Title:
Associate Professor

Institute:
McGill University

Department:
Rosalind and Morris Goodman Cancer Research Centre
Departments of Medicine, Biochemistry and Anatomy & Cell Biology

Province:
Quebec

Training:
Postdoctoral fellow, Cell Biology Program, Memorial Sloan-Kettering Cancer Centre, New York, New York, USA
PhD, Biology Department, McMaster University, Hamilton, Ontario, Canada
BSc, Molecular Biology Program, McMaster University, Hamilton, Ontario, Canada

Research interests:
Molecular mechanisms promoting breast cancer growth; Identifying molecular mediators of site-specific breast cancer metastasis; Designing/testing therapeutic agents against target molecules important for metastasis.

Recognitions:
Damon Runyon-Walter Winchell Post-Doctoral Fellow
Harold E. Johns Award, NCIC (2004-2010)
FRSQ Junior-2 Research Scholar (2010-2012)

Research Projects

Project title:
Defining Mechanisms by which CCN3 Promotes the Formation of Osteolytic Bone Metastases

Funding period:
2011-2013

Program:
Operating Grant (Basic Research)

Summary:
Breast cancer is the most frequently diagnosed and the second most lethal cancer affecting woman in Canada. Once breast cancer cells have spread from the primary site to distant organs, the disease is largely incurable. The skeleton is a common site for breast cancer metastasis. Using a mouse model of breast cancer metastasis to bone, we have identified a protein called CCN3 that is highly expressed in cells capable of metastasizing to bone. We have also demonstrated that CCN3 is expressed in bone metastatic lesions of breast cancer patients, making it a potential target in the management of bone metastatic breast cancer. CCN3 favors the formation of bone destructive metastases through its ability to regulate two major types of cells found in the bone microenvironment. The research described in this proposal will focus on the role of the different domains within CCN3 that promote bone metastasis. In addition, we will determine if CCN3 can be detected in primary breast tumors from patients that have experienced relapse to bone.

CRS publications:

Y. He, J.J. Northey, M. Primeau, R.D. Machado, R. Trembath, P.M. Siegel and N. Lamarche-Vane (2011). CdGAP is required for Transforming Growth Factor β- and Neu/ErbB-2-induced breast cancer cell motility and invasion. Oncogene. 30(9):1032-1045.

Kristin Roovers, Simona Wagner, Christopher J. Storbeck, Paul O’Reilly, Jason Northey, Juliann Chmielecki, William J. Muller, Peter M. Siegel and Luc A. Sabourin (2009). The Ste20-like kinase SLK is required for ErbB2-driven motility of mammary epithelial cells. Oncogene 28(31):2839-2848.

J.J. Northey, J. Chmielecki, E. Ngan, C. Russo, M.G. Annis, W.J. Muller and P.M. Siegel (2008). Signaling through ShcA is required for TGF-β and Neu/ErbB-2 induced breast cancer cell motility and invasion. Mol Cell Biol. 28(10): 3162-3176.

A.A. Mourskaia, J.J. Northey and P.M. Siegel. (2007) Targeting aberrant TGF-β signaling in pre-clinical models of cancer. Anti-Cancer Agents in Medicinal Chemistry, 7(5): 504-514.

Past CRS projects:

2007 ErbB-2/TGF-β signaling pathway interactions in breast cancer

2005 ErbB-2/TGF-β signaling pathway interactions in breast cancer