The Bush lab studies basic mechanisms by which signaling between cells coordinates mammalian morphogenesis. Understanding this control has significance beyond its fundamental importance in development since birth defects are the leading cause of death for infants during the first year of life. We utilize multiple approaches based in mouse genetics to understand fundamental signaling processes as they relate to development and disease with particular foci in the craniofacial and respiratory systems. In addition to mouse genetics approaches, we utilize human ESCs/iPSCs, biophysical approaches, genomics, and live imaging to understand the cellular and molecular control of morphogenesis.

The Goga Lab seeks to understand how specific oncogenes alter the cell cycle, miRNA and metabolic signaling pathways to drive tumorigenesis. We study how cancer signaling pathways are activated in breast and liver cancers and hematopoietic malignancies, amongst the most prevalent and deadly forms of human cancer. We are particularly focused on the MYC oncogene, the downstream pathways it activates, and synthetic-lethal strategies to target MYC overexpressing cancers. Using a variety of model systems we seek to develop anti-cancer therapeutics to selectively inhibit cancer signaling pathways.

The Hutchins Lab seeks to map how post-transcriptional regulation controls developmental pluripotency and cell fate decisions in vivo, using vertebrate neural crest as a model. Neural crest cells are an essential stem cell population in the vertebrate embryo. Dysregulated post-transcriptional regulatory linkages in neural crest can lead to congenital malformations and cancer in humans, and a thorough understanding of the mechanisms underlying these fundamental processes can provide new therapeutic targets for biomedical intervention. By leveraging systems-level approaches and cutting-edge developmental biology techniques to understand how neural crest cell state transitions are achieved post-transcriptionally to drive cell fate choices, we can begin to understand how these programs fail during development or may be hijacked during disease.

Dr. Barbie Klein, MS, PhD, is an Assistant Professor with joint appointments in the School of Dentistry and the School of Medicine. Dr. Klein teaches gross anatomy, human embryology, histology, and neuroanatomy to health professional students and continuing education healthcare learners. She is the anatomy and embryology Discipline Director for second-year medical student courses and Co-Director with Dr. Joyce of the Biomedical Sciences curriculum for dental students. Her research explores innovations in curriculum development, interprofessional anatomy education, instructional design principles, and the use of technology to improve anatomy education.

The Kutys Lab spans disciplinary boundaries between cell biology and engineering to answer fundamental questions in tissue morphogenesis and mechanobiology. We develop and apply biomimetic human tissue models, along with cellular and molecular technologies, to identify mechanisms across biological scales that govern cell-tissue structure and function. We aim to use these discoveries to inform the selection of candidate therapies and the design of next gen preclinical models for human cancer and cardiovascular disease. Current research thrusts include the role of Notch1 in multicellular mechanobiology and tumor suppression, chemo-mechanical signaling at adherens junctions during morphogenesis, and microfluidic human organoid platforms for developmental modeling.

The primary focus of Dr. Sneddon’s research is the niche in pancreatic development and Type I Diabetes. Her research group employs the tools of stem cell biology, developmental biology, genomics, and tissue engineering. Dr. Sneddon’s laboratory studies the underlying biology of the cellular microenvironment, including the cellular diversity and lineage relationships of the non-epithelial compartment of the pancreas in the context of organogenesis, adult organ function, and disease. The hope is that a deeper understanding of the identity and biology of non-epithelial “niche” cell types within the pancreas will enable a more directed and efficient attempt at replacing lost cell and organ function via regenerative medicine.