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META2 SIGNED

METAbolism of bone METAstasis (META2): Metabolic interactions between disseminated breast cancer cells and osteoblast lineage cells drive bone metastases formation

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 META2 project word cloud

Explore the words cloud of the META2 project. It provides you a very rough idea of what is the project "META2" about.

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Project "META2" data sheet

The following table provides information about the project.

Coordinator
KATHOLIEKE UNIVERSITEIT LEUVEN 

Organization address
address: OUDE MARKT 13
city: LEUVEN
postcode: 3000
website: www.kuleuven.be

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 Belgium [BE]
 Total cost 178˙320 €
 EC max contribution 178˙320 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-06-01   to  2021-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KATHOLIEKE UNIVERSITEIT LEUVEN BE (LEUVEN) coordinator 178˙320.00

Map

Leaflet | Map data © OpenStreetMap contributors, CC-BY-SA, Imagery © Mapbox

 Project objective

Triple negative breast cancer cells (TNBC) metastasize to the bone, resulting in progressive bone destruction and severe complications for the patient. TNBC colonize the bone already much earlier, but they often stay dormant for several years and remain undetectable. Recent studies showed that at this early stage, TNBC cells are in close proximity to bone-forming cells (osteoblasts), and this interaction promotes TNBC survival and proliferation. Interestingly, recent findings also indicate that the metabolism of tumor cells not only drives primary tumor growth, but also determines which cells will metastasize to lung or liver, indicating metabolic interactions of TNBC with their microenvironment. This concept may also apply to TNBC in bone, but insight in the metabolism of TNBC colonizing the bone is lacking. I hypothesize that to survive and thrive in the bone TNBC cells rely on a specific profile that is complementary in nutrient needs to osteoblasts. Accordingly, preliminary results of the lab showed that targeting glutamine pathway impaired bone metastasis formation. Thus, my objective is to characterize the metabolism of TNBC in bone at early time points and to validate that targeting this metabolism will limit or prevent bone metastasis. I will first perform metabolite dosage and transcriptomics on TNBC recovered at early stages of preclinical (mouse) models of bone metastasis. In parallel, I will decipher metabolic interactions in vitro between osteoblasts and TNBC using metabolomics. These two complimentary approaches will deliver fundamental insights into metabolic adaptations of TNBC during bone metastasis, and identification of the most interesting enzymes to target. I will then validate these targets through functional studies in preclinical models and analysis of expression levels in patient tumor samples. This better understanding of the metabolism of TNBC in the bone is essential for the development of new diagnostic tools and therapeutic targets.

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The information about "META2" are provided by the European Opendata Portal: CORDIS opendata.

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