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Arthur S Tischler Department of Pathology and Laboratory Medicine, Tufts Medical Center and Tufts University School of Medicine, Boston, Massachusetts, USA

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Judith Favier Université Paris cité, Inserm UMR970 PARCC, Equipe Labellisée par la Ligue contre le cancer, Paris, France

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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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Jaesung (Peter) Choi
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Reena Desai
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Yu Zheng
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Mu Yao ANZAC Research Institute, Discipline of Endocrinology, Department of Anatomical Pathology, University of Sydney, Sydney, New South Wales 2139, Australia

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Qihan Dong ANZAC Research Institute, Discipline of Endocrinology, Department of Anatomical Pathology, University of Sydney, Sydney, New South Wales 2139, Australia

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Geoff Watson ANZAC Research Institute, Discipline of Endocrinology, Department of Anatomical Pathology, University of Sydney, Sydney, New South Wales 2139, Australia

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David J Handelsman
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Ulla Simanainen
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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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Hema Parmar University of California, 3rd and Parnassus, Department of Anatomy, HSW 1323, San Francisco, CA 94143, USA

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Gerald R Cunha University of California, 3rd and Parnassus, Department of Anatomy, HSW 1323, San Francisco, CA 94143, USA

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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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Xinyu Wu 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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Shiaoching Gong 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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Pradip Roy-Burman 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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Peng Lee 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
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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Zoran Culig 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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Sarah A Dabydeen 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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Priscilla A Furth Departments of Oncology, Medicine, Lombardi Comprehensive Cancer Center, Georgetown University, 3970 Reservoir Road NW, Research Building, Room 520A, Washington, District of Columbia 20057, USA
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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Lawrence S Kirschner Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, and Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 420 West 12th Avenue, TMRF 544, Columbus, Ohio 43210, USA

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Zhirong Yin Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, and Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 420 West 12th Avenue, TMRF 544, Columbus, Ohio 43210, USA

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Georgette N Jones Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, and Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 420 West 12th Avenue, TMRF 544, Columbus, Ohio 43210, USA

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Emilia Mahoney Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, and Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, 420 West 12th Avenue, TMRF 544, Columbus, Ohio 43210, USA

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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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Maho Shibata Departments of Medicine, Genetics and Development, Urology, and Systems Biology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York 10032, USA

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Michael M Shen Departments of Medicine, Genetics and Development, Urology, and Systems Biology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, New York, New York 10032, USA

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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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S Latteyer Department of Endocrinology, Diabetes and Metabolism, University of Duisburg-Essen, Essen, Germany

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S Christoph Clinic for Bone Marrow Transplants, University of Duisburg-Essen, Essen, Germany

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S Theurer Institute of Pathology, University of Duisburg-Essen, Essen, Germany

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G S Hönes Department of Endocrinology, Diabetes and Metabolism, University of Duisburg-Essen, Essen, Germany

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K W Schmid Institute of Pathology, University of Duisburg-Essen, Essen, Germany

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D Führer Department of Endocrinology, Diabetes and Metabolism, University of Duisburg-Essen, Essen, Germany

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L C Moeller Department of Endocrinology, Diabetes and Metabolism, University of Duisburg-Essen, Essen, Germany

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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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R Serra Department of Cell Biology, University of Alabama at Birmingham, 1918 University Boulevard, Birmingham, AL 35294-0005, USA

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M R Crowley Department of Cell Biology, University of Alabama at Birmingham, 1918 University Boulevard, Birmingham, AL 35294-0005, USA

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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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Amruta Ashtekar Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA

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Danielle Huk Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA

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Alexa Magner Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA

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Krista La Perle Department of Veterinary Biosciences and Comparative Pathology & Mouse Phenotyping Shared Resource, The Ohio State University, Columbus, Ohio, USA

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Xiaoli Zhang Department of Biostatistics, The Ohio State University, Columbus, Ohio, USA

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José I Piruat Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain

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José López-Barneo Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío CSIC Universidad de Sevilla, Seville, Spain

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Sissy M Jhiang Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio, USA

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Lawrence S Kirschner Department of Cancer Biology and Genetics, The Ohio State University, Columbus, Ohio, USA
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

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