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John Essigmann is the William R. (1956) and Betsy P. Leitch Professor in Residence of Chemistry in the MIT Department of Chemistry and Professor of Toxicology and Biological Engineering in the MIT Department of Biological Engineering. He was the Associate Head of the Department of Chemistry until 2012, responsible for graduate and undergraduate education, and from 2012 until 2019 he was the Director of the MIT Center for Environmental Health Sciences. John was brought up in Medford, MA, a suburb of Boston and is a lifelong resident of the Boston area.
During his undergraduate years at Northeastern University, John worked in the chemistry group at Arthur D. Little, Inc., an industrial consulting company with longstanding ties to MIT. He received his Ph.D. from MIT with Professor Gerald Wogan, a pioneer in the field of toxicology. In the Wogan laboratory, John applied his expertise at the chemistry-biology interface to study the metabolic activation and DNA binding characteristics of aflatoxin B1 and related fungal toxins. These toxins are strongly associated with the lethal and cancer causing effects of natural products in developing areas of the world. Much of the work during this portion of his career was done in collaboration with Professor George Büchi, a chemist renown for his ability to make complex molecules by direct and elegant routes. George and Jerry, in addition to being professional mentors, became close friends of the Essigmann family owing to their mutual love of skiing in the White Mountains of New Hampshire.
As a faculty member at MIT, John used his abilities in chemistry to synthesize oligonucleotides containing DNA adducts formed by environmental toxins and chemotherapeutic drugs. His group developed a means to introduce these oligonucleotides into the genomes of viruses, which were then replicated inside cells. For a host of drugs and environmental carcinogens, the Essigmann group has defined the type and amount of mutations induced. They have also defined the genetic requirements for these mutational changes. Finally, they have applied similar techniques to probe the mechanisms by which the DNA damage formed by existing anticancer drugs cause cells to die. The drug design strategy of "lethal mutagenesis" or "viral decay acceleration" of Koronis Pharmaceuticals is based upon work done in the laboratories of Lawrence Loeb, James Mullins and John Essigmann. Kronis' lead compound, KP-1212, has reached Phase II clinical trial status.
During his undergraduate years at Northeastern University, John worked in the chemistry group at Arthur D. Little, Inc., an industrial consulting company with longstanding ties to MIT. He received his Ph.D. from MIT with Professor Gerald Wogan, a pioneer in the field of toxicology. In the Wogan laboratory, John applied his expertise at the chemistry-biology interface to study the metabolic activation and DNA binding characteristics of aflatoxin B1 and related fungal toxins. These toxins are strongly associated with the lethal and cancer causing effects of natural products in developing areas of the world. Much of the work during this portion of his career was done in collaboration with Professor George Büchi, a chemist renown for his ability to make complex molecules by direct and elegant routes. George and Jerry, in addition to being professional mentors, became close friends of the Essigmann family owing to their mutual love of skiing in the White Mountains of New Hampshire.
As a faculty member at MIT, John used his abilities in chemistry to synthesize oligonucleotides containing DNA adducts formed by environmental toxins and chemotherapeutic drugs. His group developed a means to introduce these oligonucleotides into the genomes of viruses, which were then replicated inside cells. For a host of drugs and environmental carcinogens, the Essigmann group has defined the type and amount of mutations induced. They have also defined the genetic requirements for these mutational changes. Finally, they have applied similar techniques to probe the mechanisms by which the DNA damage formed by existing anticancer drugs cause cells to die. The drug design strategy of "lethal mutagenesis" or "viral decay acceleration" of Koronis Pharmaceuticals is based upon work done in the laboratories of Lawrence Loeb, James Mullins and John Essigmann. Kronis' lead compound, KP-1212, has reached Phase II clinical trial status.
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Jie Wang,Nathania A. Takyi,Yun-Chung Hsiao,Qi Tang, Yi-Tzai Chen,Chih-Wei Liu, Jian Ma,Rui Qi,Ke Bian, Zhiyuan Peng,John M. Essigmann,Kun Lu,
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