Дисертації з теми "BREAST PROGRESSION"
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Chuprovska, Yu Ya. "Characteristics of breast cancer progression." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18208.
Повний текст джерелаKinnard, Krista. "Human Tandem Repeats in Breast Cancer Progression." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146036.
Повний текст джерелаLopez, Jose Ignacio. "CD44 Attenuates Metastasis During Breast Cancer Progression." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/193882.
Повний текст джерелаPandey, Puspa Raj. "ROLES OF LIPOGENESIS IN BREAST CANCER PROGRESSION." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/490.
Повний текст джерелаGreen, Margaret. "Prognostic factors in breast and colorectal cancer." Thesis, University of Surrey, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298045.
Повний текст джерелаRose, April. "The role of GPNMB in breast tumor progression." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96876.
Повний текст джерелаLe cancer du sein est le cancer le plus fréquemment diagnostiqué et la seconde cause de mortalité associée au cancer chez les femmes canadiennes. Le développement de métastases est la cause majeure de la morbidité et de la mortalité dûes à cette maladie. Le cancer du sein est une maladie très hétérogène qui peut toutefois être traité par l'utilisation de thérapie ciblée ; toutefois, les thérapies actuellement disponibles ont un effet limité sur la formation des métastases. Dans le but d'identifier de nouveaux médiateurs moléculaires associés à la formation de métastases osseuses dérivées du cancer du sein et qui pourraient être utilisés comme cibles thérapeutiques, nous avons soumis les cellules de carcinome mammaire 4T1 à un processus de sélection in vivo dans des souris Balb/c. Nous avons ainsi isolé des sous-populations de cellules caractérisées par leur agressivité à former des métastases osseuses. L'étude de l'expression génique de ces cellules a mis en évidence que le gène codant pour la Glycoprotéine NMB (GPNMB), aussi connu sous le nom de Ostéoactivine, est très fortement exprimé dans les lignées de cancer du sein métastatiques pour l'os.GPNMB est une protéine de surface transmembranaire de type I qui possède des domaines RGD et PKD extracellulaires ainsi qu'un motif hemITAM de signalisation cytoplasmique et n'avait encore jamais été rapportée comme impliquée dans le cancer du sein.Nous avons démontré que l'expression ectopique de GPNMB était suffisante pour promouvoir la migration et l'invasion de cellules de cancer du sein in vitro ainsi que la formation de métastases in vivo.Par la suite, nous avons analysé les niveaux d'expression des ARNm et de la protéine GPNMB dans des centaines de tumeur du sein humain et avons observé que l'expression de GPNMB corrèle positivement avec un risque accru de présence de métastases ainsi qu'une réduction du temps moyen de survie. Nous avons également démontré que GPNMB est le plus fréquemment exprimé dans des tumeurs mammaires appartenant au sous-type triple négatif pour lequel il n'y a actuellement aucune thérapie ciblée disponible.Par ailleurs, nous montrons pour la première fois que CDX-011, une drogue conjuguée à un anticorps monoclonal reconnaissant GPNMB, était capable, in vitro, d'éradiquer spécifiquement les cellules de cancer du sein exprimant GPNMB ainsi que d'induire une régression tumorale in vivo.Finalement, nous avons déterminé les effets de GPNMB sur la progression des tumeurs primaires et avons observé que GPNMB inhibait l'apoptose des cellules tumorales tout en augmentant l'angiogenèse et la croissance tumorale in vivo. Nous avons démontré que le domaine extracellulaire de GPNMB (ECD) pouvait être clivé de façon protéolytique par ADAM10 et ainsi être libéré de la surface cellulaire des cellules de cancer du sein. Nous avons postulé que la forme extracellulaire clivée (ECD) de GPNMB pourrait être impliquée dans certains des effets pro-angiogénique et avons montré que cet ECD était capable d'induire la migration de cellules endothéliales in vitro.L'ensemble des travaux décrits dans cette thèse implique pour la premier fois est le premier à identifier GPNMB comme médiateur fonctionnel de la croissance du cancer du sein et de ses métastases. Ce travail identifie GPNMB comme une importante cible thérapeutique pour le traitement des patients atteints du cancer du sein.
Perera, Kaluarachchige Upamali Lakshika. "The role of lamellipodin in breast cancer progression." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-lamellipodin-in-breast-cancer-progression(0a983ebb-e6e8-43e6-bf91-9258a50849bd).html.
Повний текст джерелаZelenko, Zara. "The Role of Hyperinsulinemia in Breast Cancer Progression." Thesis, Icahn School of Medicine at Mount Sinai, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10129345.
Повний текст джерелаWomen with Type 2 diabetes (T2D) have a 49% increase in breast cancer related mortality compared to women without T2D. Epidemiological studies report that increased endogenous insulin levels and increased insulin receptor (IR) expression are associated with poor survival in breast cancer patients. Therefore, it is essential to investigate the role of endogenous hyperinsulinemia on breast cancer progression. Presented in this thesis are contributions to understanding the effect of insulin in a mouse model of hyperinsulinemia (MKR mouse). First, data is shown that highlights the significant increase in primary MVT-1 tumors and pulmonary metastasis in the MKR mouse compared to Wild Type mice. The studies presented show that the primary tumors from the MKR mice have significantly higher Vimentin protein expression compared to primary tumors from control mice. Next, the studies determine that silencing Vimentin expression in the tumor cells leads to either decreased number of pulmonary metastasis in the hyperinsulinemic mice. The work in this thesis also establishes a novel immunodeficient hyperinsulinemic (Rag/MKR) mouse model that enabled the study of the effects of endogenous insulin on the progression of human cancer cells. The hyperinsulinemia of the Rag/MKR mice promoted a significant increase in tumor growth of MDA-MB-231 and LCC6 cells. The knockdown of the insulin receptor in the LCC6 cells led to primary tumors that were significantly smaller in both the hyperinsulinemic Rag/MKR and Rag/WT control mice compared to the tumors from the LCC6 control cells. Finally, it is shown for the first time that the knockdown of the IR promotes a reversal of the epithelial-mesenchymal phenotype by repressing mesenchymal markers and re-expressing epithelial markers in the LCC6 insulin receptor knockdown tumors. The data presented in this thesis highlight a potential contribution to the understanding of the role of insulin in the setting of hyperinsulinemia and provide potential targets for therapy to improve survival in women with breast cancer and hyperinsulinemia.
Chen, Hsiu-Hsi. "Mathematical models for progression of breast cancer and evaluation of breast cancer screening." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388263.
Повний текст джерелаKarp, Cristina M. "HRPAP20 a novel tumor progression regulator in breast cancer /." Cincinnati, Ohio : University of Cincinnati, 2005. http://www.ohiolink.edu/etd/view.cgi?acc%5Fnum=ucin1108156644.
Повний текст джерелаNeel, Jean-Charles. "Role of TGFß-regulated microRNA in breast cancer progression." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=123017.
Повний текст джерелаLe cancer du sein, le cancer féminin le plus répandu au monde, dont l'incidence augmente au cours des dernières décennies a eu une baisse de mortalitégrace aux nouvelles thérapies. Le sous-type de cancer du sein, répondant différemment aux traitements. Le sous-type triple-négatif, du à l'absence de trois marqueurs moléculaires, de dispose actuellement d'aucun traitement efficace. Le "transforming growth factor β" (TGFβ) est impliquée dans de nombreux processus biologiques allant du dévelopement embryonnaire à la croissance, la différentiation, à l'homéostasie et a un rôle majeur dans le cancer où il joue un rôle double. Dans les cellules normales et dans les cancers de stade précoce, le TGFβ conserve son aptitude à maintenir l'homéostasie et agit ainsi tel un suppresseur de tumeur. Suite à d'autres mutations, certaines de ses réponses biologiques sont perdues et le TGFβ favorise alors la progression tumorale et les métastases. La cytokine TGFβ joue alors un rôle majeur puisqu'elle promeut la progression tumorale vers les stades métastatiques.Le chapitre d'introduction explique les diverses approches tentées pour bloquer la voie de signalisation du TGFβ. Toutes ont échoué suite aux effets secondaires non négligeables. Après la découverte des microARN, et leur dérégulation dans le cancer, l'espoir d'une nouvelle thérapie à base de microARN est née. Des études initiales ont revelé in vivo que la modification de leurs taux d'expression modifiait le comportement cellulaire. Ce travail de doctorat a pour but d'élucider le rôle des microARN régulés par le TGFβ.Ce travail illustre l'utilisation d'oligonucléotides modifiés afin d'interférer avec les effets délétères du TGFβ. Les cancers du sein métastatiques sont souvent inopérables et peu répondants aux traitements systémiques. Les cancers métastatiques triple-négatifs entrainent une forte mortalité. Dans les deuxième et troisième chapitres de ce mémoire, j'ai demontré que l'inhibition du miR-181 et la surexpression du miR-30, à l'aide d'oligonucléotides synthétiques, diminuaient les effets du TGFβ in vitro. Ces résultats indiquent que la thérapie à base de microARN est une nouvelle stratégie thérapeutique prometteuse pour les sous-types actuellement intraitables. Une étude plus vaste révele qu'une grande proportion des miARN est regulée par le TGFβ. Ces miARN sont potentiellement des cibles d'intérêt thérapeutique comme le suggère les résultats préliminaires détaillés dans le quatrième chapitre de ce travail. J'ai testé l'effet du TGFβ sur le microRNome, identifié une cinquantaine de miARN régulés par la cytokine et ai commencé à les caractériser fonctionnellement. Ce travail servira de base pour de nombreux projets à venir sur la voie de signalisation du TGFβ.Cette recherche doctoratale démontre que le TGFβ est moteur de la progression tumorale du cancer du sein et que l'utilisastion d'ARN exogènes peut ralentir la progression cancéreuse. J'ai montré à deux reprises que le fait de cibler les miARN interférait avec la signalisation du TGFβ. Cette étude contribute au développement de nouvelles stratégies thérapeutiques. Au cours de la derniere décennie, il a été montré que les cellules cancéreuses étaient souvent dépendantes d'oncogènes. Je pense qu'elles le sont également d'oncomiARN tels le miR-181. Lorsque notre compréhension des relations entre miARN et leurs messagers cibles s'affinera, il sera possible de créer des miARN synthétiques capables de cibler les voies oncogéniques particulières. De tels régulateurs majeurs du transcriptome vont être des acteurs clefs des nouvelles générations de thérapies du cancer.
Balcazar, Lopez Carlos. "Breast cancer progression and phytoestrogen interactions with estrogen receptors." Thesis, University of Westminster, 2017. https://westminsterresearch.westminster.ac.uk/item/q3834/breast-cancer-progression-and-phytoestrogen-interactions-with-estrogen-receptors.
Повний текст джерелаStankevicins, Luiza. "MicroRNAs in Breast Cancer Progression and DNA Damage Response." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T041.
Повний текст джерелаBreast tumors are characterized by their high heterogeneity. Breast cancer is a complex disease, which has its development strongly influenced by environmental factors, combined with a progressive accumulation of genetic mutations and epigenetic dysregulation of critical pathways. Changes in gene expression patterns may be a result of a deregulation in epigenetic events as well as in post-transcriptional regulation driven by RNA interference endogenously represented by microRNA (miRNA). These mechanisms are capable to promote the initiation, maintenance and progression of carcinogenesis and are also implicated on the development of therapy resistance. miRNAs form a class of non-coding RNAs, which have emerged in recent years as one of the major regulators of gene expression through its capacity to silence messenger RNAs (mRNAs) containing a partially complementary sequence. The importance of regulation mediated by miRNAs was observed on their ability to regulate a wide range of biological processes, including cell proliferation, differentiation and apoptosis.To gain insights into the mechanisms involved in breast cancer initiation and progression we conducted a miRNA global expression on 21T series that are an in vitro model of breast cancer progression, comprising cell lines derived from the same patient, which include a normal epithelia (16N), primary in situ ductal carcinoma (21PT and 21NT) and cells derived from pleural effusion of lung metastasis (21MT-1 and 21MT-2). Considering the importance of miRNAs in the regulation of apoptosis, and that irradiation in different spectra is commonly used in diagnostic procedures, as mammography and on radiotherapy, we evaluated the miRNA expression after cell low and high energy irradiation and doxorubicin treatment to determine whether miRNAs are useful biomarkers to detect cell response after DNA damage. The experiments were done on the non-tumoral cell lines MCF-10A and HB-2 and on the breast carcinoma derived cell lines MCF-7 and T-47D. We observed that low energy X-rays is able to promote DNA strand breaks and apoptosis and to slightly change the expression of miRNAs involved on this pathway, such as let-7a, miR-34a and miR-29b. Regarding DNA stress response pathways, an upregulation on miR-29b expression, that in normal conditions is downregulated in tumor cell lines could be observed after all treatments. The microRNAome of 21T series revealed a significant downregulation of miR-205, an enrichment of the pro-metastatic factor ZEB-1, potential target for miR-205 and the consequent reduction of e-cadherin levels in 21MT cells checked by western blot. Our results indicate that miR-29b is a possible biomarker of genotoxic stress and that miR-205 can participate on the metastatic potential of 21T cells
Jin, Dexter X. "Molecular determinants of mammary differentiation and breast cancer progression." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117874.
Повний текст джерелаCataloged student-submitted from PDF version of thesis.
Includes bibliographical references.
The mammary epithelium is an architecturally complex tissue comprising of multiple cell lineages. Development and maintenance of this tissue are carefully orchestrated by balancing stem and progenitor cell self-renewal and differentiation. The mammary epithelium must also endure the successive regenerative cycles of pregnancy and lactation. Therefore, it is not surprising that the fidelity of these processes is of the utmost importance to ensure proper homeostasis of this tissue. In fact, dysregulation of these processes frequently results in progression toward cancer, and later, potentially metastatic disease. The clinical relevance of metastasis is hard to overstate, as it is responsible for over 90% of cancer-related deaths. In this thesis, I have identified a number of determinants involved in breast cancer progression and mammary differentiation. First, I describe SMARCE, a SWI-SNF component, as a prognostic factor of carcinoma progression. We show that SMARCE1 cooperates with ILF3 to regulate a basement membrane module and that it is functionally required to degrade basement membrane. Afterwards, I describe CREB3L1 as a key mediator of PERK-driven metastasis. We also showed that the unique mode of action of CREB3L1 provides a therapeutic opportunity to drug invasive breast cancers. Finally, I describe a 3D differentiation screen which identified the collagen receptor tyrosine kinase, DDR1, as a regulator of mammary stem cell differentiation. Mechanistically, we coupled ex vivo functional assays with single cell transcriptomic sequencing to show that DDR1 is required for basal fate commitment to activate JAG1 expression, which indirectly stimulates luminal NOTCH1 signaling to drive lobulogenesis. Collectively, these data provide insight into key molecular regulators of breast cancer progression and mammary differentiation.
by Dexter X. Jin.
Ph. D.
Stankevicins, Luiza da Cunha. "MicroRNAs in breast cancer progression and DNA damage response." Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9187.
Повний текст джерелаOs tumores de mama são caracterizados pela sua alta heterogeneidade. O câncer de mama é uma doença complexa, que possui o seu desenvolvimento fortemente influenciado por fatores ambientais, combinada a uma progressiva acumulação de mutações genéticas e desregulação epigenética de vias críticas. Alterações nos padrões de expressão gênica podem ser resultado de uma desregulação no controle de eventos epigenéticos, assim como, na regulação pós-transcricional pelo mecanismo de RNA de interferência endógeno via microRNA (miRNA). Estes eventos são capazes de levar à iniciação, à promoção e à manutenção da carcinogênese, como também ter implicações no desenvolvimento da resistência à terapia Os miRNAs formam uma classe de RNAs não codificantes, que durante os últimos anos surgiram como um dos principais reguladores da expressão gênica, através da sua capacidade de regular negativamente a atividade de RNAs mensageiros (RNAms) portadores de uma seqüencia parcialmente complementar. A importância da regulação mediada por miRNAs foi observada pela capacidade destas moléculas em regular uma vasta gama de processos biológicos incluindo a proliferação celular, diferenciação e a apoptose. Para avaliar a expressão de miRNAs durante a progressão tumoral, utilizamos como modelo experimental a série 21T que compreende 5 linhagens celulares originárias da mesma paciente diagnosticada com um tumor primário de mama do tipo ErbB2 e uma posterior metástase pulmonar. Essa série é composta pela linhagem obtida a partir do tecido normal 16N, pelas linhagens correspondentes ao carcinoma primário 21PT e 21NT e pelas linhagens obtidas um ano após o diagnóstico inicial, a partir da efusão pleural no sítio metastatico 21MT1 e 21MT2. O miRNAoma da série 21T revelou uma redução significativa nos níveis de miR-205 e nos níveis da proteina e-caderina e um enriquecimento do fator pró-metastático ZEB-1 nas células 21MT. Considerando a importância dos miRNAs na regulação da apoptose, e que a irradiação em diferentes espectros é comumente usada em procedimentos de diagnóstico como mamografia e na radioterapia, avaliamos a expressão de miRNAs após irradiação de alta e baixa energia e do tratamento doxorrubicina. Para os ensaios foram utilizados as linhagens não tumorais MCF-10A e HB-2 e as linhagens de carcinoma da mama MCF-7 e T-47D. Observou-se que raios-X de baixa energia são capazes de promover quebras na molécula do DNA e apoptose assim como, alterar sensivelmente miRNAs envolvidos nessas vias como o let-7a, miR-34a e miR-29b. No que diz respeito à resposta a danos genotóxicos, uma regulação positiva sobre a expressão de miR-29b, o qual em condições normais é regulado negativamente foi observada uma regulação positiva sobre miR-29b expressão após todos os tratamentos em células tumorais. Nossos resultados indicam que miR-29b é um possível biomarcador de estresse genotóxico e que miR-205 pode participar no potencial metastático das células 21T.
Breast tumors are characterized by their high heterogeneity. It is a complex disease, which has its development strongly influenced by environmental factors, combined with a progressive accumulation of genetic mutations and epigenetic dysregulation of critical pathways. Changes in gene expression patterns may be a result of a deregulation in epigenetic events as well as in post-transcriptional regulation driven by RNA interference endogenously represented by microRNA (miRNA) these mechanisms are capable to promote the initiation, maintenance and progression of carcinogenesis; they are also implicated on the development of therapy resistance. miRNAs form a class of non-coding RNAs which have emerged in recent years as one of the major regulators of gene expression through its capacity to silence messenger RNAs (mRNAs) containing a partially complementary sequence. The importance of regulation mediated by miRNAs was observed on their ability to regulate a wide range of biological processes including cell proliferation, differentiation and apoptosis.To gain insights into the mechanisms involved in breast cancer initiation and progression conducted a miRNA global expression on 21T series that are an in vitro model of breast cancer progression comprising cell lines derived from the same patient which include a normal epithelia (16N), primary in situ ductal carcinoma (21PT and 21NT) and cells derived from pleural effusion of lung metastasis (21MT-1 and 21MT-2). Considering the importance of miRNAs in the regulation of apoptosis, and that irradiation in different spectra is commonly used in diagnostic procedures as mammography and on radiotherapy, we evaluate the miRNA expression after cell low and high energy irradiation and doxorubicin treatment to determine whether miRNAs are useful biomarkers to detect cell response after DNA damage. The experiments were done on the non-tumoral cell lines MCF-10A and HB-2 and on the breast carcinoma derived cell lines MCF-7 and T-47D. We observed that of low energy X-rays is able to promote DNA strand breaks and apoptosis and to slightly change the expression of miRNAs involved on this pathway such as let-7a, miR-34a and miR-29b. Regarding DNA stress response pathways an upregulation on miR-29b expression, that in normal conditions is downregulated in tumor cell lines could be observed after all treatments. The microRNAome of 21T series revealed a significant downregulation of miR-205, an enrichment of the prometastatic factor ZEB-1, potential target for miR-205 and the consequent reduction of ecadherin levels in 21MT cells checked by western blot. Our results indicate that miR-29b is biomarkers of genotoxic stress and that miR-205can participate on the metastatic potential of 21T cells.
Borcherding, Nicholas. "Noncanonical Wnt signaling in breast cancer initiation and progression." Thesis, University of Iowa, 2014. https://ir.uiowa.edu/etd/1294.
Повний текст джерелаHenry, Luke Alexander. "Characterisation of the role of endoglin in breast cancer progression." Thesis, Institute of Cancer Research (University Of London), 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511168.
Повний текст джерелаPusterla, Tobias. "HMGB1 and its role in breast cancer progression and malignancy." Thesis, Open University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499456.
Повний текст джерелаSnyder, Kimberly Ashley. "The role of podocalyxin in breast cancer progression and metastasis." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/46014.
Повний текст джерелаZielinska, Hanna. "Hyperglycemia and fironectin : the criminal partnership during breast cancer progression." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.752733.
Повний текст джерелаFoglesong, Grant. "Lifestyle Improvements Enhance Metabolic Function and Mitigate Breast Cancer Progression." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1490266217799202.
Повний текст джерелаMARTINO, VALENTINA. "THE ROLE OF MIR199A IN BREAST CANCER PROGRESSION AND METASTASIS." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/217467.
Повний текст джерелаMichelatti, Daniela. "Oncogenic enhancer reprogramming in triple negative breast cancer tumour progression." Doctoral thesis, Università degli studi di Trento, 2022. http://hdl.handle.net/11572/327998.
Повний текст джерелаShaaban, Abeer M. "Risk of breast neoplasia progression : analysis of morphological and molecular markers." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403232.
Повний текст джерелаBaldwin, Gouri Seetharaman. "The CD151-α3β1 axis and its role in breast cancer progression". Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3372/.
Повний текст джерелаEscudero-Esparza, Astrid. "Role of Claudin-5 in the progression of human breast cancer." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/55020/.
Повний текст джерелаTan, Keely. "Investigating the role of acetyl-CoA carboxylases in breast cancer progression." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/26585.
Повний текст джерелаAlzaabi, Adhari Abdullah. "Identification and Characterization of Serum Biomarkers Associated with Breast Cancer Progression." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6452.
Повний текст джерелаNimishakavi, Sheela. "Alcohol consumption and breast cancer: a proposed mechanism for alcohol-caused breast cancer initiation, promotion, and progression." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12542.
Повний текст джерелаBreast cancer is the second leading cause of death in women in the United States. Several modifiable behaviors are known to place women at increased risk of developing breast cancer, one of which is consuming alcoholic beverages. The relationship between alcohol ingestion and breast cancer has been well established through epidemiological and experimental research; however, a mechanism describing the interaction and onset of carcinogenesis has not been determined. There are several proposed mechanisms currently being investigated, which fall into one of four general categories: DNA damage induced by alcohol metabolites, by hormone elevation, by oxidative stress, or by interfering with proper DNA methylation. An important goal is to determine how these various proposed mechanisms mediate alcohol-caused breast cancer through its initiation, promotion, and progression. This study reviewed current breast cancer literature, looking at both epidemiological data investigating a relationship between breast cancer onset and survival, and experimental data examining the mechanisms of alcohol and cell interaction. This paper looks at alcohol-mediated breast cancer from the broader point of view of alcohol's effect on the various stages of cancer, and determines a mechanism for each step. Data indicates that alcohol-mediated breast cancer initiation is caused by alcohol metabolites, namely acetaldehyde and its derivatives, forming DNA adducts that cause lesions in the DNA. Oxidative stress also brought on by the presence of alcohol and its metabolites initiates lipid peroxidation and the production of highly reactive aldehydes, such as trans-4-hydroxy-2-nonenal, that disrupt the DNA repair system. Together, there is DNA damage and prevention of repair, which results in the initiation of cancer. Breast cancer promotion is mediated by elevated levels of the hormones leptin and estrogen, which form complexes regulating the cell cycle and promoting cell replication and survival in these damaged cells. Cancer progression then proceeds as alcohol increases insulin sensitivity in breast cancer cells and encourages replication resulting in a mass. Furthermore, extracellular matrix proteins degrade and the cancer cells take on characteristics of migratory cells. Next, cell adhesion signals are enhanced, allowing cancer cells to follow a protein scaffold and migrate into neighboring tissue. Although there is still much more research to be done, by determining a mechanism for how alcohol mediates breast cancer through its various stages, treatments can be developed that target various stages in the mechanism to prevent carcinogenesis or increase survival chances.
Sasser, Amy Kate. "The role of stromal fibroblasts and IL-6 in breast cancer progression." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1172866243.
Повний текст джерелаFancher, Karen. "Transcriptional Alterations during Mammary Tumor Progression in Mice and Humans." Fogler Library, University of Maine, 2008. http://www.library.umaine.edu/theses/pdf/FancherK2008.pdf.
Повний текст джерелаOjemann, Alexandra. "Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model." ScholarWorks @ UVM, 2017. http://scholarworks.uvm.edu/graddis/741.
Повний текст джерелаO'Neill, Christine F. "Notch Regulation of Human Breat Cancer Progression: Contrasting Roles for Notch Signaling." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/O'NeillCF2007.pdf.
Повний текст джерелаSHUKLA, MANASI NARENDRA. "HRPAP20: A NOVEL CALMODULIN-BINDING PHOSPHOPROTEIN INVOLVED IN TUMOR PROGRESSION." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1175629479.
Повний текст джерелаPark, Keon-Young. "Predicting patient-to-patient variability in proteolytic activity and breast cancer progression." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/53479.
Повний текст джерелаMahmood, Sardar. "Identification of New Oncogenes Involved in the Tumoral Progression of Breast Carcinoma." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T021.
Повний текст джерелаAvailability of both large scale transcriptomic and genomic data of tumours now allows to identify relatively easily candidate oncogenes that are over-expressed as a consequence of DNA amplification. These candidate oncogenes have then to be functionally validated and studied for their role in the normal and cancer cell.In this study, we mainly focused on breast cancer, the most common cancer among women and the second leading cause of cancer deaths in women around the world. In France, 52,000 new cases with 12,000 deaths of breast cancer were estimated in 2010 accounting for 34% of all new cases of cancer in women. In breast cancer the main altered chromosomes include chromosome 8, 11 and 17 which contain the 17q12 (ERBB2) and the 11q13 (CCND1) amplicons. Development of “herceptin” against ERBB2 illustrates the potential of cancer genomics in identifying therapeutic targets. Several studies have identified other amplicons with candidate oncogenes. However very few studies reported functional validation of identified candidates, thus highlighting the need of large scale functional analyses of different amplicons in breast cancer to identify new driver genes which may be used for development of therapeutic strategies for breast cancer. In recent years, RNAi has become a tool of choice for high-throughput screening to characterize gene function in cultured cells. In this study we performed high-throughput RNAi based functional screening of 127 amplified and over-expressed genes from 11 major amplicons on chromosome 8, 11 and 17 in breast cancer. This resulted in the identification of 8 driver genes from 5 amplicons. Further functional validation of 5 of these genes demonstrated that 4 genes, RAD21, EIF3H, TANC2 and CHRAC1 from 3 amplicons, regulate breast cancer cell proliferation, apoptosis and transformation. Regions of genetic alteration in one cancer may be altered in multiple cancer types. One such example includes the 8p11-p12 amplicon which has been reported to be amplified in breast, pancreatic, lung and bladder cancer. Also common amplicons from different cancers may harbor common driver oncogenes. To investigate this hypothesis we evaluated the possible involvement in 8p11-12 amplified pancreatic and lung cancer cell lines of two oncogenes namely, PPAPDC1B and WHSC1L1 that have been described to be driver genes of the 8p11-12 amplicon in breast cancer and furthermore in lung cancer for WHSC1L1. Inhibition of both genes reduced cell survival and anchorage independent growth in amplified pancreatic and lung cancer cell lines. This finding highlights the importance of these two genes in multiple cancers and therapeutic potential interest to inhibit these enzymes in multiple cancers with 8p11-p12 amplification.Transgenic mouse models play an important role to investigate in vivo function of candidate genes. To evaluate in vivo role of PPAPDC1B, we established a transgenic mouse model over-expressing PPAPDC1B under the Keratin 5 promoter. Transgenic mice developed two unexpected phenotypes including development of hair follicles along front teeth and acute inflammation of salivary glands, lymph nodes, bladder and pancreas. This is an ongoing study that may help to understand the mechanism of action of PPAPDC1B in vivo
Dumont, Nancy, Yongping Crawford, Mahvash Sigaroudinia, Shefali Nagrani, Matthew Wilson, Gertrude Buehring, Gulisa Turashvili, et al. "Human mammary cancer progression model recapitulates methylation events associated with breast premalignancy." BioMed Central, 2009. http://hdl.handle.net/10150/610113.
Повний текст джерелаVoguel, González Marina 1993. "Zinc homeostasis and disease : Impact on breast cancer progression and infection severity." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/672613.
Повний текст джерелаEl zinc es un elemento traza esencial con papeles estructurales, catalíticos y de señalización en nuestro organismo. A nivel celular, la homeostasis del zinc participa en funciones fundamentales. Así, una desregulación de su concentración a nivel sistémico o celular puede causar enfermedad en humanos. El primer objetivo de esta tesis es explorar el papel del zinc durante la metástasis del cáncer de mama triple negativo al cerebro. Para ello, usamos células MDA-MB-231 y sus derivadas MDA-MB-231-BrM2, metastásicas cerebrales. Modulamos su zinc interno y probamos su contribución en marcadores metastásicos. Encontramos un impacto relevante de la concentración de zinc en la modulación del microambiente cerebral y en la capacidad de sus células madre para generar un tumor secundario. Además, la homeostasis del zinc es fundamental para el funcionamiento correcto del sistema inmune. Desde el brote de la pandemia de COVID-19, otro objetivo de este trabajo ha sido estudiar el potencial papel terapéutico de la suplementación de zinc y sus ionóforos esta enfermedad. Experimentos in vitro usando células VeroE6 y un estudio observacional con pacientes señalaron que un bajo nivel de zinc es un factor de riesgo para el fatal desenlace de la infección por SARS-CoV2. Además, demostramos que la cloroquina y la hidroxicloroquina no son ionóforos de zinc, cuestionando más el uso de estos medicamentos en el tratamiento de la COVID-19. En general, los resultados de esta tesis destacan la importancia de mantener la homeostasis del zinc para la salud de los individuos.
Kaymak, Aysegul [Verfasser]. "Zrf1’s role in mESC differentiation and breast cancer progression / Aysegul Kaymak." Mainz : Universitätsbibliothek Mainz, 2017. http://d-nb.info/1137181745/34.
Повний текст джерелаYu, Yang. "The role of hCLCA2 and hCLCA4 in suppression of breast cancer progression." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/871.
Повний текст джерелаKashyap, Abhishek S. "In vitro functional characterisation of IGF-I : VN-induced breast cancer progression." Thesis, Queensland University of Technology, 2012. https://eprints.qut.edu.au/62165/1/Abhishek_Kashyap_Thesis.pdf.
Повний текст джерелаJenkinson, Sarah Rhiannon. "In vitro models to study the role of S100A4 in mammary epithelial cell metastasis." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367678.
Повний текст джерелаBitter, Eliza Esther King. "Investigation of Thymidine Kinase 1 in Cancer Progression." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/9104.
Повний текст джерелаZhou, Wenjing. "Aspects of Progression in Breast Carcinoma : from ductal carcinoma in situ to invasive cancer." Doctoral thesis, Uppsala universitet, Institutionen för kirurgiska vetenskaper, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-166745.
Повний текст джерелаPai, Vaibhav Prakash. "Serotonin Regulation of Mammary Gland Involution and its Role in Breast Cancer Progression." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1237565289.
Повний текст джерелаGooding, 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.
Повний текст джерелаMercado-Matos, Jose R. "A Mechanistic Investigation of Insulin Receptor Substrate 2 Function in Breast Cancer Progression." eScholarship@UMMS, 2017. http://escholarship.umassmed.edu/gsbs_diss/918.
Повний текст джерелаChristensen, Kimberly Laura. "The developmental regulator SIX1 plays multiple roles in breast cancer initiation and progression /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 115-132). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
Hsieh, Szu-Min (Lintell). "Breast cancer progression is modulated by inherited genetic variance in multiple independent cohorts." Thesis, Griffith University, 2010. http://hdl.handle.net/10072/366638.
Повний текст джерелаThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Horm, Teresa Marie. "The Roles of MUC1 and EGFR in Breast Cancer Progression and Mammary Lactation." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/293562.
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