Ken Cadwell, Ph.D., New York University School of Medicine, has been given a 2013 ICAAC Young Investigator Award for his exceptional work in the fields of infectious diseases and pathogenesis. His nominator, Heran Darwin, notes that Cadwell’s findings have already had a “profound impact on the fields of infectious disease and immunity.”
Cadwell received his undergraduate degree in Biology, with Honors, from Northwestern University. He then joined the laboratory of Laurent Coscoy in the Department of Molecular Cell Biology at the University of California, Berkeley where he received his Ph.D. Coscoy describes Cadwell as an exceptional scientist and quick learner who has a “real passion for science and a genuine concern for his peers.” As part of his dissertation research, he identified a novel type of protein modification catalyzed by the Kaposi’s Sarcoma Herpesvirus. Following the completion of his Ph.D., he joined the laboratory of Herbert “Skip” Virgin at Washington University School of Medicine where he received an esteemed postdoctoral fellowship from the Damon Runyon Cancer Foundation to investigate how aberrant host-pathogen interactions lead to inflammatory disease.
As part of his postdoctoral research, he generated and characterized mice with a mutation in Atg16L1, a gene that is linked to inflammatory bowel disease and essential for the cellular pathway of autophagy. He found that these mice developed intestinal pathologies similar to the human disorder, but only upon infection with a norovirus. Virgin calls this discovery a “new paradigm for understanding how complex inflammatory diseases can be induced in a combinatorial fashion.” In recognition of this finding, he received the Dale F. Frey Award for Breakthrough Scientists, which is awarded by the Damon Runyon Foundation for individuals with great potential.
In 2010, he joined the Department of Microbiology at New York University School of Medicine as a faculty member of the prestigious Skirball Institute of Biomolecular Medicine. Using the tools that he previously established, he is continuing to examine the role of Atg16L1 and autophagy in immune responses to pathogens. In addition to examining the mechanism by which a virus triggers intestinal disease, he is also investigating how autophagy deficiency alters resistance to bacterial infections. He is especially interested in revealing new roles for autophagy during inflammation that can be exploited for improving treatment of infectious and immunological disease.