John Thomas Pinto is Professor of Biochemistry and Molecular Biology at New York Medical College in Valhalla, New York. His training in Nutritional Biochemistry began in 1974 at the Institute of Human Nutrition, Columbia University. In 1980, he joined the staff at Memorial Sloan-Kettering Cancer Center (MSKCC) as Assistant Laboratory Member and was appointed Assistant Professor of Nutrition in Medicine, Weill Medical College of Cornell University in New York City. During that time (1980-83), he was awarded the Future Leader's Award from the Nutrition Foundation. From 1989 until 1996, he co-directed the Metabolism and Oncology Core Laboratory within the Clinical Nutrition Research Unit (CNRU) at MSKCC and until 2002, also directed the Nutrition Research Laboratory. In 2002 to 2004, he re-established the CNRU at the Institute for Cancer Prevention (Formerly, the American Health Foundation) until its closure and then joined the staff at the Cornell-Burke Medical Research Institute in White Plains, New York. In 2007, he joined the faculty at New York Medical College in his current rank as Professor of Biochemistry and Molecular Biology. His adjunct teaching appointments include the Human Nutrition Program at the University of New Haven and the Nutrition and Behavioral Studies Program at Teachers College, Columbia University in New York City. He is a member of The American Institute of Nutrition, The American Society for Clinical Nutrition, and the American Association for Cancer Research. Dr. Pinto serves as a reviewer for the American Journal of Clinical Nutrition, Nutrition and Cancer, the Journal of Nutrition, and Analytical Biochemistry.
His research focuses on identifying chemopreventive strategies for diminishing primary and secondary cancer risks. His particular investigations examine the effects of organosulfur, selenium and polyphenolic compounds on redox responsive metabolic pathways within human prostate, breast, and colon cancer cells. Dr. Pinto has identified epigenetic mechanisms by which these diet-derived constituents exert control over cell growth and proliferation through sulfhydryl-disulfide regulation of signal proteins, affecting transcription factors of gene expression, and inhibition of histone deacetylation. Histone deacetylase inhibitors are highly sought after agents that control diseases where inappropriate gene activation is a causal feature, namely viral replications and in cancer prevention and control.