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Dr. Floyd:

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Dr. Floyd's CV in brief

Publications

Experimental Therapeutics Research Laboratory

Robert A. Floyd, Ph.D. Member, Experimental Therapeutics Research Laboratory Merrick Foundation Chair in Aging Research Adjunct Professor, Department of Biochemistry and Molecular Biology, University   of Oklahoma Health Sciences Center

Research Interests
The research in my laboratory involves the role of reactive nitrogen species (RNS) and reactive oxygen species (ROS) in processes associated with the development of important diseases of aging with primary focus on events that occur in early phases of cancer development. Specific nitrones have very potent biological action in curtailing the production of ROS and RNS, which are important in the development of many diseases of aging. Excess ROS and RNS production occur in many pathological conditions, including localized areas of the brain undergoing specific neurodegenerative conditions, such as stroke, Alzheimer’s disease and Parkinson’s disease. Over a decade ago, we discovered that specific nitrones were effective in preventing the brain damage caused by stroke in an experimental model. As a result of these discoveries, the nitrones have undergone 12 years of commercial development for the treatment of neurodegenerative diseases, especially stroke. The experimental nitrone drug NXY-059 has now undergone over three years’ development in Phase III clinical trials for acute ischemic stroke.

Our recent effort has focused on the role of excess ROS and RNS production in the initiation and progression of cancers. We have discovered that certain nitrones will inhibit experimental liver cancer development. Specific research focus has been on the preventive action of a-phenyl-tert-butylnitrone (PBN) in liver cancer development in rats. The results have shown that PBN inhibits hepatocellular carcinoma formation. Cur-rent research is devoted to understanding at the molecular level the inhibiting action of PBN in this animal model. The most fascinating observation we have made involves the demonstration that PBN enhances the death of cells localized in preneoplastic islands in this experimental liver cancer model. We consider that the enhanced apoptosis of these cells caused by PBN is due to the decreased production of an agent that acts to inhibit death processes in these cells thus allowing tumor development to occur. Our research has shown that nitric oxide acts to inhibit apoptosis in the cells of the preneoplastic cellular islands. The action of PBN involves the inhibition of inducible nitric oxide synthase (iNOS) expression in the hepatocytes thereby ceasing the production of nitric oxide and allowing the preneoplastic nodule cells to apoptose. Studies have led to the mechanistic basis of nitric oxide in allowing these precancerous cells to develop into cancer cells is because this agent acts to inactivate specific enzymes thereby preventing cancer cell death, enhancing oncogenic cell growth and enhancing DNA mutation processes, all of which enhance the development of cancer.

Joined OMRF Scientific Staff in 1974.

Mailing Address
Experimental Therapeutics Research Laboratory
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, Oklahoma 73104

Contact Information
Phone: (405) 271-7580
Fax: (405) 271-1795
E-mail: Robert-Floyd@omrf.org