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IVORIaN

RAS/C-RAF interaction: A new pharmacological target in Kras-driven lung cancer.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 IVORIaN project word cloud

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

krasg12c    function    oncogenic    loop    approximately    crosstalk    25    consists    mapk    inhibitors    mice    model    maintenance    technologies    activating    gene    demonstrates    reducing    relevance    binding    tumourigenesis    reactivating    domain    lung    detrimental    kinase    allosteric    tumour    strategies    normal    flipo    host    lsl    insights    advantage    frequent    kras    cancer    outcome    disrupt    cascade    groups    ago    actually    requirement    conditionally    clinical    harbour    innovative    inhibition    ras    inhibited    trying    effector    cells    surprisingly    erk    p53    molecules    regardless    tumours    treatment    cre    frt    unfortunately    proteins    druggable    patients    subtype    physiology    krasg12d    loxp    interaction    small    mutations    investigations    mouse    question    mek    therapy    moment    progressed    adenocarcinoma    interacts    rbd    resistance    emerged    signalling    vivo    raf    inducing    kinases    feedback   

Project "IVORIaN" data sheet

The following table provides information about the project.

Coordinator
THE FRANCIS CRICK INSTITUTE LIMITED 

Organization address
address: 1 MIDLAND ROAD
city: LONDON
postcode: NW1 1AT
website: www.crick.ac.uk

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 United Kingdom [UK]
 Project website https://www.crick.ac.uk/research/labs/julian-downward
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-06-01   to  2019-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE FRANCIS CRICK INSTITUTE LIMITED UK (LONDON) coordinator 183˙454.00

Map

 Project objective

Lung adenocarcinoma is the most frequent subtype of lung cancer and patients harbour activating mutations in the KRAS gene in approximately 25% of the cases. Unfortunately, regardless of the outcome of recent studies identifying specific KRASG12C inhibitors, so far, oncogenic KRAS is not a druggable target yet. The best-characterized KRAS effector pathway, the ERK cascade consists of RAF, MEK and ERK proteins that can be inhibited with small molecules targeting their kinase activities. As the development of RAF and MEK kinases inhibitors progressed, feedback loop reactivating the ERK cascade have emerged, inducing resistance to treatment. Thus, new innovative strategies are needed to achieve a more long-term inhibition of this signalling pathway, while reducing detrimental side effects due to MAPK inhibition in normal cells. It has been described more than 20 years ago that RAF directly interacts with RAS through its Ras Binding Domain (RBD), and many research groups have been trying to disrupt this interaction developing allosteric inhibitors as a cancer therapy. At the moment, those molecules need to be improved in order to achieve a strong inhibition of this pathway. Surprisingly, no mouse model actually demonstrates the requirement of RAS/RAF interaction during KRAS-induced lung tumourigenesis. Here, we propose to investigate this crucial question using a new mouse model allowing us to conditionally disrupt RAS/RAF interaction in vivo. Using the leading mouse model to study lung cancer (LSL-KrasG12D/; p53-/- mice), we will take advantage of both Cre/LoxP and FLIPo/Frt technologies to investigate the role of RAS/RAF interaction during lung tumours maintenance, as well as its function in tumour/host crosstalk and normal physiology. All together, these investigations will provide important insights into the clinical relevance of developing RAS interaction inhibitors for the treatment of RAS-driven tumours.

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