

► The tetrahydroisoquinoline (THIQ) core structure is explored as a steroidomimetic nucleus with attractive pharmaceutical properties. A library was synthesised employing Pomeranz-Fritsch, Pictet-Spengler, Bischler-Napieralski strategies yielding… (more)

▼ The tetrahydroisoquinoline (THIQ) core structure is explored as a steroidomimetic nucleus with attractive pharmaceutical properties. A library was synthesised employing Pomeranz-Fritsch, Pictet-Spengler, Bischler-Napieralski strategies yielding 77 final targets, substituted at every position, for biological evaluation. Complementary strategies overcame synthetic difficulties, sometimes yielding two products in a single cyclisation. Three compounds were initially tested against a panel of 19 nuclear receptors (NRs) and exhibited broad substitution-dependent activity. 2-(4-Chlorophenyl)-1-isopropyl-1,2,3,4-tetrahydroisoquinolin-6-ol fully inhibited every NR at 100 µM, confirming the THIQ as a lead for optimisation. Compounds were evaluated for cytotoxicity against 60 cell lines by the NCI (USA), exhibiting moderate to insignificant cytotoxicity. Three compounds showed ca. 30-90% of average growth inhibition and were selected for a five dose test. Off-target evaluation highlighted compounds with activity against glucagon-like peptide 1 secretion, calcitonin gene-related peptide receptor antagonism and with >100% inhibition against the metabotropic glutamate receptor 2. Estrogen receptor-related receptor α (ERRα), a constitutively active orphan NR, is a hormone-dependent cancer target and diethylstilboestrol (DES), a known inverse agonist, possesses similarities to THIQs. THIQs tested against ERRα revealed no general SAR rules, but showed a lower degree of efficacy in a commercial TR-FRET assay, with 1-benzyl-2-(4-chlorophenyl)-4-methyl-1,2,3,4-tetrahydroisoquinolin-6-ol showing 79% efficacy at 100 µM as an inverse agonist, being more active than DES (64% at 100 µM). Inhibition of steroidogenic enzymes like 17β-hydroxysteroid dehydrogenase type 1 (17β-HSD1) is an emerging approach for the treatment of HDBC, compared to other current clinical strategies. THIQs evaluated against 17β-HSD1 showed good activity in both whole cell and cell lysate assays, with the best inhibitor, 2-(4-chlorophenyl)-4-isopropyl-1,2,3,4-tetrahydroisoquinolin-6-ol, possessing an IC50 value of 336 nM. The value of THIQ as a drug-like steroidomimetic scaffold is thus established and this work reveals straightforward strategies to optimise potency and selectivity for a range of potential targets by structural and stereochemical iteration.

Subjects/Keywords: 616.99; tetrahydroisoquinoline; 17 beta-HSD1; estrogen receptor related receptor alpha; ERRalpha; Pomeranz-Fritsch; Bischler-Napieralski; Pictet-Spengler

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

APA (6^th Edition):

Mottinelli, M. (2014). Targeting estrogen biosynthesis and hormone receptor pathways for the treatment of cancer. (Doctoral Dissertation). University of Bath. Retrieved from https://researchportal.bath.ac.uk/en/studentthesis/targeting-estrogen-biosynthesis-and-hormone-receptor-pathways-for-the-treatment-of-cancer(0d0587d8-61c3-4d06-8ae2-77d3d9be1a78).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.642016

Chicago Manual of Style (16^th Edition):

Mottinelli, Marco. “Targeting estrogen biosynthesis and hormone receptor pathways for the treatment of cancer.” 2014. Doctoral Dissertation, University of Bath. Accessed January 22, 2021. https://researchportal.bath.ac.uk/en/studentthesis/targeting-estrogen-biosynthesis-and-hormone-receptor-pathways-for-the-treatment-of-cancer(0d0587d8-61c3-4d06-8ae2-77d3d9be1a78).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.642016.

MLA Handbook (7^th Edition):

Mottinelli, Marco. “Targeting estrogen biosynthesis and hormone receptor pathways for the treatment of cancer.” 2014. Web. 22 Jan 2021.

Vancouver:

Mottinelli M. Targeting estrogen biosynthesis and hormone receptor pathways for the treatment of cancer. [Internet] [Doctoral dissertation]. University of Bath; 2014. [cited 2021 Jan 22]. Available from: https://researchportal.bath.ac.uk/en/studentthesis/targeting-estrogen-biosynthesis-and-hormone-receptor-pathways-for-the-treatment-of-cancer(0d0587d8-61c3-4d06-8ae2-77d3d9be1a78).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.642016.

Council of Science Editors:

Mottinelli M. Targeting estrogen biosynthesis and hormone receptor pathways for the treatment of cancer. [Doctoral Dissertation]. University of Bath; 2014. Available from: https://researchportal.bath.ac.uk/en/studentthesis/targeting-estrogen-biosynthesis-and-hormone-receptor-pathways-for-the-treatment-of-cancer(0d0587d8-61c3-4d06-8ae2-77d3d9be1a78).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.642016

Vanderbilt University

23. Palmisano, Brian T. Cholesteryl Ester Transfer Protein Modulates Liver Sex Hormone Signaling to Alter Triglyceride Metabolism in Male and Female Transgenic Mice.

Degree: PhD, Molecular Physiology and Biophysics, 2016, Vanderbilt University

URL: http://hdl.handle.net/1803/13947

► Elevated plasma triglycerides (TGs) increase risk of cardiovascular disease, especially in women. Estrogen treatment raises plasma TGs in women, but molecular mechanisms remain poorly understood.… (more)

Subjects/Keywords: CETP; beta-oxidation; Low Density Lipoprotein Receptor; LDLR; ER alpha; Estrogen Receptor alpha; SHP; Small Heterodimer Partner; VLDL; Estrogen; TGs; Triglycerides; Cholesteryl Ester Transfer Protein

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

APA (6^th Edition):

Palmisano, B. T. (2016). Cholesteryl Ester Transfer Protein Modulates Liver Sex Hormone Signaling to Alter Triglyceride Metabolism in Male and Female Transgenic Mice. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13947

Chicago Manual of Style (16^th Edition):

Palmisano, Brian T. “Cholesteryl Ester Transfer Protein Modulates Liver Sex Hormone Signaling to Alter Triglyceride Metabolism in Male and Female Transgenic Mice.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed January 22, 2021. http://hdl.handle.net/1803/13947.

MLA Handbook (7^th Edition):

Palmisano, Brian T. “Cholesteryl Ester Transfer Protein Modulates Liver Sex Hormone Signaling to Alter Triglyceride Metabolism in Male and Female Transgenic Mice.” 2016. Web. 22 Jan 2021.

Vancouver:

Palmisano BT. Cholesteryl Ester Transfer Protein Modulates Liver Sex Hormone Signaling to Alter Triglyceride Metabolism in Male and Female Transgenic Mice. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/1803/13947.

Council of Science Editors:

Palmisano BT. Cholesteryl Ester Transfer Protein Modulates Liver Sex Hormone Signaling to Alter Triglyceride Metabolism in Male and Female Transgenic Mice. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/13947

University of Guelph

24. Clipperton Allen, Amy Elizabeth. Food, friends and foes: estrogens and social behaviour in mice.

Degree: PhD, Department of Psychology, 2012, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3275

► This thesis investigates estrogens' modulation of three aspects of social cognition (aggression and agonistic behaviour, social learning, and social recognition). Sex-typical agonistic behaviour (males: overt… (more)

▼ This thesis investigates estrogens' modulation of three aspects of social cognition (aggression and agonistic behaviour, social learning, and social recognition). Sex-typical agonistic behaviour (males: overt attacks, females: more subtle dominance behaviours) was increased in gonadectomized mice by estrogen receptor alpha (ERα) agonist 1,3,5-tris(4-hydroxyphenyl)-4-propyl-1H-pyrazole (PPT), while non-overt agonistic behaviour was increased in male and female gonadally intact mice by ERβ agonist 7-Bromo-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol (WAY-200070). Estrogens also affected the social transmission of food preferences (STFP). Acute estrogen and ERβ agonists WAY-200070 and 2,3-bis(4-hydroxyphenyl)propionitrile (DPN) prolonged the preference for the demonstrated food when administered pre-acquisition, likely by affecting motivation or the nature of the social interaction, while acute PPT blocked the STFP. All mice receiving any of the three treatments chronically showed a prolonged demonstrated food preference, suggesting a loss of ER specificity. Individual differences in social recognition may relate to increased oxytocin (OT) and vasopressin (AVP) mRNA, and ERα and ERβ gene activation, in the medial preoptic area, and decreased mRNA for ERs, OT receptor (OTR), AVP and AVP receptors 1a and 1b in the lateral amygdala. Additionally, dorsolateral septum ERs, progesterone receptor, and OTR may relate to social interest without affecting social recognition. Our and others' results suggest that estrogens, OT and AVP are all involved in social behaviours and mediate social recognition, social learning, social interactions, and aggression. ERs differently modulate the two types of social learning investigated here: ERα is critical for social recognition, but impairs social learning, while ERβ is less important in social recognition, and prolongs the demonstrated food preference in the STFP. This may be due to differences in receptor brain distributions or in downstream neurochemical systems that mediate these behaviours. The results of this thesis suggest that estrogens, through the various systems they modulate, have a key role to play in social behaviour. Further investigations of how estrogens effect change in these systems at the molecular and cellular level, as well as the critical brain areas and downstream effectors involved in these complex behaviours, are needed, and could contribute to therapeutic interventions in socially-based, sexually dimorphic disorders, like the autism spectrum disorders, and women receiving hormone replacement therapy for negative peri- or post-menopausal symptoms. Advisors/Committee Members: Choleris, Elena (advisor).

Subjects/Keywords: social learning; social transmission of food preferences; social recognition; social interaction; resident-intruder test; estrogen receptor alpha; estrogen receptor beta; PPT; DPN; WAY-200070

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

APA (6^th Edition):

Clipperton Allen, A. E. (2012). Food, friends and foes: estrogens and social behaviour in mice. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3275

Chicago Manual of Style (16^th Edition):

Clipperton Allen, Amy Elizabeth. “Food, friends and foes: estrogens and social behaviour in mice.” 2012. Doctoral Dissertation, University of Guelph. Accessed January 22, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3275.

MLA Handbook (7^th Edition):

Clipperton Allen, Amy Elizabeth. “Food, friends and foes: estrogens and social behaviour in mice.” 2012. Web. 22 Jan 2021.

Vancouver:

Clipperton Allen AE. Food, friends and foes: estrogens and social behaviour in mice. [Internet] [Doctoral dissertation]. University of Guelph; 2012. [cited 2021 Jan 22]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3275.

Council of Science Editors:

Clipperton Allen AE. Food, friends and foes: estrogens and social behaviour in mice. [Doctoral Dissertation]. University of Guelph; 2012. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3275

25. Poppe, Ana Carolina Machado. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.

Degree: Mestrado, Obstetrícia e Ginecologia, 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;

►

Introdução: A endometriose é uma doença ginecológica comum caracterizada pela presença de estroma e/ou glândula endometrial fora da cavidade uterina, e que não possui sua… (more)

▼

Introdução: A endometriose é uma doença ginecológica comum caracterizada pela presença de estroma e/ou glândula endometrial fora da cavidade uterina, e que não possui sua etiopatogenia bem estabelecida. A transição epitélio-mesênquima (TEM) é um processo que consiste em uma série de mudanças no fenótipo de células epiteliais que fazem com que estas células assumam características de células mesenquimais. Assim como observado na TEM, as células endometriais no contexto da endometriose apresentam capacidade migratória, invasibilidade e elevada resistência à apoptose. As moléculas de adesão têm adquirido crescente relevância na TEM, pois relacionam-se à perda de adesão célula-célula com o aumento da invasão e metástase. O objetivo deste estudo foi investigar a expressão de marcadores relacionados com a TEM na endometriose superficial, ovariana e profunda. Pacientes e Métodos: Foram selecionadas 103 mulheres que preenchiam os critérios de inclusão estabelecidos, constituindo 2 grupos de estudo independentes entre si: 18 mulheres com endometriose peritoneal, ovariana e profunda concomitantes; 85 mulheres com endometriose ovariana e/ou profunda, dividido em 44 mulheres com endometriose ovariana e 41 com endometriose intestinal. Através de reações de imunoistoquímica, a expressão proteica dos marcadores e-caderina, n-caderina, betacatenina, receptor de estrogênio e receptor de progesterona foram avaliados nos tecidos de interesse em cada grupo de estudo. Além dos locais de doença, as mulheres foram avaliadas quanto à relação com a fase do ciclo e à classificação histológica da doença. Resultados: As lesões de endometriose de ovário mostraram uma menor expressão de n-caderina em comparação às lesões de intestino e peritônio (p=0,032). O receptor de estrogênio e receptor de progesterona se mostraram significativamente menos expressos no componente epitelial da doença de ovário do que no epitélio da endometriose de peritônio e intestino (p=0,002; p=0,48). A expressão da n-caderina apresentou uma correlação direta com a expressão do receptor de estrogênio no estroma da endometriose de intestino (p=0,036). Conclusão: Estes resultados sugerem que a transição epitélio-mesênquima esteja envolvida na etiopatogenia da endometriose, demonstrando que a doença de ovário se comporta de maneira diferente da doença superficial e da doença infiltrativa profunda, sendo a n-caderina um importante fator envolvido neste processo possivelmente influenciada pela ação do estrogênio

Background: Endometriosis is a common gynecological disease defined as the presence of ectopic endometrial glands and stroma outside the uterine cavity, and its pathogenesis is not well established. The epithelial to mesenchymal transition (EMT) is a process consisting of a series of changes in the phenotype of epithelial cells that make these cells assume the characteristics of mesenchymal cells. As observed in the EMT, endometrial cells in the context of endometriosis have the capacity of migration, invasiveness and high resistance to apoptosis. . The adhesion…

Advisors/Committee Members: Abrão, Mauricio Simões.

Subjects/Keywords: beta-catenin; Beta-catenina; E-caderinas; E-cadherin; Endometriose; Endometriosis; Epithelial-mesenchymal transition; Estrogen receptor; N-caderinas; N-cadherin; Progesterone receptor; Receptores de progesterona; Receptores estrogênicos; Transição epitélial-mesenquimal

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

APA (6^th Edition):

Poppe, A. C. M. (2013). Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;

Chicago Manual of Style (16^th Edition):

Poppe, Ana Carolina Machado. “Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.” 2013. Masters Thesis, University of São Paulo. Accessed January 22, 2021. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;.

MLA Handbook (7^th Edition):

Poppe, Ana Carolina Machado. “Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica.” 2013. Web. 22 Jan 2021.

Vancouver:

Poppe ACM. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Jan 22]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;.

Council of Science Editors:

Poppe ACM. Avaliação de marcadores relacionados à transição epitélio-mesênquima na endometriose pélvica. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/5/5139/tde-20022014-092016/ ;

26. Χαντζή, Νίκη. Ανάπτυξη μεθόδων μέτρησης των υποδοχέων οιστρογόνων ERβ1 και ERβ2 και αξιολόγηση τους ως δεικτών πρόγνωσης του καρκίνου του μαστού.

Degree: 2011, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/25328

►

Estrogen action is primarily mediated by the two subtypes of estrogen receptor (ER), ERα and ERβ. There are at least five ERβ isoforms in humans,… (more)

▼

Estrogen action is primarily mediated by the two subtypes of estrogen receptor (ER), ERα and ERβ. There are at least five ERβ isoforms in humans, of which two, namely ERβ1 and ERβ2, are primarily expressed in breast tissue, with ERβ1 being the only isoform that is able to bind hormone with high affinity. While ERα is established since long ago as a marker of favorable breast cancer prognosis and response to hormone therapy, the clinical significance of ERβ1 and ERβ2 is not clear as yet. In addition, little is known about the role of ERβ1 and ERβ2 in benign hyperplastic lesions of the breast and, in particular, the breast cancer risk of these lesions. To study the role of ERβ1 and ERβ2 in breast cancer and benign breast lesions, we characterized a series of new monoclonal and polyclonal antibodies using cells transiently or stably trasnfected with ERα, ERβ1 or ERβ2, including e.g. clones of human embryonic kidney cells HEK-293 engineered to stably express ERα and ERβ1. Using antibodies characterized as most suitable for immunohistochemistry, we found that, compared to ERα and ΕRβ2, ERβ1 is more frequently expressed in hyperplastic (HUT) and non-invasive neoplastic lesions (ADH, DCIS) of human breast. We also found that, while the percentage of ERα-expressing cells increases progressively from HUT to ADH and DCIS, that of ERβ2-expressing cells decreases from normal breast to ADH. In addition, we found that expression of Ki-67 was associated with ERα positivity in HUT and inversely associated with ERβ2 positivity in DCIS. These findings are taken to indicate that ERβ2 expression is dynamically regulated during mammary carcinogenesis and that ERβ2 could have a protective role with respect to DCIS progression. In ERα-negative breast cancer, ERβ1(+) was detected in 66 out of 97 (68%) cases and ERβ2(+) in 65 out of 96 (68%) cases. Tumour grade was significantly higher in ERβ1-negative cases compared to positive cases, while ERβ2 expression was positively correlated with lymph node metastasis. We did not find any relation between ERβ1 expression and patient overall or disease free survival. In contrast, ERβ2 has emerged as the most important prognostic variable after tumour grade. Patients with ERα-negative breast carcinomas that overexpress ERβ2 had lower disease free survival, independent of the type of post-operative treatment.

Τα οιστρογόνα ασκούν τη δράση τους μέσω των υποδοχέων οιστρογόνων τύπου άλφα και βήτα (ERα και ERβ). Στον άνθρωπο υπάρχουν 5 τουλάχιστον ισομορφές του ERβ, εκ των οποίων στο μαστό εκφράζονται κυρίως δύο (ERβ1 και ERβ2), ενώ μόνο μια (ERβ1) μπορεί να προσδέσει 17β-οιστραδιόλη με υψηλή χημική συγγένεια. Ο ERα είναι καθιερωμένος δείκτης πρόγνωσης και πρόβλεψης ανταπόκρισης σε ορμονοθεραπεία του καρκίνου του μαστού. Η κλινική σημασία της έκφρασης των ERβ1 και ERβ2 στο καρκίνο του μαστού δεν έχει ακόμα διευκρινισθεί, ενώ ακόμη λιγότερο γνωστά είναι η έκφραση και ο ρόλος τους σε καλοήθεις υπερπλαστικές αλλοιώσεις του μαστού. Για τη μελέτη του ρόλου των ERβ1 και ERβ2 στο καρκίνο και στις καλοήθεις…

Subjects/Keywords: Οιστρογονικοί υποδοχείς τύπου β; Καλοήθεις παθήσεις μαστών; Μη διηθητικό καρκίνωμα μαστού; Διηθητικό καρκίνωμα μαστού; Αντισώματα κατά των oιστρογονικών υποδοχέων τύπου α, β1 & β2; Ανοσοϊστοχημεία; Estrogen receptor beta; Benign breast lesions; Non-invasive breast carcinoma; Invasive breast carcinoma; Antibodies to estrogen receptors alpha, beta1 & beta2; Immunohistochemistry ( IHC)

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

APA (6^th Edition):

Χαντζή, . �. (2011). Ανάπτυξη μεθόδων μέτρησης των υποδοχέων οιστρογόνων ERβ1 και ERβ2 και αξιολόγηση τους ως δεικτών πρόγνωσης του καρκίνου του μαστού. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/25328

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):

Χαντζή, Νίκη. “Ανάπτυξη μεθόδων μέτρησης των υποδοχέων οιστρογόνων ERβ1 και ERβ2 και αξιολόγηση τους ως δεικτών πρόγνωσης του καρκίνου του μαστού.” 2011. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed January 22, 2021. http://hdl.handle.net/10442/hedi/25328.

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

MLA Handbook (7^th Edition):

Χαντζή, Νίκη. “Ανάπτυξη μεθόδων μέτρησης των υποδοχέων οιστρογόνων ERβ1 και ERβ2 και αξιολόγηση τους ως δεικτών πρόγνωσης του καρκίνου του μαστού.” 2011. Web. 22 Jan 2021.

Vancouver:

Χαντζή �. Ανάπτυξη μεθόδων μέτρησης των υποδοχέων οιστρογόνων ERβ1 και ERβ2 και αξιολόγηση τους ως δεικτών πρόγνωσης του καρκίνου του μαστού. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2011. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10442/hedi/25328.

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

Council of Science Editors:

Χαντζή �. Ανάπτυξη μεθόδων μέτρησης των υποδοχέων οιστρογόνων ERβ1 και ERβ2 και αξιολόγηση τους ως δεικτών πρόγνωσης του καρκίνου του μαστού. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2011. Available from: http://hdl.handle.net/10442/hedi/25328

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

27. Piperigkou, Zoi. Μελέτη ρυθμιστικών μηχανισμών έκφρασης βιομορίων, λειτουργικών ιδιοτήτων και μορφολογικών χαρακτηριστικών των καρκινικών κυττάρων μαστού.

Degree: 2018, University of Patras; Πανεπιστήμιο Πατρών

URL: http://hdl.handle.net/10442/hedi/43995

► Estrogen receptors (ERs) have pivotal roles in breast cancer growth and progression. Even though the contribution of ERα in the modulation of breast cancer cells'… (more)

▼ Estrogen receptors (ERs) have pivotal roles in breast cancer growth and progression. Even though the contribution of ERα in the modulation of breast cancer cells' behavior is thoroughly studied, the biological functions of its isoform, ERβ, are less elucidated. In the present doctoral thesis, we demonstrated that ERβ suppression in the highly aggressive, ERβ-positive MDA-MB-231 breast cancer cells (shERβ MDA-MB-231) resulted in profound phenotypic changes, inhibition of EMT process and major changes in the properties as well as in gene and protein expression levels of certain functional matrix components of breast cancer cells in a 17-β-estradiol (E2)-independent manner. As observed by scanning electron microscopy, ERβ suppression strongly affects the morphology of shERβ MDA-MB-231 cells, which is followed by downregulated expression levels of the mesenchymal markers fibronectin and vimentin, whereas it increases the expression levels of epithelial marker E-cadherin and cell-cell junctions. These alterations are followed by reduced levels of cell functional properties that promote the aggressiveness of these cells, such as proliferation, migration, spreading capacity, invasion and adhesion. Notably, ERβ suppression reduces the migration of MDA-MB-231 breast cancer cells via EGFR/IGF-IR and JAK/STAT signaling pathways. Moreover, our findings revealed that ERβ has a crucial role in modulation of mRNA levels and protein expression of several matrix mediators, including the transmembrane syndecans and intracellular serglycin, several MMPs, plasminogen activation system components and receptor tyrosine kinases. These data clearly demonstrate that ERβ plays a crucial role in mediating cell behavior and ECM composition of the highly aggressive MDA-MB-231 cells and it opens a new area of research to further understand its role and to improve pharmaceutical targeting of the non-hormone-dependent breast cancer.The epigenetic alterations are responsible for the ability of the tumor cells to metastasize. In the present study, we demonstrated that ER status is associated with distinct miRNA expression profiles in MCF-7 and MDA-MB-231 breast cancer cells, and that mainly miR-10b (oncogenic miRNA) and miR-200b (EMT inhibitor) are the key regulators of MDA-MB-231 cell behavior. Notably, the expression profiles of these miRNAs are mediated through EGFR/IGF-IR crosstalk with E2. Moreover, growing ERα-positive, MCF-7, and ERβ-positive, MDA-MB-231, cells in estrogen-free medium resulted in a diverse impact on miRNA expression and the behavior of these cells, suggesting the specific effect of E2 on the miRNAs expression profile, depending on the ER status of breast cancer cells. Specifically, ERβ suppression in MDA-MB-231 breast cancer cells results in significant changes in the expression profiles of specific miRNAs that regulate breast cancer progression, including miR-10b, miR-200b and miR-145 (tumor-suppressive miRNA). Enhanced miR-10b expression or miR-145 silencing in shERβ MDA-MB-231 cells revealed that these miRNAs can regulate…

Subjects/Keywords: Καρκίνος μαστού; Οιστρογονοϋποδοχείς; Οιστρογονοϋποδοχέας β; MicroRNAs; Mετασχηματισμός από επιθηλιακό σε μεσεγχυματικό φαινότυπο; Εξωκυττάριος χώρος; Κυτταρική σηματοδότηση; Μεταλλοπρωτεϊνάσες; Πρωτεογλυκάνες; Breast cancer; Estrogen receptors; Estrogen receptor beta; MicroRNAs; Epithelial-to-mesenchymal-transition; Extracellular matrix; Cellular signaling; Matrix metalloproteinases; Proteoglycans

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

APA (6^th Edition):

Piperigkou, Z. (2018). Μελέτη ρυθμιστικών μηχανισμών έκφρασης βιομορίων, λειτουργικών ιδιοτήτων και μορφολογικών χαρακτηριστικών των καρκινικών κυττάρων μαστού. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/43995

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):

Piperigkou, Zoi. “Μελέτη ρυθμιστικών μηχανισμών έκφρασης βιομορίων, λειτουργικών ιδιοτήτων και μορφολογικών χαρακτηριστικών των καρκινικών κυττάρων μαστού.” 2018. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed January 22, 2021. http://hdl.handle.net/10442/hedi/43995.

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

MLA Handbook (7^th Edition):

Piperigkou, Zoi. “Μελέτη ρυθμιστικών μηχανισμών έκφρασης βιομορίων, λειτουργικών ιδιοτήτων και μορφολογικών χαρακτηριστικών των καρκινικών κυττάρων μαστού.” 2018. Web. 22 Jan 2021.

Vancouver:

Piperigkou Z. Μελέτη ρυθμιστικών μηχανισμών έκφρασης βιομορίων, λειτουργικών ιδιοτήτων και μορφολογικών χαρακτηριστικών των καρκινικών κυττάρων μαστού. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2018. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10442/hedi/43995.

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

Council of Science Editors:

Piperigkou Z. Μελέτη ρυθμιστικών μηχανισμών έκφρασης βιομορίων, λειτουργικών ιδιοτήτων και μορφολογικών χαρακτηριστικών των καρκινικών κυττάρων μαστού. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2018. Available from: http://hdl.handle.net/10442/hedi/43995

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

University of Helsinki

28. Mäkinen, Lotta. Estrogen receptors in ovarian granulosa cell tumors.

Degree: Medicinska fakulteten, 2017, University of Helsinki

URL: http://hdl.handle.net/10138/184200

► Granulosa cell tumor (GCT) is a rare ovarian malignancy, which is considered to be of low malignant potential but has a tendency to recurrence. In… (more)

Subjects/Keywords: Granulosa cell tumor; Cancer; Estrogen receptor beta; Immunohistochemistry; Granuloosasolukasvain; Estrogeenireseptori beeta; Immunohistokemia; Obstetrics and Gynecology; Naistentaudit ja synnytykset; Kvinnosjukdomar och förlossningar

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

APA (6^th Edition):

Mäkinen, L. (2017). Estrogen receptors in ovarian granulosa cell tumors. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/184200

Chicago Manual of Style (16^th Edition):

Mäkinen, Lotta. “Estrogen receptors in ovarian granulosa cell tumors.” 2017. Masters Thesis, University of Helsinki. Accessed January 22, 2021. http://hdl.handle.net/10138/184200.

MLA Handbook (7^th Edition):

Mäkinen, Lotta. “Estrogen receptors in ovarian granulosa cell tumors.” 2017. Web. 22 Jan 2021.

Vancouver:

Mäkinen L. Estrogen receptors in ovarian granulosa cell tumors. [Internet] [Masters thesis]. University of Helsinki; 2017. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/10138/184200.

Council of Science Editors:

Mäkinen L. Estrogen receptors in ovarian granulosa cell tumors. [Masters Thesis]. University of Helsinki; 2017. Available from: http://hdl.handle.net/10138/184200

University of Western Ontario

29. Carrier, Alexandra. Investigating the Role of Extracellular Matrix Proteins in Ovarian Folliculogenesis and Ovarian Cancer.

Degree: 2016, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/3869

► The extracellular matrix (ECM) is a highly organized, dynamic structure that maintains tissue integrity and regulates biological processes involved in organ development and function. To… (more)

▼ The extracellular matrix (ECM) is a highly organized, dynamic structure that maintains tissue integrity and regulates biological processes involved in organ development and function. To explore the role of ECM proteins in ovarian physiology and pathology, my thesis characterizes ECM proteins aberrantly overexpressed in the Estrogen Receptor (ER)β-null (βERKO) mouse ovary and epithelial ovarian cancer (EOC). The ECM undergoes extensive physical changes, and influences numerous cell functions, throughout folliculogenesis. This study identifies a role for ERβ in ovarian development earlier than previously believed. Nidogen 2 and Collagen 11a1 are aberrantly overexpressed in βERKO ovaries as early as postnatal day 13, and this dysregulation continues into adulthood, as determined by qPCR and immunofluorescence. Collagen IV, Nidogen 1 and Laminin are also more highly expressed in the βERKO ovary than in the wildtype ovary, suggesting that the repression of several ECM proteins in the ovary is ERβ-dependent. The molecular mechanisms that initiate gene repression by ERβ are not well understood; therefore a potential mechanism by which ERβ may act as a transcriptional repressor in the ovary is investigated. I characterized a novel ERβ transcriptional corepressor – transcription factor 21 (TCF21). In transient transfection and reporter assays, TCF21 represses ERβ transactivation of synthetic and natural estrogen-responsive promoters in various cell lines. As in the βERKO ovary, when the mechanisms regulating ECM dynamics during normal organ function are disrupted, the ECM becomes disorganized. This disorganization is associated with various pathologies, including cancers. The ECM protein, Spondin 1 (SPON1), is overexpressed in ovarian cancers and has been identified as a promising ovarian cancer marker, particularly for high-grade serous carcinomas; yet, its cellular functions and related mechanisms in EOC progression remain unknown. This study shows that SPON1 is expressed and secreted by immortalized EOC cell lines and human primary ascites-derived EOC cells. Treatment with exogenous SPON1 reduces EOC cell adhesion, viability and proliferation but not migration. Experiments utilizing a non-adherent culture surface suggest SPON1 does not effect EOC spheroid formation but is involved in spheroid anchoring and cell dispersion. These findings support an important role for ECM proteins in ovarian development and progression of ovarian carcinomas.

Subjects/Keywords: extracellular matrix protein; folliculogenesis; granulosa cell; ovarian cancer; transcriptional coregulator; estrogen receptor beta; Other Cell and Developmental Biology

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

APA (6^th Edition):

Carrier, A. (2016). Investigating the Role of Extracellular Matrix Proteins in Ovarian Folliculogenesis and Ovarian Cancer. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/3869

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):

Carrier, Alexandra. “Investigating the Role of Extracellular Matrix Proteins in Ovarian Folliculogenesis and Ovarian Cancer.” 2016. Thesis, University of Western Ontario. Accessed January 22, 2021. https://ir.lib.uwo.ca/etd/3869.

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

MLA Handbook (7^th Edition):

Carrier, Alexandra. “Investigating the Role of Extracellular Matrix Proteins in Ovarian Folliculogenesis and Ovarian Cancer.” 2016. Web. 22 Jan 2021.

Vancouver:

Carrier A. Investigating the Role of Extracellular Matrix Proteins in Ovarian Folliculogenesis and Ovarian Cancer. [Internet] [Thesis]. University of Western Ontario; 2016. [cited 2021 Jan 22]. Available from: https://ir.lib.uwo.ca/etd/3869.

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

Council of Science Editors:

Carrier A. Investigating the Role of Extracellular Matrix Proteins in Ovarian Folliculogenesis and Ovarian Cancer. [Thesis]. University of Western Ontario; 2016. Available from: https://ir.lib.uwo.ca/etd/3869

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. Cacioppo, Joseph. The role of endothelin-2 in ovulation.

Degree: PhD, VMS - Comparative Biosciences, 2015, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/78629

► During ovulation, the oocyte and associated cumulus cells are expelled from the ovary and travel to the ampulla of the oviduct where fertilization occurs. Concurrently,… (more)

▼ During ovulation, the oocyte and associated cumulus cells are expelled from the ovary and travel to the ampulla of the oviduct where fertilization occurs. Concurrently, granulosa and theca cells of an ovulating follicle luteinize and form lutein cells of the highly vascular corpus luteum, which secrete progesterone for pregnancy maintenance. Just prior to ovulation, the gene endothelin-2 (Edn2) is highly yet transiently expressed for a two-hour window. Mature endothelin-2 protein (EDN2) is a 21 amino acid peptide that is classically described as a potent vasoconstrictor. EDN2 is produced exclusively by the granulosa cells of mature follicles, and is an important factor in ovulation; mice that are pharmacologically treated to block action of the two endothelin receptors ovulate fewer oocytes and form fewer corpora lutea. Similar effects are seen in mice that globally lack Edn2, though they also expire at a young age. While it is clear that EDN2 plays a vital role in ovulation, the exact role for EDN2 has yet to be elucidated. Previous work suggests that EDN2 may cause contraction of mature follicles during rupture, but may also be involved in the critical processes of angiogenesis and leukocyte migration. To understand the pattern of expression, an Edn2-iCre mouse was generated and Edn2 expression was characterized throughout the body; Edn2 has widespread expression, particularly throughout the skin and ovary, with additional punctate expression in the GI tract, uterus, brain, kidney, and pituitary. This mouse model will be a useful tool for examining EDN2 signaling targets. Next, to address the role of EDN2 in ovarian contraction, the effect of EDN2 on ovaries from cats, dogs, and chickens was compared; all species’ ovaries exhibit a strong and sustained contraction relative to the amount of smooth muscle present in the ovary. Thus EDN2 has an evolutionarily conserved contractile response. To further characterize EDN2 action in the ovary, Edn2 was removed from either the whole ovary, or only the granulosa cells using a novel Esr2-iCre model. In each model, loss of EDN2 prevents follicle rupture but not folliculogenesis or corpus luteum formation. RT-PCR revealed that expression of genes critical in angiogenesis and leukocyte action are not modified by Edn2-ablation, implying no significant involvement of EDN2 in these ovulatory biological processes. To determine whether endothelin receptor A (Ednra, EDNRA, ETA) mediates EDN2 contractile action during ovulation, a conditional gene knockout approach was employed to selectively ablate Ednra in smooth muscle cells through a tamoxifen-inducible Cre recombinase system. However, all mice including wild type controls treated with tamoxifen had severely impaired ovulation; while ovulation occurred, the role of EDNRA cannot yet be determined. Alternatively, available data indicate that granulosa cell-specific loss of Ednra causes subfertility, indicating that EDN2 likely exerts an effect through EDNRA receptors on granulosa cells. Lastly, temporal regulation of Edn2 expression… Advisors/Committee Members: Ko, CheMyong J (advisor), Ko, CheMyong J (Committee Chair), Flaws, Jodi A. (committee member), Mahoney, Megan M. (committee member), Raetzman, Lori T. (committee member), Mitchell, Mark A (committee member).

Subjects/Keywords: endothelin-2 (edn2); Ovulation; Ovary; estrogen receptor-beta (esr2); edn2-icre; esr2-icre; follicle rupture; oocyte release; contraction

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Cacioppo, J. (2015). The role of endothelin-2 in ovulation. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/78629

Chicago Manual of Style (16^th Edition):

Cacioppo, Joseph. “The role of endothelin-2 in ovulation.” 2015. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 22, 2021. http://hdl.handle.net/2142/78629.

MLA Handbook (7^th Edition):

Cacioppo, Joseph. “The role of endothelin-2 in ovulation.” 2015. Web. 22 Jan 2021.

Vancouver:

Cacioppo J. The role of endothelin-2 in ovulation. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2015. [cited 2021 Jan 22]. Available from: http://hdl.handle.net/2142/78629.

Council of Science Editors:

Cacioppo J. The role of endothelin-2 in ovulation. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2015. Available from: http://hdl.handle.net/2142/78629

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Open Access Theses and Dissertations