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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.

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

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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