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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.

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

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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