Carl E. Clay, Ph.D.

Medical Director and Senior Medical Writer

Complete Healthcare Communications, Inc.

Chadds Ford, PA

Email: carlclay@hotmail.com

Education:

Washington University School of Medicine, Post-doctoral Fellow, 2002-2003

Wake Forest University School of Medicine-Wake Forest University, Ph.D., 2002

University of Colorado, BS, 1996

Research Interests:

Apoptosis in breast cancer cells.

Publications:

Hankin JA, Clay CE, Murphy RC. (1998) The Effects of Ethanol and Acetaldehyde on the Metabolism of Prostaglandin E₂ and Leukotriene B₄ in Isolated Rat Hepatocytes. Journal of Pharmacology and Experimental Therapeutics 285, 155-161.

Clay CE, Namen AM, Atsumi G, Willingham MC, High KP, Kute TE, Trimboli AJ, Fonteh AN, Dawson PA, Chilton FH. (1999) Influence of J Series Prostaglandins on Apoptosis and Tumorigenesis of Breast Cancer Cells. Carcinogenesis 20, 1905-1911.

Trimboli AJ, Atsumi G, High KP, Kute TE, Clay CE, Fonteh AN, Chilton FH. (1999) The effects of CoA-IT inhibition on cell cycle progression of breast cancer cells. Cancer Research 59, 6171-6177.

Clay CE, Namen AM, Fonteh AN, Atsumi G, High KP, Chilton FH. (2000) 15deoxyD^12,14PGJ₂ induces diverse biological responses via PPAR_g activation in cancer cells. Prostaglandins and Other Lipid Mediators 62, 23-32.

Clay CE, Namen AM, Atsumi G, Trimboli AJ, Fonteh AN, High KP, Chilton FH. (2001) The magnitude of PPAR_g activation is associated with important and seemingly opposite biological responses in breast cancer cells. Journal of Investigational Medicine 49, 413-420.

Clay CE, Atsumi G, High KP, Chilton FH. (2001) Early de novo gene expression is required for 15deoxyD^12,14 prostaglandin J₂ induced apoptosis in breast cancer cells.  The Journal of  Biological Chemistry 276, 47131-47135.

Monjazeb AM, Clay CE, High KP, Chilton FH. (2002) Antineoplastic properties of arachidonic acid and its metabolites. Prostaglandins Leukot Essent Fatty Acids. 66, 5-12.

Clay CE, Thorburn J, High KP, Chilton FH. (2002) 15deoxyD^12,14 prostalgandin J₂-induced apoptosis does not require PPAR_g breast cancer cells. The Journal of  Lipid Research. 43, 1818-1828.

O'Flahrety JT, Rogers LC, Paumi CM, Hantgan RR, Clay CE, Chen YQ, Willingham MC, Smitherman PK, Kute TE, Rao A, Cramer SD, Morrow CS. (2005) Bidirectional effects of 5-HETE analogs on the proliferation of cancer cells. 1736, 228-236.

Ortmeyer HK, Clay CE, Fried SK, Hansen BC. (2005) Transcriptional regulation of lipoprotein lipase in obese and calorie restricted rhesus monkeys. (in preparation).

Book Chapters:

Chilton FH III, Chilton FH Jr, Clay CE, Trimboli AJ, Fonteh AN, Influence of Arachidonic Acid Metabolism on Cell Proliferation and Apoptosis. In: Winkler JD, ed. Apoptosis and Inflammation. Switzerland: Birkhauser Verlag, 1998.

Abstracts:

Influence of J series prostaglandins on cell cycle, apoptosis and tumorigenesis in breast cancer cells. Keystone Symposium on Lipid Mediators Special Section on PPAR Activators. Keystone, CO, April 1-7, 1999.

Influence of J series prostaglandins on cell cycle, apoptosis and tumorigenesis in breast cancer cells. Wake Forest University Apoptosis Symposium, Winston-Salem, NC, April 21, 1999.

PPAR_g induced apoptosis requires de novo gene expression that is suppressed by a dominant negative mutant in breast cancer cells. FASEB: Receptors and Signal Transduction, Copper Mountain, CO July 2-9, 2000.

15deoxyD^12,14PGJ₂ inhibits breast cancer cell proliferation via PPAR_g activation. International Society for Preventive Oncology, 5^th International Meeting, Geneva, Switzerland, October 28-31, 2000, Satellite Symposium October 29, 2000.

PPAR_g induced apoptosis requires de novo gene expression that is suppressed by a dominant negative mutant in breast cancer cells. Wake Forest University, Breast Cancer Center of Excellence, Winston Salem, NC, November 16, 2000.

g induced apoptosis requires de novo gene expression that is suppressed by a dominant negative mutant in breast cancer cells. Keystone Symposium: PPARs a transcription odyssey, Keystone, CO, February 2-9, 2001.

Mechanisms of 15deoxyD^12,14PGJ₂ induced apoptosis in breast cancer cells. Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Related Diseases, Nashville, TN October 14-17, 2001.

PPAR_g does not mediate apoptosis in breast cancer cells: role for lipid and protein modification. South Eastern Regional Lipid Conference, Cashiers, NC, November 7-9, 2001.

15deoxyD^12,14Prostaglandin J₂ and PPAR_g: Potential therapeutic targets for breast cancer treatment and prevention. Department of Defense Era of Hope Breast Cancer Research Meeting, Orlando, FL, September 25-28, 2002.

Activation of nuclear transcription factor PPAR_g by the novel triterpenoid CDDO as a targeted therapy in breast cancer. Keystone Symposium: Nuclear Receptor Superfamily, Snowbird, UT, April 13-19, 2002.

PPAR_g modulates the cardiac hypertrophic phenotype. PPARs: Transcriptional Regulators of Metabolism and Metabolic Disease, Keystone, CO, February 4-9, 2003.