Fabien Boudia
- Acute Myeloid Leukemia Research
- Protein Degradation and Inhibitors
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Chronic Myeloid Leukemia Treatments
- Renal and related cancers
- Cancer Genomics and Diagnostics
- Prenatal Screening and Diagnostics
- Ubiquitin and proteasome pathways
- Advanced biosensing and bioanalysis techniques
- Pluripotent Stem Cells Research
- Chronic Lymphocytic Leukemia Research
- Cell death mechanisms and regulation
- Lymphoma Diagnosis and Treatment
- Genomics and Chromatin Dynamics
- Pancreatic and Hepatic Oncology Research
Inserm
2019-2024
Université Paris-Saclay
2020-2024
Institut Gustave Roussy
2019-2024
La Ligue Contre le Cancer
2019-2022
Délégation Paris 7
2019
Université Paris Cité
2019
Fusion oncogenes are prevalent in several pediatric cancers, yet little is known about the specific associations between age and phenotype. We observed that fusion oncogenes, such as ETO2-GLIS2, associated with acute megakaryoblastic or other myeloid leukemia subtypes an age-dependent manner. Analysis of a novel inducible transgenic mouse model showed ETO2-GLIS2 expression fetal hematopoietic stem cells induced rapid whereas adult bone marrow resulted shift toward transformation strikingly...
Acute megakaryoblastic leukemia of Down syndrome (DS-AMKL) is a model clonal evolution from preleukemic transient myeloproliferative disorder requiring both trisomy 21 (T21) and GATA1s mutation to driven by additional driver mutations. We modeled the megakaryocyte differentiation defect through stepwise gene editing GATA1s, SMC3+/–, MPLW515K, providing 20 different T21 or disomy (D21) induced pluripotent stem cell (iPSC) clones. profoundly reshaped iPSC-derived hematopoietic architecture...
Supplemental Digital Content is available in the text
Several fusion oncogenes showing a higher incidence in pediatric acute myeloid leukemia (AML) are associated with heterogeneous megakaryoblastic and other features. Here we addressed how developmental mechanisms influence human leukemogenesis by ETO2::GLIS2, dismal prognosis.
<div>Abstract<p>Fusion oncogenes are prevalent in several pediatric cancers, yet little is known about the specific associations between age and phenotype. We observed that fusion oncogenes, such as <i>ETO2–GLIS2</i>, associated with acute megakaryoblastic or other myeloid leukemia subtypes an age-dependent manner. Analysis of a novel inducible transgenic mouse model showed <i>ETO2–GLIS2</i> expression fetal hematopoietic stem cells induced rapid whereas...
<p>Supplementary Figures and Legends</p>
<p>Supplementary Figures and Legends</p>
<div>Abstract<p>Fusion oncogenes are prevalent in several pediatric cancers, yet little is known about the specific associations between age and phenotype. We observed that fusion oncogenes, such as <i>ETO2–GLIS2</i>, associated with acute megakaryoblastic or other myeloid leukemia subtypes an age-dependent manner. Analysis of a novel inducible transgenic mouse model showed <i>ETO2–GLIS2</i> expression fetal hematopoietic stem cells induced rapid whereas...