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Role of RAS mutant subclones in the development of High Hyperdiploid B-ALL

Project description

Understanding the role of RAS-mutated subclones in leukaemia progression

High hyperdiploid acute lymphoblastic leukaemia (HeH ALL) features RAS-mutant subclones that may drive disease progression. While this common childhood ALL subtype has a favourable prognosis, it is prone to relapse. HeH ALL is marked by multiple chromosome gains and RAS mutations, which could be potential therapeutic targets. Supported by the Marie Skłodowska-Curie Actions programme, the RasWayToALL project will analyse the molecular profiles of HeH ALL clones using single-cell multi-omic technologies. It will focus on RAS subclonal alterations and assess their in vivo impact using patient-derived xenograft (PDX) models and RAS-targeting drugs. It aims to identify expression patterns in RAS-mutated subclones that clarify their role in leukaemia progression and their potential as targets for personalised therapy.

Objective

In high hyperdiploid acute lymphoblastic leukemia (HeH ALL), RAS-mutant subclones may represent the “RASwaytoALL”, a critical evolutionary route that fuels leukemic progression. HeH ALL is the most common subtype of childhood ALL. Despite its generally favorable prognosis, it remains a major cause of relapse. Genetically, this leukemia is characterized by the gain of multiple chromosomes (51–68 in total) and an intriguing genetic mystery: single-cell DNA sequencing performed by the host laboratory revealed that all studied HeH ALL patients harbor subclonal mutations in RAS pathway genes, arising from the hyperdiploid clone. The biological and clinical significance of these RAS-mutant subclones remains unknown. I hypothesize that RAS-mutant subclones actively contribute to HeH ALL progression and may represent a therapeutically targetable vulnerability. The project has two main objectives: (i) characterize the molecular profile of HeH ALL clones using single-cell multi-omic technologies, focusing on the function of RAS subclonal alterations (ii) assess the functional impact of RAS subclonal alterations in vivo by establishing patient-derived-xenograft (PDX) models and using RAS targeting drugs. I expect to identify expression patterns in RAS-mutated subclones that explain their role in leukemia progression and demonstrate their potential as targets for personalized therapy. The proposal builds on my expertise in omics data analysis, ALL clinical and genetics, and PDX models, along with the pioneering work of the host lab in single-cell technologies, in vivo modelling, and mechanistic studies of ALL. The host institution offers access to cutting-edge facilities and strong collaborative networks. This project will enhance my experimental skills, consolidating my profile as an independent researcher at the interface of genomics, cancer biology, and translational hematology.

Fields of science (EuroSciVoc)

Keywords

Programme(s)

Topic(s)

Funding Scheme

HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

(opens in new window) HORIZON-MSCA-2025-PF

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Coordinator

VIB VZW
Net EU contribution
€ 200 400,00
Address
SUZANNE TASSIERSTRAAT 1
9052 ZWIJNAARDE - GENT
Belgium
Region
Vlaams Gewest Prov. Oost-Vlaanderen Arr. Gent
Activity type
Research Organisations
Links
Total cost
No data