Dr. Robert Rottapel
Co-lead, Ovarian Cancer TRI
The Rottapel laboratory uses functional genetic screens (both shRNA and CRISPR/Cas9) to identify novel vulnerabilities in ovarian cancer as a strategy to develop new therapeutic targets. They focus on understanding signal transduction pathways that operate in normal and cancer cells and the regulatory processes that control protein function. The lab is particularly interested in targeting adaptive stress pathways that support the transformed cancer state as a strategy to find new anti-cancer therapies.
Other areas of research pursued in the laboratory focus on signal transduction pathways in the immune system and the study of monogenic human diseases that control inflammation, bone homeostasis and metabolism.
- Co-lead, OICR Ovarian Cancer TRI;
- Senior Scientist and Amgen Chair for Cancer Research, Princess Margaret Cancer Centre;
- Professor, Departments of Medicine, Immunology and Medical Biophysics, University of Toronto;
- Rheumatologist, Department of Medicine, St. Michael’s Hospital, Toronto.
- Cancer functional genetics;
- Synthetic lethal screens;
- Signal transduction;
- Regulation of protein function;
- Ovarian cancer;
- Pancreatic cancer.
Mauricio Medrano, Laudine Communal, Marcin Iwanicki, Joshua Paterson, Kevin Brown, Fabrice Sircoulomb, Paul Krzyzanowski, Josee Normand, Sasha Anita Doodnauth, Marian Novak, Fernando Suarez, Jane Cullis, Benjamin G. Neel, John McPherson, Jason Moffat, Ronny Drapkin, Laurie Ailles, Anne-Marie Mes-Mason, and Robert Rottapel.
Interrogation of functional cell surface markers identifies CD151 dependency in high-grade serous ovarian cancer.
Cell Report, In Press, 2017.
Fine N, Dimitriou ID, Rullo J, Sandí MJ, Petri B, Haitsma J, Ibrahim H, La Rose J, Glogauer M, Kubes P, Cybulsky M, Rottapel R.
GEF-H1 is necessary for neutrophil shear stress-induced migration during inflammation.
J Cell Biol. 2016 Oct 10;215(1):107-119.
Meiri D, Marshall CB, Mokady D, LaRose J, Mullin M, Gingras AC, Ikura M, Rottapel R.
Mechanistic insight into GPCR-mediated activation of the microtubule-associated RhoA exchange factor GEF-H1.
Nat Commun. 2014 Sept 11;5:4857. Doi:10.1038/ncomms5857.
Guettler S, LaRose J, Gish G, Petsalaki E, Scotter A, Pawson T, Rottapel R, Sicheri F.
Structural basis and sequence rules for substrate recognition by Tankyrase explain the basis for cherubism disease.
Cell. 2011; 9; 147(6):1340-54.
Levaot N, Voytyuk O, Dimitriou I, Sircoulomb F, Chandrakumar A, Deckert M, Krzyzanowski PM, Scotter A, Gu S, Janmohamed S, Cong F, Simoncic PD, Ueki Y, La Rose J, Rottapel R.
Loss of Tankyrase-mediated destruction of 3BP2 is the underlying pathogenic mechanism of cherubism.
Cell. 2011; 9:147(6):1324-39.
- Program Director, Innovation in Target Validation, OICR;
- Amgen Chair for Cancer Research, University Health Network.
Opportunities to collaborate
- Target validation in ovarian cancer;
- Development of novel small molecule or antibody based therapeutics;
- Mechanism of transformation underlying ovarian cancer;
- CRISPR/CAS9 functional genetic screens;
- Drug sensitizing screens.
For more information about Dr. Rottapel’s research, please visit The Rottapel Lab.
Donna De Francesco