Peter Siegel


Image of Dr. Peter Siegel


Peter Siegel, Ph.D.

Associate Professor, Departments of Medicine, Biochemistry, and Anatomy and Cell Biology
Associate Director, Rosalind and Morris Goodman Cancer Research Centre

McGill University

1160 Pine Avenue, West, Room 513, Montreal, Quebec, H3A 1A3

Tel: 514-398-4259


peter.siegel [at]
Siegel Lab

Biographical Sketch

Dr. Peter Siegel received his Ph.D. degree from McMaster University and pursued his post-doctoral training at the Memorial Sloan-Kettering Cancer Center. He is currently an Associate Professor in the Department of Medicine at McGill University and a full member of the Goodman Cancer Research Centre, where he serves as Associate Director. Since beginning his independent academic career at McGill, Dr. Siegel has held career awards from the CCS (Harold Johns Award), FRQS (Junior II research scholar) and is currently a McGill University William Dawson Scholar. Dr. Siegel’s research focuses on the fundamental mechanisms that control organ-selective cancer metastasis and employs pre-clinical animal models and clinical material to identify molecular mediators and cellular process that promote cancer metastasis to distinct sites such as the bone, lung, liver and brain, with a particular emphasis on breast cancer. His research has been funded by the Canadian Institutes of Health Research, the Canadian Breast Cancer Research Alliance, the Canadian Cancer Society Research Institute, the Terry Fox Foundation, the US Army Department of Defense and the Cancer Research Society.


Breast Cancer, Migration/Invasion, Metastasis, Tumor Microenvironment, Tumor/stromal interactions, experimental therapeutics

Research or Clinical Activities

Dr. Siegel’s laboratory is focused on elucidating the cellular and molecular mechanisms that promote cancer metastasis, which represents the most deadly aspect of the disease. His research program can be divided into three broad themes: the first is the identification of key tumor cell intrinsic molecules, signalling pathways and metabolic strategies that enable cancer cells to migrate, invade and metastasize. The second theme investigates the interactions between cancer cells and the primary and metastatic microenvironments in which they grow. The immediate tumor microenvironment includes the extracellular matrix components, resident parenchymal cells that comprise different organs/tissues and the infiltrating innate and adaptive immune cells, all of which influence the growth and spread of cancer cells. The third theme focuses on how these key molecules; pathways or tumor/stromal interactions can be targeted therapeutically.

Selected Recent Publications

1.      S. Andrzejewski, E. Klimcakova, R.M Johnson, S. Tabariès, M.G. Annis, S. McGuirk, J.J. Northey, V. Chénard, U. Sriram, D. Papadopoli, P.M. Siegel* and J. St-Pierre* (2017). PGC-1α promotes breast cancer metastasis and confers bioenergetic flexibility against metabolic drugs. Cell Metabolism. 26(5): 778-787. *Co-corresponding Authors.

2.      E. Ngan, K. Stoletov, H.W. Smith, J. Common, W.J. Muller, J.D. Lewis and P.M. Siegel. (2017). LPP is a Src substrate required for invadopodia formation and efficient breast cancer lung metastasis. Nat Comm. 8: 15059.

3.      A.A.N. Rose, M.G. Annis, D.T. Frederick, Z. Dong, L. Kwong, L. Chin, T. Keler, T. Hawthorne, I.R. Watson K.T. Flaherty, and P.M. Siegel. (2016). MAPK Pathway Inhibitors Sensitize B-RAF Mutant Melanoma to an Antibody-Drug Conjugate Targeting GPNMB. Clin Cancer Res. 22(24): 6088-6098.

4.      F. Dupuy, S. Tabariès, S. Andrzejewski, Z. Dong, J. Blagih, M.G. Annis, A. Omeroglu, D. Gao, S. Leung, E. Amir, M. Clemons, A. Aguilar-Mahecha, M. Basik, E.E. Vincent, J. St.-Pierre, R.G. Jones* and P.M. Siegel*. (2015). PDK1-dependent metabolic reprogramming dictates metastatic potential in breast cancer. Cell Metabolism. 22(4):577-89. *Co-corresponding Authors.

5.      S. Tabariès, V. Ouellet, M.G. Annis, B.E. Hsu, A.A.N. Rose, L. Meunier, Euridice Carmona, C.E. Tam, A-M. Mes-Masson and P.M. Siegel. (2015). Granulocytic immune infiltrates are essential for the efficient formation of breast cancer liver metastases. Breast Cancer Res. 17(1): 45.

PubMed Publications – P. Siegel


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