Relevant bibliographies by topics / Mouse model and breast cancer

Academic literature on the topic 'Mouse model and breast cancer'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Mouse model and breast cancer"

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Wu, Min, and Murray O. Robinson. "Human-in-Mouse breast cancer model." Cell Cycle 8, no. 15 (August 2009): 2317–18. http://dx.doi.org/10.4161/cc.8.15.9206.

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Dabydeen, Sarah A., and Priscilla A. Furth. "Genetically engineered ERα-positive breast cancer mouse models." Endocrine-Related Cancer 21, no. 3 (January 30, 2014): R195—R208. http://dx.doi.org/10.1530/erc-13-0512.

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The majority of human breast cancers are estrogen receptor-positive (ER+), but this has proven challenging to model in genetically engineered mice. This review summarizes information on 21 mouse models that develop ER+ mammary cancer. Where available, information on cancer pathology and gene expression profiles is referenced to assist in understanding which histological subtype of ER+ human cancer each model might represent.ESR1,CCDN1, prolactin,TGFα,AIB1,ESPL1, andWNT1overexpression,PIK3CAgain of function, as well as loss ofP53(Trp53) orSTAT1are associated with ER+ mammary cancer. Treatment with the PPARγ agonist efatutazone in a mouse withBrca1andp53deficiency and 7,12-dimethylbenz(a)anthracene exposure in combination with an activated myristoylated form of AKT1 also induce ER+ mammary cancer. A spontaneous mutant in nude mice that develops metastatic ER+ mammary cancer is included. Age of cancer development ranges from 3 to 26 months and the percentage of cancers that are ER+ vary from 21 to 100%. Not all models are characterized as to their estrogen dependency and/or response to anti-hormonal therapy. Strain backgrounds include C57Bl/6, FVB, BALB/c, 129S6/SvEv, CB6F1, and NIH nude. Most models have only been studied on one strain background. In summary, while a range of models are available for studies of pathogenesis and therapy of ER+ breast cancers, many could benefit from further characterization, and opportunity for development of new models remains.
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Alfred, Jane. "A new mouse model of BRCA1 breast cancer?" Molecular Medicine Today 5, no. 7 (July 1999): 284. http://dx.doi.org/10.1016/s1357-4310(99)01520-8.

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Hennighausen, Lothar. "Mouse models for breast cancer." Oncogene 19, no. 8 (February 2000): 966–67. http://dx.doi.org/10.1038/sj.onc.1203346.

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Burney, Maryam, Lata Mathew, Anjali Gaikwad, Elizabeth K. Nugent, Anneliese O. Gonzalez, and Judith A. Smith. "Evaluation Fucoidan Extracts From Undaria pinnatifida and Fucus vesiculosus in Combination With Anticancer Drugs in Human Cancer Orthotopic Mouse Models." Integrative Cancer Therapies 17, no. 3 (November 20, 2017): 755–61. http://dx.doi.org/10.1177/1534735417740631.

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Objective: To determine the activity of fucoidan from Undaria pinnatifida (UPF) and Fucus vesiculosus (FVF) when given in combination of chemotherapy drugs using selected human breast or ovarian cancer orthotopic mouse models. Methods: Mice were inoculated with 1 × 106 cells of TOV-112d, MCF-7, or ZR-75 subcutaneously or SKOV3-GFP-Luc intraperitoneally on day 0. MCF-7 and ZR-75 mice were administered with estradiol valerate 2 mg/kg in 0.2 mL castor oil subcutaneously two days prior to cell inoculation. Mice were randomized to one of six arms (N = 10/arm) paclitaxel, UPF/paclitaxel, FVF/paclitaxel, tamoxifen, UPF/tamoxifen, or FVF/tamoxifen. Tumors were measured three times per week for 28 days. Results: Improved activity was observed with UPF or FVF in combination with tamoxifen in both the MCF-7 and ZR-75D breast cancer mouse models. Decreased activity of paclitaxel was observed when given in combination with UPF or FVF in both breast cancer mouse models. The combination of FVF/tamoxifen in the TOV-112d ovarian cancer mouse model had improved activity but no there was difference observed with the UPF/tamoxifen in either ovarian cancer mouse model. No difference was observed with combination of UPF or FVF with paclitaxel in human ovarian cancer SKOV3 or TOV-112d orthotopic mouse models. Conclusion: This study did confirm that UPF/FVF in combination with tamoxifen did not decrease tamoxifen activity in both breast and ovarian cancer, with some potential to improve activity compared to tamoxifen alone in breast cancers. Previous in vitro studies had suggested UPF and FVF had overall synergistic activity with paclitaxel; however, in the current in vivo human cancer mouse model studies there was no change in paclitaxel activity when given in combination with UPF or FVF in either of the two human ovarian cancer models. Furthermore, this study demonstrated that UPF or FVF given in combination with paclitaxel had a potential antagonistic effect in breast cancer models. Additional studies are warranted to delineate mechanisms contributing to variation in the in vivo activity when given in combination with paclitaxel. As a first step, a clinical pharmacokinetic study evaluating impact of FVF/UPF given in combination with chemotherapy in patients with solid tumors is underway.
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Hámori, Lilla, Gyöngyi Kudlik, Kornélia Szebényi, Nóra Kucsma, Bálint Szeder, Ádám Póti, Ferenc Uher, et al. "Establishment and Characterization of a Brca1−/−, p53−/− Mouse Mammary Tumor Cell Line." International Journal of Molecular Sciences 21, no. 4 (February 11, 2020): 1185. http://dx.doi.org/10.3390/ijms21041185.

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Breast cancer is the most commonly occurring cancer in women and the second most common cancer overall. By the age of 80, the estimated risk for breast cancer for women with germline BRCA1 or BRCA2 mutations is around 80%. Genetically engineered BRCA1-deficient mouse models offer a unique opportunity to study the pathogenesis and therapy of triple negative breast cancer. Here we present a newly established Brca1−/−, p53−/− mouse mammary tumor cell line, designated as CST. CST shows prominent features of BRCA1-mutated triple-negative breast cancers including increased motility, high proliferation rate, genome instability and sensitivity to platinum chemotherapy and PARP inhibitors (olaparib, veliparib, rucaparib and talazoparib). Genomic instability of CST cells was confirmed by whole genome sequencing, which also revealed the presence of COSMIC (Catalogue of Somatic Mutations in Cancer) mutation signatures 3 and 8 associated with homologous recombination (HR) deficiency. In vitro sensitivity of CST cells was tested against 11 chemotherapy agents. Tumors derived from orthotopically injected CST-mCherry cells in FVB-GFP mice showed sensitivity to cisplatin, providing a new model to study the cooperation of BRCA1-KO, mCherry-positive tumor cells and the GFP-expressing stromal compartment in therapy resistance and metastasis formation. In summary, we have established CST cells as a new model recapitulating major characteristics of BRCA1-negative breast cancers.
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Son, Yeseon, Changwook Lee, In Tag Yu, Mijin Lee, and Hangun Kim. "Evaluation of Anti-cancer Efficacy of Potassium Usnate using NIR Imaging of Orthotopic Breast Cancer Mouse Model." Yakhak Hoeji 66, no. 5 (October 31, 2022): 278–82. http://dx.doi.org/10.17480/psk.2022.66.5.278.

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Mouse cancer models are useful tools for evaluating in vivo tumor growth and metastasis, providing valuable information for preclinical testing. In this process, optical imaging enables the mouse models to easily identify the progress of disease in a non-invasive way. Here, we established an experimental bioimaging animal model of near-infrared (NIR) fluorescence by using a fluorescence-labeled organism bioimaging instrument (FOBI) and evaluated the anti-cancer effect of potassium usnate (KU) in an orthotopic breast cancer model. The cell viability assay revealed that KU had cytotoxicity with half maximal inhibitory concentration of approximately 138.57, 167.69, and 144.17 μM in 4T1-Fluc-Neo/iRFP-Puro (4T1-iRFP), MDA-MB-231, and MCF-7 cells, respectively. The measurement of NIR fluorescence from the 4T1-iRFP cells in a microtube via FOBI exhibited a strong correlation between cell number and fluorescence intensity, and the minimal detection limit was 10⁵ cells. Accordingly, NIR imaging was performed on the orthotopic breast cancer mouse model by using FOBI, and regression of tumor progression through intraperitoneal KU administration was successfully monitored. Our results demonstrated the establishment of NIR imaging in the orthotopic breast cancer animal model for evaluating the anti-cancer effect of KU.
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Lanari, Claudia, Caroline A. Lamb, Victoria T. Fabris, Luisa A. Helguero, Rocío Soldati, María Cecilia Bottino, Sebastián Giulianelli, Juan Pablo Cerliani, Victoria Wargon, and Alfredo Molinolo. "The MPA mouse breast cancer model: evidence for a role of progesterone receptors in breast cancer." Endocrine-Related Cancer 16, no. 2 (June 2009): 333–50. http://dx.doi.org/10.1677/erc-08-0244.

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More than 60% of all breast neoplasias are ductal carcinomas expressing estrogen (ER) and progesterone receptors (PR). By contrast, most of the spontaneous, chemically or mouse mammary tumor virus induced tumors, as well as tumors arising in genetically modified mice do not express hormone receptors. We developed a model of breast cancer in which the administration of medroxyprogesterone acetate to BALB/c female mice induces mammary ductal carcinomas with a mean latency of 52 weeks and an incidence of about 80%. These tumors are hormone-dependent (HD), metastatic, express both ER and PR, and are maintained by syngeneic transplants. The model has been further refined to include mammary carcinomas that evolve through different stages of hormone dependence, as well as several hormone-responsive cell lines. In this review, we describe the main features of this tumor model, highlighting the role of PR as a trigger of key signaling pathways mediating tumor growth. In addition, we discuss the relevance of this model in comparison with other presently used breast cancer models pointing out its advantages and limitations and how, this model may be suitable to unravel key questions in breast cancer.
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Gkikopoulou, Evi, Anthi Kolokotroni, Vagelis Rinotas, Martina Rauner, and Eleni Douni. "Investigating breast cancer in an osteoporotic TgRANKL mouse model." Bone Reports 16 (May 2022): 101378. http://dx.doi.org/10.1016/j.bonr.2022.101378.

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Cuellar-Vite, Leslie, Kristen L. Weber-Bonk, Fadi W. Abdul-Karim, Christine N. Booth, and Ruth A. Keri. "Focal Adhesion Kinase Provides a Collateral Vulnerability That Can Be Leveraged to Improve mTORC1 Inhibitor Efficacy." Cancers 14, no. 14 (July 11, 2022): 3374. http://dx.doi.org/10.3390/cancers14143374.

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The PI3K/AKT/mTORC1 pathway is a major therapeutic target for many cancers, particularly breast cancer. Everolimus is an mTORC1 inhibitor used in metastatic estrogen receptor-positive (ER+) and epidermal growth factor receptor 2-negative (HER2-) breast cancer. However, mTORC1 inhibitors have limited efficacy in other breast cancer subtypes. We sought to discover collateral sensitivities to mTORC1 inhibition that could be exploited to improve therapeutic response. Using a mouse model of breast cancer that is intrinsically resistant to mTORC1 inhibition, we found that rapamycin alters the expression of numerous extracellular matrix genes, suggesting a potential role for integrins/FAK in controlling mTORC1-inhibitor efficacy. FAK activation was also inversely correlated with rapamycin response in breast cancer cell lines. Supporting its potential utility in patients, FAK activation was observed in >50% of human breast cancers. While blocking FAK in mouse models of breast cancer that are highly responsive to rapamycin had no impact on tumor growth, FAK inhibition sensitized rapamycin-resistant tumors to mTORC1 inhibition. These data reveal an innate dependency on FAK when mTORC1 signaling is lost in tumors that are resistant to mTORC1 inhibitors. They also suggest a precision medicine approach to improving mTORC1 inhibitor efficacy in resistant cancers by suppressing FAK signaling.
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Dissertations / Theses on the topic "Mouse model and breast cancer"

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Herschkowitz, Jason I. Perou Charles M. "Breast cancer subtypes, mouse models, and microarrays." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1728.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum of Genetics and Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.
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Lesurf, Robert. "Molecular pathway analysis of mouse models for breast cancer." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32499.

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Human breast cancer is an extremely heterogeneous disease, consisting of a number of different subtypes with varying levels of aggressiveness reflected by distinct, but largely undefined, molecular profiles. Here we have analyzed several novel mouse models for breast cancer in the context of the human subtypes, and have shown parallels between the mice and humans at numerous biologically relevant levels. In addition, we have developed a statistical framework to help elucidate the individual molecular components that are at play across a panel of human breast or murine mammary tumors. Our results indicate that, while no mouse model captures all aspects of the human disease, they each contain components that are shared by a subset of human breast tumors. Furthermore, our statistical framework provides numerous advantages over previous methodologies, in helping to reveal the individual molecular pathways that make up the biology of the tumors.
Le cancer du sein est connue pour être une maladie très hétérogène, composé d'un nombre de différents sous-types avec différents niveaux de l'agressivité et distinctes, mais indéfini, profils moléculaires. Ici, nous avons analysé plusieurs nouveaux modèles de souris pour le cancer du sein, dans le cadre des sous-types, et nous avons trouver des parallèles à un certain nombre de niveaux pertinents biologiques. En outre, nous avons développé une méthodologie statistique pour aider à élucider les différents composants moléculaires qui sont à jouer dans un groupe de tumours de sein d'humains ou mammaires murins. Nos résultats indiquent que, même si aucun modèle de souris capte tous les aspects de la maladie chez l'homme, chacun contiennent des composants qui sont partagées par un sous-ensemble de tumeurs mammaires humaines. En outre, notre outil statistique offre de nombreux avantages par rapport aux précédentes méthodes, pour aider à révéler les voies moléculaires qui composent la biologie des tumeurs.
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Simpson, Peter Thomas. "Differential gene expression analysis in a transgenic mouse model of metastatic breast cancer." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343681.

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Alhazmi, Aiman. "Role of Nucleosome Remodeling Factor (NURF) in Tumorigenesis Using a Breast Cancer Mouse Model." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/379.

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Understanding the impact of epigenetic mechanisms on tumorigenesis is essential, as epigenetic alterations are associated with tumor initiation and progression. Because epigenetic changes are reversible, they are potential targets for cancer therapy. Nucleosome Remodeling Factor (NURF) is a chromatin-remodeling complex that regulates gene expression by changing nucleosome positioning along the DNA sequence. Previous studies have shown a role for NURF in embryonic development as well as regulating genes involved in tumor progression. In this work we investigated the impact of eliminating NURF function in tumorigenesis in vivo. BALB/c mice challenged with syngeneic 67NR breast cancer cell lines, injected into the mammary fat pad, lacking NURF, due to knockdown of its essential subunits Bptf, showed reduction in tumor growth comparing to control tumors. The observed reduction in tumor growth was abrogated in immunodeficient mice lacking a functional immune system. Bptf KD and control 67NR cells grew at similar rates in vitro. Similar findings were observed in our lab using 66cl4 breast cancer cell lines. Using immunofluorescence staining, no significant difference in CD8+, CD4+, NK and MDSC cells infiltrations into the tumor microenvironment was observed in 66cl4 tumors. Preliminary results from 67NR tumors suggested more CD4+ and CD8+ cells. Gene expression profile of tumor tissues from BALB/c mice injected with 67NR and 66cl4 cell lines showed enrichment of genes associated with immune response. Our findings suggested a role of the immune system in targeting tumor cells lacking Bptf in vivo.
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Robey, Ian, and Natasha Martin. "Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer." BioMed Central, 2011. http://hdl.handle.net/10150/610344.

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BACKGROUND:The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations.METHODS:We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA), a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231), we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB) therapies chronically.RESULTS:Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment.CONCLUSIONS:DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment.
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Pochampalli, Mamata Rani. "Characterization of Effects of Muc1 Expression on Epidermal Growth Factor Receptor Signaling in Breast Cancer." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/194355.

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EGF receptors are key regulators of cell survival and growth in normal and transformed tissues. Ligand binding results in formation of homo/hetero dimers of these receptors, followed by activation of the kinase activity and subsequent tyrosine phosphorylation of many downstream molecules. The activation of these receptors is not only mediated by the binding of their cognate ligands, but by transactivaton by other molecules as well. Recent studies have identified an oncogenic glycoprotein MUC1 as a binding partner for EGFR and that MUC1 expression can potentiate EGFR-dependent signal transduction. After receptor activation, EGFR is typically downregulated via an endocytic pathway that results in receptor degradation or recycling. We report here that MUC1 expression inhibits the degradation of ligand-activated erbB1. In addition, MUC1 expression results in prolonged activation of Akt, but not ERK1,2 MAPKinase. The MUC1-mediated protection against degradation occurs with a decrease in EGF-stimulated ubiquitination of erbB1, and an increase in erbB1 recycling. We then utilized the WAP-TGFα transgenic mouse model of breast cancer and determined that a loss of Muc1 expression dramatically alters mammary tumor progression. While 100% of WAP-TGFα/Muc1^(+/+) mice form mammary gland tumors, only 37% of WAP-TGFα/Muc1^(-/-) form tumors. Furthermore, expression of cyclin D1 expression is significantly suppressed in tumors derived from WAPTGFα/Muc1^(-/-) animals, and loss of Muc1 expression resulted in a significant inhibition in the formation of hyperplastic lesions in the mammary gland. We also observed metastatic pulmonary adenocarcinoma (1/29) and perivascular lymphoma of unknown origin (28/29) in the WAP-TGFα transgenic mice but not in the WAP TGFα/Muc1^(-/-) animals. To determine the effects of Muc1 expression on metastasis in a model lacking perivascular lymphoma, we crossed MMTV-Wnt-1 and MMTV-MUC1 transgenic mice and evaluated interactions between Muc1 and EGFR. Although the MMTV-Wnt-1 mice are non-metastatic, a majority (6/10) of the bitransgenic MMTVWnt- 1/MMTV-MUC1 formed pulmonary metastases. Furthermore, overexpression of MUC1 increases the breast cancer cell invasion in vitro. The MUC1 induced increase in invasion is found to be EGF and EGFR-kinase dependent. Collectively, these data indicate that MUC1 expression contributes to many of the hallmarks of cancer and in addition, is an important modulator of EGFR-associated mammary tumor progression.
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Ke, Jia-Yu. "Bioactivity of Naringenin in Metabolic Dysregulation and Obesity-Associated Breast Cancer in a Mouse Model of Postmenopause." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1437479457.

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Heilmann, Katharina [Verfasser], and Karin [Akademischer Betreuer] Müller-Decker. "Epigenetic characterization of the C3(1) SV40T mouse model of human breast cancer / Katharina Heilmann ; Betreuer: Karin Müller-Decker." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1178008134/34.

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Balderstone, Lucy Anne. "Use of fluorescent imaging to monitor drug responses in mouse models of tumourigenesis." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/17859.

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As our understanding of the complexities of cancer biology has increased, the ability to exploit unique features of tumour cells with molecularly targeted therapies has become a reality. However, despite unprecedented volumes of new molecules in clinical trials, the number of highly effective drugs approved by the regulatory authorities remains disappointingly low. Moreover, oncology drug development is plagued by high levels of attrition in late phase clinical development. Failure due to poor efficacy and toxicity issues are not believed to be a result of the development of molecules with inadequate pharmaceutical properties, but rather due to a lack of understanding of their full mechanism of action. All of this points to imprecise analysis of the drugs during the preclinical phase, highlighting the need for better preclinical drug development tools. Animal models provide a key preclinical tool, and as a therapeutic area, oncology is characterised by models which are not predictive of the true human pathology. Overexpression of the human epidermal growth factor receptor two (HER2) oncogene, and inactivation of the phosphatase and tensin (PTEN) tumour suppressor, are two important events in human breast cancer. A novel conditional mouse model driven by overexpression of HER2 coupled with / without the loss of PTEN has been characterised to interrogate the importance of these two cellular perturbations. Multifocal tumours arose in mice from both lines, while luminal tumour characteristics were shown to be reduced and basal characteristics increased with a reduction in PTEN expression. Disruption of PTEN rapidly accelerated tumour onset (from 138 to 82 days) and tumour growth (with the time from tumour onset to maximum tumour size reduced from 38 to 21 days), significantly reducing overall survival (from 165 to 102 days). The ability of tumour cells to colonize the lungs was not significantly affected by the loss of PTEN. Tumours arising in both mice genotypes were utilized to generate cell lines. These failed to provide an in vitro representation of the tumours, and found little utility in drug efficacy studies with HER family targeted agents, a situation which could be improved by the use of different culture methods. Since suppression of apoptosis is a hallmark of human cancer, and a desired endpoint of many anticancer therapies is the induction of cell death, the generation of cell lines inherently capable of sensing caspase-mediated apoptotic cell death would be a valuable drug development tool. Given that fluorescence imaging is also emerging as a potentially powerful modality for preclinical drug development, a novel fluorescent in house apoptosis reporter construct was generated (pCasFSwitch). Initial validation of pCasFSwitch by transient transfection into murine mammary carcinoma cells proved difficult due to transfection associated toxicity, yet proof-of-principle was indicated. Transfer of pCasFSwitch into a retroviral backbone vector enabled the generation of stably transfected squamous carcinoma cells more suitable for further analysis. Incubation of lysates from these cells with recombinant enzymes revealed the construct could be cleaved by caspase-3, but not by other members of the cysteine protease family. Furthermore, assessment of apoptosis levels in the cells upon staurosporine treatment proved the utility of the construct to quantify cell death, and was validated against data generated with a commercial competitor, NucView. Further comparison of the specificity of the imaging agents using caspase inhibitors was limited by the functionality of currently available inhibitors, but did reveal that in common with NucView, construct quantified levels of apoptosis were affected by inhibition. This thesis details the development of two preclinical drug development tools. A novel mouse model enables biological interrogation of two key events in human breast carcinogenesis. Since PTEN loss is associated with resistance to HER2 targeted therapies, it is ideally suited for efficacy testing to overcome such resistance. The in house fluorescent apoptosis imaging agent allows a temporal read-out of drug effects in live single cells. While the use of intravital imaging of stable cell lines implanted under imaging windows would allow in vivo validation of in vitro data. Taken together, such facilitation of thorough evaluation of therapies at the preclinical stage, will reduce the adverse effects felt by the pharmaceutical industry of failure late in the drug development pipeline.
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Milliken, Erin L. "USE OF A TRANSGENIC MOUSE MODEL OF OVARIAN HYPERSTIUMLUATION TO IDENTIFY THERAPEUTIC TARGETS AND MECHANISMS IN HORMONE-INDUCED MAMMARY CANCER." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1121273034.

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Books on the topic "Mouse model and breast cancer"

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O'Connell, Fiona Claire. Morphology and gene expression in the postnatal mouse mammary gland. Dublin: University College Dublin, 1997.

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Rintala, Anne C. DNA repair in a radioresistant breast cancer model system. Sudbury, Ont: Laurentian University, 2000.

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Moelleken, Brent Roderick Wilfred. Tamoxifen - 5-fluorouracil synergy in human breast cancer cell lines: Correlating in vitro synergy with the current estrogen receptor model. [New Haven: s.n.], 1985.

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The mammary gland as an experimental model: A subject collection from Cold Spring Harbor perspectives in biology. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2011.

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Kogan, Ilana. An in vivo model for PSA production by breast cancer cell-lines growing as xenografts in scid mice. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Pearce, Andrews G. The generation and characterization of a radiation resistant model system to study radioresistance in human breast cancer cells. Sudbury, Ont: Laurentian University, Chemistry and Biochemistry Department, 2000.

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Cheung, Alison Min Yan. Characterization of the biological functions of breast cancer gene BRCA2 using conditionally-inactivated mouse models. 2003.

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Tamimi, Rulla, Susan Hankinson, and Pagona Lagiou. Breast Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0016.

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Most of the established reproductive risk factors for breast cancer, like age at menarche or parity, are not appropriate for public health intervention. Several lines of evidence, like the associations with birthweight and early exposure to radiation, support an important influence of early-life events on subsequent breast cancer risk. The best established modifiable risk factors for the disease include postmenopausal hormone use, moderate alcohol intake, and adult weight gain. More recently, we have come to appreciate that instead of a single disease, breast cancer is rather a heterogeneous group of subtypes with different etiologies. Yet the wealth of available epidemiologic information can be synthesized into a consistent and testable, albeit still hypothetical, causal model. With our increasing knowledge on the relation between endogenous hormones and breast cancer, and the development of selective estrogen receptor modulators, as well as aromatase inhibitors, chemoprevention will likely become more common in the future.
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Zai, Clement. Generation of a mouse model for colorectal cancer. 2004.

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Yin, Hong. Human Mouse Mammary Tumor Virus-Like Elements and Their Relation to Breast Cancer. Uppsala Universitet, 1999.

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Book chapters on the topic "Mouse model and breast cancer"

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Couto, Joana Pinto, and Mohamed Bentires-Alj. "Mouse Models of Breast Cancer: Deceptions that Reveal the Truth." In Breast Cancer, 49–60. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48848-6_6.

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Sakamoto, Kazuhito, Jeffrey W. Schmidt, and Kay-Uwe Wagner. "Mouse Models of Breast Cancer." In Methods in Molecular Biology, 47–71. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2297-0_3.

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McAllister, Sandra S. "Systemic Instigation: A Mouse Model to Study Breast Cancer as a Systemic Disease." In Mouse as a Model Organism, 145–62. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0750-4_9.

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Medina, Daniel. "Mouse Models for Mammary Cancer." In Methods in Mammary Gland Biology and Breast Cancer Research, 3–17. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4295-7_1.

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Chakrabarti, Rumela, and Yibin Kang. "Transplantable Mouse Tumor Models of Breast Cancer Metastasis." In Methods in Molecular Biology, 367–80. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2297-0_18.

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Imagawa, W., G. Bandyopadhyay, M. Spencer, J. Li, and S. Nandi. "Regulation of Mammary Epithelial Cell Proliferation: An In Vitro Mouse Mammary Epithelial Cell Model System." In Breast Cancer: Origins, Detection, and Treatment, 31–41. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2309-9_3.

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Thiagarajan, Praveena S., and Ofer Reizes. "Mouse Models to Study Leptin in Breast Cancer Stem Cells." In Energy Balance and Cancer, 127–51. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-16733-6_7.

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Rottenberg, Sven, Marina Pajic, and Jos Jonkers. "Studying Drug Resistance Using Genetically Engineered Mouse Models for Breast Cancer." In Methods in Molecular Biology, 33–45. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-416-6_3.

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Witt, Kristina, and Andreas Lundqvist. "Evaluation of Breast Cancer and Melanoma Metastasis in Syngeneic Mouse Models." In Methods in Molecular Biology, 197–206. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8979-9_14.

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Hoffman, Robert M. "The First Patient-Derived Orthotopic Xenograft (PDOX) Mouse Models of Cancer: Cancer of the Colon, Pancreas, Lung, Breast, Ovary, and Mesothelioma." In Molecular and Translational Medicine, 79–87. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57424-0_7.

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Conference papers on the topic "Mouse model and breast cancer"

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Sawyer, Travis W., Photini F. Rice, Jennifer W. Koevary, Jennifer K. Barton, Denise C. Connolly, and Kathy Q. Cai. "In vivo multiphoton imaging of an ovarian cancer mouse model." In Diseases in the Breast and Reproductive System V, edited by Melissa C. Skala, Darren M. Roblyer, and Paul J. Campagnola. SPIE, 2019. http://dx.doi.org/10.1117/12.2505825.

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Bowman, Tyler, Kinan Alhallak, Tanny Chavez, Kamrul Khan, Dakory Lee, Narasimhan Rajaram, Jingxian Wu, Avishek Chakraborty, Keith Bailey, and Magda El-Shenawee. "Terahertz imaging of freshly excised breast cancer using mouse model." In 2017 42nd International Conference on Infrared, Millimeter, and Terahertz Waves (IRMMW-THz). IEEE, 2017. http://dx.doi.org/10.1109/irmmw-thz.2017.8067153.

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Rajhans, R., V. Cortez, SS Nair, RR Tekmal, R. Kumar, and RK Vadlamudi. "Novel mouse model for studying role of ER-nongenomic actions in breast cancer." 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-601.

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DeAngel, R., O. Tolstykh, K. Nameer, R. Jayarajan, S. Perkins, R. Tekmal, L. DeGraffenried, and S. Hursting. "Effects of obesity on anastrozole response in a mouse model of postmenopausal breast cancer." 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-1146.

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Jonkers, J. "ES2-2: Mouse Models of Basal-Like Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-es2-2.

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Bhardwaj, Anjana, Matthew D. Embury, Raniv D. Rojo, Constance Albarracin, and Isabelle Bedrosian. "Abstract 20: Fluvastatin inhibits the development of breast cancer in SV40C3Tag mouse model of triple negative breast cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-20.

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Shaw, Aubie K., Rachelle Johnson, Julie Sterling, Greg Mundy, and Hal Moses. "Abstract 1956: A novel mouse model of breast cancer metastasis to bone." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1956.

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Krause, Silva, Heather Tobin, Heidi L. Lurvey, and Donald E. Ingber. "Abstract 3273: A robust transgenic mouse model to study male breast cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3273.

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Chen, Wenhong, John Olson, Christine N. McMahan, Mayur Choudhary, Hannah Caldas, and Linda J. Metheny-Barlow. "Abstract 473: Generation of a mouse model of breast cancer brain metastasis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-473.

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Bhala, Rhea, Anjana Bhardwaj, Alexander Koh, Zhenlin Ju, Jing Wang, and Isabelle Bedrosian. "Long-term avasimibe treatment abolishes the breast cancer preventative efficacy of statin in a spontaneous mouse model of breast cancer." In Leading Edge of Cancer Research Symposium. The University of Texas at MD Anderson Cancer Center, 2022. http://dx.doi.org/10.52519/00044.

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Reports on the topic "Mouse model and breast cancer"

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Parrinello, Simona, and Judith Campisi. Aging, Breast Cancer, and the Mouse Model. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417918.

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Donehower, Laurence A. The p53-Deficient Mouse as a Breast Cancer Model. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/ada368272.

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Weilbaecher, Katherine, and Ross Cagan. Assessing a Drosophila Metastasis Model in Mouse and Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada488819.

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Jarvis, Gary A. Efficacy of Galectin-3C in Mouse Model of Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada383096.

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Weilbaecher, Katherine, and Ross Cagan. Assessing a Drosophila Metastasis Model in Mouse and Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2009. http://dx.doi.org/10.21236/ada625288.

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VAN Golen, Kenneth L. The RhoC Transgenic Mouse as a Realistic Model of Inflammatory Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada398977.

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Boka, Valerie. A Mouse Model to Investigate the Role of DBC2 in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada452752.

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Boka, Valerie. A Mouse Model to Investigate the Role of DBC2 in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada434065.

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Van Golen, Kenneth L. The RhoC Transgenic Mouse as a Realistic Model of Inflammatory Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada411463.

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Boka, Valerie. A Mouse Model to Investigate the Role of DBC2 in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada463478.

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