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Professor Kamal Badr

Dr. Kamal Badr was born in Beirut, Lebanon in 1954. He attended elementary and high school at International College in Beirut and then obtained a B.S (with distinction) and then the MD degree (with distinction) from the American University of Beirut (AUB) in 1980. Following two years of residency at AUB Medical Center, he joined the Division of Nephrology at the Brigham and Women’s Hospital, Harvard Medical School in Boston under the mentorship of Dr. Barry Brenner, where he completed a research and clinical fellowship in nephrology. He was on the faculty at Vanderbilt University (1986 to 1992) and Emory University (1992 to 2000), following which he became Chairman of the Department of Internal Medicine at the American University of Beirut (2000 to 2007). He is currently Founding Dean of the “Gilbert and Rose-Marie Chagoury School of Medicine” at Lebanese American University, Byblos, Lebanon.

Dr Badr’s initial inquiries focused on defining the mechanisms whereby inflammatory injury led to organ dysfunction in the kidney. Specifically, his research, which he conducted at Harvard, sought to define the link between the presence of inflammatory reactions in the renal glomerulus (filtering structure) and the attendant failure of filtration function which characterizes patients with ‘glomerulonephritis’, a disease affecting children and adults. His work led to the discovery that leukotrienes, vasoactive mediators of leukocyte activation, were central to that phenomenon. In the early eighties his laboratory was the first to identify the release mechanisms, hemodynamic actions, receptor characteristics, and signal transduction mechanisms for leukotrienes in these diseases. He then demonstrated in animal models, and later in human studies, that antagonism of leukotriene formation or receptor blockade led to marked salutary effects on renal function in animals and humans with glomerulonephritis, leading to large scale human trials.

During his work on leukotriene biology in the renal glomerulus, Dr Badr explored the potential role of a then newly discovered class of molecules formed through combined catalysis of arachidonic acid by 5 and 15-lipoxygenase enzymes, the lipoxins. His work was the first to demonstrate that these compounds were natural (endogenous) antagonists for leukotrienes in the kidney. Dr Badr’s laboratory demonstrated formally the precise mechanisms whereby these pathways not only acted in a “counter-regulatory” manner at the functional level, but also were endogenous competitors for the same receptor in renal cells and exerted opposing effects at several components of the inflammatory response. He further demonstrated in vitro the mechanisms governing the regulation of the expression and activity of the genes and products of the 5 and 15-lipoxygenase enzymes in the renal glomerulus and human leukocytes and demonstrated that selective in vivo transfection of one kidney with the15-lipoxygenase gene was associated with marked improvement in renal function in that kidney during experimentally induced inflammatory injury. The discoveries on endogenous anti-inflammatory pathways in Dr Badr’s lab during the eighties and nineties were a major contributor to the emerging field of what was being rapidly appreciated as a new biology in inflammation, namely that this crucial biological response was, like many others, governed by an endogenous balance between pro and counter-regulatory pathways which can be exploited to develop new strategies for treating inflammatory disorders such as arthritis, dermatitis, and atherosclerosis. This area of human biology has now expanded markedly in breadth and depth, leading to the development of topical and systemic molecules for the treatment of human diseases characterized by undesirable inflammatory reactions.

During his work on the regulation of the15-lipoxygenase enzyme in human leukocytes, Dr Badr discovered the highly selective induction of this enzyme by the T-cell derived cytokine, interleukin-13. Furthermore, closer study of the regulation of its gene expression led to a series of studies which uncovered an unexpected interaction between 15-lipoxygenase and the tumor suppressor gene p53, the genes for both of which were localized in overlapping proximity on chromosome 17. These discoveries led to a series of studies in Dr Badr’s laboratory in the mid-to-late nineties which demonstrated that15-lipoxygenase regulated the expression of p53 in vivo and that this regulation proposes a role for the 15-lipoxygenase pathway in carcinogenesis. These discoveries uncovered a new role for this pathway in prostate cancer in humans.

Sample of Academician's Research

Having previously demonstrated that the enzyme 15-lipoxygenase (15-LOS) is induced by mutant forms of the tumor suppressor gene p53 [ Proc Natl Acad Sci U.S.A.  96(8): 4378-4383, 1999], Dr Badr’s laboratory demonstrated that injection of prostate cancer cells (PC3) into mice resulted in very large tumors when cancer cells also carry the 15-LOS gene (mice in panel C above), average sized tumors in mice injected with the cancer cells and a mock 15-LOS gene (panel B) and very small or no tumors whne mice are injected with an cancer cells having an “anti-sense” molecule which antagonizes 15-LOS (panel A), thereby demonstrating in vivo that this enzyme plays a role in promoting cancer growth.

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