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Janet E. Mertz, Ph.D.

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J. Mertz photo Professor of Oncology

B.S., B.S., 1970, Life Sciences/Electrical Engineering, Massachusetts Institute of Technology
Ph.D., 1975, Biochemistry, Stanford University
Postdoctoral research: Medical Research Council Laboratory of Molecular Biology, Cambridge, England

Office: 713A McArdle Laboratory
Office - (608) 262-2383; Lab - (608) 262-2335
Email: mertz@oncology.wisc.edu

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Research Interests: Transcriptional regulation in DNA tumor viruses and breast cancer

Research Description: One of our group's long-term interests involves regulation of gene expression and mechanisms of oncogenesis by DNA tumor viruses implicated in a variety of human cancers. Recently, we have identified the cellular transcription factor ZEB-1 as a key player in establishment and maintenance of latency following primary infection, reactivation out of latency and, possibly, malignant transformation of cells by the human herpesvirus Epstein-Barr virus. These studies could lead to the development of new ZEB-based therapies for the treatment of EBV-associated diseases such as infectious mononucleosis, nasopharyngeal carcinoma, and some lymphomas.

Our group's second area of research concerns the roles of the human estrogen-related receptor a (ERRa) in regulation of estrogen responsiveness and breast carcinogenesis. We have found that ERRa can function as either a down-modulator or a constitutive activator of estrogen response element-directed transcription, with its activity regulated in part by post-translational phosphorylations occurring via EGFR/ErbB2 (HER2) signaling pathways. ERRa-positivity has been shown to be associated with poor prognosis and tamoxifen resistance in breast cancer. This finding is likely due to the active form of ERRa substituting for estrogen receptor to activate genes regardless of the presence of ligands. We are currently working to develop reagents that specifically detect the activator form of ERRa in primary breast tumors for use in prognosis and determination of best currently available therapeutic options for treatment of individual breast cancers. We also hope to identify drugs that can interfere with ERRa's functional activities for use as a novel therapy, especially for the treatment of ER-negative and tamoxifen-resistant breast cancers for which there are currently a paucity of good therapeutic options.

Selected recent publications

Iempridee, T., Reusch, J. A., Riching, A., Johannsen, E. C., Dovat, S., Kenney, S. C., and Mertz, J. E.  Epstein-Barr Virus Utilizes Ikaros in Regulating Its Latent-Lytic Switch in B Cells.  J. Virol., 88(9): 4811-4827, 2014.

Kenney, S. C., and Mertz, J. E.  Regulation of the Latent-Lytic Switch in Epstein-Barr Virus.  Semin. Cancer Biol., in press, 2014 [Epub ahead of print Jan 20 2014].

Pahlke, E., Shibley Hyde, J., and Mertz, J. E.  The Effects of Single-Sex Compared with Coeducational Schooling on Mathematics and Science Achievement:  Data from Korea.  J. Educ. Psychol., 105(2): 444-452, 2013.

Das, S., Becker, B. N., Hoffmann, F. M., and Mertz, J. E.  Reversal of Transforming Growth Factor-β Induced Epithelial-to-Mesenchymal Transition and the ZEB Proteins.  Fibrogenesis Tissue Repair, 5(Suppl 1): S28, 2012.

Esch, A. M., Thompson, N. E., Lamberski, J. A., Mertz, J. E., and Burgess, R. R.  Production and Characterization of Monoclonal Antibodies to Estrogen-Related Receptor Alpha (ERRα) and Use in Immunoaffinity Chromatography.  Protein Expr. Purif., 84:  47-58, 2012.

Kane, J. M., and Mertz, J. E. Debunking Myths About Gender and Mathematics Performance. Notices of the Am. Math. Soc., 59: 10-21, 2012. http://www.ams.org/notices/201201/rtx120100010p.pdf

Ma, S.-D., Yu, X., Mertz, J. E., Gumperz, J. E., Reinheim, E., Zhou, Y., Tang, W., Burlingham, W. J., Gulley, M. L., and Kenney, S. C.  An Epstein-Barr Virus (EBV) Mutant with Enhanced BZLF1 Expression Causes Lymphomas with Abortive Lytic EBV Infection in a Humanized Mouse Model.  J. Virol., 86: 7976-7987, 2012.

Yu, X., McCarthy, P. J., Wang, Z., Gorlen, D. A., and Mertz, J. E.  Shutoff of BZLF1 Gene Expression Is Necessary for Immortalization of Primary B Cells by Epstein-Barr Virus.  J. Virol., 86: 8086-8096, 2012.

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