George Beck Jr., PhD

Associate Professor of Medicine

Department of Medicine

Office: WMRB 1026

Phone: 404-727-1340

Fax: 404-727-1300

Email: gbeck2@emory.edu

Biography

Education:

1985-1990 University of Delaware B.A. Psychology/Philosophy

1995-2000 Temple University Ph.D. Molecular Biology and Genetics

Postdoctoral Training:

2000 Temple University - Laboratory of Dr. Elizabeth Moran, Cell growth and differentiation

National Cancer Institute Scholar:

NCI-Frederick 2000 - 2005 Transcriptional regulation of differentiation

Appointments:

2005-present Assistant Professor of Medicine, Division of Endocrinology, Metabolism and Lipids. Emory University School of Medicine, Atlanta GA.

2000 - 2005 NCI Scholar (CA84573): National Cancer Institute, Center for Cancer Research, Laboratory of Cancer Prevention, Frederick, MD.

2000 - 2000 Post-doctoral Research Associate: Temple University School of Medicine.

1995 - 2000 Doctoral Student: Graduate Program in Molecular Biology and Genetics, Temple University School of Medicine.

1996 - 1997 Graduate Trainee: Program in Cancer Research (T32-CA09214). Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine.

1992 - 1995 Research Associate: SmithKline Beecham Pharmaceuticals, Department of Cardiovascular Pharmacology.

1990 - 1992 Research Associate: Alfred I. DuPont Institute, Department of Medical Cell Biology.

Research

The effects of Thiazolidinediones on Marrow Stem Cells and Bone Quality in Diabetic Subjects: Thiazolidinediones (TZDs) are commonly prescribed oral agents for the treatment of diabetes. They act as agonists for the peroxisome proliferator-activated receptor-gamma (PPAR-?) which regulates the transcription of several genes, encoding proteins that modulate glucose and lipid metabolism, as well as genes that promote differentiation of adipocytes. Recent studies have reported an association between TZD treatment and an increased risk of fractures in patients with prediabetes and type 2 diabetes. The underlying mechanisms for this association are not known. Dr. Beck, in collaboration with Drs. Guillermo Umpierrez and Natasha Khazai (Emory and Grady Hospital), is currently investigating the mechanism(s) by which TZDs alter bone quality in diabetic subjects with a focus on the effect of TZDs on osteoblasts, adipocytes and osteoclasts.

Inorganic phosphate regulated proliferation, transformation and tumorigenesis: Over the past decade, Dr. Beck and his collaborators have studied the mechanisms by which elevated inorganic phosphate regulates both mineralization by osteoblasts and enhanced proliferation associated with a number of cancer models. Recent studies have extended these cell culture studies to begin to define the potential risk of increased dietary phosphate consumption on cancer risks in mouse models. Currently, the research is focused on elucidating how changes in serum phosphate regulate a number of disease states including cancer and osteoporosis and planned studies include incorporating cardiovascular disease and diabetes. Although it is becoming increasingly apparent that diet can have profound effects on functional genomics, to date the molecular and cellular responses to changes in serum Pi levels have only begun to be investigated.

Biological Actions and Cellular Targeting of Nanoparticles for Medical Applications: The unique combination of semi-structured extracellular matrix, biomechanical properties, and active remodeling makes bone a unique tissue particularly suited for targeting by nanoparticles. Dr. Beck and colleagues, Dr. Neale Weitzmann (Emory) and Dr. Jin-Kyu Lee at Seoul National University in Korea, are investigating the molecular and cellular mechanisms by which specific silica–based nanoparticles regulate bone cell metabolism including the identification of specific intracellular mechanisms by which the particles influence cell behavior. One particular novel nanoparticle formulation possesses a potent stimulatory effect on the formation of osteoblasts, the cells responsible for bone formation, and concomitant inhibitory effect on the formation of osteoclasts, the cells responsible for bone breakdown (resorption). This nanoparticle therefore, may have the potential to be developed into a powerful dual anticatabolic and proanabolic agent for the treatment of numerous osteoporotic diseases.