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Michael L. Gatza , Ph.D.

Assistant Professor
Tel: 732-235-8751 
Emai: : Michael.gatza@cinj.rutgers.edu  

Education:

    • Postdoctoral Training: University of North Carolina at Chapel Hill and Duke University
    • Ph.D., Baylor College of Medicine, Houston, TX
    • B.S., Virginia Polytechnic Institute and State University, Blacksburg, VA

Research Interests:

The main research focus of the Gatza laboratory is to investigate oncogenic mechanisms driving breast and ovarian tumor development, progression, and response to therapy. Human cancers, including breast cancer and ovarian cancer, are not a single disease. This is true both clinically where different subsets of patients respond differently to specific therapies, and at a molecular level where tumorigenesis is driven by a combination of inherited and acquired genetic alterations resulting in a complex and heterogeneous disease. The ability to dissect this heterogeneity is critical to understand the relevance of these alterations for disease phenotypes and also to enable the development of rational therapeutic strategies that can match the characteristics of the individual patient’s tumor. We are interested in understanding the genomic alterations that drive oncogenic pathway activity and therapeutic response in human cancers, and in particular, identifying those essential alterations that may represent therapeutic opportunities for personalized cancer treatment.

To address these questions, we use a number of experimental approaches including RNA sequencing (RNAseq), gene expression microarrays, DNA whole exome sequencing, DNA copy number analysis, proteomics, cell / tissue culture, and xenograft mouse models. Thus our research utilizes a combination of genomics and computational strategies to interrogate data from human patient samples coupled with experimental genetic models to replicate human tumor alterations in order to investigate mechanisms of disease both in vitro and in vivo.

Selected Peer-Reviewed Publications for the Recent 5 Years:

    • Ciriello G*, Gatza ML*, Beck AH, Wilkerson MD, Rhie SK, Pastore A, Zhang H, McLellan M, Yau C, Kandoth C, Bowlby R, Shen H, Hayat S, Fieldhouse R, Lester SC, Tse GMK, Factor RE, Collins LC, AllisonKH, Chen Y, Jensen K, Johnson NB, Oesterreich S, Mills GB, Cherniack AD, Robertson G, Benz C, Sander C, Laird PW, Hoadley KA, King TA, The Cancer Genome Atlas Network, and Perou CM. (2015).Comprehensive molecular characterization of invasive lobular breast tumors. Cell. Epub October 8, 2015. *Authors contributed equally.
    • Silva GO, He X, Parker JS, Gatza ML, Carey LA, and Perou CM (2015). Across Species DNA Copy Number Analyses Identifies Subtype-Specific Drivers of Breast Cancer Development. Breast Cancer Research and Treatment. 152: 347-356.
    • Young CD, Zimmerman LJ, Hoshino D, Formisano L, Hanker AB, Gatza ML, Morrison MM, Moore PD, Whitwell CA, Dave B, Stricker T, Bhola NE, Silva GO, Patel P, Brantley-Sieders DM, Levin M, Palma NA, Wang K, Stephens PJ, Perou CM, Weaver AM, O’Shaughnessey JA, Chang JC, Park BH, Liebler DC, Cook RS, Arteaga CL (2015). Activating PIK3CA mutations induce an EGFR/ERK paracrine signaling axis in basal-like breast cancer. Molecular and Cellular Proteomics. 14:1959-1976.
    • Tian H, Liu J, Chen J, Gatza ML, Blobe GC (2015). Fibulin-3 is a Novel TGF-β pathway Inhibitor in the Breast Cancer Microenvironment. Oncogene. Epub March 2015.
    • Gatza ML, Silva GO, Fan C, Parker JS, and Perou CM. (2014). An integrated genomics approach identifies drivers of proliferation in luminal subtype human breast cancer. Nature Genetics. 46(10): 1051-105.
    • Shats I, Gatza ML, Angus SP, Liu B, and Nevins JR. (2013). Cooperation between E2F1 and FOXO transcription factors provides a mechanism for control of E2F1-mediated transcription by survival signaling. Cancer Research. 73(19):6056-67.
    • Liu B, Shats I, Angus S, Gatza ML, and Nevins JR (2013). Interaction of E2F7 with E2F1 and C-terminal binding protein (CtBP) provides a mechanism for E2F7-dependent transcription repression. Journal of Biological Chemistry. 288(34):245281-24589.
    • Mythreye K, Knelson EH, Gatza CE, Gatza ML, and Blobe GC. (2013). TβRIII/β-arrestin2 suppresses epithelial derived cancer progression by regulating integrin α5β1 trafficking, function, and localization. Oncogene. 32 (11): 1416–1427.
    • Gatza ML*, Kung HN*, Blackwell KL, Dewhirst MW, Marks JR, and Chi JT. (2011). Analysis of tumor environmental response and oncogenic pathway activation identifies distinct basal and luminal features in HER2-related breast tumor subtypes. Breast Cancer Research. 13(3):R62 (Article designated as Highly Accessed).*Authors contributed equally.
    • Chang JT, Gatza ML, Lucas JE, Barry WT, Vaughn P, and Nevins JR. (2011). SIGNATURE: A workbench for gene expression signature analysis. BMC Bioinformatics. 12(1):443. (Article designated as Highly Accessed).
    • Gatza CE, Holtzhausen A, Kirkbride KC, Morton A, Gatza ML, Datto MB, and Blobe GC. (2011). The Type III TGF-β Receptor enhances colon cancer cell migration and anchorage independent growth. Neoplasia. 13(8): 758-770.
    • Shats I, Gatza ML, Chang JT, Mori S, Wang J, Rich J, and Nevins JR. (2011). Using a stem cell-based signature to guide therapeutic selection in cancer. Cancer Research. 71(5): 1772-1780.
    • Gatza ML, Lucas JE, Barry WT, Kim JW, Wang Q, Crawford M, Datto MB, Kelley M, Mathey-Prevot B, Potti A, and Nevins JR. (2010). A pathway based classification of human breast cancer. Proc. Nat’l. Acad. Sci. 107(15):6994-6.