Impact of genetic alterations on acute leukemia development
of our research axis
Acute leukemia are cancers of the bone marrow associated with a poor prognosis, mainly sporadic, very rarely some of them having a genetic origin. The development of these cancers results from successive acquisition of mutations (generally between 1 and 5).
We are analyzing the biological mechanisms by which mutations in hematopoietic key genes (mainly PAX5 in B differentiation, GATA2 in myeloid differentiation and USP7 and CHK1 in cell cycle) reprogram normal progenitors to establish a pre-leukemic state and initiate leukemic transformation. Our team uses a multidisciplinary approach on patient samples and mouse models, using CRISPR-Cas9 mutagenesis, ex vivo and in vivo functional assays, flow cytometry, transcriptome and mutation analysis (by next generation sequencing) and high throughput drug screening.
This combined approach allows us to study normal hematopoietic development and the biology of hematopoietic stem cells as well as the oncogenic reprogramming and oncogenic process induced by genomic mutations.
This work is thus part of a fundamental and translational research, with the perspective of identifying new therapeutic agents improving the treatment of acute leukemia, in particular the targeting of leukemic stem cells.
Hematopoietic Transcription factors
Cell cycle actors
Somatic and Germline mutations
Acute Myeloid and B-cell Leukaemia (AML and B-ALL)
Myelodysplastic syndromes (MDS)
National registry of patients
Study of germline alterations of transcription factors in acute leukemia
Genomic analysis of acute leukemia
Functions of CHK1 kinase and USP7 deubiquitinylase in normal and leukemic hematopoiesis.
Characterization and targeting of pre-leukemic stem cells from B-acute lymphoblastic leukemia
Leukemic development of hemopathies with germline alterations of GATA2
partnerships & Funding
Centre de Recherches en Cancérologie de Toulouse (Oncopole)
Toulouse – FR
05 82 74 15 75
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