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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... ver más

31/07/2025

STICHTING AMSTERDA...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

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

TRL 4-5

Ver 4 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2020-07-15

ERC-2019-COG: ERC Consolidator Grant

I+D

Cerrada hace 5 años

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4 Participantes

STICHTING AMSTERDAM UMC

1.65M€ | Lider

PREMO

196.10K€ | Participante

THE CLEVELAND CLINIC FOUNDAT...

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Duración del proyecto: 60 meses Fecha Inicio: 2020-07-15
Fecha Fin: 2025-07-31

Líder del proyecto

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

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto 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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