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SEE-MAGIC

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Giant-leaps during tumorigenesis: Dissecting saltatory evolution in cancer ‘in t...

Giant-leaps during tumorigenesis: Dissecting saltatory evolution in cancer ‘in the making’ Tumorigenesis is an evolutionary process driven by gradual mutation acquisition to confer selective advantages to somatic cells. DNA rearrangements are the most common cancer driver mutation, outnumbering base substitutions. Rearr... ver más

31/03/2029

EMBL

3M€

Presupuesto del proyecto: 3M€

Líder del proyecto

EUROPEAN MOLECULAR BIOLOGY LABORATORY No se ha especificado una descripción o un objeto social para esta compañía.

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-10-13

ERC-2022-ADG: ERC ADVANCED GRANTS Scope:Objectives

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Cerrada hace 2 años

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

1 Participantes

EMBL

3.43M€ | Lider

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Duración del proyecto: 65 meses Fecha Inicio: 2023-10-13
Fecha Fin: 2029-03-31

Líder del proyecto

EUROPEAN MOLECULAR BIOLOGY LABORATORY No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 3M€

Descripción del proyecto Tumorigenesis is an evolutionary process driven by gradual mutation acquisition to confer selective advantages to somatic cells. DNA rearrangements are the most common cancer driver mutation, outnumbering base substitutions. Rearrangements amplify, disrupt and fuse genes or alter their gene regulation, ultimately driving adaptive changes to initiate cancer, metastasis and therapy resistance. Cancer genomics has revealed that most of these alterations arise as complex genomic rearrangements (CGRs), where a multitude of changes arise in a short time. While in most cases deleterious to the cell, in rare cases CGRs confer an adaptive malignant phenotype in one giant-leap through saltatory evolution events (SEEs) – reminiscent of the hopeful monsters theorised by Goldschmidt. Given their potential to overcome strong selective barriers, it has been proposed that SEEs draw the line between benign lesions and lethal cancer, and understanding their mechanisms is thus fundamental to tumour biology. However, the identity of cells undergoing SEEs has remained elusive, with cancer genomics studies focusing typically on long-established cancers rather than early or even initiating cancer cells. Intriguingly, CGRs are largely explained by cascades of atypical cell nuclei (i.e., nuclear atypias) fueling rearrangement formation, providing an opportunity to study SEEs. Building a novel automated AI-driven framework that couples imaging and single-cell multi-omics, we will leverage nuclear atypias as a phenotypic indicator to dissect principles and mechanisms of SEEs ‘in the making’, and advance fundamental cancer biology. Using highly controllable cell lines and organoid models of colorectal cancer (CrC), a tumour thought to be driven by SEEs, we will unravel pathways, genetic contexts and chromosome-level constraints determining SEEs. Finally, via validation in patient samples we will pave the way to determining SEEs in future clinical studies to advance precision oncology.

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