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Raymond L. Konger, MD

Raymond L. Konger, MD

Associate Professor of Pathology and Laboratory Medicine
Associate Professor of Dermatology
Indiana University School of Medicine

Associate Director, Special Chemistry Laboratory, IU Health Laboratory
Medical Director, Clinical Chemistry Laboratory, Richard L. Roudebush VA Medical Center

Director of Clinical Laboratories, IU Health North Hospital
1120 South Drive

Fesler Hall, room 403
Indianapolis, IN 46202-4108

Telephone: 317-274-4154
FAX: 317-274-8153
email: rkonger@iupui.edu

 

Research Interests: Skin cancer chemoprevention and treatment. 

My research is focused primarily on bioactive lipid hormones produced in response to chemical carcinogenes or ultraviolet B (UVB) light exposure and how activation of their respective receptors modulate the DNA damage response, DNA repair, inflammation, and carcinogenesis. Past work has focused on prostaglandin E receptors and their role in keratinocyte proliferation, keratinocyte senescence, photocarcinogenesis and tumor invasiveness. More recently, my work has focused on two major areas:

1.) UVB-induced oxidized glycerophosphocholines (ox-GPCs).  Specifically, ox-GPCs have been identified that exhibit potent agonist activities for the peroxisome proliferator activated receptor gamma (PPARg) and the platelet activating factor receptor (PAFR). Work by our group has shown that UVB exposure activates both PPARg and the PAFR through the production of ox-GPCs. Moreover, using mice with germ-line deletion of the PAFR or epidermal specific deletion of PPARg, we show that the loss of these receptors results in increased apoptosis, inflammation, and carcinogenesis in response to either chemical carcinogens or UVB.  Current work is focused on determining the downstream mechanisms linking UVB-induced PPARg activation to the suppression of photocarcinogenesis. Future work will determine whether exogenous anti-diabetic PPARg agonists have chemopreventive activity in human non-melanoma skin cancer.

2.) In collaboration with the laboratory of Young Kim, Ph.D. at Purdue University, we are examining the ability of a novel non-invasive optical imaging device to detect areas of dermal inflammatory angiogenesis.  These areas are observed as foci of persistent hyperemia that persist and expand long after cessation of carcinogenic exposure. Importantly, early data indicate that these persistent hyperemic foci predict sites of future tumor formation as well as the chemopreventive activity of a known chemopreventive agent (Celecoxib). Ongoing studies are examining the mechanisms through which these foci are initiated as well as the mechanism that drives their persistence. The ability of other chemopreventive agents (e.g. PPARg agonists) to suppress the formation and persistence of these hyperemic foci are also underway.    

Recent Publications:

Web of Knowledge: https://apps.webofknowledge.com/summary.do?SID=3Bld2KOlJFIkK5DcLKD&product=UA&qid=1&search_mode=GeneralSearch

 

1.         Zhang, Q., Southall, M.D., Mezsick, S.M., Johnson, C., Murphy, R.C., Konger, R.L., and J.B. Travers.  Epidermal Peroxisome Proliferator – activated Receptor g as a Target for Ultraviolet B Radiation.  J. Biol. Chem., 280(1):73-79, (2005).  http://www.jbc.org/content/280/1/73.long

2.         Travers, J.B., Edenberg, H.J., Zhang, Q., Al-Hassani, M., Yi, Q., Baskaran, S.,  and Konger, R.L.. Augmentation of Ultraviolet B Radiation-mediated Early Gene Expression by the Epidermal Platelet-activating Factor Receptor.  J Invest Dermatology, 128(2):455-460 (2007). http://www.nature.com/jid/journal/v128/n2/full/5701083a.html

3.            Brouxhon, S., Konger, R.L., VanBuskirk, J., McGrath, K.H., Tanck, C., Almudevar, A., Breyer, R., Scott, G., and A.P. Pentland.  Deletion of prostaglandin E2 EP2 receptor protects against ultraviolet (UV) induced carcinogenesis, but increases tumor aggressiveness.  J Invest Dermatol, 127(2):439-446 (2007). http://www.nature.com/jid/journal/v127/n2/full/5700547a.html 

4.         Konger, R.L., G.K. Marathe, Q. Zhang, and J.B. Travers.  Oxidized Glycerophosphocholines as Biologically Active Mediators for Ultraviolet Radiation-Mediated Effects. Prostaglandins and other Lipid Mediators. 87:1-8 (2008). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3343742/?tool=pubmed 

5.         Zhang, Q. Yao, Y. Konger, R.L., Sinn, A., Cai, S., Pollok, K.E., and Travers, J.B..  UVB Radiation-Mediated Inhibition of Contact Hypersensitivity Reactions Is Dependent on the Platelet-Activating Factor System. J Invest Dermatol, 128, 1780 – 1787 (2008). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643301/?tool=pubmed 

6.         Yao, Y.,  Wolverton, J., Zhang, Q.,  Marathe, G.K.,  Al-Hassani, M.,  Konger, R.L. and J.B. Travers. Ultraviolet B Radiation Generated Platelet-activating Factor Receptor Agonist Formation Involves EGF-R-mediated Reactive Oxygen Species. J. Immunol., 182:2842-2848 (2009). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750830/?tool=pubmed 

7.         Konger, R.L., Martel, K.C.,  Thompson, A.B.,  Jernigan, D., Zhang, Q., and J.B. Travers. The peroxisome proliferator-activated receptor gamma system regulates Ultraviolet B-induced prostaglandin E2 production in human epidermal keratinocytes. PPAR Res, vol. 2010, Article ID 467053, 8 pages, (2010). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873656/?tool=pubmed

8.         Travers, J.B., Berry, D., Yao, Y., Yi, Q., Konger, R.L., and J.B. Travers. Ultraviolet B Radiation of Human Skin Generates Platelet-activating Factor Receptor Agonists. Photochem Photobiol., 86(4): 949–954 (2010). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910152/?tool=pubmed

9.         J. Liu, Z. Xu, Q. Song, R.L. Konger, and Y.L. Kim, "Enhancement factor in low-coherence enhanced backscattering and its applications for characterizing experimental skin," Journal of Biomedical Optics, 15(3), 037011, (2010). http://dx.doi.org/10.1117/1.3443795

10.       DaSilva, S. C., Sahu, R.P., Konger, R.L., Southall, M.D., Perkins, S.M., Kaplan, M.H., and J.B. Travers. Increased skin barrier disruption by sodium lauryl sulfate in mice expressing a constitutively active STAT6 in T cells. Arch Dermatol Res., 304(1):65-71 (2012).  http://www.springerlink.com/content/8446602v046h3248/?MUD=MP 

11.       Sahu, R.P., Kozman, A., Yao, Y., DaSilva, S.C., Resania, S., Martel, K.C., Warren, S., Travers, J.B., and R.L. Konger.  Loss of the Platelet Activating Factor Receptor in mice augments PMA-induced inflammation and cutaneous chemical carcinogenesis. Carcinogenesis, 33(3):694-701 (2012). http://carcin.oxfordjournals.org/content/33/3/694.long 

12.       Sahu, R.P., Yao, Y., Konger, R.L., and J.B. Travers. Platelet-activating Factor does not Mediate UVB-induced Local Immune Suppression. Photochem Photobiol, 88: 490–493 (2012). http://onlinelibrary.wiley.com/doi/10.1111/j.1751-1097.2011.01071.x/abstract;jsessionid=74F6A6C817671D5E09A164A1C2A38C9F.d01t02 

13.       Yao, Y., Harrison, K.A., Al-Hassani, M., Murphy, R.C., Rezania, S., Konger, R.L., and J.B. Travers. Platelet-activating factor agonists mediate Xeroderma Pigmentosum A photosensitivity. J. Biol. Chem., 287 ( 12): 9311–9321 (2012). http://www.jbc.org/content/287/12/9311.long 

14.       Sahu, R.P., DaSilva, S., Rashid, B., Martel, K.C., Jernigan, D., Rezania, S., Bradish, J.R., Armstrong, A.B., Warren, S., and R.L. Konger. Mice lacking epidermal PPARγ exhibit a marked augmentation in photocarcinogenesis associated with increased UVB-induced apoptosis, inflammation and transepidermal water loss.  Int. J. Cancer, in press, doi: 10.1002/ijc.27562 (2012). http://onlinelibrary.wiley.com/doi/10.1002/ijc.27562/abstract 

15.       Sahu, R.P., Turner, M.J., DaSilva, S.C., Rashid, B.M. Ocana, J.A., Perkins, S.M. Konger, R.L., Touloukian, C.E., Kaplan, M.H.,  and J.B. Travers. The environmental stressor ultraviolet B radiation inhibits murine antitumor immunity through its ability to generate platelet-activating factor agonists. Carcinogenesis, in press, doi:10.1093/carcin/bgs152  (2012). http://carcin.oxfordjournals.org/content/early/2012/05/06/carcin.bgs152.long 

 

 

Currently Active Funding:

1. Principal Investigator:

Raymond Konger / Jeffrey Travers (Co-PI)

Source:

NIH  R01 HL062996  

Title of Project (and/or Subproject):

Platelet Activating Factor and Epidermal Cytotoxicity

Dates of Approved/Proposed

04/01/2009 – 03/31/2014

 

2. Principal Investigator:

Young L. Kim (Konger (co-investigator))

Source:

NIH  R03 CA153982-01

Title of Project (and/or Subproject):

Hotspot imaging for risk stratification of non-melanoma skin cancer in a pilot study

Dates of Approved/Proposed

07/09/2009 – 06/30/2014

 

3. Principal Investigator:

Raymond Konger (PI)

Source:

NIH  R21 ES020965

Title of Project (and/or Subproject):

Characterization of persistent hyperemic foci and their role in photocarcinogenesis

Dates of Approved/Proposed

07/01/2012 – 06/30/2014

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Completed Research Support (last 3 years):

05/10-08/10     NIH 3R21ES017497-01S1, Konger, Raymond L. (PI). ARRA NIEHS Summer Supplement. Tumor Suppresion Through Oxidized Glycerophosphocholines.

07/09 – 06/11  NIH R21 ES017497-01, Konger, Raymond L. (PI). Tumor Suppresion Through Oxidized Glycerophosphocholines.

07/07-07/10     Prevent Cancer Foundation, Konger, Raymond L. (PI).  PPARgamma as a target for UVB-induced photocarcinogenesis

07/07-06/09     NIH R03 AR053710-01, Konger, Raymond L.(PI).  “Role of PPARgamma in ultraviolet stress responses”.

Dept. of Pathology & Laboratory Medicine Administration Office | Van Nuys Medical Science Building | 635 Barnhill Drive, room A-128 | Indianapolis, IN 46202 Indiana University Health Pathology Laboratory: 350 W. 11th Street, Indianapolis, Indiana 46202