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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.

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

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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