Pal Gooz is a Research Assistant Professor in the Division of Rheumatology & Immunology. He received his M.D. from the Semmelweis University of Medicine, Faculty of Medicine at Budapest, Hungary in 1993. He then worked with Dr. Gyorgy Nagy at the Department of Anatomy, and Developmental Biology at the Semmelweis University as a graduate student. He then worked with Dr. Stephen Frawley at the Department of Cell Biology at the Medical University of South Carolina as a postdoctoral fellow from 1997. He joined Dr. Stanley Hoffman’s laboratory at Division of Rheumatology & Immunology in 1999 as a postdoctoral fellow. Dr. Gooz’s primary research interest is the role of metalloproteinases in angiogenesis. Emerging evidence shows that metalloproteinases play central role in angiogenesis during normal development and numerous patological processes. However the therapeutic exploitation of this group of enzymes to inhibit or enhance angiogenesis (for example in tumors or cardiovascular diseases respectively) is obstructed by the redundancy in the function and the very much limited knowledge about the regulation and mechanism of action of individual metalloproteinases. His research focuses on one of the metalloproteinases, ADAM-17 (A Disintegrin And Metalloproteinase-17), that plays a central role in the regulation of endothelial cell responses to Vascular Endothelial Growth Factor (VEGF). These studies aim to determine how ADAM-17 activity is regulated by VEGF and to discover novel molecular pathways of ADAM-17 activity during angiogenesis. The results are analyzed with special emphasis on the identification of potential therapeutical targets that can be exploited to treat diseases where angiogenesis inhibition (for example tumors) or angiogenesis stimulation (myocardial infarct) would be beneficial. The second area of Dr. Gooz’s research focus is genomic variation in scleroderma. Scleroderma (SSc) is a rare but devastating disease. The pathogenesis of SSc is currently unknown but the role of environmental effects superimposed on enabling genetic background is proposed. It is likely, that variations in multiple genes constitute a genomic profile that makes an individual susceptible to SSc. Dr. Gooz’s studies aim to associate single nucleotide polymorphism and gene deletion in enzyme families that play a role in oxidative stress (such as glutathione-S-transferases) with SSc and its various clinical manifestations. Dr. Gooz's Curriculum Vitae (PDF Format)* * Note in order to view this document you will need to have the free Adobe Reader®  installed on your computer. More on Adobe Acrobat®.
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