Canada Research Chair in Stem Cell Signalling
Associate Professor, Department of Biochemistry and Biomedical Sciences
Location: MDCL 5031
“Wnt signalling has been linked to numerous human diseases including several types of cancer, Alzheimer’s disease, schizophrenia, type II diabetes and obesity. Thus, it is important to understand the details of how Wnt signalling works, as this information will be valuable in developing or improving therapies for Wnt-associated diseases.”
Dr. Brad Doble’s research program is focused on studying normal and aberrant cell signalling in order to understand the mechanisms of tumorigenesis. The Doble lab is particularly interested in studying the Wnt signalling pathway and those cancers in which Wnt has been implicated – cancers including blood, breast, colon and lung.
The Doble lab is gaining new insights into Wnt signalling mechanisms through the use of gene knockout, and gene knock-in approaches. Another key approach used in Dr. Doble’s lab is proteomic analysis. In collaboration with other research groups, proteomic techniques are being used to investigate the mechanisms regulating Wnt signalling networks and to identify new Wnt pathway components.
Ultimately, Dr. Doble wants to further our understanding of the role of Wnt signalling in stem cell regulation and cancer. Through this work, Dr. Doble is seeking to develop targeted cancer therapies that will address the abnormal cell signalling networks required to initiate and sustain specific sub-types of cancer.
Demonstrating the ability of the Wnt pathway to suppress tumour progression in childhood medulloblastoma, thus establishing activated Wnt signaling as a novel treatment paradigm.
The potential to identify new pathway modulators that could be used in therapies for diseases in which the Wnt pathway is hyperactivated.
Isolating new targets for the development of novel cancer therapeutics that block β-catenin’s nuclear function.
Identifying Tcf/Lef partners that regulate their functional output has the potential to provide new therapeutic targets which could be exploited in cancers with hyperactive Wnt signalling.
Cell Stem Cell. 2011 Feb 4; 8(2): 214-227.
Functional redundancy of GSK-3α and GSK-3β in Wnt/β-catenin signaling shown by using an allelic series of embryonic stem cell lines.
Developmental Cell. 2007 June 5; 12(6): 957-971.