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        Eppley Institute for Cancer Research

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Kay-Uwe Wagner, Ph.D.

Appointments: 

7/01/2004-present Associate Professor, Eppley Institute for Cancer Research, University of Nebraska Medical Center, Omaha, NE

7/01/2005-present

Associate Professor (Courtesy) Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha NE

7/01/2000-6/30/2004 

Assistant Professor, Eppley Institute for Cancer Research, University of Nebraska Medical Center, Omaha, NE

 

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1991

M.Sc., Animal Science, University of Leipzig (Germany)

1995

1995 - Ph.D. (summa cum laude), Animal Genetics, University of Halle (Germany)

1995-2000

Post Doctoral Fellow, NIDDK, NIH, Bethesda, MD 

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University of Nebraska Medical Center
986805 Nebraska Medical Center Rm. 8009
Omaha, NE 68198-6805
Tel: (402) 559-3288 (office) -3289 (lab)
Fax: (402) 559-4651
E-mail: kuwagner@unmc.edu

Web: http://www.unmc.edu/wagnerlab

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RO1 CA117930  Wagner (PI)                                         02/01/06-01/31/11

NIH/NCI - “Growth-Regulatory Signaling Networks in Breast Cancer”

Major goals: The major goal of the project is to examine whether the Janus kinase 2 (Jak2) is a potential target for breast cancer prevention and/or therapy in prolactin and Her2/neu-induced tumor models.

 

RO1 CA101841  Rui (PI)         Wagner (Co-PI)              06/23/04-05/31/09

NIH/NCI - “Stat5 as a gatekeeper in human breast cancer metastasis
Major goals: Analysis of the biological functions of Stat5 in breast cancer metastasis. Dr. Wagner has a subcontract of $38,390 (direct costs) in this NCI-funded project.

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For an updated list see: http://www.unmc.edu/wagnerlab/publications/index.html

Bierie, B.; D.G. Stover; T.W. Abel; A. Chytil; A.E. Gorska; M. Aakre; E. Forrester; L. Yang; K.-U. Wagner and H.L. Moses (2008): Transforming Growth Factor-b Regulates Mammary Carcinoma Cell Survival and Interaction with the Adjacent Microenvironment. Cancer Research 68 (6): 1809-19

Wagner, K.-U.  and H. Rui  (2008): Jak2/Stat5 signaling in mammogenesis, breast cancer initiation and progression. Journal of Mammary Gland Biology and Neoplasia 13 (1): 93-103  

Lin, D.I.; M.D. Lessie1; A.B. Gladden; C.H. Bassing; K.-U. Wagner and J. Alan Diehl (2008): Disruption of cyclin D1 nuclear export and proteolysis accelerates mammary carcinogenesis. Oncogene 27 (9): 1231–1242 (Epub 2007 Aug 27)

Feng, Y.; D. Manka; K.-U. Wagner and S. Khan (2007): ERa expression in the mammary epithelium is required for ductal and alveolar morphogenesis in pubertal, pregnant and lactating mice. Proc. Natl. Acad. Sci. U.S.A. 104 (37): 14718-14723  

Neilson, L.M.; J. Zhu; J. Xie; M.G. Malabarba; K. Sakamoto; K.-U. Wagner; R.A. Kirken and H. Rui (2007): Coactivation of janus tyrosine kinase (Jak)1 positively modulates prolactin-Jak2 signaling in breast cancer: recruitment of ERK and signal transducer and activator of transcription (Stat)3 and enhancement of Akt and Stat5a/b pathways. Molecular Endocrinology 21 (9): 2218–2232

Pecha, J.; D. Ankrapp; C. Jiang; W. Tang; K. Bruck; K.-U. Wagner and H. Xiao (2007): Deletion of Tip30 leads to rapid immortalization of murine mammary epithelial cells and ductal hyperplasia in the mammary gland. Oncogene 26 (53): 7423-7431

Sakamoto, K; B.A. Creamer; A.A. Triplett and K.-U. Wagner (2007): The Janus kinase 2 (Jak2) is required for expression and nuclear accumulation of Cyclin D1 in proliferating mammary epithelial cells. Molecular Endocrinology 21 (8): 1877-1892  

Oh, K.B.; M.J. Stanton; W.W. West; G.L. Todd and K.-U. Wagner (2007): Tsg101 is upregulated in a subset of invasive human breast cancers and its targeted overexpression in transgenic mice reveals weak oncogenic properties for mammary cancer initiation. Oncogene 26 (40): 5950–5959  

Matulka, L.A.; A.A. Triplett and K.-U. Wagner (2007): Parity-induced mammary epithelial cells are multipotent and express cell surface markers associated with stem cells. Developmental Biology 303 (1):  29–44   

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  • PREVIOUS GRADUATE STUDENTS/POST-DOCTORAL FELLOWS (present location):

KyungRan Park, M.D., Ph.D. (2000-2001), post-doctoral fellow; current position: Assistant Professor, Chungnam National University in Korea

Andrea Krempler, Ph.D. (2000-2002), post-doctoral fellow; current position: Staff Scientist, University of the Saarland, Homburg, Germany

Yongyue Qi, M.D. (2002-2003), post-doctoral fellow; current position: Douglas County Health Department

Keon Bong Oh, Ph.D. (2003-2006), post-doctoral fellow; current position: Scientist, KRIBB, Taejeon (Korea)

Laurice Matulka-Brandl, Ph.D. (2004-2007) current position: Scientists, Benchmark Biolabs in Lincoln, NE

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For specific projects see : http://www.unmc.edu/wagnerlab/projects/index.html

Summary:  The research objectives of the lab are to elucidate the mechanisms regulating the normal development of the mammary gland and to identify genetic pathways that control the development of breast cancer. Mammary development is a fascinating process that is unique in several aspects: First, proliferation and differentiation of mammary epithelial cells occur primarily postnatally. Second, mammary development is dependent upon the synergistic action of systemic hormones and local growth factors. Third, a full-functionally differentiated mammary gland requires a complex 3-D structure of epithelial and stromal compartments. Fourth, the mammary gland can serve as an excellent in vivo model for cell proliferation, differentiation, genome stability, and programmed cell death as it develops in defined steps during reproductive cycles.

Numerous genes have been identified that are crucial for normal mammary development and breast cancer. Their role is being studied in our research group through their deregulated expression in mammary tissue of transgenic animals or gene transfer using adenoviral vectors, and through their deletion from the mouse genome by homologous recombination. Specifically, our laboratory has the expertise to delete genes in a tissue-specific and temporally controlled fashion using the Cre-loxP recombination system. Current projects include the analysis of prolactin signaling through the Jak2-Stat5 pathway, the cloning of a new mammary epithelial population from parous females, and studying the role of the Tsg101 gene during cell cycle regulation and neoplastic transformation.

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No information available.

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