Dr. Ming Zhang received his PhD from the State University of New York at Albany in 1992. Following postdoctoral fellowships at both Duke University medical school and the Dana Farber Cancer Institute/ Harvard Medical School, Zhang accepted a faculty appointment at Baylor College of Medicine in 1997. Zhang joined Northwestern University in January 2007. His work has received grant supports from National Cancer Institute, the Prostate Cancer Foundation, and the Susan G. Komen Breast Cancer Foundation. Zhang laboratory has now focused on two research directions: 1) determining role of tumor suppressors in development and cancer progression, 2) and identifying immune components that control breast cancer metastasis.

The main focus of my research program is to study roles of tumor suppressors in normal development and in breast and prostate cancer progression, focusing on Maspin and an Ets transcription factor PDEF. Maspin is a unique member of SERPIN family that plays roles in normal tissue development, tumor metastasis, and angiogenesis. Genetic studies by my laboratory using maspin transgenic and knockout mice demonstrated an important role of maspin in normal mammary, prostate, and embryonic development. Recently, we have identified several new properties of maspin. As a protein that is present on cell surface, maspin controls cell-ECM adhesion. This function is responsible for maspin-mediated suppression of tumor cell motility and invasion. We have also discovered that maspin is involved in the induction of tumor cell apoptosis through a mitochondrial death pathway. The long-term goals of these projects are to elucidate the molecular mechanisms by which maspin and PDEF control tumor metastasis and to identify their physiological functions in development. These analyses are not only important for basic biology and but also may lead to a therapy for cancer and other developmental diseases.

Another focus of research in Zhang lab is to identify immune components that control breast cancer metastasis. Chronic inflammation not only increases neoplastic transformation but also drives the inhibition of the immune response in a protective negative-feedback mechanism. Suppressive immune cells are recruited to the sites of inflammation and function to inhibit both innate and adaptive immune responses, enabling tumor tolerance and unmitigated tumor progression. To study the interplay between tumor and immune cells, Zhang lab has developed a unique animal model of breast cancer that reproduces different stages of breast cancer bone metastasis. Molecules that control tumor-immune cell interaction and immunosuppression have been identified. We are currently studying roles of these genes in tumor-driven evolution that control chronic inflammation and immunosuppression. We hypothesize that these key pro-inflammatory genes are upregulated during cancer progression, which function synergistically to recruit and activate suppressive MDSCs, TAMs and Tregs, inducing chronic inflammation and an immunosuppressive tumor microenvironment conducive to metastatic progression.

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