608-265-5182 (office); 608-262-1258 (lab)
6505 WI Institute Medical Research
BSC, 1982, Biochemistry, University of Aberdeen, Scotland
PhD, 1985, Cell Biology and Biochemistry, University of Kent, England
Postdoctoral Research, Imperial Cancer Research Fund, London and UC-San Fransisco
Professor of Oncology
Developmental Therapeutics, UW Carbone Cancer Center
We are studying aspects of mammary gland biology and neoplasia using transgenic mouse models. Particularly, we have found that Wnt signaling dysregulates mammary stem cells, and that this precedes the formation of differentiated, bilineal tumors. Wnt signaling is highly oncogenic to mammalian epithelia, and indeed comprises one of the main sources of human tumor initiation identified to date. Our hypothesis is that the transforming potential of Wnt signaling is unique to stem/progenitor cells. Our work aims at elucidating how and when adult somatic stem cells can be recruited as tumor precursor cells. Current projects include:
- The discovery of the molecular and cellular mechanism that underlies the tumor resistance phenotype illustrated by mice with a mutation in the heparan sulfate proteoglycan, syndecan-1 (Sdc1) (McDermott et al 2006).
- Modeling of stem cell-based breast cancer
- The activation of stromal cells and their recruitment to tumor development during Wnt-induced tumorigenesis
- The analysis of adult stem cell responses during tumor initiation
- Determination of how Wnt signaling supports normal mammary stem cell function
- An investigation of cell-cell interactions in mammary gland, using microchannel cultures to identify endogenous growth promoting and inhibiting substances secreted by minor sub-populations
Ad-Hoc service for National Institutes of Health: Molecular Oncology Study Section and National Institutes of Health: Basic Translational Special Emphasis Study Section.