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Dietary Influences on Metastasis: How, When, and Why

Total Cost €


EC-Contrib. €






 LIPOMET project word cloud

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

carcinomas    levels    geographical    signature    almost    attach    therapeutic    anti    fatty    answer    dietary    effect    models    cell    integrative    metabolism    prolonged    exclusive    epigenetic    cd36    exploring    acid    cancer    unmet    consumption    diet    generate    link    causes    influence    fundamental    located    cells    metabolic    express    preclinical    quantities    medical    channel    predisposition    single    metastasis    mechanisms    metastases    transplanted    vivo    2017    mics    fat    breast    metastatic    sites    exquisitely    types    position    patientderived    sensitive    patients    computational    behavior    cellular    proteomics    lipid    tumor    functional    melanoma    nature    molecular    initiating    intriguingly    circulation    questions    inhibition    completely    location    western    influenced    oral    acids    3d    tumors    tackle    risk    diets    metabolomics    abolishes    underlying    transcriptomic    insights    lipids    quantitative    genetic    revert    combine    expand    deaths   

Project "LIPOMET" data sheet

The following table provides information about the project.


Organization address
postcode: 8028

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 Spain [ES]
 Total cost 2˙370˙625 €
 EC max contribution 2˙370˙625 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-ADG
 Funding Scheme ERC-ADG
 Starting year 2018
 Duration (year-month-day) from 2018-08-01   to  2023-07-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

We have recently identified metastasis-initiating cells (MICs) in several types of tumors (Nature, 2017)1. Intriguingly, MICs: (i) are exclusive in their ability to generate metastases when transplanted; (ii) express the fatty acid channel CD36 and have a unique lipid metabolic signature; (iii) are exquisitely sensitive to the levels of fat in circulation, thus providing a link between the predisposition of metastasis and dietary fat; (iv) are highly sensitive to CD36 inhibition, which almost completely abolishes their metastatic potential.

We still do not know how MICs promote metastasis or how MICs are influenced by dietary fat. In particular: (A) where are MICs located within the tumor, and does this location influence their behavior? How and where do they attach and expand at metastatic sites? (B) Why are MICs so sensitive to specific dietary lipids, and how do these lipids promote metastasis at the molecular and cellular levels? (C) Is the prolonged consumption of a high-fat diet a risk factor for developing metastatic tumors? If so, what are the underlying genetic and epigenetic causes for this effect? Can we revert these causes? To answer these questions, we will combine state-of-the-art in vivo functional models of metastasis, with quantitative metabolomics and proteomics, epigenetic and geographical position (3D) single-cell transcriptomic studies, as well as integrative computational analyses, using preclinical models and patientderived carcinomas of melanoma, oral cancer and breast cancer.

We expect our project to provide fundamental insights into the mechanisms of metastasis, and how they are influenced by diet. This is highly relevant as 1) large quantities of fatty acids are typically consumed in Western diets; and 2) metastasis is the leading cause of cancer-related deaths. We also tackle a timely medical unmet need by exploring the therapeutic anti-metastatic potential of targeting fatty acid metabolism in cancer patients.


year authors and title journal last update
List of publications.
2018 Alexandra Avgustinova, Aikaterini Symeonidi, Andrés Castellanos, Uxue Urdiroz-Urricelqui, Llorenç Solé-Boldo, Mercè Martín, Ivan Pérez-Rodríguez, Neus Prats, Ben Lehner, Fran Supek, Salvador Aznar Benitah
Loss of G9a preserves mutation patterns but increases chromatin accessibility, genomic instability and aggressiveness in skin tumours
published pages: 1400-1409, ISSN: 1465-7392, DOI: 10.1038/s41556-018-0233-x
Nature Cell Biology 20/12 2020-04-01
2018 Andras Ladanyi, Abir Mukherjee, Hilary A. Kenny, Alyssa Johnson, Anirban K. Mitra, Sinju Sundaresan, Kristin M. Nieman, Gloria Pascual, Salvador Aznar Benitah, Anthony Montag, S. Diane Yamada, Nada A. Abumrad, Ernst Lengyel
Adipocyte-induced CD36 expression drives ovarian cancer progression and metastasis
published pages: 2285-2301, ISSN: 0950-9232, DOI: 10.1038/s41388-017-0093-z
Oncogene 37/17 2020-04-01
2018 Gloria Pascual, Diana Domínguez, Salvador Aznar Benitah
The contributions of cancer cell metabolism to metastasis
published pages: dmm032920, ISSN: 1754-8403, DOI: 10.1242/dmm.032920
Disease Models & Mechanisms 11/8 2020-04-01

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