Grace Egan

At A Glance

• We study the distinct biology of acute myeloid leukemia arising in children and young adults, with a particular focus on how age, developmental context, and genomic architecture shape leukemia biology and treatment response.
• We use functional genomics, bioinformatics, proteomics, and patient-derived leukemia models to identify the molecular pathways that paediatric and young adult AML cells depend on for their growth and survival.
• Our goal is to translate these biological discoveries into new therapeutic strategies and biomarkers that improve treatment for children and young adults with AML.

Short Bio

Dr. Egan is an Assistant Professor at the University of Toronto and a clinician-scientist and staff oncologist at The Hospital for Sick Children. She completed medical school at the University of Limerick in Ireland, followed by paediatric residency at New York University and a clinical fellowship in paediatric haematology/oncology at The Hospital for Sick Children in Toronto. She subsequently completed her PhD at the University of Toronto. Her research uses genomic and bioinformatic approaches to identify and therapeutically target the proteins and pathways driving paediatric, adolescent, and young adult AML.

Research Synopsis

Acute myeloid leukemia occurs throughout the lifespan, but the biological features of the disease differ considerably with age. AML arising in infants, children and adolescents is frequently driven by fusion oncogenes and develops within a distinct developmental hematopoietic context. In contrast, AML in older adults more commonly develops through the progressive accumulation of somatic mutations. Despite these differences, most therapeutic strategies have historically been developed through the study of adult AML.

Our laboratory aims to understand how the distinct developmental and molecular biology of paediatric and adolescent/young adult AML creates therapeutic vulnerabilities. A central focus of our research is nucleocytoplasmic transport, the tightly regulated movement of proteins and RNA between the nucleus and cytoplasm. We investigate how dysregulated nuclear transport intersects with ribosome biogenesis and DNA repair to support leukemia growth, survival, and treatment resistance. We are particularly interested in these pathways because our work suggests that aspects of these pathways are upregulated in younger patients and may represent targetable dependencies. Given the molecular heterogeneity of paediatric/AYA AML, we aim to distinguish pathways that are broadly shared across the disease from those that are specific to particular genomic subtypes, with the ultimate goal of developing more effective and biologically informed therapies.

We combine transcriptomic analyses of large patient datasets with functional genomics, patient-derived samples, and preclinical leukemia models. Our goal is to translate the distinct biology of paediatric and AYA AML into biomarkers and therapeutic strategies that improve outcomes for patients with AML.

Recent Publications

1. Egan G, Tasian SK. Precision Medicine for High-Risk Gene Fusions in Pediatric AML: a focus on KMT2A, NUP98, and GLIS2 Rearrangements. Blood, doi: 10.1182/blood.2024026598. 
2. Egan G, Tasian SK. Relapsed pediatric acute myeloid leukaemia: state-of-the-art in 2023.  Haematologica, 108(9): 2275-2288
3. Egan G, Schimmer AD. Contribution of metabolic abnormalities to acute myeloid leukemia pathogenesis. Trends Cell Biol, 33(6):455-462 (2022).
4. Thomas GE*, Egan G*, Garcia-Prat L, Botham A, Voisin V, Patel PS, Chin J, Nachmias B, Kaufmann KB, Khan DH, Hurren R, MacLean N, Wang X, Gronda M, Singh RP, Hoff FW, Harding SM, Raught B, Arruda A, Minden M, Bader GD, Hakem R, Kornblau S, Dick JE, Schimmer AD. The metabolic enzyme Hexokinase 2 localizes to the nucleus in AML and normal hematopoietic stem/progenitor cells to maintain stemness. Nature Cell Biology, 24(6): 872-884 (2022). *Contributed equally.   
5. Egan G, Khan DH, Lee JB, Mirali S, Zhang L, Schimmer AD. Mitochondrial and metabolic pathways regulate nuclear gene expression to control differentiation, stem cell function, and immune response in leukemia. Cancer Discov, 11(5): 1052-1066 (2021).  
6. Egan G, Chopra Y, Mourad S, Chiang KY, Hitzler J. Treatment of acute myeloid leukemia in children – a practical perspective. Pediatric Blood & Cancer, 68(7):e28979 (2021).

See a full list of Dr Egan’s publications

Graduate Students

TBD