Jack C. Yalowich
Professor and Chair
532 Parks Hall


  • Cancer Pharmacology
  • DNA Topoisomerase Inhibitors
  • Therapy-Related Myeloid Leukemias: Chemoprevention
  • Drug Resistance

Professional Interests

Recent studies are focused on understanding the mechanisms by which the clinically effective anticancer agent etoposide (VP-16), a phenolic compound, and the environmental carcinogen, benzene, can cause therapy-related acute myelogenous leukemia (t-AML). The central testable hypothesis is that redox cycling of VP-16 and phenolic benzene metabolites initiated by myeloperoxidase (MPO) in bone marrow precursors amplifies the genotoxicity and carcinogenicity of these compounds via enhanced inhibition/poisoning of DNA topoisomerase II. Nutritional antioxidants such as vitamin C and vitamin E homologs are under investigation as a mechanism-based chemoprevention strategy to eliminate VP-16- and benzene-induced AML by reducing production of MPO-dependent free radical and electrophilic metabolites. The long-term goal of these studies is to increase the clinical efficacy of VP-16 in the treatment of cancer, and to prevent benzene leukemogenesis.


  • Postdoctoral Fellow, 1980-1983, Medical College of Virginia
  • PhD, 1980, Biochemical Pharmacology, SUNY at Buffalo
  • Bachelor of Arts, 1974, Chemistry/Biology, Lehigh University

Recent Publications

Recent Publications