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CrispSCNAs

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Dissecting the Functional and Therapeutic Impact of Somatic Copy Number Alterati...

Dissecting the Functional and Therapeutic Impact of Somatic Copy Number Alterations SCNAs In 1914 Theodor Boveri described abnormal chromosome counts in cancer cells and speculated that these alterations are the driving force of cancer. Almost 100 years later it became clear that somatic copy number alterations (SCNAs)... ver más

31/12/2025

UKHD

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

UNIVERSITATSKLINIKUM HEIDELBERG No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Ver 3 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2020-11-06

ERC-2020-STG: ERC STARTING GRANTS

I+D

Cerrada hace 5 años

0% 100% 100%

Información adicional privada

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

3 Participantes

UKHD

1.40M€ | Lider

CASTELLBLANCH

GERMAN CANCER RESEARCH CENTE...

100.00K€ | Participante

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Duración del proyecto: 61 meses Fecha Inicio: 2020-11-06
Fecha Fin: 2025-12-31

Líder del proyecto

UNIVERSITATSKLINIKUM HEIDELBERG No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto In 1914 Theodor Boveri described abnormal chromosome counts in cancer cells and speculated that these alterations are the driving force of cancer. Almost 100 years later it became clear that somatic copy number alterations (SCNAs) are one of the most striking characteristics of cancer genomes. SCNAs comprise deletions and amplifications of whole chromosome arms and therefore alter the expression patterns of several hundred genes simultaneously. These alterations show defined patterns suggesting selective pressure, and thus likely contain multiple driver genes, which can shape several tumorigenic properties. Therefore, studying how these events contribute to tumor development will be fundamental to understand cancer biology and develop targeted cancer therapies. However, whereas the function of recurrently mutated driver genes can be readily assessed, studying SCNAs remains challenging so far. This project will overcome these limitations by combining our unique ability to model liver cancer in vivo and in vitro with innovative CRISPR-based genomic engineering technologies. First, we will generate large chromosomal deletions in murine livers and human-derived liver organoids by CRISPR technologies and assess their functional role in cancer development. Furthermore, synthetic lethal interactions generated by these deletions will be evaluated on their therapeutic potential. Additionally, driver genes and driver gene-combinations of amplified chromosomal regions will be investigated using a novel CRISPR/Cas9-based mouse model for endogenous gene activation and chromosome engineering. Finally, we will exploit a novel concept for targeting cancer cells with specific amplifications. Our unique approach will for the first time systematically investigate the functional role of SCNAs in tumor pathobiology, identify new therapeutic strategies specifically tailored for individual SCNAs, and will therefore have high impact for future efforts to understand and combat cancer.

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