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Single cell tracking of malignant transformation in GATA2 deficiency

Project description

Insights into the complexity of GATA2 deficiency

GATA2 is a transcription factor with a key role in haematopoietic development. Mutations in the GATA2 gene affect haematopoietic progenitor cells and may lead to bone marrow failure and an increased risk of leukaemia. The EU-funded scGATA2track project is investigating the phenotype variability of families with GATA2 deficiency. The main aim will be to decipher the genetic and epigenetic mechanisms at single cell level to determine the key players of progressive disease. Results will assist early detection of leukaemia and lead to the design of novel personalised therapeutic strategies.

Objective

Precision medicine has improved overall survival of cancer patients; unfortunately, not all diseases can benefit from this practice due to a scarce understanding of their molecular mechanisms. This is the case of GATA2 deficiency, a complex multi-system disorder characterized by bone marrow failure, immunodeficiency and high risk to develop myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Chemotherapy and allogenic hematopoietic stem cell (HSC) transplantation are the only available treatments, underlining the lack of predictive tools as a clear medical need.
Penetrance and expressivity within GATA2 families is often variable, suggesting that cooperating somatic mutations and epigenetic events are required to trigger the disease. Here I propose to unravel the molecular mechanisms of malignant progression of GATA2 deficiency by combining single cell multi-OMICs approaches with groundbreaking functional assays in human induced pluripotent stem cells (hiPSCs).
First, to identify pathogenic single nucleotide variations and small insertion-deletions, I will perform an integrative analysis combining whole exome sequencing with whole-genome bisulfite sequencing to analyze the methylation status genome wide on 15 well-annotated GATA2 carriers.
Then, I will model the stepwise progression of normal cells to MDS through the sequential introduction of recurrent GATA2 mutations and known second driver mutations in hiPSCs by CRISPR/Cas9 genome editing. The hiPSC-derived hematopoietic progenitors will be used for simultaneous profiling of transcriptome and chromatin accessibility at single cell resolution to decipher the underlying gene regulatory networks among the different genetic backgrounds.
A thorough understanding of the genetic and epigenetic features of GATA2 carriers and the transcriptional dynamics during cancer initiation/progression will provide valuable insight into early detection and the design of novel personalized therapeutic strategies.

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MSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)

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(opens in new window) H2020-MSCA-IF-2020

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Coordinator

FUNDACIO INSTITUT D'INVESTIGACIO BIOMEDICA DE BELLVITGE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 160 932,48
Address
AVENIDA GRAN VIA HOSPITALET 199-203
08908 L'Hospitalet De Llobregat
Spain

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Region
Este Cataluña Barcelona
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Research Organisations
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 160 932,48
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