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Experimental models including xenografts and cell lines derived from multiple human tumors provide a critical foundation for preclinical cancer research. These are complemented by mouse models engineered to develop tumors that faithfully
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ERα dependent pathways in mouse EC ( Vilgelm et al . 2006 ). The goal of this study was to investigate the role of AR-mediated androgen actions in PTEN inactivation induced experimental uterine cancer. To achieve our goal, we have generated and
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midventral aspect of the embryo. In the mouse at embryonic day (E)16, cell proliferation at the tip of the mammary bud elicits elongation of the primary duct, which grows toward the mammary fat pad precursor. The primary mammary duct invades the mammary fat
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Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
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Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
Department of Pathology, Arthritis and Tissue Degeneration Program, Laboratory of Molecular Biology, Department of Pathology, Department of Urology, NYU Cancer Institute, New York Harbor Healthcare System, Department of Urology, New York University School of Medicine, New York, NY, USA
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eventually become castration-resistant PCa (CRPC), which remains the primary cause of PCa-related death. Therefore, continued generation of new PCa mouse models is necessary to enhance our understanding of PCa development and progression to metastasis
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Departments of Oncology, Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Road NW, Research Building, Room 520A, Washington, District of Columbia 20057, USA
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rats exposed to chemical carcinogens develop ER+ mammary cancer and have been used in different types of in vivo experiments exploring pathogenesis and treatment ( Shull 2007 ). Genetic engineering of mouse models to produce ER+ mammary cancer
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appreciate the complexity of PKA signaling, significant work has been invested in generating mouse models with genetic manipulation of the PKA system. Although these systems are all to some extent artificial, they allow specific investigation of various
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progression of prostate cancer to castration-resistance is of fundamental importance for the development of reliable biomarkers and effective treatments. Studies using genetically engineered mouse (GEM) models have revealed that the normal prostate contains
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therefore important to study the effects of T 3 and T 4 on cancer progress in vivo . Here, we demonstrate in an orthotopic mouse model that T 4 promotes growth of murine non-small-cell lung cancer (NSCLC) cells. Materials and methods Cell
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Introduction Development of the mouse mammary gland begins at embryonic day 11 (E11) as an invagination of the ectoderm into the underlying ventral mesoderm ( Imagawa et al. 1994 , Hennighausen & Robinson 2001 , Silberstein 2001
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Division of Endocrinology, Diabetes, and Metabolism, Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA
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, we generated tissue-specific knockout of Sdhd in the mouse thyroid gland. These in vivo studies were complemented by in vitro analyses of human thyroid cancer cells with knockdown of SDHD. Together, these studies reveal the ability of SDHD