subject:(Mammary cancer)

Penn State University

1. Mathers, Jessica. TRACKING MAMMARY EPITHELIAL CELL LINEAGE AND CELL DIVISIONS IN THE NORMAL MAMMARY GLAND AND MAMMARY NEOPLASIA USING TRANSGENIC MICE .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/12179

► With as many as 1 in 8 women diagnosed with breast cancer in their lifetime, breast cancer is the most commonly diagnosed cancer in women… (more)

▼ With as many as 1 in 8 women diagnosed with breast cancer in their lifetime, breast cancer is the most commonly diagnosed cancer in women in the Western Hemisphere and the second most common cause of cancer-related death in females. Decades of study have uncovered causative exposures and mutations that transform normal mammary epithelial cells (MECs) into breast cancer cells. Nonetheless, the cellular mechanisms that define the clinical behavior of breast cancers remain incompletely defined. Lineage commitment pathways yield diverse MEC cell types within the breast, and recent findings suggest these MEC lineage hierarchies may persist within breast cancers, perhaps helping to explain the cellular heterogeneity seen in tumors. To extend these studies, models are needed that permit cell fate tracking in the discrete MEC compartments of both normal and malignant mammary tissue. In this work, we describe novel transgenic mouse models that permit temporally-regulated, MEC compartment-restricted expression of a histone-fused eGFP (H2B-eGFP) reporter in both normal and malignant mammary epithelium. Transactivator transgenes expressed in either the luminal or basal layer of mammary ducts drove widespread H2B-eGFP labeling of luminal or basal MECs, respectively. We tested whether the H2B-eGFP reporter could be used to track cell divisions within labeled MEC compartments. Indeed, when H2B-eGFP transgene expression was switched off in pulse-chase experiments, washout of label depended on partitioning of labeled histones between daughter cells during MEC proliferation. Moreover, the H2B-eGFP nuclear label was readily detectable in live MECs, enabling live cell imaging of MECs propagated in culture. H2B-eGFP labeling was used for short-term lineage tracing of MECs during lobuloalveolar development. Hormones of pregnancy trigger the development of bi-layered alveolar outgrowths that are believed to arise from luminal progenitor cells. Contrasting with this model, we found that labeled cells from both the luminal and basal MEC compartments contribute to alveolar outgrowths. Furthermore, both luminal and basal MECs proliferated while contributing to alveologenesis, and did not merely migrate into alveoli or become incorporated as “bystanders”. These findings clarify a lineage commitment pathway operative during a key, hormonally-driven stage of mammary gland development. In separate studies, we labeled either basal or luminal MECs residing in the secretory epithelium of lactating mice to examine whether a subset of these MECs persist throughout the mammary gland remodeling program triggered by weaning. Remarkably, substantial numbers of both luminal and basal MECs survived mammary gland involution and contributed to remodeled ducts. These findings have implications for understanding how a lactation-involution cycle protects against breast cancer in rodents and humans. In other studies, the H2B-eGFP labeling strategy was applied in the context of Wnt1-driven transgenic mouse models of breast cancer. Here, we sought to use pulse-chase… Advisors/Committee Members: Edward Joseph Gunther, Dissertation Advisor/Co-Advisor, Edward Joseph Gunther, Committee Chair/Co-Chair, Sarah Bronson, Committee Member, Gary Alan Clawson, Committee Member, Jiyue Zhu, Committee Member.

Subjects/Keywords: mammary stem cell; breast cancer; mammary gland

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

APA (6^th Edition):

Mathers, J. (2011). TRACKING MAMMARY EPITHELIAL CELL LINEAGE AND CELL DIVISIONS IN THE NORMAL MAMMARY GLAND AND MAMMARY NEOPLASIA USING TRANSGENIC MICE . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/12179

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):

Mathers, Jessica. “TRACKING MAMMARY EPITHELIAL CELL LINEAGE AND CELL DIVISIONS IN THE NORMAL MAMMARY GLAND AND MAMMARY NEOPLASIA USING TRANSGENIC MICE .” 2011. Thesis, Penn State University. Accessed March 04, 2021. https://submit-etda.libraries.psu.edu/catalog/12179.

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

MLA Handbook (7^th Edition):

Mathers, Jessica. “TRACKING MAMMARY EPITHELIAL CELL LINEAGE AND CELL DIVISIONS IN THE NORMAL MAMMARY GLAND AND MAMMARY NEOPLASIA USING TRANSGENIC MICE .” 2011. Web. 04 Mar 2021.

Vancouver:

Mathers J. TRACKING MAMMARY EPITHELIAL CELL LINEAGE AND CELL DIVISIONS IN THE NORMAL MAMMARY GLAND AND MAMMARY NEOPLASIA USING TRANSGENIC MICE . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Mar 04]. Available from: https://submit-etda.libraries.psu.edu/catalog/12179.

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

Council of Science Editors:

Mathers J. TRACKING MAMMARY EPITHELIAL CELL LINEAGE AND CELL DIVISIONS IN THE NORMAL MAMMARY GLAND AND MAMMARY NEOPLASIA USING TRANSGENIC MICE . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/12179

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

University of Adelaide

2. Noor Din, Siti Mariam. Effect of C1q null mutation on mammary gland development and breast cancer susceptibility.

Degree: 2017, University of Adelaide

URL: http://hdl.handle.net/2440/113260

► The complement protein C1q promotes rapid macrophage-mediated clearance of dying cells and tolerance to self antigens. mRNA encoding C1q is a key gene upregulated during… (more)

▼ The complement protein C1q promotes rapid macrophage-mediated clearance of dying cells and tolerance to self antigens. mRNA encoding C1q is a key gene upregulated during mammary gland regression, and we hypothesise that C1q complement protein promotes mammary gland tumourigenesis through induction of tolerance to tumour antigens. We have investigated the role of C1q in normal mammary gland development, hormone-mediated regression, and in tumour development using two different mammary tumour mouse models together with C1q ⁻ʹ⁻ mice. In the absence of C1q, mammary gland development proceeds normally during puberty, with a similar abundance of terminal end buds and rate of epithelial cell proliferation at 6 weeks of age compared to wildtype C1q ⁺ʹ⁺ mice. However, deficiency in C1q perturbed mammary gland regression, with 45% increased number of ductal branch points 24 hours following progesterone receptor antagonist RU486 (also known as mifepristone)-induced epithelial cell apoptosis in C1q ⁻ʹ⁻ mice compared to C1q ⁺ʹ⁺ mice (p=0.027, n=7-11). There was a reduction of macrophage abundance (p=0.002, n=6-7) and a 3.5-fold increase of TUNEL positive apoptotic cells (p=0.011, n=5-6) in the ductal epithelium of C1q ⁻ʹ⁻ mice compared to C1q ⁺ʹ⁺ mice 24 hours following RU486 administration. To investigate the role of C1q in mammary tumour development, MMTV-PyMT transgenic mice were crossed with C1q ⁻ʹ⁻ mice and monitored weekly from 6 weeks by palpation to determine tumour latency, and mammary tumours dissected to assess total tumour burden. Lack of C1q did not affect development of mammary hyperplasia at 10 weeks, however development of palpable tumours was increased by 1 week in PyMT⁺/C1q ⁻ʹ⁻ mice compared to PyMT⁺/C1q ⁺ʹ⁺ mice (p=0.012, n=43-45). The number of tumours was significantly reduced in 15-week old PyMT⁺/C1q ⁻ʹ⁻ mice compared to PyMT⁺/C1q ⁺ʹ⁺ mice (p=0.028, n=15-16). There was also a significant reduction in the total tumour burden in PyMT⁺/C1q ⁻ʹ⁻ mice compared to PyMT⁺/C1q ⁺ʹ⁺ mice at 15 weeks of age (p=0.036, n=15-16). The frequency of tumours that had progressed to carcinoma stage was also reduced in PyMT⁺/C1q ⁻ʹ⁻ mice at 15 weeks of age (p=0.05, n=11-15) and 18 weeks of age (p=0.003, n=28-29). Carcinogen-induced mammary tumourigenesis was also investigated in mice administered 7,12-dimethylbenz[α]anthracene (DMBA) by oral gavage for 6 weeks. DMBA-treated C1q ⁻ʹ⁻ mice were highly resistant to mammary tumourigenesis, with tumours detected in only 2 of 20 mice over the 30 week monitoring period, compared to 10 of 20 DMBA-treated C1q ⁺ʹ⁺ mice (p=0.02). T lymphocytes were skewed to the CD4⁺ subset, with a significant increase in IFNG-producing CD4⁺ T cells in the mammary gland draining lymph nodes in DMBA-treated C1q ⁻ʹ⁻ mice (p=0.014, n=6-10). These findings suggest that C1q promotes tissue remodeling and clearance of dying cells during mammary gland regression, and increases mammary cancer susceptibility and tumour progression. Advisors/Committee Members: Ingman, Wendy Vanessa (advisor), Robertson, Sarah Anne (advisor), Adelaide Medical School (school).

Subjects/Keywords: C1q; mammary gland; breast cancer

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APA (6^th Edition):

Noor Din, S. M. (2017). Effect of C1q null mutation on mammary gland development and breast cancer susceptibility. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/113260

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):

Noor Din, Siti Mariam. “Effect of C1q null mutation on mammary gland development and breast cancer susceptibility.” 2017. Thesis, University of Adelaide. Accessed March 04, 2021. http://hdl.handle.net/2440/113260.

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

MLA Handbook (7^th Edition):

Noor Din, Siti Mariam. “Effect of C1q null mutation on mammary gland development and breast cancer susceptibility.” 2017. Web. 04 Mar 2021.

Vancouver:

Noor Din SM. Effect of C1q null mutation on mammary gland development and breast cancer susceptibility. [Internet] [Thesis]. University of Adelaide; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/2440/113260.

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

Council of Science Editors:

Noor Din SM. Effect of C1q null mutation on mammary gland development and breast cancer susceptibility. [Thesis]. University of Adelaide; 2017. Available from: http://hdl.handle.net/2440/113260

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

University of New South Wales

3. Junankar, Simon. The role of inhibitor of DNA binding 4 (Id4) in mammary gland development and breast cancer.

Degree: Garvan Institute of Medical Research, 2012, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/52241 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10911/SOURCE01?view=true

► The inhibitor of DNA binding (Id) proteins Id1-4 are transcriptional regulators that control many cell fate and developmental processes and are often deregulated in cancer.… (more)

▼ The inhibitor of DNA binding (Id) proteins Id1-4 are transcriptional regulators that control many cell fate and developmental processes and are often deregulated in cancer. In this dissertation I examine the role of Id proteins in mammary development and neoplasia. Initially the role of Id1 in regulating the immune response to senescent tumour cells was examined, before a more thorough investigation into the role of Id4 during mammary gland development and breast cancer. Prior to the studies described in this thesis, the role for Id4 during mammary gland development had not been investigated and its role in breast cancer was controversial. Id4 expression patterns in the mammary gland were analysed throughout development by immunohistochemistry and the phenotype of Id4 loss was determined using the Id4 knockout mouse. The function of Id4 was further analysed using the normal mouse mammary epithelial cell line Comma-Db. Id4 expression was examined in breast cancer cell lines and a number of cohorts of breast cancer patients. The results presented here show that Id4 is a critical regulator of mammary gland development through its control of differentiation, proliferation and extracellular matrix (ECM) remodelling pathways. Id4 expression is restricted to the myoepithelial cells of the mammary gland and its loss leads to impaired mammary gland development. Overexpression and knockdown studies utilising the Comma-Db cells demonstrated that Id4 inhibited luminal differentiation and was required for cell proliferation. Furthermore Id4 overexpression promoted neoplastic transformation of the normal Comma-Db cell line in vivo. Transcript profiling experiments further demonstrated Id4 regulated a number of ECM remodelling genes. Our results from examining patient cohorts demonstrate that Id4 expression associates with the Her2 and basal-like subtypes of breast cancer and that high expression significantly correlates with improved patient survival. Despite high Id4 expression associating with improved survival, our combined results demonstrate that Id4 nonetheless has the capacity to promote tumourigenesis. Advisors/Committee Members: Swarbrick, Alexander, Garvan Institute of Medical Research, Faculty of Medicine, UNSW, Ormandy, Christopher, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.

Subjects/Keywords: Development; Mammary; Breast; Cancer

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APA (6^th Edition):

Junankar, S. (2012). The role of inhibitor of DNA binding 4 (Id4) in mammary gland development and breast cancer. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52241 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10911/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Junankar, Simon. “The role of inhibitor of DNA binding 4 (Id4) in mammary gland development and breast cancer.” 2012. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/52241 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10911/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Junankar, Simon. “The role of inhibitor of DNA binding 4 (Id4) in mammary gland development and breast cancer.” 2012. Web. 04 Mar 2021.

Vancouver:

Junankar S. The role of inhibitor of DNA binding 4 (Id4) in mammary gland development and breast cancer. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/52241 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10911/SOURCE01?view=true.

Council of Science Editors:

Junankar S. The role of inhibitor of DNA binding 4 (Id4) in mammary gland development and breast cancer. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52241 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:10911/SOURCE01?view=true

University of Louisville

4. Le, Saasha. Congenic and functional analysis of rat mammary cancer susceptibility.

Degree: PhD, 2016, University of Louisville

URL: 10.18297/etd/2379 ; https://ir.library.louisville.edu/etd/2379

► Breast cancer is a complex disease affected by genetic, epigenetic and environmental factors. The genetic architecture of breast cancer comprises of high to low… (more)

Subjects/Keywords: rat; mammary cancer susceptibility; Mcs; genetics; Genetics

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APA (6^th Edition):

Le, S. (2016). Congenic and functional analysis of rat mammary cancer susceptibility. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/2379 ; https://ir.library.louisville.edu/etd/2379

Chicago Manual of Style (16^th Edition):

Le, Saasha. “Congenic and functional analysis of rat mammary cancer susceptibility.” 2016. Doctoral Dissertation, University of Louisville. Accessed March 04, 2021. 10.18297/etd/2379 ; https://ir.library.louisville.edu/etd/2379.

MLA Handbook (7^th Edition):

Le, Saasha. “Congenic and functional analysis of rat mammary cancer susceptibility.” 2016. Web. 04 Mar 2021.

Vancouver:

Le S. Congenic and functional analysis of rat mammary cancer susceptibility. [Internet] [Doctoral dissertation]. University of Louisville; 2016. [cited 2021 Mar 04]. Available from: 10.18297/etd/2379 ; https://ir.library.louisville.edu/etd/2379.

Council of Science Editors:

Le S. Congenic and functional analysis of rat mammary cancer susceptibility. [Doctoral Dissertation]. University of Louisville; 2016. Available from: 10.18297/etd/2379 ; https://ir.library.louisville.edu/etd/2379

Vanderbilt University

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

Degree: PhD, Pathology, 2018, Vanderbilt University

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

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

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

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

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

APA (6^th Edition):

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

Chicago Manual of Style (16^th Edition):

Ludwik, Katarzyna Anna. “RSKy Business in the Mammary Gland.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/11180.

MLA Handbook (7^th Edition):

Ludwik, Katarzyna Anna. “RSKy Business in the Mammary Gland.” 2018. Web. 04 Mar 2021.

Vancouver:

Ludwik KA. RSKy Business in the Mammary Gland. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/11180.

Council of Science Editors:

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

University of Manchester

6. Jobling, Stephanie. The Notch and EDAR signalling pathways in mammary gland development and tumourigenesis.

Degree: 2011, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:126178

► Worldwide, more than 1,000,000 women develop breast cancer each year, and more than 400,000 die because of it. Basal-like breast cancers, which account for 8%… (more)

▼ Worldwide, more than 1,000,000 women develop breast cancer each year, and more than 400,000 die because of it. Basal-like breast cancers, which account for 8% to 20% of all breast cancer cases, represent the most aggressive of breast cancers with the majority resistant to existing targeted therapies. Accumulating lines of evidence implicate the Notch pathway in the aetiology of these basal-like breast cancers; while current work in our lab supports the notion that signalling through the Ectodermal Dysplasin Receptor (EDAR) pathway is also important. Notch signalling functions in normal development to control cell fate decisions and is mediated primarily, although not exclusively, through the CBF1 / RBP-Jĸ transcription factor. Aberrant Notch signalling leads to mammary tumourigenesis in mice; however at the outset of this work it was unclear whether signalling through RBP-Jĸ and / or through alternative pathways is required. This thesis presents novel data showing that elevated Notch signalling through the RBP-Jĸ-dependent pathway alone in murine mammary glands causes a number of developmental defects, including reduced ductal outgrowth, increased ductal side branching at puberty and, most significantly, is sufficient to induce mammary tumourigenesis. The data presented also provide supporting evidence that Notch signalling through RBP-Jĸ likely contributes to tumourigenesis, at least in part, via the suppression of apoptosis. At the outset of this thesis far less was known regarding the role(s) of the EDAR pathway within the mammary gland. Despite its recognised function in the development of ectodermal appendages it has been predominantly studied in the context of hair and tooth development. We show here that elevated Edar signalling affects the morphology of numerous ectodermally-derived glands, including the mammary gland, where in general, it results in glands that are enlarged or more elaborately branched. Most significantly, we show that elevated Edar signalling causes mammary tumourigenesis in mice, and provide data to support the hypothesis that elevated EDAR signalling might also be important in a subset of basal-like breast cancers in humans. The murine mammary gland phenotypes seen in response to elevated Edar signalling, including the squamous metaplasia within Edar-induced tumours, are very similar to those observed when Wnt signalling is increased. We provide data to support a positive correlation between activation of the EDAR and Wnt pathways in murine mammary tumourigenesis and provide data to support a comparable interaction in the aetiology of basal-like breast cancer showing squamous differentiation in humans. In summary, this thesis identifies the EDAR pathway as a novel potential therapeutic target in the treatment of a subset of basal-like breast cancers, and provides evidence that signalling through the RBP-Jĸ-dependent Notch pathway is sufficient to induce mammary tumourigenesis, most likely through the suppression of apoptosis. Advisors/Committee Members: Brennan, Keith.

Subjects/Keywords: Notch; Edar; Breast cancer; Mammary gland

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APA (6^th Edition):

Jobling, S. (2011). The Notch and EDAR signalling pathways in mammary gland development and tumourigenesis. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:126178

Chicago Manual of Style (16^th Edition):

Jobling, Stephanie. “The Notch and EDAR signalling pathways in mammary gland development and tumourigenesis.” 2011. Doctoral Dissertation, University of Manchester. Accessed March 04, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:126178.

MLA Handbook (7^th Edition):

Jobling, Stephanie. “The Notch and EDAR signalling pathways in mammary gland development and tumourigenesis.” 2011. Web. 04 Mar 2021.

Vancouver:

Jobling S. The Notch and EDAR signalling pathways in mammary gland development and tumourigenesis. [Internet] [Doctoral dissertation]. University of Manchester; 2011. [cited 2021 Mar 04]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:126178.

Council of Science Editors:

Jobling S. The Notch and EDAR signalling pathways in mammary gland development and tumourigenesis. [Doctoral Dissertation]. University of Manchester; 2011. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:126178

University of Toronto

7. Wright, Katherine Louise. Stat3 Enhances Metastatic Dissemination of Pik3ca and Ras-induced Mammary Tumors.

Degree: PhD, 2014, University of Toronto

URL: http://hdl.handle.net/1807/94536

►

Most human breast tumors harbor mutations in the phosphatidylinositol 3' kinase (PI3K) pathway. Recent studies have also highlighted the importance of Signal Transducer and Activator… (more)

▼

Most human breast tumors harbor mutations in the phosphatidylinositol 3' kinase (PI3K) pathway. Recent studies have also highlighted the importance of Signal Transducer and Activator of Transcription 3 (Stat3) protein in breast cancer. Stat3 can be phosphorylated on two sites, and these appear to control alternative functions for the protein - transcription and oxidative phosphorylation. Both Stat3 phosphoforms have been implicated in breast cancer: Stat3 phosphorylation on Y705 has been associated with good prognosis in human breast cancer, whereas Stat3 pS727 is elevated in breast cancer stem-like cells and is associated with poor prognosis. Notably, this paradox has yet to be probed biologically, either in a mouse model or through molecular profiling. Also, the role of S727 phosphorylation has not been tested in an in vivo model for breast cancer. Stat3 phosphosite mutants, involving both tyrosine 705 and serine 727, can be used as a platform to help delineate the role of each phosphorylated species. To this end, I generated an allelic series of mice, ectopically expressing wild type or mutant Stat3 cDNAs in response to Cre-recombinase expression. In this way, I was able to probe the role of Stat3 +/-phosphorylation on Y705 or S727 in Pik3ca-induced breast cancer through targeted expression of wild type and mutant alleles to mammary epithelium by crossing R26-Stat3-C, R26-Stat3Y705F-S727E and R26-Stat3wt mice to MMTV-Cre mice, as well as to R26- Pik3camutant mice. Here, I show that Pik3camutant-induced tumors are dependent on Stat3 signaling, and that they can be induced to metastasize at a low frequency through expression of activated Stat3 (Stat3-C). In contrast, tumors induced by transgenic expression of mutant Pik3ca or Stat3-C plus activated K-Ras are highly metastatic. Overall, I have shown that Stat3 is essential for Pik3ca-induced breast cancer, and that it interacts cooperatively with Ras signaling in metastatic dissemination.

2018-06-13 00:00:00

Advisors/Committee Members: Egan, Sean E, Molecular and Medical Genetics.

Subjects/Keywords: cancer; mammary; metastasis; Pik3ca; Ras; Stat3; 0369

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APA (6^th Edition):

Wright, K. L. (2014). Stat3 Enhances Metastatic Dissemination of Pik3ca and Ras-induced Mammary Tumors. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/94536

Chicago Manual of Style (16^th Edition):

Wright, Katherine Louise. “Stat3 Enhances Metastatic Dissemination of Pik3ca and Ras-induced Mammary Tumors.” 2014. Doctoral Dissertation, University of Toronto. Accessed March 04, 2021. http://hdl.handle.net/1807/94536.

MLA Handbook (7^th Edition):

Wright, Katherine Louise. “Stat3 Enhances Metastatic Dissemination of Pik3ca and Ras-induced Mammary Tumors.” 2014. Web. 04 Mar 2021.

Vancouver:

Wright KL. Stat3 Enhances Metastatic Dissemination of Pik3ca and Ras-induced Mammary Tumors. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1807/94536.

Council of Science Editors:

Wright KL. Stat3 Enhances Metastatic Dissemination of Pik3ca and Ras-induced Mammary Tumors. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/94536

University of Minnesota

8. Forsman, Cynthia. Development and Cancer: The role of Twisted Gastrulation in mammary gland development and in cancer.

Degree: PhD, Molecular, Cellular, Developmental Biology and Genetics, 2014, University of Minnesota

URL: http://hdl.handle.net/11299/185180

► It is becoming increasingly clear that the molecular mechanisms that maintain and promote pluripotency during development reemerge as important mediators of tumorigenicity. Bone morphogenetic proteins… (more)

Subjects/Keywords: BMP; Cancer; Mammary gland; Twisted gastrulation

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

APA (6^th Edition):

Forsman, C. (2014). Development and Cancer: The role of Twisted Gastrulation in mammary gland development and in cancer. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/185180

Chicago Manual of Style (16^th Edition):

Forsman, Cynthia. “Development and Cancer: The role of Twisted Gastrulation in mammary gland development and in cancer.” 2014. Doctoral Dissertation, University of Minnesota. Accessed March 04, 2021. http://hdl.handle.net/11299/185180.

MLA Handbook (7^th Edition):

Forsman, Cynthia. “Development and Cancer: The role of Twisted Gastrulation in mammary gland development and in cancer.” 2014. Web. 04 Mar 2021.

Vancouver:

Forsman C. Development and Cancer: The role of Twisted Gastrulation in mammary gland development and in cancer. [Internet] [Doctoral dissertation]. University of Minnesota; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11299/185180.

Council of Science Editors:

Forsman C. Development and Cancer: The role of Twisted Gastrulation in mammary gland development and in cancer. [Doctoral Dissertation]. University of Minnesota; 2014. Available from: http://hdl.handle.net/11299/185180

Clemson University

9. Elliott, Kathryn Adrian. A Comprehensive Model and Modulation of Cellular Signaling Involved in Early Mammary Development and Aggressive Cancer Using a Novel Recombinant Protein of the G3 Domain of Laminin-5.

Degree: PhD, Biological Sciences, 2017, Clemson University

URL: https://tigerprints.clemson.edu/all_dissertations/2071

► The mammary gland is a unique and specialized epidermal organ; mammary organogenesis begins in the embryo but is not fully complete until puberty. As such,… (more)

▼ The mammary gland is a unique and specialized epidermal organ; mammary organogenesis begins in the embryo but is not fully complete until puberty. As such, formation of the mammary gland depends on temporally and spatially regulated developmental steps that require coordination of multiple biological and cell signaling processes; many of which have parallels with cancer development. Research describing the events that occur between birth and puberty is lacking and little is known about human breast development of youth. Since mammary gland development requires a coordinated balance between cell growth, proliferation, and apoptosis, it is critical to understand which signaling pathways are utilized to relay developmental signals, and how these pathways and their targets interact and cooperate with age. Additionally, interactions between integrin molecules and their laminin ligands, especially Laminin-5 (Ln-5; also known as Laminin-332), regulate multiple facets of both embryonic development and tumor growth, invasion, and metastasis.Â Î±6Î²4 integrin serves as a marker to detect distant metastases in the early stages of specific malignanciesÂ andÂ Î²4 integrin overexpression has been found in basal-like breast cancers, correlating with aggressiveness to institute a prognostic Î²4 signature that increases with tumor grade. The mechanismÂ Î±6Î²4 integrin utilizes to modulate oncogenic signaling through association with Ln-5 molecules in the ECM is the basis for the recombinant protein (rG3, the third of five G domains of Ln-5) produced for the work reported in this dissertation.Â Here, it is shown there are specific transcriptional differences and a unique interaction of a gene set over time that contributes to postnatal mammary gland development, and this model clearly shares similarities and signaling pathways with oncogenic development. Especially important are pathways of the adaptive and innate immunities, ECM remodeling and integrin interactions, and extrinsic and intrinsic TP53-mediated apoptosis, greater understanding of which could lead to early detection of potential tumorigenic growth and identification of potential treatment avenues. Presented is a comprehensive model of early mammary development along with several panels of biomarkers that possess a role in normal mammary development, are involved in aggressive cancers, and are affected by apoptosis induced by rG3 treatment. rG3 has proven to be a valuable tool to study apoptotic pathways and the crosstalk among those pathways. Advisors/Committee Members: Dr. Thomas Scott, Committee Chair, Dr. Zhicheng Dou, Dr. Scott Pratt, Dr. William Bridges.

Subjects/Keywords: Breast cancer; Development; Integrin; Laminin; Mammary; TNBC

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APA (6^th Edition):

Elliott, K. A. (2017). A Comprehensive Model and Modulation of Cellular Signaling Involved in Early Mammary Development and Aggressive Cancer Using a Novel Recombinant Protein of the G3 Domain of Laminin-5. (Doctoral Dissertation). Clemson University. Retrieved from https://tigerprints.clemson.edu/all_dissertations/2071

Chicago Manual of Style (16^th Edition):

Elliott, Kathryn Adrian. “A Comprehensive Model and Modulation of Cellular Signaling Involved in Early Mammary Development and Aggressive Cancer Using a Novel Recombinant Protein of the G3 Domain of Laminin-5.” 2017. Doctoral Dissertation, Clemson University. Accessed March 04, 2021. https://tigerprints.clemson.edu/all_dissertations/2071.

MLA Handbook (7^th Edition):

Elliott, Kathryn Adrian. “A Comprehensive Model and Modulation of Cellular Signaling Involved in Early Mammary Development and Aggressive Cancer Using a Novel Recombinant Protein of the G3 Domain of Laminin-5.” 2017. Web. 04 Mar 2021.

Vancouver:

Elliott KA. A Comprehensive Model and Modulation of Cellular Signaling Involved in Early Mammary Development and Aggressive Cancer Using a Novel Recombinant Protein of the G3 Domain of Laminin-5. [Internet] [Doctoral dissertation]. Clemson University; 2017. [cited 2021 Mar 04]. Available from: https://tigerprints.clemson.edu/all_dissertations/2071.

Council of Science Editors:

Elliott KA. A Comprehensive Model and Modulation of Cellular Signaling Involved in Early Mammary Development and Aggressive Cancer Using a Novel Recombinant Protein of the G3 Domain of Laminin-5. [Doctoral Dissertation]. Clemson University; 2017. Available from: https://tigerprints.clemson.edu/all_dissertations/2071

University of Edinburgh

10. Artibani, Mara. WT1 role in mammary gland and breast cancer biology.

Degree: PhD, 2015, University of Edinburgh

URL: http://hdl.handle.net/1842/21036

► The Wilms' Tumour Suppressor gene 1, WT1, encodes for a complex protein which is essential in mammals throughout life. Its roles vary with the developmental… (more)

▼ The Wilms' Tumour Suppressor gene 1, WT1, encodes for a complex protein which is essential in mammals throughout life. Its roles vary with the developmental stages: in the embryo, it regulates the epithelial-mesenchymal balance required for a correct organogenesis and acts as a tumour suppressor; in the adult, it is involved in the maintenance of tissue homeostasis and has been controversially considered as an oncogene. Breast cancer is one of the adult tumours in which WT1 oncogenic function was first hypothesised. This malignancy is the most common in women, with more than one million cases being diagnosed worldwide every year, and represents the leading cause of cancer related deaths. Because of its major health burden, this disease has been extensively studied and special attention has also been paid to normal mammary gland biology: several works have shown that breast cancer can be divided into many molecular subtypes, which may reflect the cell of origin of the tumour; moreover, many genes involved in the normal development of the mammary gland have been proven to also play a role in breast tumorigenesis. WT1 expression has been previously reported in both healthy mammary glands and breast cancer samples, however, its function in this context is not well understood and the evidence gathered so far is extremely contradictory. This thesis aimed to investigate the exact role played by WT1 in both mammary gland and breast cancer biology, using a combination of in vivo and in vitro techniques. Following flow cytometry isolation, Wt1 mRNA expression was detected in the myoepithelial and stem cell subpopulations of the healthy gland. To investigate the effects of WT1 loss, Wt1 conditional mice were crossed with two different mammary specific Cre lines: the knockout animals developed, bred and lactated normally, however, they showed a significant increase of ductular branches during pregnancy, suggesting that WT1 may be involved in the regulation of branching morphogenesis. In order to study WT1 role in mammary tumours, the gene was knocked out in a breast cancer mouse model and knocked down in several breast cancer cell lines, using both constitutive and inducible lentivirus-based systems. WT1 loss did not seem to affect cell proliferation, but resulted in a significant increase in cell migration in vitro and in the upregulation of mesenchymal markers. Furthermore, bioinformatics analysis showed that the WT1-positive tumours mainly belong to the luminal/ER-positive subtypes and express lower levels of mesenchymal markers than the WT1-negative tumours. As a whole, the findings of this thesis characterise WT1 expression in the healthy mammary gland and provide the first evidence of its possible function in this organ; moreover, this work seems to rule out an oncogenic role for WT1 in breast cancer, while suggesting that it could be an upstream regulator of cell migration. Additional experiments are required to confirm this result in vivo and verify whether it could lead to any clinical application.

Subjects/Keywords: 616.99; Wt1; mammary gland; breast cancer

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APA (6^th Edition):

Artibani, M. (2015). WT1 role in mammary gland and breast cancer biology. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/21036

Chicago Manual of Style (16^th Edition):

Artibani, Mara. “WT1 role in mammary gland and breast cancer biology.” 2015. Doctoral Dissertation, University of Edinburgh. Accessed March 04, 2021. http://hdl.handle.net/1842/21036.

MLA Handbook (7^th Edition):

Artibani, Mara. “WT1 role in mammary gland and breast cancer biology.” 2015. Web. 04 Mar 2021.

Vancouver:

Artibani M. WT1 role in mammary gland and breast cancer biology. [Internet] [Doctoral dissertation]. University of Edinburgh; 2015. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1842/21036.

Council of Science Editors:

Artibani M. WT1 role in mammary gland and breast cancer biology. [Doctoral Dissertation]. University of Edinburgh; 2015. Available from: http://hdl.handle.net/1842/21036

University of Louisville

11. denDekker, Aaron D. Genetic mapping and mechanism of action of rat mammary carcinoma susceptibility quantitative trait locus Mcs1b.

Degree: PhD, 2013, University of Louisville

URL: 10.18297/etd/330 ; https://ir.library.louisville.edu/etd/330

► Breast cancer is a complex disease that involves genetic, epigenetic, and environmental components. High and moderate penetrant genes have been identified that affect risk to… (more)

▼ Breast cancer is a complex disease that involves genetic, epigenetic, and environmental components. High and moderate penetrant genes have been identified that affect risk to developing breast cancer; however, these risk alleles are present in a small percentage of breast cancer cases. Low penetrant modifier genes have risk-associated alleles that are common in the population. Although these genes have lower penetrance, it is expected that the majority of genetic risk to developing breast cancer is controlled by common genetic variation. Studying mechanisms of common genetic variants on breast cancer risk is difficult due to their small individual effects and overlapping contribution of other risk factors; thus, animal models are commonly used. The rat mammary carcinoma susceptibility quantitative trait locus (QTL) Mcs1b was identified between mammary carcinoma-resistant Copenhagen (COP) and susceptible Wistar Furth (WF) rats on chromosome 2. This rat QTL is an ortholog of a human breast cancer-associated locus identified on human chromosome 5q; therefore, the rat Mcs1b model can be used to identify mechanisms and causative factors contributing to breast cancer risk associated with human breast cancer-associated locus 5q. The goal of the work presented in this dissertation is to identify quality candidate breast cancer risk genetic elements associated with the rat Mcs1b locus. This project utilized a well-defined rat mammary carcinogenesis system and congenic rat model to fine map and characterize the rat Mcs1b locus. My studies reduced the number of candidate genes by narrowing the rat Mcs1b locus from a 13 megabase (Mb) to a 1 Mb containing nine annotated transcripts. I determined that Mcs1b-conferred mammary carcinoma resistance is being controlled by a cell type within the mammary gland. This is an important finding because mammary carcinogenesis is dependent on both mammary gland-extrinsic and -intrinsic factors. I also found that the transcript Mier3 is differentially expressed between resistant and susceptible rat mammary glands with or without carcinogen exposure providing genetic evidence that Mier3 is a strong mammary carcinoma susceptibility gene. Taken together, these results provide insight into the mechanism by which Mier3 controls mammary carcinogenesis and implicate human MIER3 as a potential target for breast cancer prevention. Advisors/Committee Members: Samuelson, David J..

Subjects/Keywords: Breast cancer susceptibility; MIER3; Mammary carcinogenesis; Mcs1b

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APA (6^th Edition):

denDekker, A. D. (2013). Genetic mapping and mechanism of action of rat mammary carcinoma susceptibility quantitative trait locus Mcs1b. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/330 ; https://ir.library.louisville.edu/etd/330

Chicago Manual of Style (16^th Edition):

denDekker, Aaron D. “Genetic mapping and mechanism of action of rat mammary carcinoma susceptibility quantitative trait locus Mcs1b.” 2013. Doctoral Dissertation, University of Louisville. Accessed March 04, 2021. 10.18297/etd/330 ; https://ir.library.louisville.edu/etd/330.

MLA Handbook (7^th Edition):

denDekker, Aaron D. “Genetic mapping and mechanism of action of rat mammary carcinoma susceptibility quantitative trait locus Mcs1b.” 2013. Web. 04 Mar 2021.

Vancouver:

denDekker AD. Genetic mapping and mechanism of action of rat mammary carcinoma susceptibility quantitative trait locus Mcs1b. [Internet] [Doctoral dissertation]. University of Louisville; 2013. [cited 2021 Mar 04]. Available from: 10.18297/etd/330 ; https://ir.library.louisville.edu/etd/330.

Council of Science Editors:

denDekker AD. Genetic mapping and mechanism of action of rat mammary carcinoma susceptibility quantitative trait locus Mcs1b. [Doctoral Dissertation]. University of Louisville; 2013. Available from: 10.18297/etd/330 ; https://ir.library.louisville.edu/etd/330

University of New South Wales

12. Lee, Heather Jane. Investigations in hormonal regulation of the mammary gland.

Degree: Clinical School - St Vincent's Hospital, 2011, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/50818 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9713/SOURCE02?view=true

► During puberty and pregnancy, oestrogen, progesterone (Pg) and prolactin (PRL) drive mammary gland development via a network of transcription factors and paracrine signals. These factors… (more)

▼ During puberty and pregnancy, oestrogen, progesterone (Pg) and prolactin (PRL) drive mammary gland development via a network of transcription factors and paracrine signals. These factors not only coordinate normal mammary development but can also contribute to breast cancer. This thesis investigates interactions between oestrogen, Pg and PRL and draws implications for breast cancer.Oestrogen inhibits growth hormone (GH) signalling by inducing suppressors of cytokine signalling (SOCS). Given the similarities between GH and PRL, experiments were performed to determine whether oestrogen induces SOCS to inhibit PRL signalling in mammary cells. Although the SOCS protein, CIS, was induced by oestrogen in breast cancer cells, PRL signalling was unaffected. Similarly, oestrogen did not suppress PRL-induced milk expression in a mammary cell line. These results argue against oestrogen modulation of PRL signalling via regulation of SOCS proteins.PRL and Pg are critical for mammary alveologenesis during pregnancy. The transcription factor, Elf5, is also essential for this process and is an important mediator of PRL action. Experiments were undertaken to determine the relationship between Pg and Elf5 in vivo. Elf5 was induced by Pg and cooperated with Pg to promote alveolar bud formation. Further, RANKL was identified as a likely mediator of Pg’s effects on Elf5 expression. These results establish Elf5 as a point of convergence between PRL and Pg signalling in the mammary gland. Elf5 promoter methylation is proposed to enforce lineage commitment in the blastocyst, so experiments were undertaken to characterise Elf5 promoter methylation in mammary cells. Elf5 is expressed in luminal cells, and accordingly, promoter methylation was reduced in luminal cells relative to the stem cell containing basal population. During pregnancy, the abundance of luminal cells increases, so there was an overall decrease in Elf5 promoter methylation. Thus, the Elf5 promoter displays lineage specific methylation in the mammary gland. Loss of promoter methylation in luminal cells may be a prerequisite for hormonal induction of Elf5 expression during pregnancy.This thesis provides novel information regarding interactions between the hormonal drivers of mammary development. The implications of this work extend beyond normal development to pharmacological control of lactation and hormonal control of breast carcinogenesis. Advisors/Committee Members: Ormandy, Christopher, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW, Ho, Ken, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW.

Subjects/Keywords: Breast Cancer; Mammary development; Prolactin; Progesterone; Elf5

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APA (6^th Edition):

Lee, H. J. (2011). Investigations in hormonal regulation of the mammary gland. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/50818 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9713/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Lee, Heather Jane. “Investigations in hormonal regulation of the mammary gland.” 2011. Doctoral Dissertation, University of New South Wales. Accessed March 04, 2021. http://handle.unsw.edu.au/1959.4/50818 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9713/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Lee, Heather Jane. “Investigations in hormonal regulation of the mammary gland.” 2011. Web. 04 Mar 2021.

Vancouver:

Lee HJ. Investigations in hormonal regulation of the mammary gland. [Internet] [Doctoral dissertation]. University of New South Wales; 2011. [cited 2021 Mar 04]. Available from: http://handle.unsw.edu.au/1959.4/50818 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9713/SOURCE02?view=true.

Council of Science Editors:

Lee HJ. Investigations in hormonal regulation of the mammary gland. [Doctoral Dissertation]. University of New South Wales; 2011. Available from: http://handle.unsw.edu.au/1959.4/50818 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:9713/SOURCE02?view=true

University of Minnesota

13. Troness, Benjamin. The Effects of Tamoxifen on Mammary Organoids from Young and Old MMTV-c-neu Mice.

Degree: MS, Biological Science, 2020, University of Minnesota

URL: http://hdl.handle.net/11299/218675

► Tamoxifen, an estrogen antagonist, can prevent ER-positive tumor development in women at risk of developing breast cancer. Mouse studies demonstrate that tamoxifen can prevent ER-negative… (more)

Subjects/Keywords: breast; cancer; chemoprevention; mammary; prevention; Tamoxifen

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APA (6^th Edition):

Troness, B. (2020). The Effects of Tamoxifen on Mammary Organoids from Young and Old MMTV-c-neu Mice. (Masters Thesis). University of Minnesota. Retrieved from http://hdl.handle.net/11299/218675

Chicago Manual of Style (16^th Edition):

Troness, Benjamin. “The Effects of Tamoxifen on Mammary Organoids from Young and Old MMTV-c-neu Mice.” 2020. Masters Thesis, University of Minnesota. Accessed March 04, 2021. http://hdl.handle.net/11299/218675.

MLA Handbook (7^th Edition):

Troness, Benjamin. “The Effects of Tamoxifen on Mammary Organoids from Young and Old MMTV-c-neu Mice.” 2020. Web. 04 Mar 2021.

Vancouver:

Troness B. The Effects of Tamoxifen on Mammary Organoids from Young and Old MMTV-c-neu Mice. [Internet] [Masters thesis]. University of Minnesota; 2020. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11299/218675.

Council of Science Editors:

Troness B. The Effects of Tamoxifen on Mammary Organoids from Young and Old MMTV-c-neu Mice. [Masters Thesis]. University of Minnesota; 2020. Available from: http://hdl.handle.net/11299/218675

Rutgers University

14. Datar, Ketaki Rajendra, 1994-. The effect of alcohol consumption on mammary epithelial cell composition and mammary tumorigenesis.

Degree: MS, Microbiology and Molecular Genetics, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/61726/

► Breast cancer is the most common cancer in women worldwide and in 2019 it is estimated that approximately 41,000 women will die from the disease.… (more)

▼ Breast cancer is the most common cancer in women worldwide and in 2019 it is estimated that approximately 41,000 women will die from the disease. There are a variety of factors that increase risk for breast cancer one of which is alcohol consumption. However, the mechanism that underlies this increased risk is unknown. The mammary gland is a dynamic organ composed of a multiple cell types including adipose cells, fibroblasts, immune cells, and epithelial cells. The epithelial cells can be categorized into luminal and basal epithelial cells, whose composition is maintained and controlled by a pool of mammary stem cells. Mammary stem cells are quiescent and long lived, and therefore have the potential to accumulate mutations and transform into breast cancer stem cells. Breast cancer stem cells have the potential to maintain a tumor and may not be irradiated by conventional therapies, leading to relapse. Therefore, understanding what regulates the overall mammary epithelial cell hierarchy is key to improving breast cancer treatments. The goal of this project was to determine whether alcohol consumption alters the mammary epithelial cell composition to favor a tumorigenic state, whether alcohol consumption affects tumor latency, and whether alcohol alters the mammary tumor epithelial cell composition. The MMTV-Wnt1 mouse model is a useful model for studying the role of mammary stem cells in breast cancer, as the tumors that develop in this model arise from a stem or stem-like cell, and downstream targets of the Wnt signaling cascade have been found to be upregulated in breast cancer. To investigate the effect of alcohol on mammary epithelial cell composition and tumorigenesis, 7- week old MMTV-Wnt1 female mice were given a 20% alcohol solution in place of drinking water sweetened with 0.2% saccharin. Control animals were given a 0.12% saccharin solution for the entire duration of the study. Animals were weighed once per week and were sacrificed after either 8 weeks to analyze the preneoplastic mammary gland or after the first tumor had reached 1.5cm in diameter. Animals in the alcohol group gained more weight compared to the controls, and this difference in weight gain was due to an increase in overall caloric intake due to alcohol consumption. Mammary epithelial cells were isolated and analyzed by flow cytometry and plated for mammosphere/tumorsphere assays. Mammary glands from the alcohol group exhibited an increase in the luminal progenitor population, but a decrease in mammosphere forming efficiency. Alcohol consumption decreased tumor latency in animals that presented with tumors by 43 weeks of age, however, alcohol consumption did not effect on the tumor epithelial cell composition nor the tumorsphere forming efficiency. Alcohol consumption decreased the expression of the epithelial-mesenchymal transition (EMT) factors Snail and Twist in the mammary gland mRNA, and the proliferation marker Ki67. It also decreased expression of Snail in mRNA from the mammary tumor. Alcohol did not affect estrogen… Advisors/Committee Members: Cohick, Wendie S (chair), Belden, William J (internal member), Suh, Nanjoo (internal member), School of Graduate Studies.

Subjects/Keywords: Mammary; Breast – Cancer; Alcohol – Physiological effect

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

APA (6^th Edition):

Datar, Ketaki Rajendra, 1. (2019). The effect of alcohol consumption on mammary epithelial cell composition and mammary tumorigenesis. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/61726/

Chicago Manual of Style (16^th Edition):

Datar, Ketaki Rajendra, 1994-. “The effect of alcohol consumption on mammary epithelial cell composition and mammary tumorigenesis.” 2019. Masters Thesis, Rutgers University. Accessed March 04, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/61726/.

MLA Handbook (7^th Edition):

Datar, Ketaki Rajendra, 1994-. “The effect of alcohol consumption on mammary epithelial cell composition and mammary tumorigenesis.” 2019. Web. 04 Mar 2021.

Vancouver:

Datar, Ketaki Rajendra 1. The effect of alcohol consumption on mammary epithelial cell composition and mammary tumorigenesis. [Internet] [Masters thesis]. Rutgers University; 2019. [cited 2021 Mar 04]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61726/.

Council of Science Editors:

Datar, Ketaki Rajendra 1. The effect of alcohol consumption on mammary epithelial cell composition and mammary tumorigenesis. [Masters Thesis]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/61726/

Queens University

15. Apostoli, Anthony J. The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis .

Degree: Pathology and Molecular Medicine, 2014, Queens University

URL: http://hdl.handle.net/1974/12347

► Previous studies with peroxisome proliferator-activated receptor (PPAR)γ heterozygous mice suggest PPARγ normally suppresses 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumour progression, but the mechanisms and cell types involved… (more)

Subjects/Keywords: Knockout Mouse Model ; Chemical Carcinogenesis ; Breast cancer ; Mammary Epithelial Cells ; Mammary Secretory Epithelial Cells ; PPARγ

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APA (6^th Edition):

Apostoli, A. J. (2014). The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12347

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):

Apostoli, Anthony J. “The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis .” 2014. Thesis, Queens University. Accessed March 04, 2021. http://hdl.handle.net/1974/12347.

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

MLA Handbook (7^th Edition):

Apostoli, Anthony J. “The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis .” 2014. Web. 04 Mar 2021.

Vancouver:

Apostoli AJ. The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis . [Internet] [Thesis]. Queens University; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1974/12347.

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

Council of Science Editors:

Apostoli AJ. The Mammary Epithelial Contribution Of PPARγ In Breast Tumourigenesis . [Thesis]. Queens University; 2014. Available from: http://hdl.handle.net/1974/12347

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

University of Toronto

16. Jackson, Hartland Warren. TIMPs in Mammary Stem Cell Homeostasis and Breast Cancer Progression.

Degree: PhD, 2014, University of Toronto

URL: http://hdl.handle.net/1807/74482

►

The mammary gland repeatedly undergoes reorganization and cellular turnover in the adult female. Ductal invasion and branching morphogenesis during puberty, cyclical expansion during reproductive cycles,… (more)

Subjects/Keywords: aging; breast cancer; mammary gland; mammary stem cell; stem cell; TIMP; 0306

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APA (6^th Edition):

Jackson, H. W. (2014). TIMPs in Mammary Stem Cell Homeostasis and Breast Cancer Progression. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/74482

Chicago Manual of Style (16^th Edition):

Jackson, Hartland Warren. “TIMPs in Mammary Stem Cell Homeostasis and Breast Cancer Progression.” 2014. Doctoral Dissertation, University of Toronto. Accessed March 04, 2021. http://hdl.handle.net/1807/74482.

MLA Handbook (7^th Edition):

Jackson, Hartland Warren. “TIMPs in Mammary Stem Cell Homeostasis and Breast Cancer Progression.” 2014. Web. 04 Mar 2021.

Vancouver:

Jackson HW. TIMPs in Mammary Stem Cell Homeostasis and Breast Cancer Progression. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1807/74482.

Council of Science Editors:

Jackson HW. TIMPs in Mammary Stem Cell Homeostasis and Breast Cancer Progression. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/74482

University of Melbourne

17. Cross, Ryan N S. Investigating MYB in the context of mammary gland biology, transformation and as a therapeutic target in breast and colon cancer.

Degree: 2014, University of Melbourne

URL: http://hdl.handle.net/11343/54724

► Breast cancer is the second most common form of malignancy diagnosed in Australian women, imposing an enormous social and economic burden on society. If the… (more)

Subjects/Keywords: breast cancer; colon cancer; mammary gland stem cells; DNA vaccine; immunotherapy

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APA (6^th Edition):

Cross, R. N. S. (2014). Investigating MYB in the context of mammary gland biology, transformation and as a therapeutic target in breast and colon cancer. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/54724

Chicago Manual of Style (16^th Edition):

Cross, Ryan N S. “Investigating MYB in the context of mammary gland biology, transformation and as a therapeutic target in breast and colon cancer.” 2014. Doctoral Dissertation, University of Melbourne. Accessed March 04, 2021. http://hdl.handle.net/11343/54724.

MLA Handbook (7^th Edition):

Cross, Ryan N S. “Investigating MYB in the context of mammary gland biology, transformation and as a therapeutic target in breast and colon cancer.” 2014. Web. 04 Mar 2021.

Vancouver:

Cross RNS. Investigating MYB in the context of mammary gland biology, transformation and as a therapeutic target in breast and colon cancer. [Internet] [Doctoral dissertation]. University of Melbourne; 2014. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/11343/54724.

Council of Science Editors:

Cross RNS. Investigating MYB in the context of mammary gland biology, transformation and as a therapeutic target in breast and colon cancer. [Doctoral Dissertation]. University of Melbourne; 2014. Available from: http://hdl.handle.net/11343/54724

Universiteit Utrecht

18. Stee, Lucinda van. The growth inhibitory effect of of anti growth hormone (G144K) on canine mammary carcinomas.

Degree: 2008, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/32509

► One out of four intact bitches will develop mammary gland tumours. Current therapy is surgical removal of the neoplasm but this is insufficient in most… (more)

Subjects/Keywords: Diergeneeskunde; Canine mammary gland tumour; carcinoma; breast cancer; growth hormone; GHR

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APA (6^th Edition):

Stee, L. v. (2008). The growth inhibitory effect of of anti growth hormone (G144K) on canine mammary carcinomas. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/32509

Chicago Manual of Style (16^th Edition):

Stee, Lucinda van. “The growth inhibitory effect of of anti growth hormone (G144K) on canine mammary carcinomas.” 2008. Doctoral Dissertation, Universiteit Utrecht. Accessed March 04, 2021. http://dspace.library.uu.nl:8080/handle/1874/32509.

MLA Handbook (7^th Edition):

Stee, Lucinda van. “The growth inhibitory effect of of anti growth hormone (G144K) on canine mammary carcinomas.” 2008. Web. 04 Mar 2021.

Vancouver:

Stee Lv. The growth inhibitory effect of of anti growth hormone (G144K) on canine mammary carcinomas. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2008. [cited 2021 Mar 04]. Available from: http://dspace.library.uu.nl:8080/handle/1874/32509.

Council of Science Editors:

Stee Lv. The growth inhibitory effect of of anti growth hormone (G144K) on canine mammary carcinomas. [Doctoral Dissertation]. Universiteit Utrecht; 2008. Available from: http://dspace.library.uu.nl:8080/handle/1874/32509

Universiteit Utrecht

19. Vliet, Mariska van. Influence of genistein in a mammary cancer co-culture model.

Degree: 2009, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/32542

► Hormone dependent breast cancer is a common disease in humans as well as in dogs. In both species it concerns mostly middle aged individuals. Women… (more)

▼ Hormone dependent breast cancer is a common disease in humans as well as in dogs. In both species it concerns mostly middle aged individuals. Women have a chance of 1 in 8 to develop breast cancer and unspayed bitches even have a chance of 1 in 4. In women it is known that mammary fibroblasts produce estrone, which can stimulate estrogen receptor positive (ER+) epithelial cells when it is converted to estradiol. Estrone production is catalysed by the enzyme aromatase and this enzyme is a target in breast cancer therapy by the use of aromatase inhibitors like fadrazole. In dogs, the only used mammary cancer therapy is surgery. It is known that a lot of people, including a large group of cancer patients, take dietary supplements. Many of these supplements contain fytoestrogens like the isoflavone genistein. Different studies showed inhibiting as well as stimulating effects of genistein on breast cells. We investigated the effect of genistein on breast tissue by using a co-culture model in which primary mammary fibroblasts were co-cultured with a mammary ER+ epithelial cancer cell line (MCF-7) and a mammary epithelial cell line that represents healthy breast tissue (MCF-10A). Of special interest was to find out if genistein interferes with fadrazole therapy in breast cancer patients. We used healthy tissue derived fibroblasts as well as tumour tissue derived fibroblasts from dogs. By using healthy and tumour fibroblasts we also wanted to learn more about the influence of fibroblasts on epithelial cells and their importance in breast cancer etiology and use in a breast cancer model. Another interest was to find out if canine breast cancer shows the same characteristerics as human breast cancer and if canine primary fibroblasts can be a good alternative in a human breast cancer co-culture model. Subsequently, we wanted to learn if aromatase inhibiters might be useful in veterinary medecin as well. Furthermore we were interested in the relation of Cox-2 and Cyp19 (aromatase enzyme gene) expression. A positive correlation has been described before in human breast cancer and we wanted to know if this correlation can also be seen in canine mammary cancer. We performed aromatase assays and real time PCRs on primary canine fibroblasts and we could measure aromatase activity and its gene expression (Cyp19). Both were higher in tumour derived fibroblasts than in healthy tissue derived fibroblasts. Aromatase activity can not be increased with some known inducers of human aromatase, which suggests that Cyp19 expression is under control of different promotors in dogs. Fadrazole inhibited aromatase activity in canine fibroblasts very efficient (p<0.01), like it does in human cells and it might be useful in veterinary medicine as well. Genistein at a concentration of 30 μM did increase Cyp19 expression significantly in healthy fibroblasts, but the increase in tumour fibroblasts was not significant. In co-cultures of healthy fibroblasts with MCF-10A and MCF-7 cells, genistein exposure caused a non significant increase of… Advisors/Committee Members: Duursen, Majorie van, Niemeijer, Sandra.

Subjects/Keywords: Diergeneeskunde; mammary; cancer; phytochemical; genistein; canine; co-culture

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APA (6^th Edition):

Vliet, M. v. (2009). Influence of genistein in a mammary cancer co-culture model. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/32542

Chicago Manual of Style (16^th Edition):

Vliet, Mariska van. “Influence of genistein in a mammary cancer co-culture model.” 2009. Doctoral Dissertation, Universiteit Utrecht. Accessed March 04, 2021. http://dspace.library.uu.nl:8080/handle/1874/32542.

MLA Handbook (7^th Edition):

Vliet, Mariska van. “Influence of genistein in a mammary cancer co-culture model.” 2009. Web. 04 Mar 2021.

Vancouver:

Vliet Mv. Influence of genistein in a mammary cancer co-culture model. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2009. [cited 2021 Mar 04]. Available from: http://dspace.library.uu.nl:8080/handle/1874/32542.

Council of Science Editors:

Vliet Mv. Influence of genistein in a mammary cancer co-culture model. [Doctoral Dissertation]. Universiteit Utrecht; 2009. Available from: http://dspace.library.uu.nl:8080/handle/1874/32542

Universiteit Utrecht

20. Madsen, E.V.E. Optimized lymph node staging in breast cancer in the era of sentinel node biopsy.

Degree: 2012, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/240477

► SLNB has revolutionized staging and treatment in breast cancer patients, several issues provoked renewed attention. If small lymph node metastases are relevant, the pathologist should… (more)

▼ SLNB has revolutionized staging and treatment in breast cancer patients, several issues provoked renewed attention. If small lymph node metastases are relevant, the pathologist should detect them. The current Dutch pathology guideline is not sensitive enough to detect them. To obtain a 95% detection probability for 200μm metastasesthe interval between sections should be 200μm and the number of sections should be at least 20 from each half in a median sized SLN. Is small metastases are irrelevant, serial sectioning with 2mm is preferable. Intra-operative frozen section analysis of the SLN has the advantage of avoiding a second operation for an ALND, but it carries the risk of tissue loss and missing metastases. However, the detection probability is not negatively influenced by FS analysis in the majority of the protocols. Only in extensive protocols the detection probability diminishesdue to tissue loss. Patient- and primary tumor characteristics associated with pN0(i+) and pN1mi were studied. Younger patients, patients with larger tumors and with an intermediate BR-grade had an increased risk of pN1mi and ≥pN1a. Patients with a triple negative tumor had a decreased risk on pN1mi and ≥pN1a. The frequency of the smallest metastases was fairly constant in relation to increasing tumor size. pN0(i+) seems to bare resemblance to pN0, while the resemblance between pN1mi and ≥pN1a seems less clear. The need for removal of IM SLNs remains subject of discussion. Adjustment of post-surgical treatment as the result of IM SLNB was advised in 20% of patients in whom the IM SLN was harvested. Adjustments mainly implied expansion of the radiotherapy field. How to manage the axillais not clear for patients with exclusive IM drainage. In 1.1% of the patients exclusive IM lymphoscintigraphic drainage was observed and axillary staging by other means revealed additional axillary metastases in 4/14 patients, post-surgical treatment was adjusted in two. Staging the axilla thus appears sensible. Only a very small group of patients has metastases in the IM SLNs, therefore it is difficult to establish if they affect overall survival. In a large multicenter cohort the impact of IM metastases on outcome was addressed, they were observed in 3.5% of patients and OS was not significantly worse for these patients (HR 1.23; CI 0.75 - 2.01). ER+/her2neu negative breast tumors are associated with favorable outcome and may have an even better prognosis than based on ER positivity alone. In a large cohort three groups of ER+ patients were compared: her2neu+, her2neu- and her2neu not determined. ER+/her2- patients did have a significant better outcome than ER+/her2 not determined patients. These results suggest that the her2neu receptor should be includedin prognostic models. The use of SLNB in patients with breast cancer has definitely led to a more refined lymph node staging, but the heydays of optimal lymph node staging that started with the introduction of SLNB may soon be past Advisors/Committee Members: Borel Rinkes, I.H.M., Dalen, Th. van.

Subjects/Keywords: Geneeskunde; Geneeskunde; breast cancer; sentinel lymph node; internal mammary metastases

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APA (6^th Edition):

Madsen, E. V. E. (2012). Optimized lymph node staging in breast cancer in the era of sentinel node biopsy. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/240477

Chicago Manual of Style (16^th Edition):

Madsen, E V E. “Optimized lymph node staging in breast cancer in the era of sentinel node biopsy.” 2012. Doctoral Dissertation, Universiteit Utrecht. Accessed March 04, 2021. http://dspace.library.uu.nl:8080/handle/1874/240477.

MLA Handbook (7^th Edition):

Madsen, E V E. “Optimized lymph node staging in breast cancer in the era of sentinel node biopsy.” 2012. Web. 04 Mar 2021.

Vancouver:

Madsen EVE. Optimized lymph node staging in breast cancer in the era of sentinel node biopsy. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2012. [cited 2021 Mar 04]. Available from: http://dspace.library.uu.nl:8080/handle/1874/240477.

Council of Science Editors:

Madsen EVE. Optimized lymph node staging in breast cancer in the era of sentinel node biopsy. [Doctoral Dissertation]. Universiteit Utrecht; 2012. Available from: http://dspace.library.uu.nl:8080/handle/1874/240477

UCLA

21. Khialeeva, Elvira R. Novel Functions for Reelin Signaling in Mammary Gland Development and Breast Cancer Progression.

Degree: Molecular Biology, 2016, UCLA

URL: http://www.escholarship.org/uc/item/2wb9c5bg

► The reelin signaling pathway is a critical regulator of cell migration and positioning throughout the central nervous system. Recent studies identified non-neuronal functions for reelin,… (more)

▼ The reelin signaling pathway is a critical regulator of cell migration and positioning throughout the central nervous system. Recent studies identified non-neuronal functions for reelin, and reported alterations in reelin expression in cancers. It is not known whether the reelin signaling pathway plays a role in the development of the mammary gland or in progression of breast cancer. Using mice with mutations in reelin and Disabled-1 (Dab1), the intracellular adaptor protein activated in response to the reelin signal, we showed that the reelin signaling pathway is required for correct ductal patterning during mammary gland morphogenesis. Reelin and Dab1 are expressed in the developing and the mature mammary duct in a complementary pattern. Mutations in reelin or Dab1 resulted in delayed ductal elongation and disorganized mammary epithelium in mice. Mammary epithelial cells exhibited decreased migration in response to exogenous reelin in a Dab1-dependent manner in vitro. Using a syngeneic mouse mammary tumor transplantation model, we examined the effect of host-derived reelin on breast cancer progression. We found that transplanted tumors grew and metastasized more slowly in reelin-deficient mice. Tumors grown in reelin-deficient animals had fewer blood vessels and increased macrophage infiltration. Loss of host-derived reelin altered the balance of M1- and M2-associated macrophage markers in primary tumors, suggesting that reelin may influence the polarization of tumor-associated macrophages. These results indicated an important function for the reelin protein in progression of breast cancer. Furthermore, we found that several alternatively spliced variants of Dab1 exist in the developing and the mature mammary gland. In addition, we showed that alternative splicing of Dab1 is spatially and temporally regulated during puberty, pregnancy, and lactation. Taken together, our findings suggest that the reelin signaling pathway is an essential regulator of mammary gland development and has critical functions in progression of breast cancer.

Subjects/Keywords: Developmental biology; Breast Cancer; Dab1; Mammary Gland; Reelin

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APA (6^th Edition):

Khialeeva, E. R. (2016). Novel Functions for Reelin Signaling in Mammary Gland Development and Breast Cancer Progression. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/2wb9c5bg

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):

Khialeeva, Elvira R. “Novel Functions for Reelin Signaling in Mammary Gland Development and Breast Cancer Progression.” 2016. Thesis, UCLA. Accessed March 04, 2021. http://www.escholarship.org/uc/item/2wb9c5bg.

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

MLA Handbook (7^th Edition):

Khialeeva, Elvira R. “Novel Functions for Reelin Signaling in Mammary Gland Development and Breast Cancer Progression.” 2016. Web. 04 Mar 2021.

Vancouver:

Khialeeva ER. Novel Functions for Reelin Signaling in Mammary Gland Development and Breast Cancer Progression. [Internet] [Thesis]. UCLA; 2016. [cited 2021 Mar 04]. Available from: http://www.escholarship.org/uc/item/2wb9c5bg.

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

Council of Science Editors:

Khialeeva ER. Novel Functions for Reelin Signaling in Mammary Gland Development and Breast Cancer Progression. [Thesis]. UCLA; 2016. Available from: http://www.escholarship.org/uc/item/2wb9c5bg

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

University of California – Berkeley

22. Soignier, Yvette Marie. Oct3 and Sox2 Expression in Mammary Carcinoma Cells.

Degree: Molecular & Cell Biology, 2010, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/3037s4rx

► A complex transcriptional circuitry is essential in maintaining the self-renewal capacity and the undifferentiated state of embryonic stem cells (ESCs). Key factors in this pluripotency… (more)

▼ A complex transcriptional circuitry is essential in maintaining the self-renewal capacity and the undifferentiated state of embryonic stem cells (ESCs). Key factors in this pluripotency network include Sox2, Nanog, and Oct3/4, which form multiple positive and negative feedback loops to regulate an array of downstream genes. Although it was previously thought that pluripotency factors are downregulated upon differentiation, the phenotypic similarities between ESCs and cancer cells have led to speculation that common underlying regulatory mechanisms may exist. For example, the cancer phenotype includes a block in differentiation, limitless replicative potential and increased proliferation, characteristics that are also observed in pluripotent embryonic stem cells. Taken together, these observations regarding similarities in tumor cells and embryonic stem cells suggest regulatory mechanisms that may be shared in development and cancer. In the studies presented here, I investigated the expression, localization, and function of Nanog, Sox2, Oct4 and particularly the Oct3 splice variant protein in cancer. I performed a variety of biochemical, genetic and pharmacological experiments to elucidate potential roles of these pluripotency factors in maintaining the cancer phenotype, using a panel of breast cancer cells as a model system. Expression of Sox2 and the Oct3 isoform was detected in all breast cancer cell lines investigated, whereas Nanog and Oct4 expression were not detected. Moreover, Sox2 was localized to both the cytoplasm and nucleus, but Oct3 expression was detected exclusively the cytoplasm of breast cancer cells. This study also shows that Oct3 and Sox2 are upregulated in a number of breast cancer cell lines when compared to expression levels in mammary epithelial cells. I also determined that Src is an upstream regulator of Oct3 and Sox2 expression. Given the known function of Sox2 as a regulator of the cell cycle, I focused subsequent studies on the characterization and function of Oct3. Results showed that the Oct3 N-terminal domain contains an auto-inhibitory sequence that blocks its nuclear translocation despite the presence of a functional nuclear localization signal. Additional experiments to investigate Oct3 function suggested that Oct3 may be involved in regulating the cell cycle and that this regulation may be in concert with Sox2 and β-catenin to modulate cyclin D1 expression. However, studies of Oct3 function in cancer remain inconclusive due to technical difficulties in Oct3 RNAi that precluded achieving consistent Oct3 knockdown. Despite these difficulties, the data presented here suggest that Oct3 may play a role in maintaining the cancer phenotype, warranting further functional studies.

Subjects/Keywords: Cellular Biology; Breast Cancer; Mammary Carcinoma; Oct3/4; Sox2

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APA (6^th Edition):

Soignier, Y. M. (2010). Oct3 and Sox2 Expression in Mammary Carcinoma Cells. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/3037s4rx

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):

Soignier, Yvette Marie. “Oct3 and Sox2 Expression in Mammary Carcinoma Cells.” 2010. Thesis, University of California – Berkeley. Accessed March 04, 2021. http://www.escholarship.org/uc/item/3037s4rx.

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

MLA Handbook (7^th Edition):

Soignier, Yvette Marie. “Oct3 and Sox2 Expression in Mammary Carcinoma Cells.” 2010. Web. 04 Mar 2021.

Vancouver:

Soignier YM. Oct3 and Sox2 Expression in Mammary Carcinoma Cells. [Internet] [Thesis]. University of California – Berkeley; 2010. [cited 2021 Mar 04]. Available from: http://www.escholarship.org/uc/item/3037s4rx.

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

Council of Science Editors:

Soignier YM. Oct3 and Sox2 Expression in Mammary Carcinoma Cells. [Thesis]. University of California – Berkeley; 2010. Available from: http://www.escholarship.org/uc/item/3037s4rx

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

23. Druso, Joseph Edward. IDENTIFYING AND ANALYZING THE ROLES OF CDC42 DURING MAMMARY GLAND DEVELOPMENT AND TRANSFORMATION.

Degree: PhD, Pharmacology, 2017, Cornell University

URL: http://hdl.handle.net/1813/47715

► The small GTPase Cdc42 is an essential signaling molecule in multiple cellular processes, including proliferation, migration, division and apoptosis. The overexpression of Cdc42 is found… (more)

▼ The small GTPase Cdc42 is an essential signaling molecule in multiple cellular processes, including proliferation, migration, division and apoptosis. The overexpression of Cdc42 is found in certain breast carcinomas, bringing to question its roles in normal mammary cell function and during breast cancer progression. In this thesis, I have examined the roles of Cdc42 during mammary gland development, and then analyzed the effects of overactive Cdc42 signaling on mammary epithelial cells (MECs). To accomplish this, I used an in vivo mouse model as well as primary cell culture systems. In the initial study, the conditional-knockout of Cdc42 in the epithelia of adult mouse mammary glands resulted in the altered cellular localization of Par complex members, as well as E-cadherin. These changes accompanied a disorganization of the epithelial cells within the mammary gland, and led to insufficient lactation. This loss-of-function mouse model showed that Cdc42 is essential for the proper maintenance of both apical-basal cell polarity and E-cadherin-based cell-cell junctions in the adult mammary gland. These results raised further interest concerning the roles Cdc42 may have in breast carcinoma development, in which proper apical-basal cell polarity and cell-cell communication are commonly lost. I next examined the effects of aberrant Cdc42 signaling in primary MECs by utilizing the constitutively-active Cdc42[F28L] mutant. In a monolayer culture system, Cdc42[F28L] stimulated the formation of actin-based stress fibers, and gave rise to multi-nucleated cells, while in a three-dimensional model system it drove the primary MECs toward an invasive phenotype in an IQGAP1-dependent manner. The primary MECs expressing Cdc42[F28L] lost the proper localization of E-cadherin at cell-cell contacts and no longer formed normal, hollowed alveolar lumens, but instead began to abnormally fill the luminal space and invade out into the surrounding environment. A common phenotype exhibited by these model systems was the proper maintenance of E-cadherin-based cell-cell contacts between mammary epithelial cells. Interestingly, both the deletion of Cdc42 and its constitutive activation resulted in abnormal E-cadherin expression and localization within mammary epithelial cells. IQGAP1 is likely the primary Cdc42 effector responsible for these phenotypes, as it can both regulate E-cadherin stability at cell-cell junctions as well as bundle microtubules at the leading edge of invasive cells. These studies suggest IQGAP1 is a critical signaling effector of Cdc42 in adult mammary epithelial cells and that, when not properly regulated, it can shift the epithelia toward an invasive phenotype. Advisors/Committee Members: Cerione, Richard A (chair), Linder, Maurine E. (committee member), Kurpios, Natasza (committee member).

Subjects/Keywords: Breast cancer; Cdc42; Lactation; Mammary gland; Transformation; Cellular biology; Developmental biology

10 more images…

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APA (6^th Edition):

Druso, J. E. (2017). IDENTIFYING AND ANALYZING THE ROLES OF CDC42 DURING MAMMARY GLAND DEVELOPMENT AND TRANSFORMATION. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/47715

Chicago Manual of Style (16^th Edition):

Druso, Joseph Edward. “IDENTIFYING AND ANALYZING THE ROLES OF CDC42 DURING MAMMARY GLAND DEVELOPMENT AND TRANSFORMATION.” 2017. Doctoral Dissertation, Cornell University. Accessed March 04, 2021. http://hdl.handle.net/1813/47715.

MLA Handbook (7^th Edition):

Druso, Joseph Edward. “IDENTIFYING AND ANALYZING THE ROLES OF CDC42 DURING MAMMARY GLAND DEVELOPMENT AND TRANSFORMATION.” 2017. Web. 04 Mar 2021.

Vancouver:

Druso JE. IDENTIFYING AND ANALYZING THE ROLES OF CDC42 DURING MAMMARY GLAND DEVELOPMENT AND TRANSFORMATION. [Internet] [Doctoral dissertation]. Cornell University; 2017. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1813/47715.

Council of Science Editors:

Druso JE. IDENTIFYING AND ANALYZING THE ROLES OF CDC42 DURING MAMMARY GLAND DEVELOPMENT AND TRANSFORMATION. [Doctoral Dissertation]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/47715

Vanderbilt University

24. Vaught, David Bryan. EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis.

Degree: PhD, Cancer Biology, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/11610

► Eph receptor tyrosine kinases are membrane bound receptors often expressed by normal epithelial cells but are frequently overexpressed in many human cancers. Of the many… (more)

▼ Eph receptor tyrosine kinases are membrane bound receptors often expressed by normal epithelial cells but are frequently overexpressed in many human cancers. Of the many Eph receptors, EphA2 is present at low levels in normal mammary tissue but highly expressed in breast cancer and correlative with a poor patient prognosis. The focus of this thesis is to understand the endogenous role of EphA2 in mammary gland development and how overexpression can contribute to the poor prognosis through metastasis often seen with breast cancers overexpressing EphA2. Using EphA2-deficient animals, this thesis work demonstrates for the first time that EphA2 receptor function is required for mammary epithelial growth and branching morphogenesis. Loss of EphA2 decreased penetration of mammary epithelium into fat pad, reduced epithelial proliferation, and inhibited epithelial branching. These defects appear to be intrinsic to loss of EphA2 in epithelium, as transplantation of EphA2-deficient mammary tissue into wild-type recipient stroma recapitulated these defects. In addition, HGF-induced mammary epithelial branching morphogenesis was significantly reduced in EphA2-deficient cells relative to wild-type cells, which correlated with elevated basal RhoA activity. These results suggest that EphA2 receptor acts as a positive regulator in mammary gland development, functioning downstream of HGF to regulate branching through inhibition of RhoA. Breast cancer metastasis to bone is a major cause of morbidity and mortality in patients. Analysis of human breast-to-bone metastasis samples revealed EphA2 positive staining on tumor cells in close proximity to osteoclast at the tumor-bone interface. To define the role of EphA2 in tumor cell-host bone cell interactions, mouse tibias were injected with osteolytic breast tumor cells lacking EphA2 activity. Our data showed that inhibition of EphA2 activity significantly decreased tumor-induced osteolysis compared to controls. Further in vitro analysis revealed that blocking EphA2 function resulted in defective precursor maturation into functional osteoclasts. A human antibody targeted against EphA2 decreased breast tumor induced osteolysis in vivo. Our studies indicate the selective inhibition of EphA2 at the tumor-bone interface may be a benefit for the treatment of breast-to-bone metastases Advisors/Committee Members: Pampee Young (committee member), Charles Lin (committee member), Jin Chen (committee member), Lynn Matrisian (Committee Chair).

Subjects/Keywords: Branching Morphogenesis; Mammary Gland; Bone Metastasis; Breast Cancer; EphA2; IL-6

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APA (6^th Edition):

Vaught, D. B. (2011). EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11610

Chicago Manual of Style (16^th Edition):

Vaught, David Bryan. “EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/11610.

MLA Handbook (7^th Edition):

Vaught, David Bryan. “EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis.” 2011. Web. 04 Mar 2021.

Vancouver:

Vaught DB. EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/11610.

Council of Science Editors:

Vaught DB. EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/11610

Vanderbilt University

25. Kurley, Sarah Jean. The role of p120 catenin in mammary development and breast cancer.

Degree: PhD, Cancer Biology, 2012, Vanderbilt University

URL: http://hdl.handle.net/1803/11120

► Cadherins and catenins are important regulators of tissue homeostasis and cancer. Here, we report critical roles for p120 catenin (p120) in mammary development and breast… (more)

Subjects/Keywords: mammary gland; cadherin; catenin; p120; metastasis; breast cancer

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APA (6^th Edition):

Kurley, S. J. (2012). The role of p120 catenin in mammary development and breast cancer. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11120

Chicago Manual of Style (16^th Edition):

Kurley, Sarah Jean. “The role of p120 catenin in mammary development and breast cancer.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed March 04, 2021. http://hdl.handle.net/1803/11120.

MLA Handbook (7^th Edition):

Kurley, Sarah Jean. “The role of p120 catenin in mammary development and breast cancer.” 2012. Web. 04 Mar 2021.

Vancouver:

Kurley SJ. The role of p120 catenin in mammary development and breast cancer. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1803/11120.

Council of Science Editors:

Kurley SJ. The role of p120 catenin in mammary development and breast cancer. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/11120

Texas A&M University

26. Scribner, Kelly C. Regulation of Mammary cell Differentiation and Metabolism by Singleminded-2s.

Degree: PhD, Toxicology, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151007

► Ductal carcinoma in situ (DCIS) has been shown to be a precursor to invasive ductal cancer (IDC). Though the progression of DCIS to IDC is… (more)

▼ Ductal carcinoma in situ (DCIS) has been shown to be a precursor to invasive ductal cancer (IDC). Though the progression of DCIS to IDC is believed to be an important aspect of tumor aggressiveness, prognosis and molecular markers that predict progression are poorly understood. Therefore, determining the mechanisms by which some DCIS progress is critical for future breast cancer diagnostics and treatment. Singleminded-2s (SIM2s) is a member of the bHLH/PAS family of transcription factors and a key regulator of differentiation. SIM2s is highly expressed in mammary epithelial cells and lost in breast cancer. Loss of Sim2s causes aberrant mouse mammary development with features suggestive of malignant transformation, whereas over-expression of Sim2s promotes precocious alveolar differentiation, suggesting that Sim2s is required for establishing and enhancing mammary gland differentiation. We hypothesize that SIM2s expression must be lost in premalignant lesions for breast cancer to develop. We first analyzed Sim2s in the involuting mammary gland, which is a highly tumorpromoting environment. Sim2s is down-regulated during involution, and forced expression delays involution. We then analyzed SIM2s expression in human breast cancer samples and found that SIM2s is lost with progression from DCIS to IDC, and this loss correlates with metastasis. SIM2s expression in DCIS promoted a differentiated phenotype and suppressed genes associated with de-differentiation. Furthermore, loss of SIM2s expression in DCIS xenografts increased metastasis likely due to an increase in hedgehog signaling and matrix metalloproteinase expression. Interestingly, we found metabolic shifts with gain and loss of SIM2s in not only DCIS cells, but also MCF7 and SUM159 cells. SIM2s expression decreased aerobic glycolysis and promoted oxidative phosphorylation through direct upregulation of CDKN1a and senescence. Loss of SIM2s, conversely, promotes mitochondrial dysfunction and induction of the Warburg effect. This is the first time CDKN1a and cellular senescence have been indicated as causative to metabolic shifts within cancer cells. These studies show a new role for SIM2s in metabolic homeostasis, and this regulation is lost during tumorigenesis. These data indicate SIM2s is at the apex where aging, metabolism, and disease meet – regulating the delicate relationship between the three. Advisors/Committee Members: Porter, Weston W (advisor), Safe, Stephen (committee member), Dindot, Scott (committee member), Dees, W. Les (committee member), Phillips, Tim (committee member).

Subjects/Keywords: Breast Cancer; Warburg Effect; Metabolism; Singleminded-2s; Mammary gland

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APA (6^th Edition):

Scribner, K. C. (2013). Regulation of Mammary cell Differentiation and Metabolism by Singleminded-2s. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151007

Chicago Manual of Style (16^th Edition):

Scribner, Kelly C. “Regulation of Mammary cell Differentiation and Metabolism by Singleminded-2s.” 2013. Doctoral Dissertation, Texas A&M University. Accessed March 04, 2021. http://hdl.handle.net/1969.1/151007.

MLA Handbook (7^th Edition):

Scribner, Kelly C. “Regulation of Mammary cell Differentiation and Metabolism by Singleminded-2s.” 2013. Web. 04 Mar 2021.

Vancouver:

Scribner KC. Regulation of Mammary cell Differentiation and Metabolism by Singleminded-2s. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/1969.1/151007.

Council of Science Editors:

Scribner KC. Regulation of Mammary cell Differentiation and Metabolism by Singleminded-2s. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151007

Penn State University

27. Turbitt, William James. THE EFFECTS OF CHANGES IN ENERGY BALANCE ON IMMUNE REGULATION AND TUMOR PROGRESSION IN THE 4T1.2 MAMMARY TUMOR MODEL.

Degree: 2017, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/14336wjt5015

► One significant challenge in the field of breast cancer (BC) research is to determine how to reduce and/or eliminate the mortality associated with metastatic BC.… (more)

▼ One significant challenge in the field of breast cancer (BC) research is to determine how to reduce and/or eliminate the mortality associated with metastatic BC. Novel therapies, especially non-pharmacological, lifestyle-based interventions that prevent or slow metastatic disease with less severe side effects are greatly needed. Numerous lifestyle factors (including dietary components, body weight, and physical activity patterns) significantly impact BC risk and survival. Emerging population data suggests an inverse relation between physical activity and BC incidence, as well as an important role for exercise in the prevention of cancer recurrence and mortality. The observational nature of these studies limit the ability to determine biological mechanisms and the extent to which exercise, as opposed to changes in body weight, drive beneficial effects. Additionally, very little is known about the mechanisms contributing to the relation between physical activity and survival. Given the importance of metastases in the mortality of women with BC, understanding the role of exercise on metastatic burden may reveal important new targets for secondary and tertiary cancer prevention. The aim of study one was to control for weight and examine the effects of exercise, mild dietary restriction, or the combination of diet and exercise on the inflammation-immune axis and tumor progression in a preclinical metastatic BC model to determine the extent to which exercise or body weight contribute to cancer prevention. Dietary energy restriction-induced weight control (i.e., SED+ER mice) was effective at altering host splenic immunity and the expression of key genes in the tumor microenvironment (TME) related to immunosuppression and metastatic progression; however, this intervention failed to induce changes in primary tumor growth or spontaneous metastases. Moderate exercise in weight stable mice (EX+ER) resulted in a similar reduction in immunosuppressive and metastatic genes in the TME compared with the SED+ER mice; however, in addition, EX+ER mice had the greatest reduction in splenic immunosuppressive cells and plasma insulin-like growth factor-1 (IGF-1). The effects of moderate exercise in weight stable mice culminated in a significant delay in primary tumor growth and spontaneous metastases, suggesting that exercise-induced alterations in metabolic drivers of tumorigenesis, not simply a change in body weight, underlie the protective effects in the dual intervention group. Interestingly the exercise-induced protective effect on the emergence of immunosuppressive factors and reduced tumor burden was lost when mice continued to gain weight over the course of the study, suggesting that weight gain-induced disturbances on hormonal, inflammatory, and/or immunological function can override the exercise-induced benefits. Collectively, study one provided a deeper understanding of the extent to which exercise, and changes in body weight, underlies cancer protection. Few researchers have examined the effect of energy balance… Advisors/Committee Members: Connie Jo Rogers, Dissertation Advisor/Co-Advisor, Connie Jo Rogers, Committee Chair/Co-Chair, Matam Vijay Kumar, Committee Member, Kumble Sandeep Prabhu, Committee Member, Andrea Marie Mastro, Outside Member.

Subjects/Keywords: Cancer immunology; exercise; energy balance; 4T1.2 model; metastasis; mammary tumor model

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

APA (6^th Edition):

Turbitt, W. J. (2017). THE EFFECTS OF CHANGES IN ENERGY BALANCE ON IMMUNE REGULATION AND TUMOR PROGRESSION IN THE 4T1.2 MAMMARY TUMOR MODEL. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/14336wjt5015

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):

Turbitt, William James. “THE EFFECTS OF CHANGES IN ENERGY BALANCE ON IMMUNE REGULATION AND TUMOR PROGRESSION IN THE 4T1.2 MAMMARY TUMOR MODEL.” 2017. Thesis, Penn State University. Accessed March 04, 2021. https://submit-etda.libraries.psu.edu/catalog/14336wjt5015.

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

MLA Handbook (7^th Edition):

Turbitt, William James. “THE EFFECTS OF CHANGES IN ENERGY BALANCE ON IMMUNE REGULATION AND TUMOR PROGRESSION IN THE 4T1.2 MAMMARY TUMOR MODEL.” 2017. Web. 04 Mar 2021.

Vancouver:

Turbitt WJ. THE EFFECTS OF CHANGES IN ENERGY BALANCE ON IMMUNE REGULATION AND TUMOR PROGRESSION IN THE 4T1.2 MAMMARY TUMOR MODEL. [Internet] [Thesis]. Penn State University; 2017. [cited 2021 Mar 04]. Available from: https://submit-etda.libraries.psu.edu/catalog/14336wjt5015.

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

Council of Science Editors:

Turbitt WJ. THE EFFECTS OF CHANGES IN ENERGY BALANCE ON IMMUNE REGULATION AND TUMOR PROGRESSION IN THE 4T1.2 MAMMARY TUMOR MODEL. [Thesis]. Penn State University; 2017. Available from: https://submit-etda.libraries.psu.edu/catalog/14336wjt5015

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

Michigan State University

28. Stoica, Gheorghe. In vivo diverse spectrum of neoplasms induced in 30-day-old rats and in vitro neoplastic transformation of rat mammary epithelial cells following a single pulse of N-Ethyl-N-Nitrosourea.

Degree: PhD, Department of Pathology, 1984, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:35907

Subjects/Keywords: Carcinogens; Tumors; Mammary glands – Cancer

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

APA (6^th Edition):

Stoica, G. (1984). In vivo diverse spectrum of neoplasms induced in 30-day-old rats and in vitro neoplastic transformation of rat mammary epithelial cells following a single pulse of N-Ethyl-N-Nitrosourea. (Doctoral Dissertation). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:35907

Chicago Manual of Style (16^th Edition):

Stoica, Gheorghe. “In vivo diverse spectrum of neoplasms induced in 30-day-old rats and in vitro neoplastic transformation of rat mammary epithelial cells following a single pulse of N-Ethyl-N-Nitrosourea.” 1984. Doctoral Dissertation, Michigan State University. Accessed March 04, 2021. http://etd.lib.msu.edu/islandora/object/etd:35907.

MLA Handbook (7^th Edition):

Stoica, Gheorghe. “In vivo diverse spectrum of neoplasms induced in 30-day-old rats and in vitro neoplastic transformation of rat mammary epithelial cells following a single pulse of N-Ethyl-N-Nitrosourea.” 1984. Web. 04 Mar 2021.

Vancouver:

Stoica G. In vivo diverse spectrum of neoplasms induced in 30-day-old rats and in vitro neoplastic transformation of rat mammary epithelial cells following a single pulse of N-Ethyl-N-Nitrosourea. [Internet] [Doctoral dissertation]. Michigan State University; 1984. [cited 2021 Mar 04]. Available from: http://etd.lib.msu.edu/islandora/object/etd:35907.

Council of Science Editors:

Stoica G. In vivo diverse spectrum of neoplasms induced in 30-day-old rats and in vitro neoplastic transformation of rat mammary epithelial cells following a single pulse of N-Ethyl-N-Nitrosourea. [Doctoral Dissertation]. Michigan State University; 1984. Available from: http://etd.lib.msu.edu/islandora/object/etd:35907

University of Notre Dame

29. Kristi Marie Bray. Investigating the Role of Cdc42 in Mammary Gland Development and Breast Cancer</h1>.

Degree: Biological Sciences, 2013, University of Notre Dame

URL: https://curate.nd.edu/show/tx31qf88477

► Breast cancer is the most frequently diagnosed cancer in women and is responsible for the largest number of cancer related deaths in women across… (more)

▼ Breast cancer is the most frequently diagnosed cancer in women and is responsible for the largest number of cancer related deaths in women across the globe. Basic research into the roles of cancer-related genes in normal development is crucial to understanding their roles in cancer and will aid in developing new targeted therapies. Altered expression of the Rho GTPases and their regulators is associated with breast cancer. The focus of my project was to investigate the role of the Rho GTPase Cdc42 during normal mammary gland (MG) development to define the key cellular processes regulated by Cdc42, as deregulation of these processes may occur when the expression and activity of Cdc42 is elevated during the development and progression of breast cancer. Using novel conditional knockout (KO) and overexpression (OE) mouse MG models, my studies revealed for the first time critical roles for Cdc42 in mammary epithelial proliferation, migration, adhesion, stromal interactions, and morphogenesis and support a working hypothesis for how Cdc42 is functioning during MG development. In the context of normal levels of Cdc42 expression, Cdc42 participates in the Par/PKC zeta polarity complex to form tight junctions, establish epithelial polarity, and promote normal proliferation and morphogenesis of the mammary ductal tree. In the absence of Cdc42, the complete polarity complex cannot form, thus tight junctions and polarity cannot be established. Without these important initial steps the mammary epithelial cells (MECs) cannot properly organize and ultimately their ability to survive and/or contribute to MG morphogenesis is compromised, resulting in small dysmorphic mammary acini in vitro. In vivo, the KO MECs are rapidly outcompeted by wildtype (WT) MECs. Conversely, when Cdc42 is overexpressed, the polarity complex can form but the signaling downstream of this complex may become unbalanced. The tight, spatial and temporal control that is important for normal development may be tipped, causing increased contractility and aberrant migration, resulting in a dysmorphic hyperbranched MG. Evidence from our Cdc42 KO and Cdc42 OE mouse MG development models, together with published studies, suggest that Cdc42 plays an important role in breast cancer. Our work provides strong motivation for future studies investigating the role of Cdc42 in mouse mammary tumor models. Advisors/Committee Members: Robert Schulz, Committee Member, Suzie Bohlson, Committee Member, Crislyn D'Souza-Schorey, Committee Member, Joseph O'Tousa, Committee Member, Tracy Vargo-Gogola, Committee Chair.

Subjects/Keywords: mammary gland development; breast cancer; Rho GTPases; Cdc42

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

APA (6^th Edition):

Bray, K. M. (2013). Investigating the Role of Cdc42 in Mammary Gland Development and Breast Cancer</h1>. (Thesis). University of Notre Dame. Retrieved from https://curate.nd.edu/show/tx31qf88477

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):

Bray, Kristi Marie. “Investigating the Role of Cdc42 in Mammary Gland Development and Breast Cancer</h1>.” 2013. Thesis, University of Notre Dame. Accessed March 04, 2021. https://curate.nd.edu/show/tx31qf88477.

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

MLA Handbook (7^th Edition):

Bray, Kristi Marie. “Investigating the Role of Cdc42 in Mammary Gland Development and Breast Cancer</h1>.” 2013. Web. 04 Mar 2021.

Vancouver:

Bray KM. Investigating the Role of Cdc42 in Mammary Gland Development and Breast Cancer</h1>. [Internet] [Thesis]. University of Notre Dame; 2013. [cited 2021 Mar 04]. Available from: https://curate.nd.edu/show/tx31qf88477.

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

Council of Science Editors:

Bray KM. Investigating the Role of Cdc42 in Mammary Gland Development and Breast Cancer</h1>. [Thesis]. University of Notre Dame; 2013. Available from: https://curate.nd.edu/show/tx31qf88477

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

California State University – Sacramento

30. Abrahamsson, Ninnie Marie-Louice. Prospective identification of the pre-cancer stem cell.

Degree: MA, Biological Science (Stem Cell, 2011, California State University – Sacramento

URL: http://hdl.handle.net/10211.9/1119

► Ductal Carcinoma In Situ (DCIS) is considered the earliest form of breast cancer where cells that appear malignant develop into benign heterogneous lesions confined within… (more)

▼ Ductal Carcinoma In Situ (DCIS) is considered the earliest form of breast cancer where cells that appear malignant develop into benign heterogneous lesions confined within the epithelial membrane, yet progression to invasive ductal carcinoma frequently occurs. Therefore, treatment of the disease is equal to preventing development of invasive cancer. It has previously been suggested that the cells of DCIS may already be programmed to become invasive, which led to the speculation that a small population of cancer stem cells, sharing characteristics with normal stem cells, are responsible for the development of invasive cancer. As a mammary gland stem cell population that increases in size with tumor progression has previously been identified using FACS, along with transplantation experiments revealing a capability to regenerate the ductal tree, the goal of this project was to identify the pre-cancer stem cell population using a mouse model representative of human DCIS and previously established surface markers CD24, CD29 and CD49f. However, identification of the pre-cancer stem cells in the DCIS mouse model using the aforementioned surface markers was proven unsuccessful, and thus novel markers CD44 and CD61 were added to the selectional process to increase specificity. The results of this study revealed a putative stem cell population with a CD24low CD29high CD49fhigh expression profile within mammary glands of normal FVB mice as well as in the pre-cancer mouse model. The data further revealed an increased expression of CD44 in the same population, with respect to the DCIS mouse model as well as in normal mammary glands. However, CD61 expression was increased in a CD24negative CD29low CD49flow population, indicating a possible luminal epithelial origin. The results furthermore revealed an increase in the stem cell population with carcinoma progression through comparisons of DCIS lesions, DCIS derived tumors and a tumor cell line. In summary, the results of this study indicates that a pre-cancer stem cell population may be distinguished based on the expression of surface markers CD24, CD29, CD49f and CD44, and seems to correlate with their expansion and progression to invasive cancer. These findings should significantly improve the isolation of the pre-cancer stem cell population in DCIS, and thus may lead to new treatments aimed at eliminating the cancer stem cells. Advisors/Committee Members: Peavy, Thomas R..

Subjects/Keywords: Cancer stem cells; DCIS; Mammary stem cell surface markers

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

APA (6^th Edition):

Abrahamsson, N. M. (2011). Prospective identification of the pre-cancer stem cell. (Masters Thesis). California State University – Sacramento. Retrieved from http://hdl.handle.net/10211.9/1119

Chicago Manual of Style (16^th Edition):

Abrahamsson, Ninnie Marie-Louice. “Prospective identification of the pre-cancer stem cell.” 2011. Masters Thesis, California State University – Sacramento. Accessed March 04, 2021. http://hdl.handle.net/10211.9/1119.

MLA Handbook (7^th Edition):

Abrahamsson, Ninnie Marie-Louice. “Prospective identification of the pre-cancer stem cell.” 2011. Web. 04 Mar 2021.

Vancouver:

Abrahamsson NM. Prospective identification of the pre-cancer stem cell. [Internet] [Masters thesis]. California State University – Sacramento; 2011. [cited 2021 Mar 04]. Available from: http://hdl.handle.net/10211.9/1119.

Council of Science Editors:

Abrahamsson NM. Prospective identification of the pre-cancer stem cell. [Masters Thesis]. California State University – Sacramento; 2011. Available from: http://hdl.handle.net/10211.9/1119

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Open Access Theses and Dissertations