MultiOmic characteriZation of Acute Myeloid Leukemia Evolving From myelopRoliferative Neoplasm to Identify New Targeted Therapeutic Strategies
- Sponsor
- University Hospital, Angers
- Study ID
- NCT06022341
- Status
- Not Yet Recruiting
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Conditions
- Myeloproliferative Neoplasm
- Secondary Leukemia
Eligibility Criteria
- Sex
- ALL
- Age
- 18 Years - N/A
- Healthy Volunteers
- Not accepted
Interventions
- Multiomic characterization — OTHERMultiomics analysis include targeted-NGS with a 400-genes panel, RNA-seq and methylome. All the genomic libraries will be constructed at the genomic facility of Angers University Hospital and the sequencing will be performed on a NovaSeq6000 in the GenoBIRD Platform in Nantes. Bioinformatic analysis will be performed and will derive for each sample: SNV/Indel and CNV from DNA sequencing, expression of mRNA and lncRNA, genes fusion and splicing events from RNA-seq, and methylation beta-values from methylome.
- In vitro drug screening — OTHERThe drug screening will be performed on the 'NEXT-AML' platform at St-Louis Hospital, Paris. This platform uses a multiparametric screening strategy based on flow cytometry measurements of cell viability, cell differentiation and stem cell compartment. Primary patient cells will be cultured in a specific niche-like medium with amino-acids, cytokines and stromal cells (Dal Bello et al. 2022). Twenty-five drugs at 6 concentrations covering a 1000-fold concentration range will be studied for each sample.
Study Details
Myeloproliferative neoplasms (MPN) are chronic myeloid malignancies characterized by a risk of evolution to acute myeloid leukemia (AML). This unpredictable complication is associated with a grim outcome with median overall survival ranging between 2 to 10 months. To date, even allogeneic transplantation fails to significantly improve the prognosis. Biological and molecular mechanisms driving leukemic transformation are complex, ill-defined, and heterogeneous between patients. The investigator hypothesize that deciphering the molecular heterogeneity of post-MPN AML may lead identifying efficient drugs targeting of the most relevant leukemogenic pathways. Our main objective is to identify new targeted therapeutic approaches in post-MPN AML through in-depth characterization of the dysregulated pathways. The investigator will first characterize in an already annotated cohort of 120 post-MPN AML homogeneous patients subgroups using comprehensive multiomic analyses. Dysregulated pathways will be identified in each subgroup using the omics data and single-cell RNA-sequencing will be performed in a subset of patients in each subgroup. A customised drug-panel will be derived from the dysregulated pathway for an ex vivo drug screening, which will use a flow-cytometry read-out enabling to identity drug effect on cells survival, differentiation, and stemness. The 3 most promising drugs will be validated in a preclinical in vivo model of patient's derived xenograft (PDX) and their impact on clonal architecture will be studied in primary cell cultures using single-cell DNA-sequencing. Overall, this proposal may provide a better understanding of MPN leukemic transformation mechanisms and provide a path for personalized therapies. Our findings may therefore pave the way to drugs development in post-MPN AML that would provide a rationale for implementation of early clinical trials in these dreadful diseases.
Key Dates
- First listed
- Sep 1, 2023
- Start date
- Oct 15, 2023
- Status verified
- Aug 2023
- Primary completion
- Dec 31, 2027
- Completion
- Dec 31, 2028
Study Design
- Enrollment
- 120 participants (estimated)
- Allocation
- NA
- Intervention model
- SINGLE_GROUP
- Primary purpose
- BASIC_SCIENCE
Arms
- Other: Leukemic transformation of myeloproliferative neoplasms120 patients will be studied for : * Multiomic characterization * In vitro drug screening
Primary Outcome Measure
Ward's minimum variance criterion to minimize the intra-cluster variance [ Time Frame: 24 months ]
Central Contacts
- Damien LUQUE PAZ, PharmD. PhD.241355353
- Béatrice GABLE241356825
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