The University of Texas MD Anderson Cancer Center
Department of Melanoma Medical Oncology
The major focus of Dr. Suhendan Ekmekcioglu's research is to recognize the inflammatory pathways in melanoma progression. Her early studies revealed that inducible Nitric Oxide Synthase (iNOS) and related pathways are major contributors in melanoma growth by modulating tumor inflammation. These studies further identified tumor-derived inflammation by specific cytokine/chemokine characteristics in tumor microenvironment which drives the process of melanoma progression. As a result of these early discoveries, her research expand the area in collaborating factors, which are the basis of her current scientific interest. Immune modulation strategy for the treatment of melanoma brings a strong hope, specifically, in combinational approaches. Thus, the research projects are designed to overcome melanoma cells’ contribution to tumor growth in an inflammatory microenvironment by inhibiting inflammation; and also boosting the immune activators in one cellular cascade, which will give a unique advantage in a clinical setting. The scientific rationale is based on the understanding that all tumor progression is characterized by a complex network of interactions among different cell types that cooperatively exploit a metabolic reprograming and mutually influence their functionality. Arginine metabolism is dependent on the activity within the families of, nitric oxide synthase (NOS) and arginase (ARG) enzymes. Collectively, ARG and NOS enzymes are crucial components of immune suppression pathways, and the metabolic products of these enzymes are important moderators of T-cell function in cancer. Overall, the primary focus in her current research is to determine NO-produce effects on human melanoma cells and microenvironmental T- lymphocytes (TIL) to test the role of NOS driven arginine metabolism on the growth and immune function of the T cells, which will develop a novel area of research.
Education & Training
PhD, University of Istanbul, 1993