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Stem cell dysfunction and secondary AML
Jean Soulier
Team leader
Research themes
Clonal evolution in bone marrow failure syndrome as Fanconi anemia can result into ‘adaptive’ somatic genetic rescue, rescuing the HSC defect, or into ‘maladaptive’ evolution towards acute myeloid leukemia.
We profile patient samples at the single cell level and model bone marrow evolution using in vitro and mice experimental systems.
The adaptive or maladaptive deregulated pathways involve DNA damage response, inflammation, stem cell homeostasis and myeloid oncogenes.
Data inform on the BM dysfunction and pathway to sAML, with insights for patients staging and follow up.
Research areas
AML and MDS predisposition
Somatic genetic rescue in bone marrow failure
Featured research projects
Pathogenesis of secondary leukemias
Adaptive somatic genetic rescue in Fanconi anemia
Team members
Jean SOULIERPU-PH, UPC and APHPLise LARCHERPharD, doctorante Inserm FRMMarie DE TERSANTMD, doctorante PA InsermChristophe ANTONIEWSKIDR2, CNRS – GenomicsClaude GAZINCRCN, CNRSLoïc MAILLARDPhD, IR, CNRSLucie HERNANDEZAI, UPCVesnie ETIENNEIE, UPC – AnimalsNadia VASQUEZPhD, IG APHP, CRMR AplasieMélanie DA COSTAIG APHP, CRMR AplasieScientific publications
A clickable melphalan for monitoring DNA interstrand crosslink accumulation and detecting ICL repair defects in Fanconi anemia patient cells
Berrada et al, Nucleic Acids Res., 2023Lire la publication
Clonal hematopoiesis driven by chromosome 1q/MDM4 trisomy defines a canonical route toward leukemia in Fanconi anemia
Sébert et al, Cell Stem Cell, 2023Lire la publicationFunding
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