David Buchner, PhD
Program Director, Master of Science in Computational Genomic Medicine
Associate Professor, Department of Genetics and Genome Sciences, School of Medicine
Dr. David Buchner is an accomplished geneticist and educator whose career spans more than two decades of research and leadership in human genetics, metabolic disease, and computational genomics. He earned his PhD in Human Genetics from the University of Michigan, where his doctoral work in Dr. Miriam Meisler’s laboratory focused on identifying and characterizing a modifier gene for neurological disease—an early contribution to understanding genetic complexity in human disorders.
Following his PhD, Dr. Buchner completed postdoctoral fellowships with two leading scientists: Dr. David Ginsburg (Howard Hughes Medical Institute, University of Michigan) and Dr. Joe Nadeau (ÐÓ°ÉÊÓƵ). During this time, he leveraged animal models to uncover novel disease genes underlying bleeding disorders and metabolic disease, advancing the field’s understanding of gene–environment interactions and genetic modifiers.
Dr. Buchner continued his research as an Assistant Research Scientist in Dr. Alan Saltiel’s laboratory at the University of Michigan Life Sciences Institute, where he investigated the molecular mechanisms driving obesity and diabetes. In 2013, he joined the faculty at ÐÓ°ÉÊÓƵ School of Medicine, where he holds a primary appointment in the Department of Genetics and Genome Sciences and secondary appointments in Biochemistry and the Research Institute for Children’s Health. In 2025, he was appointed Program Director for the Master of Science in Computational Genomic Medicine, where he leads curriculum development, faculty engagement, and strategic initiatives to prepare the next generation of leaders in genomic medicine.
Dr. Buchner’s research program integrates genomics, computational biology, and experimental models to address fundamental questions in metabolic disease. His lab focuses on the role of adipocytes in obesity and type 2 diabetes, with an emphasis on the genetic and molecular pathways that regulate insulin sensitivity. By combining large-scale genomic datasets with mouse metabolic phenotyping and cell biology, his team has identified novel transcriptional regulators critical for adipocyte function and continues to dissect their roles in metabolic health.
Beyond adipocyte biology, Dr. Buchner’s group investigates the genetic architecture of complex traits, contributing to discoveries in modifier genes, context-dependent susceptibility loci, epigenetic inheritance, and gene–gene interactions (epistasis). His work exemplifies the integration of computational and experimental approaches to unravel the complexity of human disease, aligning closely with the mission of the Computational Genomic Medicine program.
As Program Director, Dr. Buchner is committed to fostering an interdisciplinary learning environment that bridges genomics, data science, and clinical application, equipping students with the skills to translate genomic insights into precision medicine solutions.
Zhenghe J Wang, PhD
Chair and Professor, Department of Genetics and Genome Sciences, School of Medicine
Dale H. Cowan M.D. – Ruth Goodman Blum Professor of Cancer Research
Co-Leader, Cancer Genomics and Epigenomics Program, Case Comprehensive Cancer Center
John Wang received his Ph.D. in Microbiology from University of Virginia in 2001. He was a postdoctoral fellow with Dr. Bert Vogelstein in the Sydney Kimmel Comprehensive Cancer Center at Johns Hopkins University. Dr. Wang joined the Department of Genetics and the Case Comprehensive Cancer Center in August, 2005. He has been co-leader of the GI cancer genetics program at Case Comprehensive Cancer Center since 2014. He was named as a co-leader of the Standup to Cancer (SU2C) Colorectal Cancer Dream Team in 2017 and Chair of the Department in 2024.
Dr. Wang’s research program focuses on defining mechanisms of oncogenesis at the molecular, regulatory and phenotypic levels and translating these discoveries to new cancer therapies.
Dr. Wang co-discovered that PIK3CA, which encodes p110α catalytic subunit of PI3 kinase, is frequently mutated in human cancers. His laboratory recently found that PIK3CA mutations render colorectal cancer dependent on glutamine. He has successfully translated these discoveries into ongoing phase I/II clinical trials. This line of research is currently funded by a SU2C colorectal cancer Dream Team award, the Case GI SPORE and an R01 from the National Cancer Institute.
Dr. Wang also is interested in defining the roles of pseudo-kinases and pseudo-phosphatases in tumorigenesis. The human genome encodes 48 pseudo-kinases and 17 pseudo-phosphatases, which are thought to be enzymatically inactive. However, his laboratory recently discovered that the pseudo-phosphatase domain of protein tyrosine phosphatase receptor T (PTPRT) is in fact an active enzyme which removes nitration (NO2) from tyrosine residues in proteins. His lab has demonstrated that this denitrase functions as a tumor suppressor.