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Dissertations / Theses on the topic 'Breast Metastasis'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Weigelt, Britta. "Molecular markers of breast cancer metastasis." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/88848.

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2

LeBedis, Christina. "Lymph node involvement in breast carcinoma metastasis." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31255.

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Since lymph node stromal cells remain largely uncharacterized with respect to cell surface markers and function, their role in regulating the growth and invasion of disseminated cancer cells, including breast carcinoma has, to date, been virtually unexplored. In the present study, we asked whether peripheral lymph node cells could modulate the growth of breast carcinoma cells and, thereby, contribute to the progression of the metastatic process. Primary cultures of rat peripheral lymph node stromal cells were obtained by limiting dilution and two sublines, STA4 and STB12, with breast carcinoma

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3

Mourskaia, Anna. "Molecular mediators of breast cancer bone metastasis." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114138.

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Breast cancer is the most frequently diagnosed and the second leading cause of cancer deaths in Canadian women. The most devastating and deadly feature of the disease is the emergence of metastases. Breast cancer most commonly metastasizes to bone, often leading to a significantly decreased quality of life in affected patients. Despite progress in understanding the underlying molecular biology of breast tumors that relapse to bone, to date there are no therapies capable of curing the disease. Hence, it is essential to gain a more in-depth knowledge of the molecular mechanisms that underlie the

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4

Lopez, Jose Ignacio. "CD44 Attenuates Metastasis During Breast Cancer Progression." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/193882.

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Progression to metastatic disease is the leading cause of deaths resulting from breast cancer. Understanding the mechanisms underlying a cell's ability to move away from its site of origin and populate a distant site is important for the future development of therapies. The interactions between a tumor cell and the microenvironment can modulate a cell's ability to invade through tissues and access distant organs. In this study we present evidence indicating the differential modulation of invasive and proliferative phenotypes by hyaluronan present in the cellular microenvironment.We establis

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5

Harihar, Sitaram. "The Role of Phosphoinositide Signaling in Breast Cancer Metastasis Suppressor 1-Mediated Metastasis Suppression of Human Breast Carcinoma Cells." DigitalCommons@USU, 2011. https://digitalcommons.usu.edu/etd/870.

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Breast cancer is the most common non-skin cancer in women and the second most common cause of cancer-related death in U.S. women. Despite numerous advances in treatment strategies against breast cancer, the presence of undetected distant metastasis of the primary tumor remains the main cause of mortality. Current screening and detection methods such as mammograms are simply not sensitive enough to detect formation of metastasis. Further, currently available therapies against metastatic breast cancer do not provide a complete cure for the disease. Thus, understanding the biology and molecular f

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6

Cunnick, Giles Harvey. "Lymphangiogenesis and lymphatic metastasis in human breast cancer." Thesis, St George's, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399219.

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7

Xing, Fei. "ROLE OF NOTCH SIGNALING IN BREAST CANCER METASTASIS." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/514.

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Notch signaling is often and aberrantly activated by hypoxia during tumor progression; however, the exact pathological role of hypoxia-induced Notch signaling in tumor metastasis is as yet poorly understood. In the first part of this study, we aimed to define the mechanism of Notch ligand activation by hypoxia in both primary tumor and bone stromal cells in the metastatic niche and to clarify their roles in tumor progression. We have analyzed the expression profiles of various Notch liagnds in 779 breast cancer patients in GEO database and found that the expression of Jagged2 among all five

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8

Leonard, Marissa. "Overcoming Breast Cancer Metastasis with Novel RNA Aptamers." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1572879601351414.

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9

Adorno-Cruz, Valery. "Identifying Stemness and Metastasis Drivers in Breast Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case158687657816132.

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10

Gooding, Alex Joseph. "Characterizing a Role for the lncRNA BORG during Breast Cancer Progression and Metastasis." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1528462540265762.

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11

Hall, Kelly L. "Angiopoietin-2 overexpression promotes hematogenous metastasis in breast cancer /." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1967985931&sid=2&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (M.S.)--Southern Illinois University Carbondale, 2009.<br>"Department of Medical Microbiology, Immunology, and Cell Biology." Includes bibliographical references (p. 97-133). Also available online.

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12

Hall, Kelly. "ANGIOPOIETIN-2 OVEREXPRESSION PROMOTES HEMATOGENOUS METASTASIS IN BREAST CANCER." OpenSIUC, 2009. https://opensiuc.lib.siu.edu/theses/154.

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Angiogenesis supports tumor growth and facilitates metastasis, the leading cause of patient mortality in breast and other types of solid tumors. Angiopoietin-2 (Ang-2) is an angiogenic factor whose overexpression is associated with increased tumor vascularity, metastasis, and decreased patient survival. We assessed the effects of Ang-2 on breast tumor vasculature by comparing vascular morphology and metastasis of orthotopically implanted metastatic breast carcinoma line MDA-MB-231 that either lacked or overexpressed Ang-2. Methods: Luciferase-tagged MDA-MB-231 breast carcinoma cells designated

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13

Zhang, Xuejing. "Targeting Thromboxane A2 Receptor Signaling in Breast Cancer Metastasis." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/518.

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Breast cancer is the most common type of cancer among women in the United States and metastasis is the leading cause of mortality in patients diagnosed with malignant breast cancer. The receptor of thromboxane A2 (TxA2), TP, is a member of the G-protein coupled receptor family. Increased expression of TP at RNA level was found to correlate with a poor prognosis in breast cancer patients; however, it is unknown how TP expression and activities are involved in breast cancer progression. Here we report that TP is expressed in breast cancer cells at both RNA and protein levels. And further, activa

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14

Suciu, Diana J. "NEURAL ACTIVITY WITHIN SOLID BREAST TUMORS AND THE IMPLICATIONS ON METASTASIS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1528117273992639.

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15

Holz, David R. "Investigating Molecular Mechanisms Driving Breast Cancer Metastasis into the CNS." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/221276.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.<br>This research project aims to identify unique candidate genes involved in breast cancer metastatic invasion into the central nervous system (CNS). The goal of this study focuses on studying and comparing the genomes of two distinct breast cancer cell lines that model a primary breast cancer and a CNS metastatic variant. These cell lines were established by Yoneda et al. by employing six serial rounds of tumor injection into mice follo

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16

Harrell, Joshua C. "Dissecting roles of estrogen receptors in breast cancer lymphatic metastasis /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Reproductive Sciences) -- University of Colorado Denver, 2007.<br>Typescript. Includes bibliographical references (leaves 125-140). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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17

Gupta, Gaorav. "Breast cancer metastasis to the lungs : from genes to mechanisms /." Access full-text from WCMC :, 2007. http://proquest.umi.com/pqdweb?did=1456287491&sid=10&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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18

Turnham, Daniel. "Understanding the role of Bcl-3 in breast cancer metastasis." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/105140/.

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Despite recent advances in the treatment and detection of breast cancer it still remains the third most common cause of death from cancer in the UK as a result of its final metastatic stage, which is currently incurable. Numerous targets have been identified in an attempt to prevent and treat this highly aggressive form of cancer with limited success, however recent work has highlighted B-cell lymphoma 3 (Bcl-3) as a promising therapeutic target. Bcl-3 is a mediator of the well characterised NF-kB signalling pathway and both have been implicated with promoting tumour growth and progression. Th

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19

Snyder, Kimberly Ashley. "The role of podocalyxin in breast cancer progression and metastasis." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46014.

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20

Werbeck, Jillian Lee. "Genetic Contributions of the Tumor Microenvironment in Breast Cancer Metastasis." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306436090.

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21

Adoki, Samson. "Involvement of scribble protein in breast cancer invasion and metastasis." Thesis, University of Essex, 2016. http://repository.essex.ac.uk/17655/.

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A common feature of cancer cells is the loss of cell polarity. Scribble is a cell polarity protein with an unknown mechanism for its role in tumour suppression. Changes in the phosphorylation pattern of four serine sites at the C-terminal of scribble, implicate scribble in breast cancer invasion and metastasis. This was due to CD74 overexpression in lymph node metastatic triple negative breast cancers. Investigating how changes in serine phosphorylation status at these sites affect the regulation of invasion and metastasis in breast cancer was the focus of this study. These sites were mutated

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22

Chen, Wanqing. "Predictors of axillary lymph node involvement in screen-detected breast cancer." Connect to full text, 2004. http://setis.library.usyd.edu.au/adt/public_html/adt-NU/public/adt-NU20050104.165451/index.html.

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Thesis (M.I.P.H.)--School of Public Health, University of Sydney, 2004.<br>"This treatise is submitted in partial satisfaction of the requirements for the Degree of Master of International Public Health (Hons), University of Sydney". Bibliography: leaves 10-15.

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23

Qazi, Romena. "The role of the urokinase family in invasion by breast cancer." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266538.

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24

Pavlovic, Milica 1985. "Identification of genetic determinants of breast cancer metastasis to the bone." Doctoral thesis, Universitat Pompeu Fabra, 2014. http://hdl.handle.net/10803/385911.

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El objetivo de esta tesis era identificar determinantes genéticos de cáncer de mama con metástasis óseas. Para ello se utilizó un enfoque integral que se sustenta en células humanas de cáncer de mama, modelos experimentales de ratón y datos clínicos. En primer lugar, nos centramos en los genes específicamente adquiridos para la metástasis ósea, altamente expresados en las lesiones de metástasis óseas, pero no enriquecidos en los tumores primarios de mama que recaen en el hueso. Entre estos genes, el factor secretado NOG destaca como altamente expresado en células de cáncer de mama, principalme

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25

Osborne, Chloe E. "Functional role of Helix pomatia binding glycans in breast cancer metastasis." Thesis, Oxford Brookes University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402293.

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26

Harvey, James R. "Blockade of breast cancer metastasis by disruption of chemokine/glycosaminoglycan interactions." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427329.

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27

Wu, Hailong. "MicroRNAs that affect breast cancer growth, metastasis and estrogen-independent growth /." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1879689221&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Thesis (Ph. D.)--Southern Illinois University Carbondale, 2009.<br>"Department of Medical Microbiology, Immunology and Cell Biology." Keywords: Breast cancer, Estrogen-independent, miRNAs, Metastasis. Includes bibliographical references (p. 92-118). Also available online.

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28

Shirure, Venktesh S. "Molecular Mechanisms of Circulating Tumor Cell Adhesion in Breast Cancer Metastasis." Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1357706517.

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29

Mancini, Stephanie Sarah Jane. "The putative role of matrix metalloproteinase 13 and oncostatin M in the establishment of bone metastases." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/4179.

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Breast cancer has a high propensity to metastasize to bone. While the genetic and epigenetic changes associated with metastatic breast cancer progression are being identified, the changes that drive metastatic progression are poorly understood. Proteases, and in particular matrix metalloproteinases (MMPs), have been shown to play a pivotal role in certain aspects of tumor metastasis by modifying the affected microenvironment. Bone matrix-depositing mouse MC3T3 osteoblasts were co-cultured with metastatic human MDA-MB-23 1 (MDA23 1) cells or the bone-homing MDA-MB 231-1 833/TR (1 833/TR) varian

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30

Lee, Kai-chung Arthur, and 李啓聰. "The prognostic significance of lymphatic and blood vessel invasion, angiogenesis and occult nodal metastasis in breast carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31981604.

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31

Cerneaz, Nicholas J. "Model-based analysis of mammograms." Thesis, University of Oxford, 1994. http://ora.ox.ac.uk/objects/uuid:a8d91bb2-429c-4da3-9f1b-6209771c61b5.

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Metastasised breast cancer kills. There is no known cure, there are no known preventative measures, there are no drugs available with proven capacity to abate its effects. Early identification and excision of a malignancy prior to metastasis is the only method currently available for reducing the mortality due to breast disease. Automated analysis of mammograms has been proposed as a tool to aid radiologists detect breast disease earlier and with greater efficiency and success. This thesis addresses some of the major difficulties associated with the automated analysis of mammograms, in particu

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32

Stillfried, Gillian Erika. "Urokinase-dependent plasminogen binding and activation on breast cancer cells an important process linked to malignancy /." Access electronically, 2007. http://ro.uow.edu.au/theses/13.

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33

Nouhi, Zaynab. "Prolactin plays a dual role in breast cancer : promoting formation of breast tumour while inhibiting its metastasis." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97983.

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Prolactin is a key mammary gland differentiation factor. However, the contribution of prolactin (PRL) to breast carcinogenesis is less clear. Accumulating evidences indicate that in established breast carcinomas autocrine/paracrine PRL can enhance growth/viability of breast cancer cells. Still, it is not known whether the ascribed pro-oncogenic activity of PRL describes fully the role of PRL in regulating breast carcinogenesis. On the other hand a critical role for Ras-Erk1/2 and TGF-beta (Transforming Growth Factor beta) pathway in breast cancer progression has already been established. Our r

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34

McIlroy, James W. "The detection and characterization of cysteine and serine proteases in breast cancer and osteosarcoma." Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318795.

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35

Donaldson, E. A. "Characterisation of the 67 kilodalton laminin receptor (67 LR) in breast cancer." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368772.

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36

Huber, Jennifer. "The role of Dock180 in ErbB2-mediated breast cancer tumorigenesis and metastasis." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97036.

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The ErbB2 receptor is found to be overexpressed and/or amplified in 20-30% of all breast cancer cases, which tend to have aggressive behaviors and often metastasize to distant organs making them difficult to treat in the clinic. It has been previously shown that the Dock180 and ELMO1 proteins work together to promote cell motility and invasion in a Rac-dependant manner under physiological and pathological conditions. Rac is a small GTPase well known to act on proliferation, migration and invasion and has been linked to development and metastasis of several types of human cancers. This prompted

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37

Arenas, Lahuerta Enrique Javier. "Identification of novel mechanisms in human breast cancer lung metastasis and chemoresistance." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/404730.

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Breast Cancer (BC) is one of the major causes of cancer deaths in women. BC is a heterogeneous disease, and within the heterogeneity of the tumor, Tumor-Initiating Cells (TICs) have been reported as important drivers in tumor initiation and progression. On the basis of these observations, we hypothesized that TICs contribute to BC metastasis, as well to chemoresistance. Through genetic, transcriptomic, molecular and therapeutic analyses of tumor xenografts, BC cell lines, and/or human tumors, in this thesis we first demonstrate that RARRES3, a lung metastatic suppressor gene, prevents adhesion

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38

Reyes, Andres. "The role of E2F3 in the macrophage assisted metastasis of breast cancer." Connect to resource, 2007. http://hdl.handle.net/1811/28359.

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Thesis (Honors)--Ohio State University, 2007.<br>Title from first page of PDF file. Document formatted into pages: contains [23] p.; also includes graphics. Includes bibliographical references. Available online via Ohio State University's Knowledge Bank.

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39

Zhu, Li, and 朱麗. "Determination of predictive markers related to micro-metastasis in breast cancer patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30330919.

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40

Zhai, Yubo. "REDEFINING THE MOLECULAR BASIS OF EPITHELIAL MESENCHYMAL TRANSITION IN BREAST CANCER METASTASIS." Master's thesis, Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/216586.

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Biochemistry<br>M.S.<br>Metastasis is a multi-step process that begins with cancer cells migrating and invading away from the primary tumor site and extravasating into distant organs to establish a secondary tumor. The loss of epithelial expression markers by neoplastic breast cancer cells in the primary tumor is believed to play a pivotal role during breast cancer metastasis. This phenomenon is the hallmark of the epithelial mesenchymal transition (EMT) process. Gene expression microarrays were performed to investigate key functional elements on an in vitro metastasis model derived from human

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41

Carthew, James Robert. "Characterising LINC complex roles in 3D epithelial migration and breast cancer metastasis." Thesis, Durham University, 2016. http://etheses.dur.ac.uk/11453/.

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Cell migration is essential for the development of multicellular organisms; with disruptions in this process contributing to diseases such as cancer, neurological disorders and musculoskeletal diseases. The LINC (Linker of Nucleoskeleton and Cytoskeleton) complex is an evolutionary conserved proteinaceous structure, critical for maintaining proper cellular migration. This multifunctional complex provides a physical connection between the nuclear interior and the cytoskeleton, with disruptions stimulating loss of directed cell migration, compromised nuclear structure and abnormal cellular signa

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42

Seachrist, Darcie Dawn. "Elucidation of Metastasis-promoting Mechanisms of Activin and BCL11A in Breast Cancer." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1600271384300217.

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43

OKAMOTO, TOMOMITSU, SHIGEKO SAITO, SHIHO TANAKA, SACHI NAGAI, YUKIKO MORI, and MAI HORIKAWA. "METASTATIC BREAST CANCER TO THE UTERINE CERVIX MIMICKING A GIANT CERVICAL LEIOMYOMA." Nagoya University School of Medicine, 2012. http://hdl.handle.net/2237/16745.

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44

Fumagalli, Debora. "Evaluation of tumor heterogeneity in breast cancer." Doctoral thesis, Universite Libre de Bruxelles, 2016. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/229735.

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Le cancer du sein est le cancer le plus fréquent chez la femme et représente la principale cause de mortalité liée au cancer. Le décés est habituellement causé par le développement de résistance aux traitements et la propagation métastatique de la maladie. Malgré la pertinence clinique, la complexité moléculaire de la maladie et sa dynamique restent à ce jour peu connues.Depuis longtemps, l’hétérogénéité du cancer du sein a été observée au niveau histologique et du profil évolutif clinique, et ces différences ont servi de base pour la classification de la maladie. Avec le développement des tec

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45

Mendes, Odete Rodrigues. "Role of MMP2, MMP3 and MMP9 in the development of breast cancer brain and lung metastasis in a syngeneic rat model." Texas A&M University, 2005. http://hdl.handle.net/1969.1/2645.

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In order to study the expression of MMP2, MMP 3 and MMP9 in breast cancer brain and lung metastasis, we used a syngeneic rat model of distant metastasis of ENU1564, a carcinogen-induced mammary adenocarcinoma cell line. At six weeks post inoculation we observed development of micro-metastasis in the brain and lung. Immunohistochemistry and Western blotting analyses showed that MMP 2, -3 and -9 protein expression is consistently significantly higher in neoplastic brain tissue compared to normal brain tissue. Lung metastases express abundant MMP2, -3 and -9 in neoplastic cell cytoplasm. In situ

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46

Keskin, Doruk. "Functional Contribution of PDGFRbeta+ Cells in Angiogenesis and Metastatic Breast Cancer." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11085.

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Tumor stroma is known to affect tumor growth and metastasis. Inhibiting PDGF signaling, with the goal of depleting PDGFRβ+ stromal cells, is a putative therapeutic approach in this context. PDGFRβ is widely accepted as a pericyte marker and targeting PDGF signaling primarily affects pericytes. Pericyte-endothelial cell interactions modulate angiogenesis and vascular stability in developmental and pathological contexts. Owing to this, pericytes are speculated to be important regulators of tumor growth and metastasis, although their role is not clear.

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47

He, Felicia Jane. "Targeting Metastatic Breast Cancer Using Dual-Ligand Nanoparticles." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499699087340348.

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48

Talvensaari-Mattila, A. (Anne). "MMP-2 immunoreactive protein in breast carcinoma and neoplastic cervical lesions:mMP-2 is a new prognostic factor in breast carcinoma." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514254023.

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Abstract Tumor invasion and metastasis are the major causes of treatment failure or death for carcinoma patients. Matrix metalloproteinases (MMPs) are zinc dependent endopeptidases implicated in tumor invasion and metastasis. The expression of MMP-2 has been previously linked to invasiveness of carcinoma cells. The MMP-2 immunoreactive protein was studied here in squamous cell carcinoma of the utrine cervix and in adenocarcinoma of the breast by using a specific monoclonal antibody in immunohistochemical stainings. Immunoreactive protein of latent MMP-2 was found to be an early event in neopla

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49

Hill, A. M. "Identification and characterisation of transcriptional targets underpinning CD44 promoted metastasis of breast cancer." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411196.

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50

Draffin, J. E. "Investigation of the molecular basis of prostate and breast cancer metastasis to bone." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419565.

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