Dr. Peters did his graduate training at the University of California at Davis followed by two postdoctoral fellowships. The first at the Institute of Toxicology and Environmental Health at UC Davis, and then in the Laboratory of Metabolism at the National Cancer Institute (NCI). Dr. Peters was recruited to Penn State after his postdoctoral fellowship at the NCI. Dr. Peters is a Distinguished Professor of Molecular Toxicology and Carcinogenesis, and the Deputy Director of the Penn State Cancer Institute. He has served on many editorial boards including The Journal of Biological Chemistry and he is the Editor-in-Chief for Toxicological Sciences.
Department or University Committees
Department of Biochemistry, Microbiology and Molecular Biology: Graduate Affairs Committee, 2014-2015
Candidacy Exam Committee, 2007-2009, 2010
Institutional Review Entity, The Pennsylvania State University, 2016-present
Co-Chair, Intercollege Graduate Degree Program in Molecular Toxicology, The Pennsylvania State University, 2005-2010
|University: Institutional Biosafety Committee, The Pennsylvania State University, Chair, 2016-present|
|Institutional Biosafety Committee, The Pennsylvania State University, Member, 2003-2016|
|Graduate Admissions Committee, 2005-2007, 2009-2010|
|Institutional Animal Care and Use Committee, The Pennsylvania State University, Member, 2005-2012|
Program or Departmental Affiliations
|The BMMB Graduate Program||The Department of Veterinary and Biomedical Sciences||The Molecular, Cellular, and Integrative Biosciences Program|
Chairperson, Cancer Drug Development and Therapeutics Special Emphasis Panel, ZRG1 OTC-T (10) B, National Cancer Institute, National Institutes of Health, 2017 - present
Member, Chemo/Dietary Prevention (CDP) Study Section, National Cancer Institute, National Institutes of Health, 2008-2012
The Center for Molecular Toxicology and Carcinogenesis
Our laboratory studies the role of the peroxisome proliferator-activated receptors (PPARs) in the regulation of homeostasis, toxicology and carcinogenesis. PPARs are members of the nuclear receptor superfamily and are critical modulators of environmental and dietary stimulii. For example fatty acids and metabolic derivatives of fatty acids derived primarily from dietary sources are known ligands that can activate PPARs. Acting as regulatory transcription factors, the PPARs modulate gene expression of target genes containing peroxisome proliferator responsive elements in response to ligand activation. Numerous genes that modulate lipid metabolism are regulated by PPARα, PPARβ/δ and PPARγ ligands/activators, and are clinically relevant for a number of diseases including diabetes, obesity, atherosclerosis and cancer. In addition to transcriptional regulation, PPARs can also epigenetically regulate transcription by interacting with other proteins including NF-κB. Our laboratory uses loss-of-function and gain-of-function mouse and human models, and high affinity agonists, antagonists, and selective, repressive ligands to delineate the roles of PPARs, with a particular interest in epithelial cancers. Through these studies, the laboratory is elucidating the molecular mechanisms by which exogenous (dietary) and endogenous (metabolic sources) lipids specifically modulate human health. We are particularly interested in delineating how natural compounds found in dietary constituents can activate PPARs with the goal of identifying new molecules/proteins that can be targeted with existing approaches to improve the efficacy of cancer chemoprevention and chemotherapy.
Honors or Awards
- Toxicology Forum, George H. Scott Memorial Award, 2018
- The Huck Award for Outstanding Achievements in Life Sciences Research, 2016
- Gamma Sigma Delta Faculty Research Award, 2016
- Fellow, Academy of Toxicological Sciences, 2012-present
- Faculty of 1000, Pharmacology and Drug Discovery Faculty, 2011-2019
- National Institutes of Health Director's Wednesday Afternoon Lecture, 2009
- Society of Toxicology Achievement Award, 2007
- Black Award for Excellence in Research, College of Ag. Sciences, Penn State University, 2007
- Teratology Society F. Clarke Fraser New Investigator Award, March 2002
- Peters, J.M., Walter, V., Patterson, A.D. and Gonzalez, F.J.. Unraveling the role of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) expression in colon carcinogenesis. Precision Oncology (2019) 3: 26; https://doi.org/10.1038/s41698-019-0098-x.
- Koga, T., Yao, P.-L., Goudarzi, M., Murray, I. A., Balandaram, G., Gonzalez, F.J., Perdew, G.H., Fornace Jr., A.J. and Peters, J.M.. Novel regulation of cytochrome P450 2B10 (CYP2B10) expression in liver by peroxisome proliferator-activated receptor-β/δ (PPARβ/δ). The Journal of Biological Chemistry (2016) 291: 25255-25263. Virtual issue of The Journal of Biological Chemistry, “Drug metabolism, transport and toxicity” (2018): [Weblink].
- Zhu, B., Ferry, C.H., Markell, L.M., Blazanin, N., Glick, A.B., Gonzalez, F.J. and Peters, J.M.. The nuclear receptor PPARβ/δ promotes oncogene-induced cellular senescence through repression of endoplasmic reticulum stress. The Journal of Biological Chemistry (2014) 289: 20102-20119.
- Yao, P.-L., Morales, J.L., Zhu, B., Kang, B.-H., Gonzalez, F.J. and Peters, J.M.. Activation of peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) inhibits human breast cancer cell line tumorigenicity. Molecular Cancer Therapeutics (2014) 1008-1017.
- Zhu, B., Bility, M.T., Ferry, C.H., Khozoie, C., Blazanin, N., Kang, B.-H., Glick, A.B., Gonzalez, F.J. and Peters, J.M.. PPARβ/δ promotes HRAS-induced senescence and tumor suppression by potentiating p-ERK and repressing p-AKT signaling. Oncogene (2014) 33: 5348-5359.
- Khozoie, C., Borland, M.G., Zhu. B., Baek, S., John, S., Hager, G.L., Shah, Y.M., Gonzalez, F.J. and Peters, J.M.. Analysis of the peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) cistrome reveals novel co-regulatory role of ATF4. BMC Genomics (2012) 13: 665.