François Mercier

ORCID: 0000-0001-5324-2167
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About
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Research Areas
  • Acute Myeloid Leukemia Research
  • Hematopoietic Stem Cell Transplantation
  • CRISPR and Genetic Engineering
  • Lysosomal Storage Disorders Research
  • Protein Degradation and Inhibitors
  • Immune Cell Function and Interaction
  • Epigenetics and DNA Methylation
  • Immunotherapy and Immune Responses
  • Cancer Genomics and Diagnostics
  • Advanced biosensing and bioanalysis techniques
  • PI3K/AKT/mTOR signaling in cancer
  • Glycosylation and Glycoproteins Research
  • Cancer Cells and Metastasis
  • HIV Research and Treatment
  • RNA modifications and cancer
  • Chronic Lymphocytic Leukemia Research
  • Multiple Myeloma Research and Treatments
  • Cancer, Hypoxia, and Metabolism
  • Monoclonal and Polyclonal Antibodies Research
  • Extracellular vesicles in disease
  • Lymphoma Diagnosis and Treatment
  • Sphingolipid Metabolism and Signaling
  • Carbohydrate Chemistry and Synthesis
  • Immune cells in cancer
  • Myeloproliferative Neoplasms: Diagnosis and Treatment

McGill University
2009-2025

Jewish General Hospital
2009-2025

Université de Montréal
2025

Massachusetts General Hospital
2014-2023

Harvard Stem Cell Institute
2014-2023

Harvard University
2013-2023

Hôpital Maisonneuve-Rosemont
2022

Jewish Hospital
2017

Boston University
2017

Novartis (Switzerland)
2012

While acute myeloid leukemia (AML) comprises many disparate genetic subtypes, one shared hallmark is the arrest of leukemic myeloblasts at an immature and self-renewing stage development. Therapies that overcome differentiation represent a powerful treatment strategy. We leveraged observation majority AML, despite their genetically heterogeneity, share in expression HoxA9, gene normally downregulated during differentiation. Using conditional HoxA9 model system, we performed high-throughput...

10.1016/j.cell.2016.08.057 article EN publisher-specific-oa Cell 2016-09-01

Defining the molecular regulators of hematopoietic stem and progenitor cells (HSPCs) requires in vivo functional analyses. Competitive bone marrow transplants (BMTs) compare control test HSPCs to demonstrate role a genetic change or chemical perturbation. BMT is enabled by antibodies that specifically recognize from congenic mouse strains due variants cell surface protein CD45, designated CD45.1 CD45.2. The current competitor strain, B6.SJL-Ptprc(a) Pepc(b)/BoyJ (CD45.1), has substantial...

10.1016/j.stemcr.2016.04.010 article EN cc-by-nc-nd Stem Cell Reports 2016-05-12

Abstract Acute myeloid leukemia (AML) is a high remission, relapse fatal blood cancer. Although mTORC1 master regulator of cell proliferation and survival, its inhibitors have not performed well as AML treatments. To uncover the dynamics activity in vivo, fluorescent probes are developed to track single proliferation, apoptosis cells bone marrow live animals quantify these activities context microanatomical localization intra-tumoral heterogeneity. When chemotherapy drugs commonly used...

10.1038/s41467-020-20491-8 article EN cc-by Nature Communications 2021-01-11

Abstract Differentiation therapy has proven to be a success story for patients with acute promyelocytic leukemia. However, the remaining subtypes of myeloid leukemia (AML) are treated cytotoxic chemotherapies that have limited efficacy and high likelihood resistance. As differentiation arrest is hallmark AML, there increased interest in developing differentiation-inducing agents enhance disease-free survival. Here, we provide comprehensive review current reports future avenues nucleic acid...

10.1038/s41375-024-02191-0 article EN cc-by Leukemia 2024-02-29

Summary Interleukin (IL)-7 and its receptor (IL-7Rα) play important roles in regulating lymphopoiesis. Previous studies have reported that human immunodeficiency virus-1 (HIV-1) viraemia affects the expression of IL-7Rα, but effects on CD4+ CD8+ T cell memory subsets not been studied. Using eight-colour flow cytometry, we compared immunophenotypic patterns expressing IL-7Rα activation markers, as well circulating IL-7 levels, three well-defined groups HIV-1-infected subjects: successfully...

10.1111/j.1365-2249.2008.03610.x article EN Clinical & Experimental Immunology 2008-02-16

The mTOR pathway is a critical determinant of cell persistence and growth wherein complex 1 (mTORC1) mediates balance between factor stimuli nutrient availability. Amino acids or glucose facilitates mTORC1 activation by inducing RagA GTPase recruitment to the lysosomal outer surface, enabling Ras homolog Rheb. Thereby, alters mTORC1-driven in times abundance scarcity. Here, we have evaluated differential nutrient-sensing dependence through hematopoietic progenitors, which dynamically drive...

10.1172/jci89452 article EN Journal of Clinical Investigation 2017-03-19

Gaucher disease (GD) is a rare autosomal recessive multisystemic lysosomal storage disorder presenting marked phenotypic and genotypic variability. GD caused by deficiency in the glucocerebrosidase enzyme. The diagnosis of remains challenging because large clinical spectrum associated with disease. Moreover, biomarkers are often not sensitive enough can be subject to polymorphic variations. main objective this study was perform metabolomic using an ultra-performance liquid chromatography...

10.3390/ijms21217869 article EN International Journal of Molecular Sciences 2020-10-23

Acute myeloid leukemia (AML) is an aggressive hematological cancer resulting from uncontrolled proliferation of differentiation-blocked cells. Seventy percent AML patients are currently not cured with available treatments, highlighting the need novel therapeutic strategies. A promising target in mammalian rapamycin complex 1 (mTORC1). Clinical inhibition mTORC1 limited by its reactivation through compensatory and regulatory feedback loops. Here, we explored a strategy to curtail these...

10.1186/s13046-022-02542-8 article EN cc-by Journal of Experimental & Clinical Cancer Research 2022-12-09

Pediatric acute megakaryoblastic leukemia (AMKL) is an aggressive blood cancer associated with poor therapeutic response and high mortality. Here we describe the development of CBFA2T3-GLIS2-driven mouse models AMKL that recapitulate phenotypic transcriptional signatures human disease. We show activating Ras mutation occurs in increases penetrance decreases latency CBF2AT3-GLIS2-driven AMKL. CBFA2T3-GLIS2 GLIS2 modulate similar networks. identify dominant oncogenic properties trigger...

10.1016/j.celrep.2023.113084 article EN cc-by-nc-nd Cell Reports 2023-09-01
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