Relevant bibliographies by topics / BREAST PROGRESSION

Academic literature on the topic 'BREAST PROGRESSION'

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Published: 11 March 2023

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Journal articles on the topic "BREAST PROGRESSION"

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Arafat, Kholoud, Elham Al Kubaisy, Shahrazad Sulaiman, Sherif M. Karam, Zeina Al Natour, Ahmed H. Hassan, and Samir Attoub. "SMARCAD1 in Breast Cancer Progression." Cellular Physiology and Biochemistry 50, no. 2 (2018): 489–500. http://dx.doi.org/10.1159/000494163.

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Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER-/PR-/ HER2-) and T47D (ER+/PR+/-/HER2-) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.
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Gespach, Christian. "Reciprocity in breast cancer progression." Oncotarget 5, no. 22 (November 30, 2014): 10967–68. http://dx.doi.org/10.18632/oncotarget.2853.

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Chen, Yinghua, and Olufunmilayo I. Olopade. "MYC in breast tumor progression." Expert Review of Anticancer Therapy 8, no. 10 (October 2008): 1689–98. http://dx.doi.org/10.1586/14737140.8.10.1689.

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Dalgin, Gul S., Gabriela Alexe, Daniel Scanfeld, Pablo Tamayo, Jill P. Mesirov, Shridar Ganesan, Charles DeLisi, and Gyan Bhanot. "Portraits of breast cancer progression." BMC Bioinformatics 8, no. 1 (2007): 291. http://dx.doi.org/10.1186/1471-2105-8-291.

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Ma, L. "Determinants of Breast Cancer Progression." Science Translational Medicine 6, no. 243 (July 2, 2014): 243fs25. http://dx.doi.org/10.1126/scitranslmed.3009587.

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SUBRAMANIAN, BALAKRISHNA, and DAVID E. AXELROD. "Progression of Heterogeneous Breast Tumors." Journal of Theoretical Biology 210, no. 1 (May 2001): 107–19. http://dx.doi.org/10.1006/jtbi.2001.2302.

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Kontomanolis, Emmanuel N., Sofia Kalagasidou, Stamatia Pouliliou, Xanthoula Anthoulaki, Nikolaos Georgiou, Valentinos Papamanolis, and Zacharias N. Fasoulakis. "The Notch Pathway in Breast Cancer Progression." Scientific World Journal 2018 (July 8, 2018): 1–11. http://dx.doi.org/10.1155/2018/2415489.

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Objective. Notch signaling pathway is a vital parameter of the mammalian vascular system. In this review, the authors summarize the current knowledge about the impact of the Notch signaling pathway in breast cancer progression and the therapeutic role of Notch’s inhibition.Methods. The available literature in MEDLINE, PubMed, and Scopus, regarding the role of the Notch pathway in breast cancer progression was searched for related articles from about 1973 to 2017 including terms such as “Notch,” “Breast Cancer,” and “Angiogenesis.”Results. Notch signaling controls the differentiation of breast epithelial cells during normal development. Studies confirm that the Notch pathway has a major participation in breast cancer progression through overexpression and/or abnormal genetic type expression of the notch receptors and ligands that determine angiogenesis. The cross-talk of Notch and estrogens, the effect of Notch in breast cancer stem cells formation, and the dependable Notch overexpression during breast tumorigenesis have been studied enough and undoubtedly linked to breast cancer development. The already applied therapeutic inhibition of Notch for breast cancer can drastically change the course of the disease.Conclusion. Current data prove that Notch pathway has a major participation and multiple roles during breast tumor progression. Inhibition of Notch receptors and ligands provides innovative therapeutic results and could become the therapy of choice in the next few years, even though further research is needed to reach safe conclusions.
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Ferreira, Sandra, Nuno Saraiva, Patrícia Rijo, and Ana S. Fernandes. "LOXL2 Inhibitors and Breast Cancer Progression." Antioxidants 10, no. 2 (February 19, 2021): 312. http://dx.doi.org/10.3390/antiox10020312.

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LOX (lysyl oxidase) and lysyl oxidase like-1–4 (LOXL 1–4) are amine oxidases, which catalyze cross-linking reactions of elastin and collagen in the connective tissue. These amine oxidases also allow the cross-link of collagen and elastin in the extracellular matrix of tumors, facilitating the process of cell migration and the formation of metastases. LOXL2 is of particular interest in cancer biology as it is highly expressed in some tumors. This protein also promotes oncogenic transformation and affects the proliferation of breast cancer cells. LOX and LOXL2 inhibition have thus been suggested as a promising strategy to prevent metastasis and invasion of breast cancer. BAPN (β-aminopropionitrile) was the first compound described as a LOX inhibitor and was obtained from a natural source. However, novel synthetic compounds that act as LOX/LOXL2 selective inhibitors or as dual LOX/LOX-L inhibitors have been recently developed. In this review, we describe LOX enzymes and their role in promoting cancer development and metastases, with a special focus on LOXL2 and breast cancer progression. Moreover, the recent advances in the development of LOXL2 inhibitors are also addressed. Overall, this work contextualizes and explores the importance of LOXL2 inhibition as a promising novel complementary and effective therapeutic approach for breast cancer treatment.
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Skinner, Kristin A., C. Alan Kachel, Raymond Sullivan, Andrew Jones, and Soudamini Kurumboor. "Progressive accumulation of DNA methylation with malignant progression in breast tissue." Journal of the American College of Surgeons 199, no. 3 (September 2004): 85. http://dx.doi.org/10.1016/j.jamcollsurg.2004.05.184.

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Artacho-Cordón, Antonia, Francisco Artacho-Cordón, Sandra Ríos-Arrabal, Irene Calvente, and María Isabel Núñez. "Tumor microenvironment and breast cancer progression." Cancer Biology & Therapy 13, no. 1 (January 2012): 14–24. http://dx.doi.org/10.4161/cbt.13.1.18869.

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Dissertations / Theses on the topic "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.

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Kinnard, Krista. "Human Tandem Repeats in Breast Cancer Progression." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146036.

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A tandemly-repeated sequence of DNA located approximately 1kb upstream of HIC1 has been identified which appears to regulate the expression of this important tumor suppressor gene. Loss of HIC1 expression in tumors, either by deletion or hypermethylation, has previously been shown to correlate with a more severe prognosis in multiple cancers. Initial data show that larger alleles of this tandem repeat do not influence incidence of disease but do appear to correspond with a heritable predisposition to more aggressive cancers, represented by earlier onset and increased metastasis. This study hypothesizes that there may be a connection between these more aggressive types of cancer but also with the deleterious BRCA mutation.
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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 establish the role of CD44, the primary receptor for hyaluronan, in breast cancer progression and metastasis through the use of transgenic mouse models of breast cancer. While no differences were seen in the onset of primary breast tumors, mice expressing CD44 had a reduced rate of pulmonary metastasis compared to mice that lacked CD44. This establishes an anti-invasive role for CD44 in breast tumor progression. We also identify a decreased population of alveolar macrophages in CD44 negative mice that could affect metastatic breast cancer cell colonization of the lungs.We then focused our study in vitro, where we assessed the invasive properties of breast cancer cells as they move through three dimensional (3D) matrices containing or lacking hyaluronan. We show that in 3D type I collagen gels, breast cancer cells invade more readily in the absence of hyaluronan compared to when hyaluronan (HA) is embedded within the gel. HA mediated inhibition of invasion is dependent on CD44 binding as demonstrated through the use of a CD44 functional blocking antibody.We also show that HA promotes differential phenotypes of breast cancer cell. HA promotes filopodia formation and invasion when soluble in the cell microenvironment. Alternatively, matrix-embedded HA inhibits invasion and promotes migration through the formation of lamellipodia. The differential HA invasive and proliferative phenotypes are mediated by differential activation of ERK or γPAK. Activation of γPAK is mediated by CD44 while ERK activation by HA occurs by CD44 independent mechanisms.We also demonstrate an inhibition of MMP9 mediated invasion by HA when embedded within a type IV collagen matrix, but not a type I collagen matrix. This differential activity indicates that it is not only the immobilization of HA in a matrix that determines its activity, but also the context in which it is present within the matrix.These data underscore the importance of studying matrix components in an environment that closely resembles in vivo conditions. HA is a prime example as it has the capability of both promoting and inhibiting invasion depending on how it is presented to a cell. Differential HA activity also underlies the importance of understanding extracelluar matrix degradation and the release of matrix components as these can adversely affect disease progression.
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Pandey, Puspa Raj. "ROLES OF LIPOGENESIS IN BREAST CANCER PROGRESSION." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/490.

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Elevated level of lipogenic enzymes and overall lipogenesis have been reported in a wide variety of cancers and blocking the lipogenic pathway by chemical inhibitors or RNA interference causes tumor cell death by apoptosis which provides a strong rationale for targeting lipogenic pathway for the treatment and prevention of cancer however the exact role of lipogenesis as a cause, facilitator or consequence is not yet clearly understood. Therefore in this dissertation research, we set up to determine the mechanism of tumor cell death by inhibiting lipogenesis and to determine the role of increased lipogenesis in the breast cancer progression. In the first part of this study, we investigated the status of fatty acid synthase (FAS) gene which is regarded as the key lipogenic gene in fatty acid biosynthetic pathway and is responsible for the synthesis of lipid molecules by facilitating the condensation reaction between acetyl-CoA and malonyl-CoA in the presence of NADPH. We observed that normal breast epithelial cells MCF10A cells have very low level of FAS expression whereas breast cancer cell lines MCF7, MDA MB231 and MDA MB231 LM have significant overexpression. Next, we observed the similar trend of FAS overexpression in breast cancer stem-like cells (CSCs) isolated from the MCF7, MDA MB231 and MDA MB231 LM cell lines using cell surface markers (CD24-/CD44+/ESA+). These cells were previously transplanted into the mammary fat pad of nude mice and the results of our limiting dilution analysis indicate that CSCs had a significantly higher ability of forming breast cancer in the injected animals which explains our rationale to use CSCs in our research. In order to exploit this lipogenic pathway for the treatment and chemoprevention of breast cancer, we then examined the effects of resveratrol on breast cancer cells. Resveratrol is a natural polyphenolic compound and has been shown to exhibit cardio-protective as well as anti-neoplastic effects on various types of cancers. However, the exact mechanism of its anti-tumor effect is not clearly defined. We observed that resveratrol significantly reduced the cell viability by inducing apoptosis in parental cells as well as in CSCs. Resveratrol also inhibited mammosphere formation which is an inherent property of CSCs. This inhibitory effect of resveratrol is accompanied by a significant reduction in lipid synthesis which is caused by the down-regulation of the FAS gene followed by up-regulation of pro-apoptotic genes, DAPK2 and BNIP3. The activation of apoptotic pathway in the cancer stem-like cells was suppressed by FAS overexpression suggesting that resveratrol-induced apoptosis is indeed through the modulation of FAS-mediated cell survival signaling. Importantly, resveratrol was able to significantly suppress the growth of CSC in an animal model of human breast cancer xenograft without showing apparental toxicity. Taken together, our results indicate that resveratrol is capable of inducing apoptosis in the CSCs through suppression of lipogenesis by modulating FAS expression, which highlights a novel mechanism of anti-tumor effect of resveratrol. Taken together, our results indicate that resveratrol is capable of inducing apoptosis in the cancer stem-like cells through suppression of lipogenesis by modulating FAS expression, which highlights a novel mechanism of anti-tumor effect of resveratrol. In the second part of research, we tried to determine the role of elevated level of lipogenesis in normal to ductal carcinoma in situ (DCIS) progression. For this, we first analyzed the expression profile of various lipogenic genes using an expression microarray and found that CSCs from DCIS.com showed significantly higher level of ATP-citrate lyase (ACLY), acetyl-CoA carboxylase (ACC) and FAS than the normal non-tumorigenic stem-like cells obtained from MCF10A. The result was also confirmed by qRT-PCR and Western blot as well as in clinical specimens of DCIS by immunohistochemistry. In the next step, we detected that SREBP1, the master regulator of lipogenic genes, is also upregulated in DCIS and further identified that SREBP1 regulates the co-ordinate expression of ACLY, ACC and FAS ultimately resulting in the elevation of lipogenesis. In order to determine the role of SREBP1 overexpression in normal to DCIS transition, we overexpressed the SREBP1 in MCF10A cells which induced a significant increase in the downstream key lipogenic genes ACLY, ACC1 and FAS which resulted in the clear upregulation of total lipid content in the cells. Furthermore, we found that this elevation of lipogenesis in MCF10A-SREBP1 stem-like cells confers proliferative advantage as well as a significant increase in mammosphere forming ability and anchorage independent growth (3D culture). Thus, our results showed a possibility that increased lipogenesis in normal stem-like cells may be responsible for providing oncogenic transformation properties which can be confirmed at least in our in vitro model. We then examined the effects of resveratrol on CSCs sorted from DCIS.com. We found that resveratrol decreased the cell viability and increased apoptosis by reducing the total lipid content by inhibiting the expression of SREBP1 and downstream lipogenic genes. Resveratrol also hindered the stemness of the DCIS CSCs by inhibiting its mammosphere forming ability. When DCIS CSCs were transplanted into mammary fat pad of nude mice which were on resveratrol treatment, we observed that resveratrol significantly suppressed the formation of DCIS by downregulating lipogenic genes and by upregulating pro-apoptotic genes, DAPK2 and BNIP3. Collectively, our results indicate that lipogenic genes SREBP1 co-ordinately regulates the overexpression of ACLY, ACC1 and FAS in DCIS CSCs at an early stage of breast tumorigenesis and thus confer proliferative and survival advantages. Anti-growth effect of resveratrol on DCIS CSCs also provides us with a strong rationale to use this agent for chemo-prevention against DCIS.
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Green, Margaret. "Prognostic factors in breast and colorectal cancer." Thesis, University of Surrey, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298045.

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Rose, 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.

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Breast cancer is the most commonly diagnosed cancer and the second leading cause of cancer related deaths among Canadian women. Development of distant metastases is the leading cause of morbidity and mortality from this disease. Breast cancer is a highly heterogeneous disease that is amenable to intervention with targeted therapeutics; however, therapies that are currently available have limited efficacy in the metastatic setting. To identify novel molecular mediators of breast cancer bone metastasis that might also serve as therapeutic targets, we subjected 4T1 mammary carcinoma cells to in vivo selection in Balb/c mice and isolated sub-populations with an aggressively bone-metastatic phenotype. Gene expression profiling of these cells revealed Glycoprotein NMB (GPNMB), also known as Osteoactivin, as a gene that was highly expressed in bone metastatic breast cancer cells. GPNMB is a type I transmembrane, cell surface expressed protein with an extracellular RGD and PKD domains and a cytoplasmic hemITAM signaling motif that had not previously been implicated in breast cancer. We demonstrate that ectopic GPNMB expression was sufficient to promote migration and invasion of breast cancer cells in vitro and the formation of bone metastases in vivo.Subsequently, we analyzed GPNMB mRNA and protein expression levels in hundreds of breast tumors and found that GPNMB expression positively correlates with increased risk of metastasis and shorter overall survival times. We have also demonstrated that GPNMB is most commonly expressed in breast tumors belonging to the triple negative subtype, for which there are no targeted therapies currently available. We showed for the first time that CDX-011, a GPNMB-targeted monoclonal antibody-drug conjugate, was capable of killing GPNMB-expressing breast cancer cells in vitro and inducing tumor regression in vivo. Finally, we investigated the effects of GPNMB on primary tumor progression and found that it inhibits tumor cell apoptosis while enhancing angiogenesis and tumor growth in vivo. We demonstrate that the extracellular domain (ECD) of GPNMB can be proteolytically cleaved and shed from the surface of breast cancer cells, which is mediated by ADAM10. We postulated that the shed extracellular domain (ECD) of GPNMB might be responsible for some of its pro-angiogenic effects and showed that this ECD was indeed capable of inducing endothelial cell migration in vitro.The body of work described in this thesis is the first to identify GPNMB as a functional mediator of breast cancer growth and metastasis and to validate it as an important clinical target in human breast cancer.
Le 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.
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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.

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Zelenko, 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.

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Women 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.

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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.

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Karp, 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.

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Books on the topic "BREAST PROGRESSION"

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1952-, Dickson Robert B., and Lippman Marc E. 1945-, eds. Mammary tumorigenesis and malignant progression: Advances in cellular and molecular biology of breast cancer. Boston: Kluwer Academic Publishers, 1994.

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Yacoub, Ninos. Molecular events involving p27kip1, p53 HER-2/neu, and ER in multistep progression of breast cancer. Ottawa: National Library of Canada, 2000.

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Lippman, Marc E., and Robert B. Dickson. Mammary Tumorigenesis and Malignant Progression: Advances in Cellular and Molecular Biology of Breast Cancer. Springer, 2012.

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Berns, P. M. J. J., Romijn J. C, and Schröder F. H, eds. Mechanisms of progression to hormone-independent growth of breast and prostatic cancer. Carnforth, Lancs, UK: Parthenon Pub. Group, 1991.

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Lippman, Marc E., and Robert B. Dickson. Mammary Tumorigenesis and Malignant Progression: Advances in Cellular and Molecular Biology of Breast Cancer. Springer, 2012.

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Apple, Sophia K., and Lawrence W. Bassett. Proliferative Lesions and Breast Cancer Histopathology. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0004.

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Breast in situ lesions and invasive carcinomas are a heterogeneous group of tumors comprising many different morphological and biological subtypes. The majority of invasive breast cancers thought to arise in the terminal ductal lobular unit (TDLU). As multidisciplinary diagnosis and detection of early breast carcinomas is the gold standard, an understanding of histopathology in correlation with radiologic findings is critical. This chapter reviews the histopathology of high-risk proliferative lesions, ductal carcinoma in situ (DCIS), lobular carcinoma in situ (LCIS), and invasive breast carcinoma. Tumor progression and some of the frequently seen invasive breast cancer subtypes are described. Histopathology of other malignancies arising from mesenchymal origin, including phyllodes tumor, is also described.
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Mammary Tumorigenesis and Malignant Progression: Advances in Cellular and Molecular Biology of Breast Cancer (Cancer Treatment and Research). Springer, 1994.

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Hopko, Derek R., Crystal C. McIndoo, Michael Gawrysiak, and Stevie Grassetti. Psychosocial Interventions for Depressed Breast Cancer Patients. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.004.

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Clinical depression affects many people and is associated with several risk factors that include being diagnosed with a serious medical illness such as breast cancer. Objectives of this chapter were to elucidate the prevalence of depression in breast cancer patients, the impact of depression as it pertains to life functioning and quality of life, highlight the bidirectional relationship of breast cancer and depression, outline assessment strategies and measurement issues relevant to assessing depression, and review the treatment outcome literature addressing the efficacy of psychosocial interventions for depressed breast cancer patients. Depression is highly prevalent among breast cancer patients, significantly impacts life functioning, may be associated with cancer progression and mortality, and is bidirectionally related to breast cancer through several pathways. Many behavioral assessment strategies may be useful for recognizing depression in breast cancer patients, and, although methodological weaknesses are evident, several psychosocial interventions show substantial promise as effective treatments for depressed breast cancer patients.
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Rodriguez-Rincon, Daniela, Brandi Leach, and Catriona Manville. Understanding the societal impact of treatment of early breast cancer: What are the non-clinical outcomes associated with disease progression? RAND Corporation, 2019. http://dx.doi.org/10.7249/rr3010.1.

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Elmore, Natasha, Sarah King, Josephine Exley, Daniela Rodriguez-Rincon, Jody Larkin, Molly Morgan Jones, and Catriona Manville. Findings from a systematic review to explore the patient and societal impacts of disease progression in women who were treated for early breast cancer: Implications for future research, policy and practice. RAND Corporation, 2019. http://dx.doi.org/10.7249/rr3010.3.

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Book chapters on the topic "BREAST PROGRESSION"

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Band, Vimla, and Ruth Sager. "Tumor Progression in Breast Cancer." In Neoplastic Transformation in Human Cell Culture, 169–78. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0411-4_18.

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Callahan, Robert. "Oncogenes and Breast Cancer Progression." In Boundaries between Promotion and Progression during Carcinogenesis, 143–56. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5994-4_13.

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Pietras, Richard J., and Mark D. Pegram. "Oncogene Activation and Breast Cancer Progression." In Endocrinology of Breast Cancer, 133–53. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-699-7_10.

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Kern, Francis G. "The Role of Fibroblast Growth Factors in Breast Cancer Pathogenesis and Progression." In Breast Cancer, 59–93. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-456-6_3.

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Shukla, Samriddhi, and Syed Musthapa Meeran. "Epigenetic Factors in Breast Cancer Progression." In Breast Cancer Metastasis and Drug Resistance, 341–65. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5647-6_19.

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Lin, Elaine Y., and Jeffrey W. Pollard. "Macrophages: Modulators of Breast Cancer Progression." In Novartis Foundation Symposia, 158–72. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470856734.ch12.

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Gul, Hira, Iqra, and Nosheen Masood. "Early-Stage Progression of Breast Cancer." In Breast Cancer: From Bench to Personalized Medicine, 113–23. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-0197-3_6.

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von Minckwitz, Gunter, and Cristina Pirvulescu. "Treatment with Trastuzumab Beyond Progression." In Drugs for HER-2-positive Breast Cancer, 61–71. Basel: Springer Basel, 2010. http://dx.doi.org/10.1007/978-3-0346-0094-1_4.

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Cardiff, R. D., D. W. Morris, L. J. T. Young, and R. Strange. "MuMTV Genotype, Protoneoplasia, and Tumor Progression." In Breast Cancer: Origins, Detection, and Treatment, 156–66. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2309-9_12.

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Sameni, Mansoureh, Stefanie R. Mullins, Kamiar Moin, Bonnie F. Sloane, and Kingsley Osuala. "Modeling Breast Cancer Progression in 4-D." In Breast Cancer Metastasis and Drug Resistance, 177–88. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5647-6_10.

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Conference papers on the topic "BREAST PROGRESSION"

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Snider, Kara E., Hormoz Ehya, Jose Russo, and Sandra V. Fernandez. "Abstract 75:NRG1andRARβhypermethylation in breast cancer progression." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-75.

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Sauter, ER, W. Qin, and S. Dasgupta. "Abstract P1-04-01: Breast milk exosomes promote breast cancer progression." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p1-04-01.

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Taghipour, S., D. Banjevic, N. Montgomery, and A. K. S. Jardine. "Modeling breast cancer progression and evaluating screening policies." In 2013 Annual Reliability and Maintainability Symposium (RAMS). IEEE, 2013. http://dx.doi.org/10.1109/rams.2013.6517766.

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Polyak, Kornelia. "Abstract IA005: Immune escape during breast tumor progression." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-ia005.

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McAllister, Sandra S. "Abstract IA07: Systemic regulation of breast cancer progression." In Abstracts: AACR Special Conference on Tumor Metastasis; November 30-December 3, 2015; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-ia07.

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Mardis, Elaine R. "Abstract IA04: Genomic studies of breast cancer progression." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-ia04.

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Chen, Cindy X., Han Sang Park, and Adam Wax. "Breast Cell Cancer Progression Characterization Through Holographic Cytometry." In Novel Techniques in Microscopy. Washington, D.C.: OSA, 2021. http://dx.doi.org/10.1364/ntm.2021.nth2c.3.

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Zhou, W., AA Muggerud, P. Vu, EU Due, T. Sørlie, A. Børresen-Dale, F. Wärnberg, and A. Langerød. "TP53mutation is an early event in breast cancer progression." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-1047.

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Man, Y., Z. Zhang, C. Wang, L. Gao, and X. Zhang. "CAPC expression correlates with breast tumor progression and invasion." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4044.

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Phoenix, KN, F. Vumbaca, and KP Claffey. "Effective metabolic intervention of breast cancer progression and metastasis." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6024.

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Reports on the topic "BREAST PROGRESSION"

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Galaktionov, Konstantin. MicroRNA and Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada480199.

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Lin, Chen-Yong. Matriptase Activation in Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada439289.

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Lin, Chen-Yong. Matriptase Activation in Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427164.

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Lin, Chen-Yong. Matriptase Activation in Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417787.

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McLeskey, Sandra W. Stromal Components of Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada354318.

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Serra, Rosa, and Andra Frost. Primary Cilia in Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada601708.

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Gerald, William L. Gene Expression Analysis of Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada437751.

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Vlodavsky, Israel. Involvement of Heparanase in Breast Carcinoma Progression. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395693.

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Zhang, Lurong. Membrane-Bound Hyaluronidase in Breast Cancer Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada398227.

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Vlodavsky, Israel, Yael Friedmann, and Tamar Peretz. Involvement of Heparanase in Breast Carcinoma Progression. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada407484.

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