Morag Park
Professor
Biochemistry
McGill University
Canada
Biography
1983 - PhD, Glasgow University
Research Interest
There is increasing evidence to support the concept that the malignant behavior of some tumors is sustained by the deregulated activation of growth factor receptors. Our work in the past few years has uncovered an important regulator of invasive cell growth, the Met receptor tyrosine kinase. In normal cells, Met acts to relay signals from the cell surface that promote tissue organisation. However when these pathways are altered in cancer cells, this acts to enhance cell invasion the first step of metastasis. Our aims are to identify what signal transduction pathways are important for the development of human cancers and how these can be targeted with drug therapies. This is a complex question that requires a full understanding of how signals are integrated in normal cells and how these signals become altered in tumor cells, in the context of other genetic alterations. My lab has focused on and will continue to address these questions using the Met receptor tyrosine kinase and oncogene as a model. We will focus on signals required for anchorage independent growth, morphological cell transformation, epithelial mesenchymal transition, cell invasion and tumorigenesis.
Publications
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Discovery of Stromal Regulatory Networks that Suppress Ras-Sensitized Epithelial Cell Proliferation. Liu H, Dowdle JA, Khurshid S, Sullivan NJ, Bertos N, Rambani K, Mair M, Daniel P, Wheeler E, Tang X, Toth K, Lause M, Harrigan ME, Eiring K, Sullivan C, Sullivan MJ, Chang SW, Srivastava S, Conway JS, Kladney R, McElroy J, Bae S, Lu Y, Tofigh A, Saleh SMI, Fernandez SA, Parvin JD, Coppola V, Macrae ER, Majumder S, Shapiro CL, Yee LD, Ramaswamy B, Hallett M, Ostrowski MC, Park M, Chamberlin HM, Leone G.
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Identification of Interacting Stromal Axes in Triple-Negative Breast Cancer. Saleh SMI, Bertos N, Gruosso T, Gigoux M, Souleimanova M, Zhao H, Omeroglu A, Hallett MT, Park M.
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Simultaneous targeting of two distinct epitopes on MET effectively inhibits MET- and HGF-driven tumor growth by multiple mechanisms. Grandal MM, Havrylov S, Poulsen TT, Koefoed K, Dahlman A, Galler GR, Conrotto P, Collins S, Eriksen KW, Kaufman D, Vande Woude GF, Jacobsen HJ, Horak ID, Kragh M, Lantto J, Bouquin T, Park M, Pedersen MW.
