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RASATaC SIGNED

Regulating RAS Activity to Target RAS-Driven Cancers

Total Cost €

EC-Contrib. €

Partnership

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RASATaC project word cloud

Explore the words cloud of the RASATaC project. It provides you a very rough idea of what is the project "RASATaC" about.

poc signalling mutant commercial oncogene standards triggers prove expressed forms drugging ras clinic treatment innovative effort quarter isoforms intensive cog completely erc cancers scaffolding genes truly class cytotoxic made cancer found strategies vivo family protein proteins oncogenes function cell considering moderate exploits successfully bind accordingly death avenues mutated more scaffold explore active mutations therapeutic patients first anti care despite

Project "RASATaC" data sheet

The following table provides information about the project.

Coordinator	TURUN YLIOPISTO Organization address address: YLIOPISTONMAKI city: Turku postcode: 20014 website: www.utu.fi contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	Finland [FI]
Total cost	0 €
EC max contribution	150˙000 € (0%)
Programme	1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
Code Call	ERC-2019-PoC
Funding Scheme	ERC-POC-LS
Starting year	2020
Duration (year-month-day)	from 2020-06-01 to 2021-11-30

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	TURUN YLIOPISTO TURUN YLIOPISTO Organization address address: YLIOPISTONMAKI city: Turku postcode: 20014 website: www.utu.fi contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	FI (Turku)	coordinator	150˙000.00

Map

Project objective

More than a quarter of all cancers are driven by mutations in the RAS family of genes. Considering the key role of these oncogenes, and despite intensive effort, no effective anti-RAS strategies have successfully made it to the clinic. In our ERC-CoG project, we found that a class of scaffold proteins, expressed in cancer, bind to active/mutated forms of RAS proteins to moderate RAS signalling. Accordingly, we find that loss of one of the scaffolding protein isoforms in RAS-mutant cancers triggers cytotoxic signalling, leading to cell death. As such, drugging this scaffold protein could not only i) represent a completely innovative approach to target RAS-driven cancers that exploits the oncogene’s function, but also ii) deliver the first truly effective cancer treatment for patients that do not respond to current standards of care. In this ERC-PoC, we aim to prove that therapeutic targeting of the scaffold protein is effective in vivo, and to explore the commercial avenues to exploit this finding.

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The information about "RASATAC" are provided by the European Opendata Portal: CORDIS opendata.