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ONCOFUM SIGNED

Integrating the tissue-specificity and chronology of hereditary renal cancer predisposition

Total Cost €

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EC-Contrib. €

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Partnership

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 ONCOFUM project word cloud

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

hlrcc    fh    tools    phenotypic    oncofum    experimental    develops    cancers    accumulation    inherit    hydratase    allele    dysregulated    uterus    skin    tissues    initially    insights    contributes    strategies    tricarboxylic    multiple    hardware    models    anticancer    biochemical    cancer    little    appropriate    mechanisms    framework    give    copy    ensuing    perform    deficiency    parallel    permissive    cellular    inactivate    cells    vitro    tumorigenesis    hypothesis    renal    prognostic    hereditary    cycle    tissue    mutations    leads    validated    wt    mitochondria    leiomyomatosis    mutation    patients    survive    generate    tumours    cell    occurs    mouse    drive    die    amongst    metabolic    unparalleled    profound    therapeutic    gives    underpin    generally    elucidate    model    unclear    mutated    wild    carriers    metabolism    vivo    tca    reprogramming    discovery    molecular    predispose    fumarate    characterised    acid    hypothesise    undergo    enzymes    diagnostic   

Project "ONCOFUM" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.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]
 Total cost 1˙998˙698 €
 EC max contribution 1˙998˙698 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-COG
 Funding Scheme ERC-COG
 Starting year 2019
 Duration (year-month-day) from 2019-03-01   to  2024-02-29

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 1˙998˙698.00

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 Project objective

Cancer cells undergo profound metabolic changes. However, little is known about whether and how metabolic changes drive cancer. The discovery that mutations of Tricarboxylic Acid (TCA) cycle enzymes in mitochondria predispose to cancer gives evidence that dysregulated metabolism could drive tumorigenesis. Amongst these, mutations in Fumarate Hydratase (FH) cause Hereditary Leiomyomatosis and Renal Cell Cancer (HLRCC), characterised by tumours of the skin and uterus, and renal cancer. Patients inherit one mutated copy of FH and loss of the wild-type (wt) allele occurs in tumours. Fumarate accumulation is the defining biochemical feature of these tumours. However, the mechanisms by which FH loss and fumarate accumulation lead to these tumours is unclear. In ONCOFUM, I want to elucidate the mechanisms that underpin tissue-specific tumorigenesis in HLRCC. I hypothesise that HLRCC occurs via a two-step process. Initially, loss of the wt allele in carriers of a FH mutation leads to FH deficiency. However, most of these cells die and only cells in tissues with the appropriate metabolic hardware survive. In the second step, FH loss in permissive tissues leads to phenotypic changes that lead to cancer. To assess this hypothesis, we will generate a mouse model where we inactivate FH in multiple tissues and elucidate the ensuing tissue-specific reprogramming. Then, using cellular models, we will investigate the molecular consequences of FH loss. In parallel, we will perform a comprehensive analysis of HLRCC tumours to find diagnostic and prognostic tools, and new anticancer targets, which will be validated in vitro and in vivo. The experimental framework developed in ONCOFUM will give unparalleled molecular insights into how cancer develops in different tissues in response to loss of FH and will lead to new therapeutic strategies for HLRCC, and, more generally for the many other cancers to which metabolic reprogramming contributes.

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