Regulating RAS Activity to Target RAS-Driven Cancers

Informacje na temat projektu

RASATaC

Identyfikator umowy o grant: 899155

DOI

10.3030/899155

Projekt został zamknięty

Data podpisania przez KE 19 Marca 2020

Data rozpoczęcia 1 Września 2020

Data zakończenia 28 Lutego 2022

Finansowanie w ramach

• EXCELLENT SCIENCE - European Research Council (ERC)

Koszt całkowity

Brak danych

Wkład UE

€ 150 000,00

Koordynowany przez

TURUN YLIOPISTO
Finland

Periodic Reporting for period 1 - RASATaC (Regulating RAS Activity to Target RAS-Driven Cancers)

Okres sprawozdawczy: 2020-09-01 do 2022-02-28

Podsumowanie kontekstu i ogólnych celów projektu

More than a quarter of all cancers exist because of mutations in the RAS family of genes. Considering the pivotal role of these oncogenes, and despite intensive efforts, no effective pan-RAS therapies have successfully made it to the clinic. Notably, these efforts have mainly focused on switching off the activity of specific RAS mutants.

In our previous ERC-funded project, we discovered that a class of neuronal proteins, called SHANKs, is present in RAS-driven cancers. The SHANK3 family member binds to active/mutant RAS proteins and dampens RAS function. In our RASATaC ERC-PoC, we investigated if targeting SHANK3 could be an effective therapy in RAS-driven cancers. We developed several approaches to monitor the effect of SHANK3 loss on RAS activity and signalling. We found a significant impact on the size of RAS-driven tumours in animals when SHANK3 was lost compared to untreated tumours. Based on our data, we have now established several avenues and collaboration with industry to find drugs to target SHANK3 and to battle RAS-driven cancers.