Stacey obtained both her BSc, Honours (biology) and MSc (cancer genetics) from Queen’s University, and her PhD (molecular cancer biology) from the University of Toronto. After graduate studies, she worked as a scientific advisor in the Intellectual Property (IP) group of a leading Canadian law firm where she gained experience drafting and prosecuting patent applications, focusing on life sciences and biotechnology patent protection. Prior to joining MaRS Innovation in 2009, she worked as IP manager and strategist for a Montreal-based biotechnology startup and also as IP scout/advisor for a Toronto teaching hospital.
Stacey's role at MaRS Innovation includes the development of IP strategy and commercialization plan for projects across a variety of sectors including therapeutics, biotechnology, imaging and healthcare IT.
Industry Expertise (3)
Areas of Expertise (4)
Intellectual Property Strategy
Access to Essential Medicines
Biotechnology Patent Protection
Early Stage Commercialization
National Brain Tumor Foundation Basic Science Award (2003) (professional)
Selected as recipient of the Society for Neuro-Oncology and National Brain Tumor Foundation basic science award for PhD thesis work exploring the interaction between p14ARF tumor suppressor and Transcription Termination Factor-1 (TTF-1).
University of Toronto: Ph.D. , Molecular Biology
Queen's University: M.Sc. , Cancer Genetics
Queen's University : B.Sc., Biology
- Canadian Cancer Society volunteer
- Terry Fox Run volunteer
Media Appearances (1)
"Intellectual property protection is a game small businesses can’t afford to lose"
Financial Post print
Dr. Stacey Ivanchuk, MaRS Innovation's director of intellectual property, was quoted in Denise Deveau's article, "Intellectual property protection is a game small businesses can't afford to lose," for the Financial Post on September 26, 2014 regarding the importance of protecting intellectual property for small businesses.
Event Appearances (5)
Intellectual Property and Commercialization
IP Osgoode Intellectual Property Law and Technology Program York University
Research Commercialization: Primer on Health Technology
cMIP-CREATE Training Program in Molecular Imaging Probes webinar
Introduction to Intellectual Property and Commercialization
St. Michael's Hospital Research Institute Retreat Rama, Ontario
Intellectual Property: What is it and how can you use it to build a business?
8th Connections ECE Graduate Symposium University of Toronto St George Campus
Improving Access to Medicines with a Pharmaceutical Patent Pool: Legal/Business and Antitrust Considerations"
Drug Patents in Canada conference Toronto, Ontario
p14ARF interacts with DAXX: effects on HDM2 and p53Cell Cycle
The p14(ARF) (ARF) tumour suppressor plays an important role in the cellular response to oncogene activation. In this report, we demonstrate an interaction between ARF and DAXX, a highly conserved protein with identified roles in the regulation of gene expression. HDM2 was shown to interact with each of ARF and DAXX upon upregulation of expression as well as at lower expression levels following transfection of ARF and DAXX. Through immunofluorescence analysis, we observed that endogenous ARF and DAXX colocalize both to nucleoli and to nuclear bodies in cell lines that co-express both proteins. Similar results were obtained upon co-transfection of ARF and DAXX. Co-expression of ARF and DAXX was further found to inhibit ARF-mediated HDM2 sumoylation and to induce sumoylation and ubiquitination of DAXX itself, implicating DAXX as a substrate of ARF-mediated post-translational events. We also observed induction of p53 sumoylation in the presence of ARF and DAXX, an effect that was inhibited by upregulation of HDM2 expression. In summary, we have identified DAXX as a novel ARF binding partner and substrate of ARF-mediated sumoylation and suggest that DAXX acts as a modifier of both p53-dependent and p53-independent ARF function.
The cell cycle: accelerators, brakes and checkpointsNeurosurgery
PROLIFERATIVE CUES TRIGGER a complex series of molecular signaling events in cells. Early in the cell cycle, cells are faced with an important decision that affects their fate. They either initiate a round of replication or they withdraw from cell division. Passage through the restriction point, or "point of no return," marks cellular commitment to a new round of division. Genetic mutations that predispose individuals to tumorigenesis often affect pathways that influence cellular proliferation. Many of the mutated genes give rise to molecules that are no longer able to appropriately regulate the mammalian cell cycle; the end result is neoplasia. In this review, the critical elements that permit cell cycle progression and the positive and negative regulators that affect the process are reviewed.
The INK4A/ARF locus: roled in cell cycle control and apoptosis and implications for glioma growthJournal of Neuro-oncology
The unique INK4A/ARF locus at chromosome 9p21 encodes two distinct proteins that intimately link the pRB and p53 tumour suppressor pathways. p16INK4A has been identified as an inhibitor of the cell cycle, capable of inducing arrest in G1 phase. p14/p19ARF on the other hand can induce both G1 and G2 arrest due to its stabilizing effects on the p53 transcription factor. In addition to their roles in growth arrest, both proteins are involved in cellular senescence and apoptosis. The frequent mutation or deletion of INK4A/ARF in human tumours as well as the occurence of tumours in the murine knockout models have identified both p16 and ARF as bona fide tumour suppressors.