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Raymond L. Konger, MD

Assistant Professor of Pathology and Laboratory Medicine
Assistant Professor of Dermatology
Indiana University School of Medicine
Medical Director, Clinical Chemistry Laboratory
Richard L. Roudebush VA Medical Center
Clarian Pathology Laboratory
350 West 11th Street, Room 5054
Indianapolis, IN 46202-4108

Telephone: 317-491-6567
FAX: 317-491-6419
email: rkonger@iupui.edu

Research Interests: Defining the mechanisms by which prostaglandin receptors are involved in malignancy, cell aging, and wound repair.

Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, are chemopreventive for both breast and skin cancer. My research focuses on understanding the mechanisms by which NSAIDS block carcinogenesis. NSAIDs inhibit the cyclooxygenase (COX) class of enzymes that produce a lipid hormone, called prostaglandins. Prostaglandins are potent mediators of inflammation, fever, and pain. The ability of NSAIDs to block cancer appears to be primarily dependent on production of a particular prostaglandin, prostaglandin E2 (PGE2). PGE2, in turn, modulates cell growth, cell differentiation, apoptosis, immune cell function, and angiogenesis. Many of these functions are thought to play a role in tumor formation. How PGE2 alters these many cellular functions is dependent on activation of one or more of four different PGE2 receptors, termed EP1, EP2, EP3, and EP4. Research from my laboratory has shown that PGE2 activation of the EP2 receptor stimulates growth of primary keratinocytes and may be important in tumor promotion. Loss of the EP2 receptor results in increased invasiveness. My laboratory is currently examining the role of the EP2 receptor on tumorigenesis and malignant progression in both breast and skin cancer. In addition, we are examining the role of the EP1, EP2, and EP3 receptors in skin cell differentiation and cellular aging.

Publications:

  1. Mehrotra S. Morimiya A. Agarwal B. Konger R. Badve S. Microsomal prostaglandin E2 synthase-1 in breast cancer: a potential target for therapy.  Journal of Pathology. 208(3):356-63, 2006 Feb.
  2. Zhang Q. Seltmann H. Zouboulis CC. Konger RL. Involvement of PPARgamma in oxidative stress-mediated prostaglandin E(2) production in SZ95 human sebaceous gland cells.  Journal of Investigative Dermatology. 126(1):42-8, 2006 Jan.
  3. Konger RL. Brouxhon S. Partillo S. VanBuskirk J. Pentland AP. The EP3 receptor stimulates ceramide and diacylglycerol release and inhibits growth of primary keratinocytes.  Experimental Dermatology. 14(12):914-22, 2005 Dec.
  4. Konger RL. Billings SD. Thompson AB. Morimiya A. Ladenson JH. Landt Y. Pentland AP. Badve S. Immunolocalization of low-affinity prostaglandin E receptors, EP and EP, in adult human epidermis.  Journal of Investigative Dermatology. 124(5):965-70, 2005 May.
  5. Zhang Q. Southall MD. Mezsick SM. Johnson C. Murphy RC. Konger RL. Travers JB. Epidermal peroxisome proliferator-activated receptor gamma as a target for ultraviolet B radiation. Journal of Biological Chemistry. 280(1):73-9, 2005 Jan 7.
  6. Cho YM. Lewis DA. Koltz PF. Richard V. Gocken TA. Rosol TJ. Konger RL. Spandau DF. Foley J. Regulation of parathyroid hormone-related protein gene expression by epidermal growth factor-family ligands in primary human keratinocytes.  Journal of Endocrinology. 181(1):179-90, 2004 Apr.
  7. Rys-Sikora KE. Pentland AP. Konger RL. Pertussis toxin-sensitive secretory phospholipase A2 expression and motility in activated primary human keratinocytes. Journal of Investigative Dermatology. 120(1):86-95, 2003 Jan.
  8. Konger RL. Scott GA. Landt Y. Ladenson JH. Pentland AP. Loss of the EP2 prostaglandin E2 receptor in immortalized human keratinocytes results in increased invasiveness and decreased paxillin expression.  American Journal of Pathology. 161(6):2065-78, 2002 Dec.
  9. Konger, R.L., Scott, G.A., Ladenson, J.H., Landt, Y., and A.P. Pentland.  Loss of the EP2  Prostaglandin Receptor in Immortalized Human Keratinocytes Results in Increased Invasiveness and Decreased Paxillin Expression.  American Journal of Pathology; 161(6): 2065-2078, 2002.