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What doesn’t kill you: primed and adaptive mechanisms of treatment resistance in...

What doesn’t kill you: primed and adaptive mechanisms of treatment resistance in ovarian cancer Cancer therapy resistance is a complex, dynamic process. Pre-existing heterogeneity in cell states provides substance for evolutionary selection, and their plasticity enables adaptation during the therapy. Recently, we discovered... ver más

31/03/2029

HELSINGIN YLIOPIST...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

HELSINGIN YLIOPISTO 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 2024-02-12

ERC-2023-COG: ERC CONSOLIDATOR GRANTS Scope:Objectives

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Cerrada hace 1 año

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1 Participantes

HELSINGIN YLIOPISTO

2.00M€ | Lider

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Duración del proyecto: 61 meses Fecha Inicio: 2024-02-12
Fecha Fin: 2029-03-31

Líder del proyecto

HELSINGIN YLIOPISTO No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Cancer therapy resistance is a complex, dynamic process. Pre-existing heterogeneity in cell states provides substance for evolutionary selection, and their plasticity enables adaptation during the therapy. Recently, we discovered a stress-related, immunocompromised cell state underpinning both intrinsic and adaptive resistance in high-grade serous ovarian cancer (HGSC) metastatic tumours, suggesting that pre-existing stress improves the resilience of cancer cells during neoadjuvant chemotherapy. To unveil how past stress responses prime cancer cells’ adaptation during therapies, I suggest a novel approach that combines dynamic stress recording with the identification of pre-existing resistant states via my novel methodology, ReSisTrace. We will apply this ground-breaking approach in patient-derived organoids to reveal how past stress signalling of a single cell is reflected in its adaptive stress responses and survival upon chemotherapy or cytotoxic immune attack. We will further characterise subclonal and spatial enrichment of the identified resistant phenotypes in longitudinal clinical specimens to incorporate the effect of tumour microenvironment in discovered mechanisms. Importantly, simultaneous characterisation of primed and adaptive resistance enables us to overcome both of them by a sequential combination of drugs where the first will drive cells to identified sensitive states prior the treatment, and the second will block identified adaptive responses during the treatment. After finding the most effective pre-sensitisers and anti-adaptive drugs in the organoids, we will validate most promising combinations in patient-derived xenograft models to pave the way for clinical translation. By targeting both pre-existing cell states and their plasticity, my novel approach will lead to a paradigm shift by providing novel, sequential therapeutic strategies to mutually overcome intrinsic and adaptive resistance in the treatment of cancer.

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