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CYNAMIS

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Clonal dynamics and mitochondrial dysfunction in hematopoiesis following chemoth...

Clonal dynamics and mitochondrial dysfunction in hematopoiesis following chemotherapy Chemotherapy can cause significant damage to healthy tissues, especially in the hematopoietic system. As a result, cancer survivors may experience bone marrow damage manifested as cytopenias, which increase the risk of infections... ver más

30/11/2026

CHARITE UNIVERSIT...

190K€

Presupuesto del proyecto: 190K€

Líder del proyecto

CHARITE UNIVERSITAETSMEDIZIN BERLIN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2024-04-12

HORIZON-MSCA-2023-PF-01-01: MSCA Postdoctoral Fellowships 2023 ExpectedOutcome:Project results are expected to contribute to the following outcomes:

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No hay información privada compartida para este proyecto. Habla con el coordinador.

1 Participantes

CHARITE UNIVERSITAETSMEDIZI...

189.69K€ | Lider

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Duración del proyecto: 31 meses Fecha Inicio: 2024-04-12
Fecha Fin: 2026-11-30

Líder del proyecto

CHARITE UNIVERSITAETSMEDIZIN BERLIN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 190K€

Descripción del proyecto Chemotherapy can cause significant damage to healthy tissues, especially in the hematopoietic system. As a result, cancer survivors may experience bone marrow damage manifested as cytopenias, which increase the risk of infections and bleeding. Despite this, there has not been a thorough examination of these events, including the clonal dynamics of hematopoiesis after chemotherapy exposure, due to a lack of methodologies to perform lineage tracing in humans in vivo. To address this, I will study the effects of chemotherapy on the clonal dynamics of hematopoiesis, mitochondrial dysfunction and genetic integrity in young cancer survivors. I will analyze samples obtained before, during, and after treatment using emerging single-cell multi-omic approaches to effectively capture mitochondrial DNA (mtDNA) genetic variation for inferences of clonal dynamics and studies of mtDNA damage. By combining mtDNA-based clonal inferences with whole-genome sequencing (WGS)-based detection of somatic nuclear DNA mutations, I will provide deep phylogenies with scalable single-cell resolved clonal measurements of perturbed hematopoiesis following chemotherapy. Moreover, orthogonal analysis of DNA methylation and chromatin accessibility data will yield new molecular insights into chemotherapy-induced accelerated aging and mitochondrial dysfunction (a hallmark of aging). This project sets out to gain quantitative and fundamental insights into the long-term molecular defects of chemotherapy in young cancer survivors, potentially paving the way for new interventions to improve the quality of life of this emergent population.

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