subject:(tamoxifen)

University of Alberta

1. Cole, Laura Kathleen. Insights into the Transcriptional Regulation and Physiological Importance of Phosphatidylethanolamine N-Methyltransferase.

Degree: PhD, Department of Biochemistry, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/m900nt98v

► Phosphatidylcholine (PC) is made in all nucleated mammalian cells via the CDP-choline pathway. Another major pathway for PC biosynthesis in liver is catalyzed by phosphatidylethanolamine… (more)

Subjects/Keywords: Tamoxifen; Sp1; Phosphatidylcholine; Cardiac Dysfunction

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

APA (6^th Edition):

Cole, L. K. (2010). Insights into the Transcriptional Regulation and Physiological Importance of Phosphatidylethanolamine N-Methyltransferase. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/m900nt98v

Chicago Manual of Style (16^th Edition):

Cole, Laura Kathleen. “Insights into the Transcriptional Regulation and Physiological Importance of Phosphatidylethanolamine N-Methyltransferase.” 2010. Doctoral Dissertation, University of Alberta. Accessed February 28, 2021. https://era.library.ualberta.ca/files/m900nt98v.

MLA Handbook (7^th Edition):

Cole, Laura Kathleen. “Insights into the Transcriptional Regulation and Physiological Importance of Phosphatidylethanolamine N-Methyltransferase.” 2010. Web. 28 Feb 2021.

Vancouver:

Cole LK. Insights into the Transcriptional Regulation and Physiological Importance of Phosphatidylethanolamine N-Methyltransferase. [Internet] [Doctoral dissertation]. University of Alberta; 2010. [cited 2021 Feb 28]. Available from: https://era.library.ualberta.ca/files/m900nt98v.

Council of Science Editors:

Cole LK. Insights into the Transcriptional Regulation and Physiological Importance of Phosphatidylethanolamine N-Methyltransferase. [Doctoral Dissertation]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/m900nt98v

Vanderbilt University

2. Reinert, Rachel Byerley. Vascular Endothelial Growth Factor A Coordinates Pancreatic Islet Vascularization, Innervation, and Function.

Degree: PhD, Molecular Physiology and Biophysics, 2012, Vanderbilt University

URL: http://hdl.handle.net/1803/14196

► Pancreatic islets are miniature endocrine organs that regulate glucose homeostasis. Islets are highly vascularized and richly innervated, but the molecular mechanisms directing this organization are… (more)

▼ Pancreatic islets are miniature endocrine organs that regulate glucose homeostasis. Islets are highly vascularized and richly innervated, but the molecular mechanisms directing this organization are incompletely defined. Vascular endothelial growth factor A (VEGF-A) is crucial for the recruitment of endothelial cells during islet development and vascularization. Once thought to be an endothelial cell-specific signaling molecule, VEGF-A can also signal directly to neurons and glia. This Dissertation defined a new role for VEGF-A in regulating islet innervation during development and expanded our understanding of VEGF-A in the maintenance of mature islet vascularization and function. First, the VEGF-Á-mediated patterning of the intraislet vasculature was found to be required for the development of islet innervation. In mature islets, nerves are closely associated with capillaries, but islet vascularization developmentally precedes islet innervation. Genetic mouse models showed that VEGF-A is a critical mediator of both processes, although VEGF-A is not a direct signal to islet nerves. Instead, islet-derived VEGF-A is required for the formation of the intraislet vasculature during embryogenesis, and postnatally, nerve fibers travel along these capillaries in a VEGF-A-independent manner to innervate islet cells. These results demonstrated that islet vascularization and innervation are developmentally interconnected, and that islet-derived VEGF-A is a principal coordinator of islet formation. Furthermore, the role of VEGF-A in maintaining the vascularization and function of mature islets was defined using a mouse model of tamoxifen-inducible gene inactivation. In development of this model, an islet transplantation bioassay was designed to demonstrate that tamoxifen-inducible Cre-loxP recombination in adult mice in vivo occurs significantly longer than suggested by prior studies, which has broad implications for the use of tamoxifen-inducible mouse models in biomedical research. In these studies, inactivation of VEGF-A in â-cells of adult mice reduced islet vascularity and impaired glucose tolerance, but surprisingly had little impact on â-cell mass maintenance, gene expression, or insulin secretion in vitro. These experiments showed that mature pancreatic â-cells can tolerate a significant and prolonged reduction in intraislet capillary density and still maintain relatively normal function. Advisors/Committee Members: Wenbiao Chen (committee member), Danny Winder (committee member), Masakazu Shiota (committee member), Patricia A. Labosky (committee member), Maureen Gannon (Committee Chair).

Subjects/Keywords: VEGF; Cre-loxP recombination; tamoxifen

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

APA (6^th Edition):

Reinert, R. B. (2012). Vascular Endothelial Growth Factor A Coordinates Pancreatic Islet Vascularization, Innervation, and Function. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14196

Chicago Manual of Style (16^th Edition):

Reinert, Rachel Byerley. “Vascular Endothelial Growth Factor A Coordinates Pancreatic Islet Vascularization, Innervation, and Function.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed February 28, 2021. http://hdl.handle.net/1803/14196.

MLA Handbook (7^th Edition):

Reinert, Rachel Byerley. “Vascular Endothelial Growth Factor A Coordinates Pancreatic Islet Vascularization, Innervation, and Function.” 2012. Web. 28 Feb 2021.

Vancouver:

Reinert RB. Vascular Endothelial Growth Factor A Coordinates Pancreatic Islet Vascularization, Innervation, and Function. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1803/14196.

Council of Science Editors:

Reinert RB. Vascular Endothelial Growth Factor A Coordinates Pancreatic Islet Vascularization, Innervation, and Function. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/14196

University of Texas Southwestern Medical Center

3. Chen, Jian. Malignant Gliomas Originate From Neural Stem/Progenitor Cells and Are Maintained By Cancer Stem Cells.

Degree: 2011, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/938

► Malignant glioma is one of the most aggressive cancers. To study the biology of glioma, our lab previously developed a series of mouse models that… (more)

▼ Malignant glioma is one of the most aggressive cancers. To study the biology of glioma, our lab previously developed a series of mouse models that phenocopy both tumor initiation and progression through stochastic tumor suppressor loss-of-heterozygosity (LOH). To determine whether the mouse models recapitulate human glioma at the molecular level, we have performed gene set enrichment analysis (GSEA) comparing the molecular signature of tumors that develop in our mouse glioma models to the gene expression profiles of a number of human tumors. Our mouse glioma models share high similarity with human GBM and showed a generally proneural marker gene expression profile. We also found that tumors from the same initial genetic mutations can be further divided into several subtypes. Previous studies suggested a neural stem/progenitor cell (NSC) origin for gliomas, however strict exprimental evidence was still lacking. To examine the role of NSCs in glioma, we developed an NSC-specific tamoxifen-inducible nestin-cre driver mouse. When crossed to the NF/p53/Pten flox mice and induced with tamoxifen at E13.5, the Nes-Cre;Nf/p53/Pten mutant mice exhibited tumor initiation and progression similar to our previous mouse model using hGFAP-cre, with complete penetrance. All analyzed mice that were induced at 4 weeks such that only adult neural stem cells were targeted, developed malignant astrocytoma 7 - 12 months after induction. These findings indicate that despite their rarity, neural stem/progenitor cells are sufficient targets for the accumulation of mutations that initiate malignant astrocytomas. Our highly physiological relevant mouse model also allowed us to address the question of how glioma is maintained in vivo: whether tumors are maintained by a subpopulation of cells with self-renewal capacity that supplies tumor bulk, or whether the majority of tumor cells have the capacity to maintain the tumor. In our spontaneous somatic mouse model of glioma, a Nestin-¦¤TK-IRES-GFP transgene labels the primary tumor cells that are required for tumorigenicity in allograft assays. Ablating endogenous Nes-¦¤TK-positive cells significantly extended the survival of tumor-bearing mice by decreasing tumor proliferation and infiltration. We show that the glioma drug, temozolomide, selectively targets endogenous CSC-derived proliferating cells. Furthermore, a combination therapy targeting both dividing cells and the CSCs arrests tumor progression. Advisors/Committee Members: Parada, Luis F..

Subjects/Keywords: Gliomas; Adult Stem Cells; Tamoxifen

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

APA (6^th Edition):

Chen, J. (2011). Malignant Gliomas Originate From Neural Stem/Progenitor Cells and Are Maintained By Cancer Stem Cells. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/938

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):

Chen, Jian. “Malignant Gliomas Originate From Neural Stem/Progenitor Cells and Are Maintained By Cancer Stem Cells.” 2011. Thesis, University of Texas Southwestern Medical Center. Accessed February 28, 2021. http://hdl.handle.net/2152.5/938.

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

MLA Handbook (7^th Edition):

Chen, Jian. “Malignant Gliomas Originate From Neural Stem/Progenitor Cells and Are Maintained By Cancer Stem Cells.” 2011. Web. 28 Feb 2021.

Vancouver:

Chen J. Malignant Gliomas Originate From Neural Stem/Progenitor Cells and Are Maintained By Cancer Stem Cells. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2011. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2152.5/938.

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

Council of Science Editors:

Chen J. Malignant Gliomas Originate From Neural Stem/Progenitor Cells and Are Maintained By Cancer Stem Cells. [Thesis]. University of Texas Southwestern Medical Center; 2011. Available from: http://hdl.handle.net/2152.5/938

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

Univerzitet u Beogradu

4. Abu Rabi, Zaki, 1980-. Značaj biološke heterogenosti karcinoma dojke za odgovor na terapiju antiestrogenima.

Degree: Biološki fakultet, 2014, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get

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Molekularna biologija kancera dojke / Molekularna biologija kancera dojke

Karcinom dojke, kao najčešći oblik malignih tumora koji se javlja kod žena, spada u grupu heterogenih… (more)

▼

Molekularna biologija kancera dojke / Molekularna biologija kancera dojke

Karcinom dojke, kao najčešći oblik malignih tumora koji se javlja kod žena, spada u grupu heterogenih oboljenja zbog čega je veoma teško utvrditi tok bolesti i uspeh potencijalne terapije. Danas endokrina terapija tamoksifenom značajno produžava vreme bez ponovnog javljanja bolesti. Ipak usled poliklonalnosti tumora, koja se ispoljava i u klinički nedetektabilnim mikrimetastazama, uspeh terapije tamoksifenom je znatno smanjen. Pojava de novo rezistencije po davanju tamoksifena se javlja čak kod 50% pacijentkinja, dok se kod većeg broja pacijentkinja gde je inicijalna terapija bila uspešna kasnije javlja stečeni oblik rezistencije. Otkrivanje novih molekularnih biomarkera, kao i analiza njihove povezanosti sa kliničkim tokom bolesti, pomogla bi u izboru inicijalne terapije (prediktivna vrednost), kao i za predviđanje toka bolesti (prognostička vrednost). Analiza biološke heterogenosti estrogen zavisnog primarnog operabilnog karcinoma dojke, pacijentkinja u postmenopauzi lečenih tamoksifenom, imala je za cilj ispitivanje njenog značaja na klinički tok bolesti. Biološka heterogenost tumora ove grupe pacijentkinja je određivana na osnovu molekularnih biomarkera tumora: ER, PR, Her2, Ki-67, apoptotski indeks, uPA, PAI-1 i VEGF. Određivanje novih visokorizičnih fenotipova vršeno je u tri vremenska perioda kliničkog praćenja toka bolesti: prvih 2.5 godine terapije kako bi se utvrdila rana (de novo) rezistencija, perioda između 2.5 i 5 godina terapije radi definisanja stečene rezistencije i praćenje od 12 godina koje ima za cilj da ukaže na prognostički značaj biomarkera. Analizama u okviru ove studije obuhvaćeno je 127 pacijentkinja kod kojih je potvrđen primarni operabilni karcinom dojke. Nakon hiruške terapije sve pacijentkinje su primale terapiju tamoksifenom u trajanju od pet godina. Steroidni receptori su određivani klasičnom biohemijskom metodom, amplifikacija Her2 gena hromogenom in situ hibridizacijom (CISH), nivo Ki-67 je utvrđen imunohistohemijskom metodom, apoptotski indeks TUNEL metodom, dok je za određivanje nivoa proteina uPA, PAI-1 i VEGF korišćen ELISA test. Praćenje kliničkog toka bolesti pacijentkinja lečenih tamoksifenom u prvih 2.5 godina ukazalo je da od kliničko-patoloških parametara veličina tumora, a od biomarkera ER, PR, uPA i PAI-1 imaju značajnu prediktivnu ulogu. Pri tome tumori veći od 2 cm, zatim negativan status ER, PR i PAI-1 definišu pacijentkinje sa lošijim odgovorom na terapiju tamoksifenom. Pozitivan status uPA definiše podgrupu sa slabijim odgovorom na terapiju. Združivanje nepovoljnih karakteristika otkriva fenotipove sa još lošijim tokom bolesti, ukazujući na de novo rezistenciju. U periodu od 2.5-5 godina terapije amplifikacija Her2 gena kod pT2,3 tumora je pokazatelj stečene rezistencije na terapiju tamoksifenom. Visokorizične podgrupe dobijene za period prvih 2.5 godina ne pokazuju isti rizik i u periodu od 2.5-5 godina terapije. Prognostički značaj parametara, posmatran u periodu od 12 godina, otkriva da…

Advisors/Committee Members: Matić, Gordana, 1953-.

Subjects/Keywords: breast cancer; tamoxifen; resistance

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

APA (6^th Edition):

Abu Rabi, Zaki, 1. (2014). Značaj biološke heterogenosti karcinoma dojke za odgovor na terapiju antiestrogenima. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:6759/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):

Abu Rabi, Zaki, 1980-. “Značaj biološke heterogenosti karcinoma dojke za odgovor na terapiju antiestrogenima.” 2014. Thesis, Univerzitet u Beogradu. Accessed February 28, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:6759/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):

Abu Rabi, Zaki, 1980-. “Značaj biološke heterogenosti karcinoma dojke za odgovor na terapiju antiestrogenima.” 2014. Web. 28 Feb 2021.

Vancouver:

Abu Rabi, Zaki 1. Značaj biološke heterogenosti karcinoma dojke za odgovor na terapiju antiestrogenima. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2021 Feb 28]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:6759/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:

Abu Rabi, Zaki 1. Značaj biološke heterogenosti karcinoma dojke za odgovor na terapiju antiestrogenima. [Thesis]. Univerzitet u Beogradu; 2014. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get

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

University of Edinburgh

5. Patel, Saloni Hiten. Inducible gene targeting in the male : tamoxifen adversely impacts postnatal testicular development and function.

Degree: PhD, 2016, University of Edinburgh

URL: http://hdl.handle.net/1842/25870

► Normal development and function of the male reproductive tract relies on the crucial balance between androgen and estrogen signalling, furthermore estrogens play an important role… (more)

▼ Normal development and function of the male reproductive tract relies on the crucial balance between androgen and estrogen signalling, furthermore estrogens play an important role in the regulation of spermatogenesis and steroidogenesis. Tamoxifen (TAM) inducible Cre-loxP systems are widely used to study testicular function. TAM is a selective estrogen receptor modulator (SERM), thereby exerting anti- and pro-estrogenic effects. Therefore, it was hypothesised that acute (single dose) TAM administration to the postnatal testis has significant long-term effects on testicular development and adult testis function, questioning its utility in inducible transgenic systems. A suitable Cre line was first validated as a tool to target the postnatal adult Leydig cell (ALC) population. The Nestin-Cre expressing stem Leydig cells (LCs) were demonstrated as a source of a subset of the ALCs. Hence, a TAM inducible Nestin- Cre line was one of the mouse lines employed for further studies. A comprehensive investigation was carried out to assess any short-and long-term testicular phenotype upon administration of high (3mg) and low (1mg, 500ug and 250ug) doses of TAM. These studies were carried out in TAM-inducible Nestin- Cre/ERT2 and PDGFRA-Cre/ERT2 mouse lines as well as C57Bl/6 mice, to ensure that the observations made were independent of transgene effects. High dose TAM treatment resulted in transgene induction, however this also caused short-term spermatogenic arrest, alterations to steroidogenesis and LC number. Spermatogenesis recovers in young adults, but LCs show delayed maturation, suggesting changes in developmental programming of the ALC population. Thus it was concluded that a single dose of TAM in early postnatal life disrupts testicular function in adulthood. Single low doses of TAM did not induce the transgene, but surprisingly also had a long-term impact on ALC development, steroidogenesis and spermatogenesis. Severity of the phenotype worsened with dose concentration, indicating dose dependent impacts of TAM on the testis. Therefore, TAM has adverse impacts on the testis at doses below the threshold of Cre induction. In order to find a substitute for TAM in transgene induction studies, Raloxifene (RAL), another SERM, was hypothesised to induce transgenes with minimal disruption of testicular function. A 3mg dose of RAL did not show the adverse impacts of TAM. However, different dose regimens were assayed to induce the transgene without success, hence ruling out RAL as a substitute for TAM. Given the severity of previously undocumented TAM-induced phenotypes elucidated in these studies, it is evident that the off-target effects of TAM are severely underappreciated and can cause long-term programming effects. These off-target effects are likely to be present in other estrogen responsive tissues. Hence TAM-inducible Cre systems should be used with rigorous controls, to ensure correct conclusions are drawn from results obtained.

Subjects/Keywords: 612.6; Tamoxifen; testis; Leydig cells

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

APA (6^th Edition):

Patel, S. H. (2016). Inducible gene targeting in the male : tamoxifen adversely impacts postnatal testicular development and function. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/25870

Chicago Manual of Style (16^th Edition):

Patel, Saloni Hiten. “Inducible gene targeting in the male : tamoxifen adversely impacts postnatal testicular development and function.” 2016. Doctoral Dissertation, University of Edinburgh. Accessed February 28, 2021. http://hdl.handle.net/1842/25870.

MLA Handbook (7^th Edition):

Patel, Saloni Hiten. “Inducible gene targeting in the male : tamoxifen adversely impacts postnatal testicular development and function.” 2016. Web. 28 Feb 2021.

Vancouver:

Patel SH. Inducible gene targeting in the male : tamoxifen adversely impacts postnatal testicular development and function. [Internet] [Doctoral dissertation]. University of Edinburgh; 2016. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1842/25870.

Council of Science Editors:

Patel SH. Inducible gene targeting in the male : tamoxifen adversely impacts postnatal testicular development and function. [Doctoral Dissertation]. University of Edinburgh; 2016. Available from: http://hdl.handle.net/1842/25870

Ruhr Universität Bochum

6. Alemi, Mohammad Aref. Endometriumveränderungen unter Tamoxifen bei Mammakarzinompatientinnen : Korrelation des sonographischen mit dem intraoperativen und histologischen Befund unter Berücksichtigung des endometrialen Rezeptorstatus.

Degree: 2014, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-42183

► Problem: In der vorliegenden Arbeit wurde untersucht, inwiefern die sonographische Diagnose mit dem hysteroskopischen und dem histologischen Befund korrelieren. Methode: Es wurden 52 hormonrezeptorpositive Mammakarzinompatientinnen… (more)

Subjects/Keywords: Gebärmutterschleimhaut / Änderung; Tamoxifen; Brustkrebs; Hormonrezeptor; Hysteroskopie

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

APA (6^th Edition):

Alemi, M. A. (2014). Endometriumveränderungen unter Tamoxifen bei Mammakarzinompatientinnen : Korrelation des sonographischen mit dem intraoperativen und histologischen Befund unter Berücksichtigung des endometrialen Rezeptorstatus. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-42183

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):

Alemi, Mohammad Aref. “Endometriumveränderungen unter Tamoxifen bei Mammakarzinompatientinnen : Korrelation des sonographischen mit dem intraoperativen und histologischen Befund unter Berücksichtigung des endometrialen Rezeptorstatus.” 2014. Thesis, Ruhr Universität Bochum. Accessed February 28, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-42183.

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

MLA Handbook (7^th Edition):

Alemi, Mohammad Aref. “Endometriumveränderungen unter Tamoxifen bei Mammakarzinompatientinnen : Korrelation des sonographischen mit dem intraoperativen und histologischen Befund unter Berücksichtigung des endometrialen Rezeptorstatus.” 2014. Web. 28 Feb 2021.

Vancouver:

Alemi MA. Endometriumveränderungen unter Tamoxifen bei Mammakarzinompatientinnen : Korrelation des sonographischen mit dem intraoperativen und histologischen Befund unter Berücksichtigung des endometrialen Rezeptorstatus. [Internet] [Thesis]. Ruhr Universität Bochum; 2014. [cited 2021 Feb 28]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-42183.

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

Council of Science Editors:

Alemi MA. Endometriumveränderungen unter Tamoxifen bei Mammakarzinompatientinnen : Korrelation des sonographischen mit dem intraoperativen und histologischen Befund unter Berücksichtigung des endometrialen Rezeptorstatus. [Thesis]. Ruhr Universität Bochum; 2014. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-42183

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

University of Otago

7. Scandlyn, Marissa Jayne. Novel drug therapies for ER- basal-like breast cancer; preclinical evaluation in a xenograft model.

Degree: 2011, University of Otago

URL: http://hdl.handle.net/10523/1688

► Basal-like breast cancers are a subgroup of breast lesions that are triple-negative for the estrogen receptor (ER), progesterone receptor and human epidermal growth factor receptor… (more)

▼ Basal-like breast cancers are a subgroup of breast lesions that are triple-negative for the estrogen receptor (ER), progesterone receptor and human epidermal growth factor receptor 2. There is currently no effective treatment for basal-like breast cancer and patients with this disease have a particularly poor prognosis. Previous work has shown that combinations of epigallocatechin gallate (EGCG) and selective estrogen receptor modulators (SERMs) are synergistically cytotoxic to MDA-MB-231 cells, a commonly used in vitro model of basal-like breast cancer. Therefore, the in vivo efficacy of EGCG and SERM combinations was investigated, using an MDA-MB-231 mouse xenograft model. MDA-MB-231 tumor volume was significantly suppressed 71% in mice treated with a combination of EGCG (25 mg/kg, i.p.) and tamoxifen (75 μg/kg, p.o.) daily for 10 weeks, whereas individual treatments failed to suppress tumor growth. Using Western blotting, EGCG and tamoxifen co-therapy was found to significantly reduce tumoral CYP1B1 protein levels 72%, which may be crucial for tumor suppression by preventing CYP1B1-mediated inactivation of 4-hydroxytamoxifen, the active tamoxifen metabolite. Contrary to expectations, raloxifene (850 μg/kg, p.o.) was far more effective at suppressing MDA-MB-231 xenograft growth individually than when used in combination with EGCG (25 mg/kg, i.p.), and tumor volume was reduced 79% and 54% by individual raloxifene and combination therapies, respectively, after 8 weeks of treatment. This finding was unexpected and suggested that EGCG may interfere with raloxifene’s metabolism. However, the activities of hepatic uridine diphospho-glucuronosyl transferase (UGT) enzymes, which metabolize raloxifene, were not altered by EGCG treatment. Because basal-like breast cancers appear dependent on epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR) signaling for survival and proliferation, Western blotting was used to investigate the expression and phosphorylation status of various signaling proteins in the MDA-MB-231 tumors. EGCG + tamoxifen combination therapy was associated with a marked reduction in tumoral EGFR, Akt, mTOR and NFκB expression compared with individual treatments, whereas raloxifene therapy did not significantly influence EGFR signaling or VEGFR expression. Therefore, modulation of growth factor signaling contributes to the growth suppression of MDA-MB-231 tumors by EGCG + tamoxifen, which shows therapeutic potential for basal-like breast cancer. Although the tumor suppression elicited by raloxifene is encouraging, further investigation is required to establish the mechanism of action. Curcumin is another natural product that has received much attention for its anticarcinogenic properties, and previous work in our laboratory has shown that curcumin displays activity toward basal-like breast cancer cells in vitro, but fails in vivo, probably due to poor bioavailability. In an attempt to improve curcumin’s bioavailability, a panel of derivatives had been developed… Advisors/Committee Members: Rosengren, Rhonda J (advisor).

Subjects/Keywords: EGCG; Breast cancer; Tamoxifen; Raloxifene; Curcumin

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

APA (6^th Edition):

Scandlyn, M. J. (2011). Novel drug therapies for ER- basal-like breast cancer; preclinical evaluation in a xenograft model. (Doctoral Dissertation). University of Otago. Retrieved from http://hdl.handle.net/10523/1688

Chicago Manual of Style (16^th Edition):

Scandlyn, Marissa Jayne. “Novel drug therapies for ER- basal-like breast cancer; preclinical evaluation in a xenograft model. ” 2011. Doctoral Dissertation, University of Otago. Accessed February 28, 2021. http://hdl.handle.net/10523/1688.

MLA Handbook (7^th Edition):

Scandlyn, Marissa Jayne. “Novel drug therapies for ER- basal-like breast cancer; preclinical evaluation in a xenograft model. ” 2011. Web. 28 Feb 2021.

Vancouver:

Scandlyn MJ. Novel drug therapies for ER- basal-like breast cancer; preclinical evaluation in a xenograft model. [Internet] [Doctoral dissertation]. University of Otago; 2011. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10523/1688.

Council of Science Editors:

Scandlyn MJ. Novel drug therapies for ER- basal-like breast cancer; preclinical evaluation in a xenograft model. [Doctoral Dissertation]. University of Otago; 2011. Available from: http://hdl.handle.net/10523/1688

8. Nkuliyingoma, Anastase. Effects of Oestrogen Receptor Status of Women with Breast Cancer Treated with Tamoxifen at University Teaching Hospital and Cancer Diseases Hospital.

Degree: 2015, University of Zimbabwe

URL: http://dspace.unza.zm/handle/123456789/4364

► The main objective of this study was to determine the prevalence of oestrogen receptor-negative breast cancers at UTH and CDH and its impact on tamoxifen… (more)

▼ The main objective of this study was to determine the prevalence of oestrogen receptor-negative breast cancers at UTH and CDH and its impact on tamoxifen management. The specific objectives of the study were to determine the prevalence of oestrogen receptor negative of breast cancer patients; to determine other clinical and epidemiological characteristics of these patients with ER negative breast cancer; and to determine the short term (six months) clinical outcome of oestrogen receptor negative breast cancer patients on tamoxifen therapy following mastectomy. The study combined cross sectional and prospective observational designs. The immunostaining include breast cancer histologically confirmed in participants not pre-treated with tamoxifen at UTH and CDH. Forty-six female breast cancer patients were recruited for this study. The impact of ER negative and management of breast cancer with tamoxifen was measured through changes observed in QOL(EuroQol Group's EQ5D) questionnaire combined with two clinical characteristics that were investigated namely chest radiography and axillary lymph nodes in relation to ER negative. The study has revealed a higher prevalence of oestrogen receptor negative among the participants. The data demonstrates that ER positive tumours accounted for about 45.7% of all tumours, whereas 54.3% were ER negative tumours. Therefore, in this study the ER positive rate was lower than that ER negative. The results about the quality of life tended to slight increase between the first and second visit and significantly decline between the second and third visits. Total quality of life in the patients declined significantly at the third visit. This trend was noted in both the ER negative and ER positive groups. But the worst results were observed in the ER negative group. Lastly, the results revealed a significant association between diabetes mellitus and ER status; patients who were diabetic were likely to be ER negative. The study has established that although the quality of life declined significantly in all the participants, the ER negative proved to be worse. These results suggest that tumour with ER negative; adjuvant tamoxifen therapy may have no benefit

Subjects/Keywords: Hormone Receptors; Breast – Cancer – Hormone Therapy; Tamoxifen

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

APA (6^th Edition):

Nkuliyingoma, A. (2015). Effects of Oestrogen Receptor Status of Women with Breast Cancer Treated with Tamoxifen at University Teaching Hospital and Cancer Diseases Hospital. (Thesis). University of Zimbabwe. Retrieved from http://dspace.unza.zm/handle/123456789/4364

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):

Nkuliyingoma, Anastase. “Effects of Oestrogen Receptor Status of Women with Breast Cancer Treated with Tamoxifen at University Teaching Hospital and Cancer Diseases Hospital.” 2015. Thesis, University of Zimbabwe. Accessed February 28, 2021. http://dspace.unza.zm/handle/123456789/4364.

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

MLA Handbook (7^th Edition):

Nkuliyingoma, Anastase. “Effects of Oestrogen Receptor Status of Women with Breast Cancer Treated with Tamoxifen at University Teaching Hospital and Cancer Diseases Hospital.” 2015. Web. 28 Feb 2021.

Vancouver:

Nkuliyingoma A. Effects of Oestrogen Receptor Status of Women with Breast Cancer Treated with Tamoxifen at University Teaching Hospital and Cancer Diseases Hospital. [Internet] [Thesis]. University of Zimbabwe; 2015. [cited 2021 Feb 28]. Available from: http://dspace.unza.zm/handle/123456789/4364.

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

Council of Science Editors:

Nkuliyingoma A. Effects of Oestrogen Receptor Status of Women with Breast Cancer Treated with Tamoxifen at University Teaching Hospital and Cancer Diseases Hospital. [Thesis]. University of Zimbabwe; 2015. Available from: http://dspace.unza.zm/handle/123456789/4364

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

University of Southern California

9. Schafer, Christopher A. The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2011, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353

► The homeobox genes Msx1 and Msx2 are set of transcription factors known to have both widespread and overlapping expression patterns throughout the developing murine embryo.… (more)

▼ The homeobox genes Msx1 and Msx2 are set of transcription factors known to have both widespread and overlapping expression patterns throughout the developing murine embryo. Conventional inactivation of either or both of these genes has been associated with a variety of congenital abnormalities including defects in calvarial osteogenesis, palate formation, cardiac development, and embryonic lethality. Here we utilize conditional and temporal gene inactivation to investigate the role of these genes in the development of the murine skull vault. ❧ Temporal inactivation of Msx2 revealed a window of requirement for cranial osteogenesis. Concerted loss of both Msx1 and Msx2 showed an unexpected ability of neural crest derived tissues to contribute to the formation of ectopic bone. Along with this we demonstrated a more extended requirement for the basic helix-loop-helix transcription factor, Twist1, which when mutated causes multiple cranial malformations including craniosynostosis. Although conditional inactivation of Msx1 and Msx2 in neural crest or mesoderm derived tissue did manifest deficient frontal and parietal bone development respectively, only mesodermal inactivation resulted in premature coronal suture fusion. However, conditional targeting of Msx1 and Msx2 using either neural crest or mesoderm driven cre recombinase illustrated phenotypes in adjacent calvarial tissues. Consistent with the view that Msx1 and Msx2 are required for specific tissue-tissue interactions in vertebrate development, here I show that these genes act upstream of BMP4 in cranial mesoderm to initiate and maintain osteogenesis in both the parietal and posterior frontal bone regions. Together my data suggest (1) that Msx1, Msx2, and Twist1 have a crucial window of requirement in the formation of the murine skull vault, (2) that mesoderm derived Msx1 and Msx2 function upstream of the morphogen BMP4 to influence posterior frontal bone osteogenesis, (3) that mesoderm derived Msx1 and Msx2 establish and maintain non-osteogenic coronal suture mesenchyme. Advisors/Committee Members: Maxson, Robert E. (Committee Chair), Chai, Yang (Committee Member), Dubeau, Louis (Committee Member).

Subjects/Keywords: skull vault; neural crest; mesoderm; tamoxifen

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APA (6^th Edition):

Schafer, C. A. (2011). The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353

Chicago Manual of Style (16^th Edition):

Schafer, Christopher A. “The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis.” 2011. Doctoral Dissertation, University of Southern California. Accessed February 28, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353.

MLA Handbook (7^th Edition):

Schafer, Christopher A. “The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis.” 2011. Web. 28 Feb 2021.

Vancouver:

Schafer CA. The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis. [Internet] [Doctoral dissertation]. University of Southern California; 2011. [cited 2021 Feb 28]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353.

Council of Science Editors:

Schafer CA. The temporal and tissue specific requirement of Msx genes in murine skull vault osteogenesis. [Doctoral Dissertation]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/636188/rec/7353

University of Southern California

10. Gordon, Michael Alexander. HER2 and co-amplified genes in breast and gastric cancer.

Degree: PhD, Pathobiology, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/315085/rec/3156

► Breast cancer is a heterogeneous disease containing numerous subtypes with disparate outcomes. Patients whose breast cancers contain HER2 gene amplification have a significantly worse prognosis;… (more)

▼ Breast cancer is a heterogeneous disease containing numerous subtypes with disparate outcomes. Patients whose breast cancers contain HER2 gene amplification have a significantly worse prognosis; the advent of HER2-targeted therapies such as trastuzumab and lapatinib has improved the survival rates for patients with HER2-positive disease, however response to non-targeted agents is variable in this subpopulation of breast cancer patients. Identifying molecular alterations which contribute to this differential response may lead to greater effectiveness in designing treatment strategies and improved patient outcomes. To address this issue, breast cancer cell lines were assessed at the genome-wide level for copy number alterations to identify genes that are co-amplified with HER2. Candidate genes were then selected and examined for their potential role in affecting disease outcome. This was accomplished by testing for the presence of gene amplification in clinical breast cancer specimens and testing for an association with response to treatment and survival. Functional assays were also conducted in breast cancer cell lines to determine if candidate genes had an impact on breast cancer cell physiology or response to anti-cancer agents. ❧ Preliminary studies identified MYST2 as a candidate gene that is co-amplified with HER2, and its amplification may have functional consequences in breast cancer outcome. Assessment of MYST2 in breast tumors showed that it is amplified in approximately 40% of HER2-positive breast cancers, and approximately 1% of HER2-negative breast cancers. In vitro knockdown of MYST2 using RNAi resulted in cells becoming sensitized to the anti-estrogen tamoxifen. Additionally, overexpression of MYST2 results in resistance to tamoxifen. These results suggest that MYST2 is a candidate driver oncogene and its amplification may impact the survival of some women with HER2-positive breast cancer. ❧ HER2 gene amplification has been reported in gastroesophageal cancer, but despite numerous clinical studies, its predictive and prognostic value in this setting remains controversial. To address this issue, patients enrolled in the INT-0116/SWOG9008 phase III gastric cancer clinical trial with available tissue specimens were retrospectively evaluated for HER2 gene amplification by FISH and overexpression by immunohistochemistry (IHC). Patients lacking HER2 gene amplification benefited from chemoradiation therapy, whereas patients with HER2 gene amplification did not benefit. In addition, HER2 was not a prognostic marker in the absence of treatment. Advisors/Committee Members: Press, Michael F. (Committee Chair), Dubeau, Louis (Committee Member), Ladner, Robert D. (Committee Member), Casey, Graham (Committee Member).

Subjects/Keywords: breast cancer; gastric cancer; HER2; MYST2; tamoxifen

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

APA (6^th Edition):

Gordon, M. A. (2013). HER2 and co-amplified genes in breast and gastric cancer. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/315085/rec/3156

Chicago Manual of Style (16^th Edition):

Gordon, Michael Alexander. “HER2 and co-amplified genes in breast and gastric cancer.” 2013. Doctoral Dissertation, University of Southern California. Accessed February 28, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/315085/rec/3156.

MLA Handbook (7^th Edition):

Gordon, Michael Alexander. “HER2 and co-amplified genes in breast and gastric cancer.” 2013. Web. 28 Feb 2021.

Vancouver:

Gordon MA. HER2 and co-amplified genes in breast and gastric cancer. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2021 Feb 28]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/315085/rec/3156.

Council of Science Editors:

Gordon MA. HER2 and co-amplified genes in breast and gastric cancer. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/315085/rec/3156

Duke University

11. Ogburn, Ryenne. Development of Data Analysis Methods and Applications for Proteome-Wide SPROX Measurements .

Degree: 2017, Duke University

URL: http://hdl.handle.net/10161/16251

► Protein-ligand interactions can be detected and quantified using protein folding stability measurements. Thus, protein folding stability changes are closely linked to protein function and… (more)

▼ Protein-ligand interactions can be detected and quantified using protein folding stability measurements. Thus, protein folding stability changes are closely linked to protein function and are an important biophysical measurement. Stability of Proteins from Rates of Oxidation (SPROX) is one approach for making proteome wide stability measurements on proteins. Previous SPROX data analysis strategies relied heavily on visual inspection of the data to identify protein stability changes. This created a bottleneck in the analysis and chances for human error. As part of this work, several new data analysis strategies were evaluated using data from previously reported ligand-binding studies. One strategy, the so-called difference analysis, was determined to be the data analysis strategy of choice as it minimized false positive and negatives. The difference analysis strategy was applied to identify protein targets of the breast cancer therapeutic tamoxifen (TAM) and its active metabolite 4-hydroxytamoxifen (4OHT) in yeast and protein targets of TAM and its most abundant metabolite n-desmethyl tamoxifen (NDT) in MCF-7 cell lysate. Several yeast protein targets of TAM and 4OHT were identified using SPROX, and they were subsequently validated using a pulse proteolysis strategy. The proteins in an MCF-7 cell line were probed for TAM- and NDT-induced stability changes using the SPROX in combination with two different quantitative proteomics strategies. Together the SPROX experiments on the proteins in an MCF-7 cell lysate enabled over 1000 proteins to be assayed for TAM- and NDT- induced protein stability changes. Ultimately, a total of 163 and 200 proteins with TAM- and NDT-induced stability changes were identified, respectively. A subset of 33 high confidence hits, including those identified using both proteomics strategies or those identified with multiples peptide probes, were assessed for experimental links to the ER using a STRING analysis. One high confidence protein hit, Y-box binding protein 1 (YBX1), was recently shown to bind the estrogen receptor, which is the known target of TAM. Preliminary results generated here using pulse proteolysis and a purified recombinant YBX1 protein construct suggest that YBX1 is a direct protein target of TAM. Proteins with altered expression levels with TAM and NDT treatment were also identified here. In total, 799 and 671 proteins were probed for TAM- and NDT- induced expression changes, respectively, and 49 and 30 proteins had altered expression. Out of the 49 and 30 proteins with TAM- and NDT- induced expression changes, 14 and 4 proteins had TAM- and NDT- induced altered stability, respectively. In addition to the above ligand-binding studies, SPROX was utilized to characterize the stability of the allergen containing proteomes of the European house dust mite, timothy grass pollen, and ragweed pollen. It was determined that the protein allergens in these proteomes were more stable and more abundant (based on transcriptomic data), than non-allergen proteins from these sources. Advisors/Committee Members: Fitzgerald, Michael C (advisor).

Subjects/Keywords: Biochemistry; Chemistry; allergens; Proteomics; SPROX; tamoxifen

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APA (6^th Edition):

Ogburn, R. (2017). Development of Data Analysis Methods and Applications for Proteome-Wide SPROX Measurements . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/16251

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):

Ogburn, Ryenne. “Development of Data Analysis Methods and Applications for Proteome-Wide SPROX Measurements .” 2017. Thesis, Duke University. Accessed February 28, 2021. http://hdl.handle.net/10161/16251.

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

MLA Handbook (7^th Edition):

Ogburn, Ryenne. “Development of Data Analysis Methods and Applications for Proteome-Wide SPROX Measurements .” 2017. Web. 28 Feb 2021.

Vancouver:

Ogburn R. Development of Data Analysis Methods and Applications for Proteome-Wide SPROX Measurements . [Internet] [Thesis]. Duke University; 2017. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10161/16251.

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

Council of Science Editors:

Ogburn R. Development of Data Analysis Methods and Applications for Proteome-Wide SPROX Measurements . [Thesis]. Duke University; 2017. Available from: http://hdl.handle.net/10161/16251

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

Clemson University

12. Elraghy, Omaima. REPRESSION OF MULTIPLE CYP2D GENES IN MOUSE USING A SINGLE SIRNA CONSTRUCT.

Degree: MS, Biological Sciences, 2011, Clemson University

URL: https://tigerprints.clemson.edu/all_theses/1149

► The CYP2D subfamily is the second most important subfamily of hepatic drug metabolizing CYPs. In mouse, there are nine CYP2D subfamily members, while humans have… (more)

Subjects/Keywords: CYP2D; P450; siRNA; Tamoxifen; Testosterone; Biology

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APA (6^th Edition):

Elraghy, O. (2011). REPRESSION OF MULTIPLE CYP2D GENES IN MOUSE USING A SINGLE SIRNA CONSTRUCT. (Masters Thesis). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_theses/1149

Chicago Manual of Style (16^th Edition):

Elraghy, Omaima. “REPRESSION OF MULTIPLE CYP2D GENES IN MOUSE USING A SINGLE SIRNA CONSTRUCT.” 2011. Masters Thesis, Clemson University. Accessed February 28, 2021. https://tigerprints.clemson.edu/all_theses/1149.

MLA Handbook (7^th Edition):

Elraghy, Omaima. “REPRESSION OF MULTIPLE CYP2D GENES IN MOUSE USING A SINGLE SIRNA CONSTRUCT.” 2011. Web. 28 Feb 2021.

Vancouver:

Elraghy O. REPRESSION OF MULTIPLE CYP2D GENES IN MOUSE USING A SINGLE SIRNA CONSTRUCT. [Internet] [Masters thesis]. Clemson University; 2011. [cited 2021 Feb 28]. Available from: https://tigerprints.clemson.edu/all_theses/1149.

Council of Science Editors:

Elraghy O. REPRESSION OF MULTIPLE CYP2D GENES IN MOUSE USING A SINGLE SIRNA CONSTRUCT. [Masters Thesis]. Clemson University; 2011. Available from: https://tigerprints.clemson.edu/all_theses/1149

13. Levinson, Nathanael Simeon. Towards the elucidation of the mechanism of the antibiotic activity of tamoxifen.

Degree: MS, Chemistry and Biochemistry, 2017, Georgia Tech

URL: http://hdl.handle.net/1853/58251

► Antibiotic resistance is increasingly a health and financial burden on the global population. Use and misuse of antibiotics has led to increased frequencies of antibiotic-resistant… (more)

Subjects/Keywords: Antibiotics; Tamoxifen

…Figure B9 – NMR of desmethyl tamoxifen 69 Figure B10 – Mass spec of NL-I-43 70 Figure B11… …of tamoxifen in SA 79 Figure C2 – MIC of tamoxifen in MRSA 79 Figure C3 – MIC of… …desmethyl tamoxifen in SA 80 Figure C4 – MIC of desmethyl tamoxifen in MRSA 80 Figure C5 – MIC… …of didesmethyl tamoxifen in SA 81 Figure C6 – MIC of didesmethyl tamoxifen in MRSA 81… …Figure C23 – MIC of 4-hydroxy tamoxifen in SA 90 Figure C24 – MIC of 4-hydroxy tamoxifen in…

11 more images…

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APA (6^th Edition):

Levinson, N. S. (2017). Towards the elucidation of the mechanism of the antibiotic activity of tamoxifen. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/58251

Chicago Manual of Style (16^th Edition):

Levinson, Nathanael Simeon. “Towards the elucidation of the mechanism of the antibiotic activity of tamoxifen.” 2017. Masters Thesis, Georgia Tech. Accessed February 28, 2021. http://hdl.handle.net/1853/58251.

MLA Handbook (7^th Edition):

Levinson, Nathanael Simeon. “Towards the elucidation of the mechanism of the antibiotic activity of tamoxifen.” 2017. Web. 28 Feb 2021.

Vancouver:

Levinson NS. Towards the elucidation of the mechanism of the antibiotic activity of tamoxifen. [Internet] [Masters thesis]. Georgia Tech; 2017. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1853/58251.

Council of Science Editors:

Levinson NS. Towards the elucidation of the mechanism of the antibiotic activity of tamoxifen. [Masters Thesis]. Georgia Tech; 2017. Available from: http://hdl.handle.net/1853/58251

University of Georgia

14. Rubin, Valeria Norma. Tamoxifen analogs bearing acidic-side chain substituents.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/20248

► The estrogen receptor (ER) ligand 4-[1-(p-hydroxyphenyl)-2-phenylethyl]phenoxyacetic acid (HPPA) was previously found to have differential bone loss suppressive effects in the ovariectomized (OVX) rat approaching those… (more)

Subjects/Keywords: tamoxifen; SERMs; osteoporosis; raloxifene; estrogen replacement therapy

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APA (6^th Edition):

Rubin, V. N. (2014). Tamoxifen analogs bearing acidic-side chain substituents. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/20248

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):

Rubin, Valeria Norma. “Tamoxifen analogs bearing acidic-side chain substituents.” 2014. Thesis, University of Georgia. Accessed February 28, 2021. http://hdl.handle.net/10724/20248.

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

MLA Handbook (7^th Edition):

Rubin, Valeria Norma. “Tamoxifen analogs bearing acidic-side chain substituents.” 2014. Web. 28 Feb 2021.

Vancouver:

Rubin VN. Tamoxifen analogs bearing acidic-side chain substituents. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10724/20248.

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

Council of Science Editors:

Rubin VN. Tamoxifen analogs bearing acidic-side chain substituents. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/20248

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

University of Louisville

15. Manavalan, Tissa Thomas. Dysregulation of microRNA expression in acquired endocrine-resistant breast cancer.

Degree: PhD, 2012, University of Louisville

URL: 10.18297/etd/897 ; https://ir.library.louisville.edu/etd/897

► MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level by repressing translation or stimulating mRNA degradation. In this study, I tested the hypothesis that miRNAs… (more)

▼ MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level by repressing translation or stimulating mRNA degradation. In this study, I tested the hypothesis that miRNAs are differentially expressed in antiestrogen-sensitive MCF-7 versus -resistant L Y2 human breast cancer cells. Microarray analyses identified 97 miRNAs that are differentially expressed between two estrogen receptor alpha (ERa) -positive human breast cancer cell lines: endocrine-sensitive MCF-7 versus -resistant L Y2 cells under basal conditions. Opposite expression of miRs-lOa,-21, -22, -12Sb, -181, -200a, -200b, -200c, -221, and -222 was confirmed between MCF-7 and L Y2 cells. The ER antagonist ICI 182,780 (fulvestrant or Faslodex) generally blocked the effect of estradiol E2 and 4-hydroxytamoxifen (4-OHT) regulated miRs, i.e .. , miR-lOa, miR-21, miR-22, miR-200a, miR-221, and miR-222, indicating that these responses in MCF-7 cells are ER-mediated. Time dependent variation in basal (ethanol, the vehicle), E2, and 4-0HT regulation of the top 8 miRNAs was detected in MCF-7 cells. Bioinformatic analyses to impute the biological significance of the identified miRNAs by identifying their computationally predicted target genes in the human genome using TargetScan, Pic Tar, and the Sanger miRBase Targets databases was performed. Thirty six putative mRNA targets were identified. Agreement in the direction of anticipated regulation was detected for 12 putative targets. These miRNAs showing opposite expression between these two breast cancer cell lines may be involved in endocrine resistance. MiR-200 family includes two clusters i.e. miR-200 a/200 b/ 429 and miR-200c/141 encoded on chromosome 1 and chromosome 12, respectively. Lower miR-200a, miR-200 b and miR-200c expression was observed in estrogen-independent LCC1 and endocrine-resistant LCC2, LCC9, and LY2 compared to the parental, endocrine-sensitive MCF-7 human breast cancer cell line. ZEB 1 protein was found to be expressed in endocrine-resistant LY2 cells but not in endocrine-sensitive MCF-7 cells. L Y2 cells did not express E-cadherin, a ZEB 1 target which is a marker for epithelial phenotype. This is the first demonstration that L Y2 cells have undergone EMT as part of their endocrine-resistant phenotype. Concomitant with miR-200 decrease, there was an increase in ZEB 1 mRNA expression m L Y2 cells. Overexpression of miR-200b or miR-200c in LY2 cells changed the cellular morphology from a mesenchymal to an epithelial appearance and sensitized cells to inhibition by 4-0HT and fulvestrant. These studies indicate that reduced expression of miR-200 and a corresponding increase in ZEB 1 protein is an indicator of endocrine-resistance in breast cancer cells. Advisors/Committee Members: Klinge, Carolyn Muriel.

Subjects/Keywords: Breast cancer; endocrine; microRNA; resistance; Tamoxifen

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

APA (6^th Edition):

Manavalan, T. T. (2012). Dysregulation of microRNA expression in acquired endocrine-resistant breast cancer. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/897 ; https://ir.library.louisville.edu/etd/897

Chicago Manual of Style (16^th Edition):

Manavalan, Tissa Thomas. “Dysregulation of microRNA expression in acquired endocrine-resistant breast cancer.” 2012. Doctoral Dissertation, University of Louisville. Accessed February 28, 2021. 10.18297/etd/897 ; https://ir.library.louisville.edu/etd/897.

MLA Handbook (7^th Edition):

Manavalan, Tissa Thomas. “Dysregulation of microRNA expression in acquired endocrine-resistant breast cancer.” 2012. Web. 28 Feb 2021.

Vancouver:

Manavalan TT. Dysregulation of microRNA expression in acquired endocrine-resistant breast cancer. [Internet] [Doctoral dissertation]. University of Louisville; 2012. [cited 2021 Feb 28]. Available from: 10.18297/etd/897 ; https://ir.library.louisville.edu/etd/897.

Council of Science Editors:

Manavalan TT. Dysregulation of microRNA expression in acquired endocrine-resistant breast cancer. [Doctoral Dissertation]. University of Louisville; 2012. Available from: 10.18297/etd/897 ; https://ir.library.louisville.edu/etd/897

University of Sydney

16. Stuart, Kirsten Elizabeth. Optimising the management of ductal carcinoma in situ of the breast: diagnosis, treatment and outcomes .

Degree: 2014, University of Sydney

URL: http://hdl.handle.net/2123/13331

► Ductal carcinoma in situ (DCIS) of the breast is common, now representing one-fifth of breast cancers detected at breast-screening; the incidence increased dramatically two decades… (more)

▼ Ductal carcinoma in situ (DCIS) of the breast is common, now representing one-fifth of breast cancers detected at breast-screening; the incidence increased dramatically two decades ago with the introduction of screening mammography. Despite treatment, ipsilateral local recurrence (LR) rates remain high; half the recurrences are invasive breast cancer. This research aimed to evaluate the management of DCIS in Australia and internationally, and by doing so, identify areas requiring optimisation. This work comprehensively appraises Australian patterns of DCIS practice in the context of National guidelines and assesses long-term outcomes of treatment. Initially, the quality of imaging reporting and a systematic review of DCIS management patterns of practice in Australia are investigated. Secondly, long-term treatment outcomes of patients with DCIS are determined with systematic review, meta-analysis and meta-regression analysis. Finally, the long-term cardiac outcomes of radiation therapy (RT) in breast cancer patients are evaluated apropos laterality. This research has found the quality of imaging reporting was greatly enhanced when a synoptic format was used, in accordance with Australian guidelines; in all reports assessed, considerable key reporting requirements were omitted. Management of DCS in Australia has improved since the release of National guidelines, particularly with increased rates of pre-operative image-guided biopsies, breast conserving surgery (BCS) and RT utilisation. However, these rates remain below recommended levels. Significantly lower LR rates were revealed with more locally intensive treatment for patients with DCIS treated by biopsy-only, BCS alone, BCS+RT or mastectomy, on meta-regression analysis of a systematic review of DCIS long-term outcomes. A linear trend for lower breast cancer-specific death rates was identified in this group with more local treatment. Further, amongst patients treated with BCS, a significant linear trend was noted for lower invasive LR rates with more adjuvant treatment. In particular, significantly fewer invasive LRs were observed with both RT and tamoxifen compared with RT alone. Ten years after patients were treated in 1995 with tangential RT for breast cancer, cardiac mortality was found not to be increased for patients from New South Wales, Australia. Breast tumour laterality did not influence this outcome. Radiotherapy techniques have since improved significantly, as has the understanding that reduced radiation dose to the heart decreases the rate of major coronary events. Overall, this work extensively analyses the management of DCIS and identifies areas of sub-optimal practice. These findings bestow a responsibility to develop further National educational strategies and support further DCIS research, particularly in the areas of diagnosis, reducing potential over- and under-treatment as well as improved methods to support patients to make informed decisions after a diagnosis of DCIS.

Subjects/Keywords: DCIS; Surgery; Radiotherapy; Tamoxifen; Outcomes; Cardiac

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APA (6^th Edition):

Stuart, K. E. (2014). Optimising the management of ductal carcinoma in situ of the breast: diagnosis, treatment and outcomes . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/13331

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):

Stuart, Kirsten Elizabeth. “Optimising the management of ductal carcinoma in situ of the breast: diagnosis, treatment and outcomes .” 2014. Thesis, University of Sydney. Accessed February 28, 2021. http://hdl.handle.net/2123/13331.

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

MLA Handbook (7^th Edition):

Stuart, Kirsten Elizabeth. “Optimising the management of ductal carcinoma in situ of the breast: diagnosis, treatment and outcomes .” 2014. Web. 28 Feb 2021.

Vancouver:

Stuart KE. Optimising the management of ductal carcinoma in situ of the breast: diagnosis, treatment and outcomes . [Internet] [Thesis]. University of Sydney; 2014. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2123/13331.

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

Council of Science Editors:

Stuart KE. Optimising the management of ductal carcinoma in situ of the breast: diagnosis, treatment and outcomes . [Thesis]. University of Sydney; 2014. Available from: http://hdl.handle.net/2123/13331

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

University of Aberdeen

17. Maley, Mary. The role of individual forms of cytochrome P450 in drug metabolism in human liver microsomes.

Degree: PhD, 1996, University of Aberdeen

URL: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152886690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327540

► Human liver microsomal metabolism of nicardipine was investigated and compared to that of another dihydropyridine, felodipine, and to published results for other compounds belonging to… (more)

Subjects/Keywords: 572; Cytochrome; Tamoxifen

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APA (6^th Edition):

Maley, M. (1996). The role of individual forms of cytochrome P450 in drug metabolism in human liver microsomes. (Doctoral Dissertation). University of Aberdeen. Retrieved from https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152886690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327540

Chicago Manual of Style (16^th Edition):

Maley, Mary. “The role of individual forms of cytochrome P450 in drug metabolism in human liver microsomes.” 1996. Doctoral Dissertation, University of Aberdeen. Accessed February 28, 2021. https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152886690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327540.

MLA Handbook (7^th Edition):

Maley, Mary. “The role of individual forms of cytochrome P450 in drug metabolism in human liver microsomes.” 1996. Web. 28 Feb 2021.

Vancouver:

Maley M. The role of individual forms of cytochrome P450 in drug metabolism in human liver microsomes. [Internet] [Doctoral dissertation]. University of Aberdeen; 1996. [cited 2021 Feb 28]. Available from: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152886690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327540.

Council of Science Editors:

Maley M. The role of individual forms of cytochrome P450 in drug metabolism in human liver microsomes. [Doctoral Dissertation]. University of Aberdeen; 1996. Available from: https://abdn.alma.exlibrisgroup.com/view/delivery/44ABE_INST/12152886690005941 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327540

18. Orias, Frédéric. Contribution à l'évaluation des risques écotoxicologiques des effluents hospitaliers : bioconcentration, bioaccumulation et bioamplification des résidus pharmaceutiques : Contribution to ecotoxicological risk assessment of hospital effluents : bioconcentration, bioaccumulation and biomagnification of pharmaceutical compounds.

Degree: Docteur es, Environnement, 2015, Vaulx-en-Velin, Ecole nationale des travaux publics

URL: http://www.theses.fr/2015ENTP0005

►

Les hôpitaux génèrent des effluents riches en résidus pharmaceutiques (RP), fonctions de leurs activités de soins et de diagnostic. Certains de ces RP sont aujourd’hui… (more)

▼

Les hôpitaux génèrent des effluents riches en résidus pharmaceutiques (RP), fonctions de leurs activités de soins et de diagnostic. Certains de ces RP sont aujourd’hui retrouvés de manière ubiquitaire dans les écosystèmes aquatiques, en raison de leurs propriétés persistantes et/ou de leur émission continue. La variété de ces RP est telle qu’il est nécessaire de les hiérarchiser, en fonction des risques qu’ils représentent pour l’Environnement, à des fins d’étude et de gestion. Un de ces risques est le transfert des RP bioaccumulables (i.e. Kow élevé et faible biodégradabilité) dans les chaînes alimentaires, via les processus de bioconcentration, de bioaccumulation et de bioamplification. L’objectif principal de cette thèse est de caractériser expérimentalement la bioconcentration et la bioaccumulation de molécules identifiées comme prioritaires dans des travaux précédents. Le composé modèle que nous avons choisi est le tamoxifen, molécule utilisée contre le cancer du sein et déjà retrouvé dans l’Environnement. Les organismes étudiés, issus des trois niveaux trophiques de la chaine alimentaire modèle, sont Pseudokirchneriella subcapitata, Daphnia magna et Danio rerio. Pour mesurer la teneur de cette molécule dans les organismes, nous avons développé une méthode d’analyse reposant sur l’utilisation d’une molécule marquée par un isotope stable, le 15N tamoxifen.Nous avons mesuré des facteurs de bioconcentration (BCF) allant de 12800 chez D. magna à 85600 dans le foie de D. rerio en passant par 21500 chez P. subcapitata. Chez ces derniers, nous avons également évalué la part du régime alimentaire dans la bioaccumulation du tamoxifen. Nous avons observé que plus la concentration dans le milieu d’exposition est faible, plus le régime alimentaire contribue à la bioaccumulation. Ces travaux de thèse présentent de nombreuses perspectives que l’on peut regrouper autour de deux axes : connaissance de l’écotoxicité des RP et de l’écotoxicologie isotopique.

Hospitals generates effluents rich in pharmaceuticals compounds (PC), notably because of careand diagnostics activities. Some of these PCs are ubiquitous in aquatic ecosystems owing to itspersistent properties and/or because of continuous releasing in environment. The diversity of thesePCs is so strong that it is necessary to prioritize them, considering risks that PCs represents forthe Environment, in order to manage and study these compounds. One of these risks is the transferof bioaccumulatives PCs (i.e. PCs with high Kow and low biodegradability) along trophic webs,via bioconcentration, bioaccumulation and biomagnification processes. The main objective of thisthesis is to characterize bioconcentration and bioaccumulation of molecules identified as priorityin previous studies. The model compound choose in our work is the tamoxifen, a molecule usedin the treatment of breast cancer and already found in Environment. Organisms studied, typicalfrom three trophic levels of the model trophic chain, are Pseudokirchneriella subcapitata, Daphniamagna and Danio rerio. In order to…

Advisors/Committee Members: Perrodin, Yves (thesis director).

Subjects/Keywords: Effluents hospitaliers; Résidus pharmaceutiques; Bioconcentration; Bioaccumulation; Isotopes stables; Tamoxifen; Hospital effluents; Pharmaceutical compounds; Bioconcentration; Bioaccumulation; Stable isotopes; Tamoxifen

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

APA (6^th Edition):

Orias, F. (2015). Contribution à l'évaluation des risques écotoxicologiques des effluents hospitaliers : bioconcentration, bioaccumulation et bioamplification des résidus pharmaceutiques : Contribution to ecotoxicological risk assessment of hospital effluents : bioconcentration, bioaccumulation and biomagnification of pharmaceutical compounds. (Doctoral Dissertation). Vaulx-en-Velin, Ecole nationale des travaux publics. Retrieved from http://www.theses.fr/2015ENTP0005

Chicago Manual of Style (16^th Edition):

Orias, Frédéric. “Contribution à l'évaluation des risques écotoxicologiques des effluents hospitaliers : bioconcentration, bioaccumulation et bioamplification des résidus pharmaceutiques : Contribution to ecotoxicological risk assessment of hospital effluents : bioconcentration, bioaccumulation and biomagnification of pharmaceutical compounds.” 2015. Doctoral Dissertation, Vaulx-en-Velin, Ecole nationale des travaux publics. Accessed February 28, 2021. http://www.theses.fr/2015ENTP0005.

MLA Handbook (7^th Edition):

Orias, Frédéric. “Contribution à l'évaluation des risques écotoxicologiques des effluents hospitaliers : bioconcentration, bioaccumulation et bioamplification des résidus pharmaceutiques : Contribution to ecotoxicological risk assessment of hospital effluents : bioconcentration, bioaccumulation and biomagnification of pharmaceutical compounds.” 2015. Web. 28 Feb 2021.

Vancouver:

Orias F. Contribution à l'évaluation des risques écotoxicologiques des effluents hospitaliers : bioconcentration, bioaccumulation et bioamplification des résidus pharmaceutiques : Contribution to ecotoxicological risk assessment of hospital effluents : bioconcentration, bioaccumulation and biomagnification of pharmaceutical compounds. [Internet] [Doctoral dissertation]. Vaulx-en-Velin, Ecole nationale des travaux publics; 2015. [cited 2021 Feb 28]. Available from: http://www.theses.fr/2015ENTP0005.

Council of Science Editors:

Orias F. Contribution à l'évaluation des risques écotoxicologiques des effluents hospitaliers : bioconcentration, bioaccumulation et bioamplification des résidus pharmaceutiques : Contribution to ecotoxicological risk assessment of hospital effluents : bioconcentration, bioaccumulation and biomagnification of pharmaceutical compounds. [Doctoral Dissertation]. Vaulx-en-Velin, Ecole nationale des travaux publics; 2015. Available from: http://www.theses.fr/2015ENTP0005

Duquesne University

19. Hasan, Mahmud. Melatonin-Tamoxifen Drug Conjugates as Breast Cancer Drugs: Pharmacological Evaluation in Phenotypically Diverse Breast Cancer Models and Pharmacokinetic Assessment in Liver Microsome and Female Mouse Models.

Degree: PhD, Pharmacology, 2020, Duquesne University

URL: https://dsc.duq.edu/etd/1935

► Tamoxifen is a first-generation selective estrogen receptor modulator, which reduces the risk of both invasive and non-invasive breast cancer (BC) as well as tumor… (more)

▼ Tamoxifen is a first-generation selective estrogen receptor modulator, which reduces the risk of both invasive and non-invasive breast cancer (BC) as well as tumor recurrence in several clinical trials. However, chronic use of tamoxifen can increase uterine cancer risk and induce tamoxifen resistance. In past studies, melatonin alone reversed tamoxifen resistance induced by light exposure at night in rodents. This study demonstrates that melatonin or melatonin-based ligands (e.g., melatonin-tamoxifen drug conjugates) may be novel BC therapies that are efficacious and free of side effects. To investigate this further, five melatonin-tamoxifen drug conjugates with different linker sizes were synthesized and screened for their anti-cancer actions in a variety of BC cells that included: MCF-7 (ER+), tamoxifen-resistant MCF-7 (TamR), MMC (HER2+), MDA-MB-231 (triple-negative), and BT-549 (triple-negative). Specifically, their actions against cell viability and migration and binding affinity to MT1 melatonin receptor (MT1Rs) and estrogen receptor 1 (ESR1) were assessed. The melatonin-tamoxifen drug conjugate linked with four (C4) or five (C5) carbons demonstrated the most favorable pharmacological characteristics with respect to potency and efficacy to inhibit BC cell viability and migration. C4 and C5 also exhibited unique binding profiles (affinity for ESR1 and MT1R) compared to the other conjugates. C4 and C5 were further assessed for their actions against tamoxifen-resistant (TamR) MCF-7 cells and patient-derived xenograft triple-negative BC cells (TU-BcX-4IC) as well as for potential mechanisms of action using selective MEK1/2, MEK5, and PI3K inhibitors. C4 and C5 inhibited TamR MCF-7 cells with equal potency and efficacy and both C4 and C5 inhibited TU-BcX-4IC cell viability. Even though both compounds demonstrated similar inhibitory actions against BC cell viability and migration, how this occurred, at a mechanistic level, was quite different between C4 and C5 in the cell lines. The underlying mechanisms of C4 and C5 in BC cell lines were context-specific and involved ERK1/2, ERK5, PI3 kinase, and NF-κB. They also exhibited unique pharmacokinetic profiles, where C4 had higher relative oral bioavailability than C5. These melatonin-tamoxifen drug conjugates show promise as novel anti-BC drugs. Advisors/Committee Members: Paula A. Witt-Enderby, David A. Johnson, Jane E. Cavanaugh, Lauren A. O’Donnell, Robert E. Stratford.

Subjects/Keywords: melatonin-tamoxifen drug conjugates; triple negative breast cancer; tamoxifen resistant breast cancer; MEK1/2; MEK5; PI3 kinase; estrogen receptors; melatonin receptors

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APA (6^th Edition):

Hasan, M. (2020). Melatonin-Tamoxifen Drug Conjugates as Breast Cancer Drugs: Pharmacological Evaluation in Phenotypically Diverse Breast Cancer Models and Pharmacokinetic Assessment in Liver Microsome and Female Mouse Models. (Doctoral Dissertation). Duquesne University. Retrieved from https://dsc.duq.edu/etd/1935

Chicago Manual of Style (16^th Edition):

Hasan, Mahmud. “Melatonin-Tamoxifen Drug Conjugates as Breast Cancer Drugs: Pharmacological Evaluation in Phenotypically Diverse Breast Cancer Models and Pharmacokinetic Assessment in Liver Microsome and Female Mouse Models.” 2020. Doctoral Dissertation, Duquesne University. Accessed February 28, 2021. https://dsc.duq.edu/etd/1935.

MLA Handbook (7^th Edition):

Hasan, Mahmud. “Melatonin-Tamoxifen Drug Conjugates as Breast Cancer Drugs: Pharmacological Evaluation in Phenotypically Diverse Breast Cancer Models and Pharmacokinetic Assessment in Liver Microsome and Female Mouse Models.” 2020. Web. 28 Feb 2021.

Vancouver:

Hasan M. Melatonin-Tamoxifen Drug Conjugates as Breast Cancer Drugs: Pharmacological Evaluation in Phenotypically Diverse Breast Cancer Models and Pharmacokinetic Assessment in Liver Microsome and Female Mouse Models. [Internet] [Doctoral dissertation]. Duquesne University; 2020. [cited 2021 Feb 28]. Available from: https://dsc.duq.edu/etd/1935.

Council of Science Editors:

Hasan M. Melatonin-Tamoxifen Drug Conjugates as Breast Cancer Drugs: Pharmacological Evaluation in Phenotypically Diverse Breast Cancer Models and Pharmacokinetic Assessment in Liver Microsome and Female Mouse Models. [Doctoral Dissertation]. Duquesne University; 2020. Available from: https://dsc.duq.edu/etd/1935

Ruhr Universität Bochum

20. Vanheiden, Svenja. Der spannungsabhängige offene Kanalblock der G-Protein-gekoppelten einwärtsgleichrichtenden Kaliumkanäle durchTamoxifen an atrialen Myozyten von Ratten.

Degree: 2014, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-43308

► Tamoxifen ist ein selektiver Östrogen-Antagonist und wird in der Therapie des hormonsensitiven Mammakarzinoms eingesetzt. In dieser Arbeit wurden die Effekte von Tamoxifen am G-Proteingekoppelten einwärtsgleichrichtenden… (more)

Subjects/Keywords: Tamoxifen; Kaliumkanal; GTP-bindende Proteine; Brustkrebs; Patch-Clamp-Methode

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APA (6^th Edition):

Vanheiden, S. (2014). Der spannungsabhängige offene Kanalblock der G-Protein-gekoppelten einwärtsgleichrichtenden Kaliumkanäle durchTamoxifen an atrialen Myozyten von Ratten. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-43308

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):

Vanheiden, Svenja. “Der spannungsabhängige offene Kanalblock der G-Protein-gekoppelten einwärtsgleichrichtenden Kaliumkanäle durchTamoxifen an atrialen Myozyten von Ratten.” 2014. Thesis, Ruhr Universität Bochum. Accessed February 28, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-43308.

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

MLA Handbook (7^th Edition):

Vanheiden, Svenja. “Der spannungsabhängige offene Kanalblock der G-Protein-gekoppelten einwärtsgleichrichtenden Kaliumkanäle durchTamoxifen an atrialen Myozyten von Ratten.” 2014. Web. 28 Feb 2021.

Vancouver:

Vanheiden S. Der spannungsabhängige offene Kanalblock der G-Protein-gekoppelten einwärtsgleichrichtenden Kaliumkanäle durchTamoxifen an atrialen Myozyten von Ratten. [Internet] [Thesis]. Ruhr Universität Bochum; 2014. [cited 2021 Feb 28]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-43308.

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

Council of Science Editors:

Vanheiden S. Der spannungsabhängige offene Kanalblock der G-Protein-gekoppelten einwärtsgleichrichtenden Kaliumkanäle durchTamoxifen an atrialen Myozyten von Ratten. [Thesis]. Ruhr Universität Bochum; 2014. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-43308

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

Universidade do Rio Grande do Norte

21. Jatobá, Carlos André Nunes. Avaliação bioquímica e hostológica de fígado de ratas wistar diabéticas e tratadas com tamoxifeno .

Degree: 2007, Universidade do Rio Grande do Norte

URL: http://repositorio.ufrn.br/handle/123456789/13111

► Tamoxifen (TX), a drug used in the treatment of breast cancer, may cause hepatic changes in some patients. The consequences of its use on the… (more)

Subjects/Keywords: Fígado; Hemossiderina; Siderose; Ferro; Tamoxifeno; Liver; Hemosiderin; Siderosis; Iron overload; Tamoxifen

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APA (6^th Edition):

Jatobá, C. A. N. (2007). Avaliação bioquímica e hostológica de fígado de ratas wistar diabéticas e tratadas com tamoxifeno . (Thesis). Universidade do Rio Grande do Norte. Retrieved from http://repositorio.ufrn.br/handle/123456789/13111

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):

Jatobá, Carlos André Nunes. “Avaliação bioquímica e hostológica de fígado de ratas wistar diabéticas e tratadas com tamoxifeno .” 2007. Thesis, Universidade do Rio Grande do Norte. Accessed February 28, 2021. http://repositorio.ufrn.br/handle/123456789/13111.

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

MLA Handbook (7^th Edition):

Jatobá, Carlos André Nunes. “Avaliação bioquímica e hostológica de fígado de ratas wistar diabéticas e tratadas com tamoxifeno .” 2007. Web. 28 Feb 2021.

Vancouver:

Jatobá CAN. Avaliação bioquímica e hostológica de fígado de ratas wistar diabéticas e tratadas com tamoxifeno . [Internet] [Thesis]. Universidade do Rio Grande do Norte; 2007. [cited 2021 Feb 28]. Available from: http://repositorio.ufrn.br/handle/123456789/13111.

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

Council of Science Editors:

Jatobá CAN. Avaliação bioquímica e hostológica de fígado de ratas wistar diabéticas e tratadas com tamoxifeno . [Thesis]. Universidade do Rio Grande do Norte; 2007. Available from: http://repositorio.ufrn.br/handle/123456789/13111

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

Penn State University

22. Blevins Primeau, Andrea Sascha. UDP-glucuronosyltransferase 2B7 glucuronidation of the active tamoxifen metabolites .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/12439

► Tamoxifen (TAM) is a non-steroidal selective estrogen receptor modulator that was approved by the FDA in 1977 for the treatment of breast cancer. Although it… (more)

▼ Tamoxifen (TAM) is a non-steroidal selective estrogen receptor modulator that was approved by the FDA in 1977 for the treatment of breast cancer. Although it is generally well tolerated, significant adverse effects have been reported, including severe hot flashes and an increased risk for venous thromboembolism and endometrial cancer. The phase I metabolism of TAM is primarily performed by CYP2D6 and CYP3A4/5, resulting in the major, active metabolites N-desmethyl-4-hydroxy-tamoxifen (endoxifen) and 4-hydroxy-tamoxifen (4-OH-TAM). Interestingly, CYP2D6 variant genotypes that result in an inactive or less active phenotype results in greater levels of circulating endoxifen and is also associated with clinical outcomes. However, despite adjusting for CYP2D6 genotype, large variability in the circulating levels of endoxifen are still observed, indicating that additional mechanisms, such as other metabolizing pathways, are involved. The UDP-glucuronosyltransferases (UGT) are a super family of phase II metabolizing enzymes that conjugate a glucuronic acid moiety to a substrate, increasing the polarity and thereby facilitating excretion. The present dissertation identified UGTs 1A8, 1A10, and 2B7 as the most active UGTs against trans-endoxifen, in vitro. In addition, UGT2B7 genotype is associated with the glucuronidation phenotype of human liver microsomes (HLM) against both trans-endoxifen and trans-4-OH-TAM. HLM specimens that were hetero- or homozygous for the polymorphic UGT2B7268Tyr allele exhibited a significant decrease in the glucuronidation of trans-endoxifen and trans-4-OH-TAM. A previous study reported the phosphorylation of UGT2B7 by the non-receptor tyrosine kinase, Src, which altered UGT2B7 enzyme activity against the endogenous substrate, 4-hydroxy-estrone. Therefore, the effect of over-expression of Src in UGT2B7 cells on the glucuronidation of trans-endoxifen and trans-4-OH-TAM was examined. Stable over-expression of Src in the wild-type UGT2B7 cells resulted in a significant decrease in the glucuronidation of both TAM metabolites, similar to the level observed in cell lines only stably expressing the polymorphic UGT2B7268Tyr. Interestingly, over-expression of Src in the variant UGT2B7268Tyr cell line did not alter glucuronidation activity. The evidence presented in this dissertation provides additional knowledge of the metabolism of TAM and specifically, how the pharmacogenetics of the UGT family of phase II metabolizing enzymes cause inter-individual differences in TAM metabolism. Advisors/Committee Members: Harriet C Isom, Dissertation Advisor/Co-Advisor, Harriet C Isom, Committee Chair/Co-Chair, Henry Joseph Donahue, Committee Member, Melvin Billinglsey, Ph D, Committee Member, John Peter Richie Jr., Committee Member, Thomas E Spratt, Committee Member.

Subjects/Keywords: pharmacogenetics; drug metabolism; breast cancer; Src; tamoxifen; UGT; polymorphisms

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

APA (6^th Edition):

Blevins Primeau, A. S. (2011). UDP-glucuronosyltransferase 2B7 glucuronidation of the active tamoxifen metabolites . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/12439

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):

Blevins Primeau, Andrea Sascha. “UDP-glucuronosyltransferase 2B7 glucuronidation of the active tamoxifen metabolites .” 2011. Thesis, Penn State University. Accessed February 28, 2021. https://submit-etda.libraries.psu.edu/catalog/12439.

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

MLA Handbook (7^th Edition):

Blevins Primeau, Andrea Sascha. “UDP-glucuronosyltransferase 2B7 glucuronidation of the active tamoxifen metabolites .” 2011. Web. 28 Feb 2021.

Vancouver:

Blevins Primeau AS. UDP-glucuronosyltransferase 2B7 glucuronidation of the active tamoxifen metabolites . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Feb 28]. Available from: https://submit-etda.libraries.psu.edu/catalog/12439.

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

Council of Science Editors:

Blevins Primeau AS. UDP-glucuronosyltransferase 2B7 glucuronidation of the active tamoxifen metabolites . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/12439

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

Queens University

23. Sellars, Erin. Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance .

Degree: Biochemistry, 2015, Queens University

URL: http://hdl.handle.net/1974/13692

► The function of the glucocorticoid receptor (GR) is crucial for the development and proliferation of normal human breast cells. The primary activity of GR is… (more)

▼ The function of the glucocorticoid receptor (GR) is crucial for the development and proliferation of normal human breast cells. The primary activity of GR is in its binding to glucocorticoids and the subsequent activation of its transcriptional target genes. However, GR is also able to transcriptionally regulate target genes in the absence of ligand in EPH4 mouse mammary cells, which is termed the unliganded activity of GR. Unliganded GR stimulates the activity of the BRCA1 and CH25H promoters and is important in modulating apoptosis and cell growth. The activity of unliganded GR in normal human breast cell lines was investigated in this study in order to validate its regulatory role. Unliganded GR did not upregulate BRCA1 or CH25H expression in the human breast cell lines MCF-10A and 184-hTERT. As well, no novel target genes of unliganded GR were identified in normal human breast cells, however both PRLR and CDKN1A were found to be negatively regulated by liganded and possibly unliganded GR respectively. The second portion of this study focused on the exploration of the role of GR in modulating tamoxifen response in ER+ breast cancer. GR was overexpressed in response to tamoxifen in ER+ breast cancer cells in the ER+ cell lines MCF-7 and T47D. As well, GSTM1 expression was increased by tamoxifen in a GR-dependent manner which suggests that downstream GR signaling is also increased in response to tamoxifen. This is crucial as it suggests that the increase in GR leads to increased GR activity and signaling. The ERα pioneer factor, FOXA1 was overexpressed by tamoxifen as well and may be responsible for activating GR overexpression. Finally, loss of GR may initiate a survival signal in ER+ cells as tamoxifen also increased the expression of cancer stem-like marker genes, EpCAM and ALDH1A3. EpCAM expression was found to be upregulated by tamoxifen and loss of GR expression and ALDH1A3 expression was increased 5-fold by tamoxifen alone. This upregulation of cancer stem-like markers suggests that tamoxifen resistance could occur through the formation of a stem-like chemotherapeutic resistant cell population.

Subjects/Keywords: Breast Cancer ; Tamoxifen Resistance ; Estrogen Receptor ; Glucocorticoid Receptor

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

APA (6^th Edition):

Sellars, E. (2015). Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/13692

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):

Sellars, Erin. “Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance .” 2015. Thesis, Queens University. Accessed February 28, 2021. http://hdl.handle.net/1974/13692.

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

MLA Handbook (7^th Edition):

Sellars, Erin. “Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance .” 2015. Web. 28 Feb 2021.

Vancouver:

Sellars E. Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance . [Internet] [Thesis]. Queens University; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1974/13692.

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

Council of Science Editors:

Sellars E. Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance . [Thesis]. Queens University; 2015. Available from: http://hdl.handle.net/1974/13692

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

University of Toronto

24. Gupta, Rashi. Tamoxifen Inhibits ERα Positive Breast Cancer Progression by Disrupting the ERα-JMJD2B Signaling Axis.

Degree: 2015, University of Toronto

URL: http://hdl.handle.net/1807/69638

►

JMJD2B is a histone demethylase for H3K9me3. Our lab has shown that JMJD2B is a co-factor of estrogen receptor in breast cancer proliferation: JMJD2B knockdown… (more)

Subjects/Keywords: Breast Cancer; Estrogen receptor; histone demethylation; JMJD2B; Tamoxifen; 0379

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

APA (6^th Edition):

Gupta, R. (2015). Tamoxifen Inhibits ERα Positive Breast Cancer Progression by Disrupting the ERα-JMJD2B Signaling Axis. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/69638

Chicago Manual of Style (16^th Edition):

Gupta, Rashi. “Tamoxifen Inhibits ERα Positive Breast Cancer Progression by Disrupting the ERα-JMJD2B Signaling Axis.” 2015. Masters Thesis, University of Toronto. Accessed February 28, 2021. http://hdl.handle.net/1807/69638.

MLA Handbook (7^th Edition):

Gupta, Rashi. “Tamoxifen Inhibits ERα Positive Breast Cancer Progression by Disrupting the ERα-JMJD2B Signaling Axis.” 2015. Web. 28 Feb 2021.

Vancouver:

Gupta R. Tamoxifen Inhibits ERα Positive Breast Cancer Progression by Disrupting the ERα-JMJD2B Signaling Axis. [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/1807/69638.

Council of Science Editors:

Gupta R. Tamoxifen Inhibits ERα Positive Breast Cancer Progression by Disrupting the ERα-JMJD2B Signaling Axis. [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/69638

Wayne State University

25. Haagenson, Kelly. Expression And Regulation Of Map Kinase Phosphatases 1 And 2 In Breast Cancer Tamoxifen Sensitivity.

Degree: PhD, Cancer Biology, 2013, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/659

► ABSTRACT EXPRESSION AND REGULATION OF MAP KINASE PHOSPHATASES 1 and 2 IN BREAST CANCER TAMOXIFEN SENSITIVITY by KELLY K. HAAGENSON May 2013 Advisor: Dr.… (more)

▼ ABSTRACT EXPRESSION AND REGULATION OF MAP KINASE PHOSPHATASES 1 and 2 IN BREAST CANCER TAMOXIFEN SENSITIVITY by KELLY K. HAAGENSON May 2013 Advisor: Dr. Malathy Shekhar Co-Advisor: Dr. Gen Sheng Wu Major: Cancer Biology Degree: Doctor of Philosophy The deregulation of cell signaling is a very important component in the development and progression of cancer. One group of signaling molecules that has been implicated in these processes is the Mitogen-Activated Protein Kinase (MAPK) family which consists of three major branches in mammalian cells: ERK, JNK and p38. The activity of these kinases has wide-ranging effects within the cell and must be tightly regulated. This is partially accomplished through the activity of Mitogen-Activated Protein Kinase Phosphatases (MKPs). The MKPs are a family of eleven dual-specificity threonine-tyrosine phosphatases that attenuate MAP Kinase signaling by dephosphorylating them. Increased ERK signaling has been shown to correlate with poor prognosis in breast cancer patients and is commonly found in tumors that are resistant to tamoxifen treatment. JNK signaling has also been shown to be increased in breast cancer tissue samples. MKP-1 overexpression in breast cancer has been connected with resistance to a number of different chemotherapeutic agents with the underlying mechanism being a decrease in JNK-mediated apoptosis, but no association with tamoxifen response has been previously studied. These observations lead to the hypothesis that MKP-1 overexpression contributes to changes in tamoxifen sensitivity via the inhibition of JNK-mediated apoptosis. The characterization of MKP-1 following its overexpression in the MCF7 cell line revealed that its expression is not changed after tamoxifen treatment, but that the expression of MKP-2 was increased following treatment with anti-estrogens. Both MKP-1 and MKP-2 decreased cell proliferation in response to estrogen and maintained the tamoxifen sensitivity of MCF7 cells. This decrease in proliferation was attributed to the elimination of ERK phosphorylation, as no JNK activation was observed in these cells. MKP-2 protein expression was shown to be constitutive in MCF7 tamoxifen resistant cells, while MKP-1 expression was not detected. All of these results suggest that MKP-2 expression is upregulated in response to tamoxifen treatment in order to dephosphorylate ERK and slow cell proliferation. In tamoxifen resistant cells, upregulation of MKP-2 expression is most likely an attempt to bring the high levels of ERK activation back down to a more normal level. Its inability to do… Advisors/Committee Members: Malathy Shekhar, Gen Sheng Wu.

Subjects/Keywords: Breast Cancer; MAP Kinase Phosphatases; Tamoxifen Sensitivity; Biology; Oncology

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

APA (6^th Edition):

Haagenson, K. (2013). Expression And Regulation Of Map Kinase Phosphatases 1 And 2 In Breast Cancer Tamoxifen Sensitivity. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/659

Chicago Manual of Style (16^th Edition):

Haagenson, Kelly. “Expression And Regulation Of Map Kinase Phosphatases 1 And 2 In Breast Cancer Tamoxifen Sensitivity.” 2013. Doctoral Dissertation, Wayne State University. Accessed February 28, 2021. https://digitalcommons.wayne.edu/oa_dissertations/659.

MLA Handbook (7^th Edition):

Haagenson, Kelly. “Expression And Regulation Of Map Kinase Phosphatases 1 And 2 In Breast Cancer Tamoxifen Sensitivity.” 2013. Web. 28 Feb 2021.

Vancouver:

Haagenson K. Expression And Regulation Of Map Kinase Phosphatases 1 And 2 In Breast Cancer Tamoxifen Sensitivity. [Internet] [Doctoral dissertation]. Wayne State University; 2013. [cited 2021 Feb 28]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/659.

Council of Science Editors:

Haagenson K. Expression And Regulation Of Map Kinase Phosphatases 1 And 2 In Breast Cancer Tamoxifen Sensitivity. [Doctoral Dissertation]. Wayne State University; 2013. Available from: https://digitalcommons.wayne.edu/oa_dissertations/659

Washington State University

26. [No author]. OVARIAN PHYSIOLOGY IN A NON-DOMESTICATED BIRD: MECHANISMS BEHIND THE ACCUMULATION AND VARIATION OF YOLK ANDROGENS IN HOUSE SPARROWS .

Degree: 2011, Washington State University

URL: http://hdl.handle.net/2376/2919

► In birds and other oviparous species, the accumulation of maternally-derived yolk androgens may represent an adaptive transgenerational information system. Researchers have found multiple effects of… (more)

Subjects/Keywords: GnRH; House sparrows; Maternal effects; Steroidogenic enzymes; Tamoxifen; Yolk androgens

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APA (6^th Edition):

author], [. (2011). OVARIAN PHYSIOLOGY IN A NON-DOMESTICATED BIRD: MECHANISMS BEHIND THE ACCUMULATION AND VARIATION OF YOLK ANDROGENS IN HOUSE SPARROWS . (Thesis). Washington State University. Retrieved from http://hdl.handle.net/2376/2919

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):

author], [No. “OVARIAN PHYSIOLOGY IN A NON-DOMESTICATED BIRD: MECHANISMS BEHIND THE ACCUMULATION AND VARIATION OF YOLK ANDROGENS IN HOUSE SPARROWS .” 2011. Thesis, Washington State University. Accessed February 28, 2021. http://hdl.handle.net/2376/2919.

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

MLA Handbook (7^th Edition):

author], [No. “OVARIAN PHYSIOLOGY IN A NON-DOMESTICATED BIRD: MECHANISMS BEHIND THE ACCUMULATION AND VARIATION OF YOLK ANDROGENS IN HOUSE SPARROWS .” 2011. Web. 28 Feb 2021.

Vancouver:

author] [. OVARIAN PHYSIOLOGY IN A NON-DOMESTICATED BIRD: MECHANISMS BEHIND THE ACCUMULATION AND VARIATION OF YOLK ANDROGENS IN HOUSE SPARROWS . [Internet] [Thesis]. Washington State University; 2011. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/2376/2919.

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

Council of Science Editors:

author] [. OVARIAN PHYSIOLOGY IN A NON-DOMESTICATED BIRD: MECHANISMS BEHIND THE ACCUMULATION AND VARIATION OF YOLK ANDROGENS IN HOUSE SPARROWS . [Thesis]. Washington State University; 2011. Available from: http://hdl.handle.net/2376/2919

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

University of Illinois – Chicago

27. Patel, Hitisha K. Novel Approaches to Endocrine Therapy in Endocrine-Independent Breast Cancer.

Degree: 2016, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/20928

► Tamoxifen, an antagonist at estrogen receptor alpha (ERα) in breast tissue, and the prototypical selective estrogen receptor modulator (SERM), is the standard of care for… (more)

▼ Tamoxifen, an antagonist at estrogen receptor alpha (ERα) in breast tissue, and the prototypical selective estrogen receptor modulator (SERM), is the standard of care for many patients with ER-positive breast cancer. However, continued tamoxifen treatment increases the risk of endometrial cancer and half of ER-positive breast cancer patients do not respond or relapse on treatment with tamoxifen. Tamoxifen-resistant tumors are often ER-positive and endocrine-independent and therefore resistant to aromatase inhibitors. Recent clinical trials have shown the efficacy of estrogen in patients who have undergone exhaustive tamoxifen therapy. Therefore, we propose the development of small molecules that mimic the actions of estradiol in ER-positive breast cancer without the uterotrophic actions of estradiol and tamoxifen: Selective human Estrogen Receptor Partial Agonists (ShERPAs). Evidence suggest that a significant subset of ER-positive breast cancers, over-expressing PKCα, and tamoxifen-resistant cancers will respond to ShERPAs. In order to design and optimize ShERPAs, tamoxifen-resistant cell lines, MCF-7:5C, T47D:A18/PKCα and T47D:A18-Tam1 were studied. The activation of classical ERα signaling by the estrogen mimics was profiled in MCF-7 cells and cell viability in 2D culture was examined. Interestingly, it was found that in MCF-7:5C cells, ShERPA induced cell death was mediated by activation of classical ERα signaling. In an effort to increase throughput and mimic the in vivo environment more closely, we assessed the ShERPAs in a new 3D spheroid model as well. ShERPAs caused decreased spheroid viability in all three models of tamoxifen resistance. Extranuclear localization of ERα after ShERPA treatment was observed. Three promising ShERPAs were evaluated in xenograft models of TAM-resistant, PKCα overexpressing breast cancer. While E2 caused regression of these tumors, a significant increase in uterine weight as predicted was observed. More importantly, ShERPA treated mice had negligible increase in uterine weight underlining the enhanced safety of these molecules. This work suggests that development of ShERPAs that retain the beneficial properties of estrogen while limiting the side effects is a feasible strategy for the treatment of tamoxifen resistant breast cancer. Advisors/Committee Members: Thatcher, Gregory (advisor), Bolton, Judy (committee member), Tonetti, Debra (committee member), Moore, Terry (committee member), Thomas, Douglas (committee member).

Subjects/Keywords: Breast cancer; estrogen receptor; tamoxifen resistance; partial agonists; therapeutics

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

APA (6^th Edition):

Patel, H. K. (2016). Novel Approaches to Endocrine Therapy in Endocrine-Independent Breast Cancer. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/20928

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):

Patel, Hitisha K. “Novel Approaches to Endocrine Therapy in Endocrine-Independent Breast Cancer.” 2016. Thesis, University of Illinois – Chicago. Accessed February 28, 2021. http://hdl.handle.net/10027/20928.

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

MLA Handbook (7^th Edition):

Patel, Hitisha K. “Novel Approaches to Endocrine Therapy in Endocrine-Independent Breast Cancer.” 2016. Web. 28 Feb 2021.

Vancouver:

Patel HK. Novel Approaches to Endocrine Therapy in Endocrine-Independent Breast Cancer. [Internet] [Thesis]. University of Illinois – Chicago; 2016. [cited 2021 Feb 28]. Available from: http://hdl.handle.net/10027/20928.

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

Council of Science Editors:

Patel HK. Novel Approaches to Endocrine Therapy in Endocrine-Independent Breast Cancer. [Thesis]. University of Illinois – Chicago; 2016. Available from: http://hdl.handle.net/10027/20928

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

University of Manchester

28. O'Brien, Ciara. Breast Cancer Initiating Cells in Tamoxifen Treatment and Resistance.

Degree: 2012, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:162494

► Resistance to endocrine treatments in oestrogen receptor positive (ER+) breast cancer (BC) significantly contribute to patient morbidity and mortality. ER+ BC constitute 60% of all… (more)

▼ Resistance to endocrine treatments in oestrogen receptor positive (ER+) breast cancer (BC) significantly contribute to patient morbidity and mortality. ER+ BC constitute 60% of all breast cancers although there is considerable clinico-pathological diversity within this group. Breast cancer initiating cells (BCICs) are implicated in tumour relapse and metastasis and are postulated to drive resistance to standard anti-cancer therapies. However little is known about the sensitivity of BCICs to endocrine therapies. We assessed the effect of tamoxifen treatment and acquired tamoxifen resistance on BCIC frequency in vitro and in vivo using breast cancer cell lines and, importantly, patient derived samples of early and metastatic ER+ breast cancer.In ER+ breast cancer, BCICs may be prospectively enriched in vitro by selecting cells by CD44+/CD24lo/ESA+ phenotype or by mammosphere initiating capacity (MIC). However the gold standard assay to determine BCIC frequency is limiting dilution transplantation in vivo. In the past it has been historically difficult to generate xenograft models of ER+ breast cancer using patient samples. In this thesis, using a novel experimental technique, patient-derived xenografts (PDX) of early and metastatic ER+ BC were generated with almost 85% efficiency in NOD/SCID IL2gammaR-/- (NSG) mice. PDX expressed ER and were able to undergo serial in vivo passage, matching the phenotype of the tumour from which they were derived. In this work, two patterns of response to tamoxifen treatment were observed in ER+ cell lines, patient derived breast cancer samples and xenografts during BCIC assays in vitro and in vivo; Limited Sensitivity (LS) or Resistance (R). In the LS group there was no change or a significant diminution in BCIC frequency in the presence of tamoxifen. In the R group, a significant increase in BCIC frequency was observed in the presence of tamoxifen. Furthermore BCIC activity was shown be enhanced by the acquisition of tamoxifen resistance using cell line models. Cellular populations enriched for BCICs in ER+ cell lines were shown to express low levels of ER compared to non-BCICs. Finally Notch (gamma-secretase inhibitor) and EGFR (gefitinib) pathway inhibitors were tested alone or in combination with tamoxifen against a panel of established and novel cell lines and ER+ patient-derived breast cancer samples for anti-BCIC activity.Tamoxifen treatment can increase BCIC frequency in vitro assays of cell lines and patient-derived samples and in vivo using patient-derived xenografts of ER+ breast cancer. However phenotypic diversity of BCIC may be present within the ER+ BC population. A pharmaceutical strategy to effectively treat BCICs alongside standard endocrine therapy is necessary for the effective future treatment of ER+ breast cancer. Advisors/Committee Members: Clarke, Robert.

Subjects/Keywords: breast cancer; tamoxifen; stem cell; treatment resistance; xenograft; oestrogen receptor

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

APA (6^th Edition):

O'Brien, C. (2012). Breast Cancer Initiating Cells in Tamoxifen Treatment and Resistance. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:162494

Chicago Manual of Style (16^th Edition):

O'Brien, Ciara. “Breast Cancer Initiating Cells in Tamoxifen Treatment and Resistance.” 2012. Doctoral Dissertation, University of Manchester. Accessed February 28, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:162494.

MLA Handbook (7^th Edition):

O'Brien, Ciara. “Breast Cancer Initiating Cells in Tamoxifen Treatment and Resistance.” 2012. Web. 28 Feb 2021.

Vancouver:

O'Brien C. Breast Cancer Initiating Cells in Tamoxifen Treatment and Resistance. [Internet] [Doctoral dissertation]. University of Manchester; 2012. [cited 2021 Feb 28]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:162494.

Council of Science Editors:

O'Brien C. Breast Cancer Initiating Cells in Tamoxifen Treatment and Resistance. [Doctoral Dissertation]. University of Manchester; 2012. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:162494

29. Abu Rabi Zaki. Significance of biological heterogeneity of breast carcinomas in response to antiestrogen therapy.

Degree: PhD, Biology, 2010, University of Belgrade

URL: http://dx.doi.org/10.2298/BG20100618ABURABI ; http://eteze.bg.ac.rs/application/showtheses?thesesId=594 ; https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=1024545458

►

Analysis of biological heterogeneity of estrogen-dependant primary operable breast cancer in postmenopausal patients treated with tamoxifen, had, as а goal, analysis of its significance in… (more)

▼

Analysis of biological heterogeneity of estrogen-dependant primary operable breast cancer in postmenopausal patients treated with tamoxifen, had, as а goal, analysis of its significance in determining clinical course of disease. Biological heterogeneity of cancers in this group of patients has been determined based on molecular biomarkers of tumor growth: ER, PR, Her-2, Ki-67, apoptotic index, and markers of invasiveness and metastatic potential of malignant tumor cells uP А, Р AI -1 and VEGF. Determination of new high risk phenotypes was conducted in three time periods of clinical course of disease follow-up: in first 2.5 years of treatment to determine early (de novo) resistance, period between 2.5 and 5 years, in order to define acquired resistance, and 12 years of follow-up in order to determine biomarker prognostic value. In this study, analysis was conducted on 127 patients diagnosed with primary operable breast cancer. After surgical treatment, all the patients were treated with tamoxifen during five years. Steroid receptors were determined by classical biochemical method, Her2 amplification was determined using chromogen in situ hybridization (CISH), levels of Ki-67 antigen were determined using immnohistochemistry, apoptotic index by using TUNEL method, while ELISA test were used to determine protein levels of uPA, PAI-1 and VEGF. Follow-up on clinical course of disease in patients treated with tamoxifen in first 2.5 years had shown that, out of clinical-pathological parameters it is the size of tumor, and in biomarkers it is ER, PR, иРА and PAI-1 that have predictive role. Tumors that are larger than 2 cm, negative status of ER (<5 fmol/mg), PR (<5 fmol/mg) and PAI-1(<4.5 ng/mg), define the worse response to tamoxifen in patients. Positive status of uPA (0.26 ng/mg≥) defmes а subgroup of patients with poor response to therapy. Unitizing of unfavoraЬle characteristics reveals phenotypes with even worse course of disease, indicating de novo resistance. In 2.5 to 5 years period of treatment, amplification of Her2 in tumors equal or larger than 2cm is indicator of acquired resistance in tamoxifen therapy. The subgroups that were proven to be high-risk for the period of first 2.5 years, do not show the same risk in period of2.5 to 5 years. Prognostic value of parameters, observed in period of 12 years, reveals that the patients older then 66 years have significantly worse prognosis, regardless of status of clinical-pathological parameters and molecular biomarkers. Positive status of ER (5 fmol/mg≥), PAI-1 (2.11 ng/mg≥) and VEGF (571 .8 pg/mg≥) are indicators of low risk patients groups. These results have show to us that reactions between biomarkers, signal pathways in the time of making diagnosis, can signify the time of resistance appearing as well as distant metastasis.

Karcinom dojke, kao najčešći oblik malignih tumora koji se javlja kod žena, spada u grupu heterogenih oboljenja zbog čega je veoma teško utvrditi tok bolesti i uspeh potencijalne terapije. Danas endokrina terapija tamoksifenom…

Subjects/Keywords: breast cancer; tamoxifen; resistance; kancer dojke; tamoksifen; rezistencija

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APA (6^th Edition):

Zaki, A. R. (2010). Significance of biological heterogeneity of breast carcinomas in response to antiestrogen therapy. (Doctoral Dissertation). University of Belgrade. Retrieved from http://dx.doi.org/10.2298/BG20100618ABURABI ; http://eteze.bg.ac.rs/application/showtheses?thesesId=594 ; https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=1024545458

Chicago Manual of Style (16^th Edition):

Zaki, Abu Rabi. “Significance of biological heterogeneity of breast carcinomas in response to antiestrogen therapy.” 2010. Doctoral Dissertation, University of Belgrade. Accessed February 28, 2021. http://dx.doi.org/10.2298/BG20100618ABURABI ; http://eteze.bg.ac.rs/application/showtheses?thesesId=594 ; https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=1024545458.

MLA Handbook (7^th Edition):

Zaki, Abu Rabi. “Significance of biological heterogeneity of breast carcinomas in response to antiestrogen therapy.” 2010. Web. 28 Feb 2021.

Vancouver:

Zaki AR. Significance of biological heterogeneity of breast carcinomas in response to antiestrogen therapy. [Internet] [Doctoral dissertation]. University of Belgrade; 2010. [cited 2021 Feb 28]. Available from: http://dx.doi.org/10.2298/BG20100618ABURABI ; http://eteze.bg.ac.rs/application/showtheses?thesesId=594 ; https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=1024545458.

Council of Science Editors:

Zaki AR. Significance of biological heterogeneity of breast carcinomas in response to antiestrogen therapy. [Doctoral Dissertation]. University of Belgrade; 2010. Available from: http://dx.doi.org/10.2298/BG20100618ABURABI ; http://eteze.bg.ac.rs/application/showtheses?thesesId=594 ; https://fedorabg.bg.ac.rs/fedora/get/o:6759/bdef:Content/get ; http://vbs.rs/scripts/cobiss?command=SEARCH&base=99999&select=ID=1024545458

University of California – San Francisco

30. Tchu, Simone Ming. Tamoxifen Pharmacogenetics: CYP2D6 and Other Variables Influencing Tamoxifen and Tamoxifen Metabolite Exposure.

Degree: Pharmaceutical Sciences and Pharmacogenomics, 2013, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/96r0s5cw

► Tamoxifen is a selective estrogen receptor modulator (SERM) that is used for the treatment of estrogen receptor positive (ER+) breast cancer, most commonly as an… (more)

▼ Tamoxifen is a selective estrogen receptor modulator (SERM) that is used for the treatment of estrogen receptor positive (ER+) breast cancer, most commonly as an adjuvant for the prevention of disease recurrence. Several retrospective studies suggest that functional CYP2D6 polymorphisms are associated with the clinical outcome of tamoxifen adjuvant therapy; variants that confer reduced enzymatic activity are associated with poorer outcomes. The biological basis for this association is that tamoxifen is a pro-drug and CYP2D6 metabolism is important for the formation of the potent anti-estrogenic metabolite, endoxifen. The general goal of this work was to investigate the effect of CYP2D6 polymorphisms and other variables on tamoxifen and tamoxifen metabolite exposure in order to clarify the best use of clinical tamoxfien pharmacogenetic test data. An LC-MS/MS assay was developed and validated for the quantitation of tamoxifen, N-desmethyltamoxifen, and endoxifen in human serum. The assay was found to be robust for the measurement of these analytes at physiologically relevant concentrations. In collaboration with the Women's Healthy Eating and Living (WHEL) study group, serum endoxifen concentrations were shown to be associated with the clinical outcome of tamoxifen adjuvant therapy, and a sub-therapeutic endoxifen risk group was defined. Extensive CYP2D6 genotypes were determined for WHEL study subjects using the Roche P450 AmpliChip, and an analysis was performed to determine the extent to which genotype cutoffs define the sub-therapeutic endoxifen risk group among Caucasian subjects. Of subjects who carried two null CYP2D6 alleles, approximately 72% fell into the sub-therapeutic endoxifen risk group, but this accounted for less than a quarter of all subjects within the risk group. Poor metabolizer phenocopies were present in all genotype groups. In addition, inter-ethnic differences in serum tamoxifen and tamoxifen metabolites were determined between Caucasian, Asian, Hispanic, and African American subjects within the WHEL cohort, with Asians and Hispanics exhibiting higher median endoxifen concentrations. Finally, an association study was performed in order to determine if variants in candidate genes (UGT2B7, ABCC2, CYP2C19) influence serum endoxifen concentrations in Caucasian subjects. Statistically significant associations were determined, but are unlikely to be clinically relevant due to small effect.

Subjects/Keywords: Pharmaceutical sciences; Genetics; Breast Cancer; CYP2D6; Endoxifen; Pharmacogenetics; Tamoxifen

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

APA (6^th Edition):

Tchu, S. M. (2013). Tamoxifen Pharmacogenetics: CYP2D6 and Other Variables Influencing Tamoxifen and Tamoxifen Metabolite Exposure. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/96r0s5cw

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):

Tchu, Simone Ming. “Tamoxifen Pharmacogenetics: CYP2D6 and Other Variables Influencing Tamoxifen and Tamoxifen Metabolite Exposure.” 2013. Thesis, University of California – San Francisco. Accessed February 28, 2021. http://www.escholarship.org/uc/item/96r0s5cw.

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

MLA Handbook (7^th Edition):

Tchu, Simone Ming. “Tamoxifen Pharmacogenetics: CYP2D6 and Other Variables Influencing Tamoxifen and Tamoxifen Metabolite Exposure.” 2013. Web. 28 Feb 2021.

Vancouver:

Tchu SM. Tamoxifen Pharmacogenetics: CYP2D6 and Other Variables Influencing Tamoxifen and Tamoxifen Metabolite Exposure. [Internet] [Thesis]. University of California – San Francisco; 2013. [cited 2021 Feb 28]. Available from: http://www.escholarship.org/uc/item/96r0s5cw.

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

Council of Science Editors:

Tchu SM. Tamoxifen Pharmacogenetics: CYP2D6 and Other Variables Influencing Tamoxifen and Tamoxifen Metabolite Exposure. [Thesis]. University of California – San Francisco; 2013. Available from: http://www.escholarship.org/uc/item/96r0s5cw

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

Open Access Theses and Dissertations