
Always prepared and organized for students.
James Amos-Landgraf is an Associate Professor of Veterinary Pathobiology in the Agricultural and Veterinary Science faculty at the University of Missouri-Columbia, College of Veterinary Medicine. He earned an A.B. from Washington University, a Ph.D. in Genetics from Case Western Reserve University in 2004, and completed a postdoctoral fellowship in Cancer Genetics at the McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, where he served as an American Cancer Society Postdoctoral Research Fellow under William Dove. Joining the University of Missouri in 2012 initially as an Assistant Professor, he advanced to Associate Professor and now holds key leadership roles, including Co-Director of the NIH-funded Mutant Mouse Resource and Research Center, Co-Investigator of the Rat Resource and Research Center, Director of the Cancer Biology track in the Translational Biosciences Program, and Executive Committee member of the Genetics Area Program. He co-teaches veterinary genomics to second-year veterinary students and contributes to the Molecular Pathogenesis and Therapeutics track.
Amos-Landgraf's research employs genetically engineered mouse, rat, and pig models to investigate human colon cancer, focusing on molecular genetic and epigenetic mechanisms driving initiation and progression. His work examines sex disparities in disease susceptibility, revealing promotion by male hormones like testosterone rather than protection by female hormones, and explores the gut microbiota's role in linking host genetics, phenotype, epigenome, and cancer development. He pioneered longitudinal in vivo monitoring and forward genetics to identify susceptibility genes and potential chemotherapeutics, discovering a novel epigenetic pathway in early adenoma formation influenced by sex and microbiome. Key publications include 'Sex disparity in colonic adenomagenesis involves promotion by male hormones, not protection by female hormones' (Proc Natl Acad Sci U S A, 2014), 'The utility of Apc-mutant rats in modeling human colon cancer' (Dis Model Mech, 2014), 'Monoallelic silencing and haploinsufficiency in early murine intestinal neoplasms' (Proc Natl Acad Sci U S A, 2012), and 'A target-selected Apc-mutant rat kindred enhances the modeling of familial human colon cancer' (Proc Natl Acad Sci U S A, 2007). His contributions enhance translatability of animal models, advancing diagnostics and prevention strategies in colon cancer research.