Dr. Sonia Cellot is an Assistant Professor in the Department of Pediatrics at Université de Montréal and an investigator in the Viral and Immune Disorders and Cancers axis at CHU Sainte-Justine Research Center. She is a clinician-scientist with a BSc in Biochemistry from McGill, an MD from the Université de Montréal, Royal College certification in both Pediatrics and Hematology, and a PhD in Molecular Biology from the Université de Montréal. She has been a pediatric hematologist in the Hematology-Oncology Division of CHU Sainte-Justine since 2009, where she is responsible for the pediatric acute myeloid leukemia (AML) program and is the Assistant Director of the Immune disorders and Cancer research axis at CHU- Sainte-Justine . Clinical duties encompass direct patient care, mainly in the hematopoietic stem cell (HSC) transplantation unit, and diagnostic test development as medical advisor in the molecular biology laboratory. Since 2010, she has been the co-investigator of the pediatric branch of the Quebec Leukemia Cell Bank, in collaboration with Dr Josée Hébert, hematologist at Hôpital Maisonneuve-Rosemont, with the mandate to collect highly annotated pediatric AML and infant leukemia samples to support and promote research projects.

Her research focus is on hematopoietic stem cell (HSC) biology and the development of human synthetic leukemia models to identify therapeutic vulnerabilities in high fatality pediatric leukemia. Long-lived HSC sustain the constant production of all mature cell lineages in the blood system, and constitute the critical cellular component of transplantation procedures performed in oncology for high risk malignancies, including leukemia. Nonetheless, factors that dictate HSC fate remain poorly defined, and their isolation and ex vivo culture remain challenging, limiting their clinical applications. The main focus of the laboratory is to study the role of chromatin methylation in human HSC biology. Accessibility of the transcriptional machinery to the genetic code is mediated through the concerted actions of chromatin modifying enzymes. The Mll (Mixed Lineage Leukemia) gene, encoding for a histone methyltransferase (of lysine 4 on histone 3, or H3K4) is involved in normal HSC maintenance and mutated in >70% of infant leukemia cases. Once thought to be irreversible, histone methylation is now regarded as a highly dynamic process, since the identification of the histone demethylase LSD1 (KDM1A) in 2004. Previous work identified that JARID1B (KDM5B), an eraser of the H3K4 epigenetic mark, regulates the expression of stemness associated genes, and its knockdown leads to HSC expansion in culture. The implication of histone demethylases (HDM) in HSC biology and cancer development is being unraveled, and under active pharmacological investigation.

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