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TENSION

Financiado

Targeting replication stress recovery pathways in oncology

Genomic instability characterizes tumors, which have no clear ‘oncogenic-driver’ mutation, including triple-negative breast cancers (TNBCs). These patients do not benefit from molecularly targeted treatment and urgently need bette... ver más

31/07/2021

UNIVERSITAIR MEDIS...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

ACADEMISCH ZIEKENHUIS GRONINGEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 2 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-07-31

Línea de financiación objetivo El proyecto se financió a través de la siguiente ayuda:

ERC-CoG-2015: ERC Consolidator Grant

I+D

Cerrada hace 9 años

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2 Participantes

UNIVERSITAIR MEDISCH CENTRUM...

1.97M€ | Lider

HYDRA POWER SL

574.73K€ | Participante

Últimas noticias

30-11-2024: Cataluña Gestión For... Se ha cerrado la línea de ayuda pública: Gestión Forestal Sostenible para Inversiones Forestales Productivas para el organismo:

29-11-2024: IDAE En las últimas 48 horas el Organismo IDAE ha otorgado 4 concesiones

29-11-2024: ECE En las últimas 48 horas el Organismo ECE ha otorgado 2 concesiones

Duración del proyecto: 60 meses Fecha Inicio: 2016-07-01
Fecha Fin: 2021-07-31

Líder del proyecto

ACADEMISCH ZIEKENHUIS GRONINGEN

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Genomic instability characterizes tumors, which have no clear ‘oncogenic-driver’ mutation, including triple-negative breast cancers (TNBCs). These patients do not benefit from molecularly targeted treatment and urgently need better treatment options. Increasing evidence points to replication stress as the driver of genomic instability. Since replication stress compromises cell viability, cells have evolved mechanisms to mitigate this threat. Recently, I discovered a novel cellular mechanism—mitotic Replication Stress Recovery (RSR)—that acts as an ‘emergency brake’ during mitosis, allowing recovery from high levels of replication stress. This machinery is critical for tumor cell survival, and therefore constitutes a promising target for anti-cancer drug development. However, it is unclear how this mitotic RSR is organized molecularly and how it can be targeted therapeutically. In this project, I aim to molecularly define and therapeutically target the Mitotic Replication Stress Recovery (RSR) machinery in triple-negative breast cancer cells. To this end, I will implement a series of complementary innovative strategies. First, I will use mass-spec-based proteomics to molecularly characterize components and wiring of the mitotic RSR machinery. Second, to identify the genetic profiles of cancer subgroups that are sensitive to inactivation of the mitotic RSR, functional genetic screens will be combined with visualization and quantification of replication stress in genomically-defined human cancer samples. Finally, my findings will be translated to the pre-clinical situation by exploring the feasibility of therapeutic inactivation of the RSR machinery in vitro and in vivo in a panel of triple-negative breast cancer models. In summary, TENSION will provide advanced insight into the composition and wiring of the mitotic RSR machinery and will reveal the potency of targeting this pathway therapeutically for TNBCs and other hard-to-treat, genomically instable cancers.

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