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Jamie Bernard, Ph.D.

Associate Professor, Pharmacology & Toxicology

Dr. Jamie Bernard
B420 Life Sciences
1355 Bogue Street
East Lansing, MI 48824

Email: jbernard@msu.edu

Phone: (517) 353-5326 | Fax: (517) 353-8915 | Location:  B420 Life Sciences

Fields of Interest: Our laboratory studies toxicological effects in everyday life that act as triggers in the formation of cancer.

  • 2004 - B.S. Neuroscience, University of Rochester
  • 2009 - Ph.D. Toxicology, University of Rochester
  • 2009-2011 - Postdoctoral fellow, University of California San Diego
  • 2011-2015 - Postdoctoral fellow, Rutgers University
  • 2015-2021 - Assistant Professor, Pharmacology and Toxicology, Michigan State University
  • 2021-present - Associate Professor, Pharmacology and Toxicology, Michigan State University

In the Bernard lab we study the mechanisms that underlie the onset of carcinogenesis, so we can find new targets for prevention. We have discovered that intra-abdominal (visceral) fat can promote carcinogenesis in in vitro models and animal models of high-fat diet-induced obesity by releasing fibroblast growth factor-2 (FGF2) and activating FGFR1. We aim to identify specific mechanisms of obesity-promoted cancer with a focus on visceral fat inflammation. We are now exploring the translational relevance of FGF2 as a biomarker of adiposity-associated cancer risk. Additionally, we have interests in screening to identify new compounds that target our pathways for chemoprevention and identifying modifiable risk factors as a biomarkers of adiposity-associated cancer that are amenable to prevention and early intervention measures. Attractive compounds for chemoprevention include natural products. Historically, natural product extracts were the source of medications. Purified natural products have advantages in terms of standardization of dose and avoidance of side effects of other products in the mixtures. We currently have collaborations and are seeking new collaborations to develop chemopreventive agents from purified natural products.The active compounds identified have the potential to lead to new scientific discoveries by providing compounds that will reveal new mechanisms and pathways of carcinogenesis as well as potential commercial licensing and spin-off opportunities for chemopreventive agents.


  • SOT Carcinogenesis Specialty
    Section Postdoctoral Fellowship 2014
  • Scala Scholar Travel Award 2013
  • Selected for Oasis Leadership and
    Professional Development Program for Faculty 2012
  • Stratacor Postdoctoral Award,
    Dermal Toxicology Specialty Section 2012
  • Albert M. Kligman Travel Fellowship 2011
  • Society for Investigative Dermatology
    Eugene M. Farber Award Travel Award 2011
  • Harold Hodge Award for best Thesis
    in the Toxicology program 2009
  • Robert N. Infurna Award for best student publication
    in the Environmental Health Sciences 2009
  • Drug Discovery Award (1st Place)
    Society of Toxicology meeting Baltimore 2009
  • Dr. William F. Newman Award
    for excellence in scholarship and citizenship 2008
  • Bristol-Myers-Squibb Award,
    for meritorious research in Toxicology 2007
  • Rochester Toxicology Scholar 2004
  • Merritt and Marjorie Cleveland Fellowship Award
    for outstanding potential for scientific contributions 2004


  • K99/R00 Pathway to Independence
    Transitional Grant from the National Cancer Institute 2014-present
  • NIEHS Toxicology Training Grant
    (T32 ES007148) Trainee 2011-2014
  • NIEHS Toxicology Training Grant
    (T32 ES07026) Trainee 2004-2007
  • Pharmaceutical Researchers and Manufacturers of America (PhRMA) Foundation,
    Advanced Predoctoral Fellowship in Pharmacology/Toxicology
  • Awards committee, Society of Toxicology, Carcinogenesis Specialty Section (2015-present)
  • Society of Toxicology (2007-present)
  • Society of Investigative Dermatology (2010-present)
  • American Society for Pharmacology and Experimental Therapeutics (2015-present)

Most recent 5 Publications

  • Bernard JJ, Lou YR, Peng QY, Li T, Lu YP.  PDE2 is a Novel Target for Attenuating Tumor Formation in a Mouse Model of UVB-induced Skin Carcinogenesis. 2014 Oct 16;9(10):e109862. doi: 10.1371/journal.pone.0109862
  • Bernard JJ, Lou YR, Peng QY, Li T, Vakil PR, et al. (2014) Parametrial Fat Tissue from High Fat Diet-Treated SKH-1 Mice Stimulates Transformation of Mouse Epidermal JB6 Cells. J Carcinog Mutagen 5:183 doi: 10.4172/2157-2518.1000183
  • Bernard JJ, Lou YR, Peng QY, Li T, Conney AH, Lu YP.  Inverse relationship between p53 and phosphor-Chk1 (Ser317) protein expression in UVB-induced skin tumors in SKH-1 mice.  Experimental and molecular pathology.  2014.  Feb; 96(1):126-31.
  • Bernard JJ, Cowing-Zitron C, Nakatsuji T, Muehleisen B, Moto J, Martinez L, Greidinger EL, Yu BD, Gallo RL. Ultraviolet radiation damages self non-coding RNA and is detected by TLR3. Nature Medicine. 2012. Aug; 18(8): 1286-90.
  • Lu YP, Lou YR, Bernard JJ, Peng, QY, Li T, Lin Y, Shih WJ, Nghiem P, Shapses S, Wagner GC, Conney AH.  Surgical removal of the parametrial fat pads stimulates apoptosis and inhibits UVB-induced carcinogenesis in mice fed a high-fat diet.  PNAS. 2012, Jun;109(23):9065-70.