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Boosting metabolism in T cells a tool to improve T cell therapy for chronic lym...

Boosting metabolism in T cells a tool to improve T cell therapy for chronic lymphocytic leukemia patients Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world. Novel targeted drugs are effective, but not curative. Moreover, prolonged use is associated with development of resistance, toxicity, and high ec... see more

31/07/2025

STICHTING AMSTERDA...

2M€

Project Budget: 2M€

Project leader

STICHTING AMSTERDAM UMC No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

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Financing granted El organismo H2020 notifico la concesión del proyecto The day 2025-07-31

ERC-2019-COG: ERC Consolidator Grant Scope:Objectives

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Cerrada does 6 years

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characteristics of the participant

Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

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4 Participantes

STICHTING AMSTERDAM UMC

1.65M€ | Leader

PREMO

196.10K€ | participant

THE CLEVELAND CLINIC FOUNDAT...

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Project duration: 60 months Date Start: 2020-07-15
End date: 2025-07-31

Project leader

STICHTING AMSTERDAM UMC No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 2M€

participation deadline Sin fecha límite de participación.

Project description Chronic lymphocytic leukemia (CLL) is the most common leukemia in the Western world. Novel targeted drugs are effective, but not curative. Moreover, prolonged use is associated with development of resistance, toxicity, and high economic cost. Allogeneic stem cell transplantation, which evokes a T cell mediated response, is potentially curative yet is associated with high graft-vs-host-related mortality. Therefore, an autologous T cell-based approach, e.g. chimeric antigen receptor T cells (CAR-T), is a highly promising strategy. However, in contrast to the success of CAR-T cells in aggressive leukemia, their effect in CLL is limited owing to a largely unexplained acquired T cell dysfunction in this disease setting. I recently found that CLL cells impose a reduction in mitochondrial fitness and altered glucose metabolism on T cells, which may underlie the acquired T cell dysfunction. Lending clinical significance to this finding, I observed that the success of CAR-T treatment in CLL patients is highly associated with their mitochondrial biogenic capacity. I therefore hypothesize that improving mitochondrial fitness of CAR-T cells may offer a path to cure CLL. I aim to: 1. Characterize the molecular mechanisms of metabolic alterations in CLL-derived T cells 2. Elucidate how CLL cells reprogram T cells metabolism 3. Increase mitochondrial biogenesis and fitness in CAR-T cells to improve therapeutic efficacy To achieve these goals, I will conduct an array of complementary molecular, metabolic, and genetic assays using patient samples and a murine model of CLL. To address therapeutic potential I will study murine and human CAR-T cells in which metabolic processes will be manipulated. This project provides crucial insight into the interplay between CLL and T cells, and the underlying failure of cancer immune surveillance. This may lead to metabolism-based curative autologous T cell based therapies in CLL, which may also be relevant for other malignancies.

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