Barry Gold, PhD

Chair and Professor, University of Pittsburgh Department of Pharmaceutical Sciences

Barry Gold, PhD

Office: 711 Salk Hall
Phone: 412-383-9593

School of Pharmacy


A.B. in Chemistry, Hunter College 1966
Ph.D. in Chemistry, University of Nebraska 1972
Post-doctorate, University of Nebraska Medical Center 1976

While I was originally trained as an organic chemist, I have been involved in the field of chemical carcinogenesis since 1976 when I took a position at the Eppley Institute for Research in Cancer at the University of Nebraska Medical Center (UNMC). My early training included in vitro and in vivo metabolism of potential carcinogens and chronic bioassays of chemical carcinogens in rodent species (mice, rats and hamsters). Accordingly, I have been interested in the relationship between exposure to genotoxic chemicals and cancer for my entire career. While chemicals in our environment are associated with a higher risk of cancer, for example the higher incidence of colorectal cancer in diets with grilled meats, normal exposure to DNA damaging agents in many animal models is not sufficient to develop cancer. For this reason, we have turned to the interaction between inflammation and chemical-induced mutagenesis and carcinogenesis. Recently we have adapted, and published, an enzymatic approach to measure stem cell mutations formed in the colon of mice treated with putative promutagenic/carcinogenic compounds. This approach has allowed us to determine whether compound(s) or treatments can generate stem cell mutations or affect the spontaneous mutation frequency presumably due to replication errors and endogenous genotoxins. We have demonstrated that inflammation induced by dextran sulfate sodium does not produce stem cell mutations proving that inflammation associated reactive oxygen/nitrogen species (RONS) are not acting via direct mutagenesis. The current grant application builds and expands on this finding using a mutagen found in grilled meats, which has been epidemiologically tied to human colorectal cancer and is known to produce colon tumors in animal models. We are proposing a novel mechanism by which RONS mediated oxidation converts the initial heterocyclic aromatic amine DNA adduct into more potent promutagenic ring-opened lesions. The analytical MS work is being conducted with my co-investigator (Robert Turesky), who is an established expert in the field of adduct analysis. We have known each other for many years and are excited to collaborate on a project of mutual interest. The proposal was developed based on extensive face-to-face and electronic meetings.

  1. Gold, B., Stone, M. P. and Marky, L. A. Looking for Waldo: A potential thermodynamic signature to DNA damage. Acc. Chem. Res. 47, 1446-1454 (2014).
  2. Whetstone, R. and Gold, B. T-Cells Enhance Stem Cell Mutagenesis in the Mouse Colon. Mutat. Res. 744, 1-5 (2015).
  3. Whetstone, R. and Gold, B. Quantification of glucose-6-phosphate dehydrogenase mutations in colonic stem cells. J. Vis. Exp., 103, doi: 10.3791/53240 (2015).
  4. Feng, Z., Kochanek, S., Close, D., Wang, L. R., Srinivasan, A., Almehizia, A. A., Iyer, P., Xie, X.-Q., Johnston, P. A. and Gold, B. Design and Activity of AP Endonuclease-1 Inhibitors. J. Chem. Biol. 8, 79-93 (2015).
  5. Whetstone, W., Wittel, U., Michels, N., Gulizia, J. A. and Gold, B. Colon carcinogenesis in wild type and immune compromised mice after treatment with azoxymethane, and azoxymethane with dextran sodium sulfate. Mol. Carcinog. doi: 10.1002/mc.22361 (2015).