Charles Murtaugh, Ph.D.

Associate Professor

Research Focus

The Murtaugh lab has a longstanding interest in how cells of the pancreas differentiate, or assume their mature program of gene expression and function, and how this differentiation process goes awry in disease. During embryonic development, a cascade of intercellular signals and transcription factors establishes the two major “compartments” of the pancreas and their cell types: the endocrine pancreas, organized into the islets of Langerhans and comprising cells producing several hormones including insulin; and the exocrine pancreas, made up of acinar cells that synthesize and secrete the digestive enzymes that break down our food, and duct cells that channel those enzymes into the intestine. Multiple pancreatic diseases, including diabetes, pancreatitis and pancreatic cancer, are associated with changes or reversals of this developmental process, and we have particularly focused on the transition of normal pancreatic cells into cancer.

Most cases of pancreatic cancer are referred to as “ductal adenocarcinoma,” because the cancer cells have some resemblance to normal duct cells, and the disease was assumed to develop from duct cells. However, our lab established a novel mouse model of pancreatic cancer in which the disease actually arises from differentiated exocrine acinar cells, which lose their normal differentiation state through a process we have termed “reprogramming.” Acinar cell reprogramming appears to represent the earliest step of pancreatic tumor formation, and we have worked to identify its underlying mechanisms. Our recent studies have focused in particular on the role of the transcription factor Ptf1a as an epigenetic tumor suppressor in the pancreas, and the possible role of gut microbiota-derived signals in promoting pancreatic inflammation and tumor development. In addition, recent genomics studies in the lab have uncovered new evidence that human pancreatic cancer also originates from acinar cells. We consider reprogramming to be a potential mediator of both inherited and environmental risk factors for human pancreatic cancer, as well as an attractive target for anti-cancer therapeutics.

Representative Publications

Krah, N.M., S.M. Narayanan, D.E. Yugawa, J.A. Straley, C.V.E. Wright, R.J. MacDonald and L.C. Murtaugh. (2019) Prevention and reversion of pancreatic tumorigenesis through a differentiation-based mechanism. Developmental Cell 50:744-754

Krah N.M., J.-P. De La O, G.H. Swift, C.Q. Hoang, S.G. Willet, P.F. Chen, G.M. Cash, M.P. Bronner, C.V. Wright, R.J. MacDonald, and L.C. Murtaugh. (2015) The acinar differentiation determinant PTF1A inhibits initiation of pancreatic ductal adenocarcinoma. eLife Jul 7;4. doi: 10.7554/eLife.07125

Baumgartner, B.K., G. Cash, H. Hansen, S. Ostler, and L.C. Murtaugh. (2014) Distinct requirements for beta-catenin in pancreatic epithelial growth and patterning. Developmental Biology 391:89-98

De La O, J.-P., L.L. Emerson, J.L. Goodman, S.C. Froebe, B.E. Illum, A.B. Curtis, L.C. Murtaugh. (2008) Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia. Proc. Natl. Acad. Sci. USA 105:18907-12

Complete list at MyBibliography


Jamie Covington
Jamie Covington

Undergraduate Student

Erik Eide
Erik Eide

Lab Specialist

Diane Hernandez
Diane Hernandez

Graduate Student

Contact Information


Office: 801.581.5958

Lab: 801.581.7599

Building/Office: EIHG 4420B