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CDK6-DrugOpp

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CDK6 in transcription turning a foe in a friend

"Translational research aims at applying mechanistic understanding in the development of ""precision medicine"", which depends on precise diagnostic tools and therapeutic approaches. Cancer therapy is experiencing a switch from no... ver más

31/08/2022

VETMEDUNI VIENNA

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

VETERINAERMEDIZINISCHE UNIVERSITAET WIEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

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Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2022-08-31

ERC-ADG-2015: ERC Advanced Grant Scope:Objectives

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Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

Información adicional privada

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2 Participantes

VETMEDUNI VIENNA

2.50M€ | Lider

ALIANET S.L

490.52K€ | Participante

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Duración del proyecto: 72 meses Fecha Inicio: 2016-08-01
Fecha Fin: 2022-08-31

Líder del proyecto

VETERINAERMEDIZINISCHE UNIVERSITAET WIEN 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 "Translational research aims at applying mechanistic understanding in the development of ""precision medicine"", which depends on precise diagnostic tools and therapeutic approaches. Cancer therapy is experiencing a switch from non-specific, cytotoxic agents towards molecularly targeted and rationally designed compounds with the promise of greater efficacy and fewer side effects. The two cell-cycle kinases CDK4 and CDK6 normally facilitate cell-cycle progression but are abnormally activated in certain cancers. CDK6 is up-regulated in hematopoietic malignancies, where it is the predominant cell-cycle kinase. The importance of CDK4/6 for tumor development is underscored by the fact that the US FDA selected inhibitors of the kinase activity of CDK4/6 as ""breakthrough of the year 2013"". Our recent findings suggest that the effects of the inhibitors may be limited as CDK6 is not only involved in cell-cycle progression: ground-breaking research in my group and others has shown that CDK6 is involved in regulation of transcription in a kinase-independent manner thereby driving the proliferation of leukemic stem cells and tumor formation. We have now identified mutations in CDK6 that convert it from a tumor promoter into a tumor suppressor. This unexpected outcome is accompanied by a distinct transcriptional profile. Separating the tumor-promoting from the tumor suppressive functions may open a novel therapeutic avenue for drug development. We aim at understanding which domains and residues of CDK6 are involved in rewiring the transcriptional landscape to pave the way for sophisticated inhibitors. The idea of turning a cancer cell's own most potent weapon against itself is novel and would represent a new paradigm for drug design. Finally, the understanding of CDK6 functions in tumor promotion and maintenance will also result in better patient stratification and improved treatment decisions for a broad spectrum of cancer types. "

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