Fatty acid synthesis is required for breast cancer brain metastasis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2021-04-01

AUTHORS

Gino B. Ferraro, Ahmed Ali, Alba Luengo, David P. Kodack, Amy Deik, Keene L. Abbott, Divya Bezwada, Landry Blanc, Brendan Prideaux, Xin Jin, Jessica M. Posada, Jiang Chen, Christopher R. Chin, Zohreh Amoozgar, Raphael Ferreira, Ivy X. Chen, Kamila Naxerova, Christopher Ng, Anna M. Westermark, Mark Duquette, Sylvie Roberge, Neal I. Lindeman, Costas A. Lyssiotis, Jens Nielsen, David E. Housman, Dan G. Duda, Elena Brachtel, Todd R. Golub, Lewis C. Cantley, John M. Asara, Shawn M. Davidson, Dai Fukumura, Véronique A. Dartois, Clary B. Clish, Rakesh K. Jain, Matthew G. Vander Heiden

ABSTRACT

Brain metastases are refractory to therapies that control systemic disease in patients with human epidermal growth factor receptor 2-positive breast cancer and the brain microenvironment contributes to this therapy resistance. Nutrient availability can vary across tissues, therefore metabolic adaptations required for brain metastatic breast cancer growth may introduce liabilities that can be exploited for therapy. Here we assessed how metabolism differs between breast tumors in brain versus extracranial sites and found that fatty acid synthesis is elevated in breast tumors growing in the brain. We determine that this phenotype is an adaptation to decreased lipid availability in the brain relative to other tissues, resulting in site-specific dependency on fatty acid synthesis for breast tumors growing at this site. Genetic or pharmacological inhibition of fatty acid synthase reduces human epidermal growth factor receptor 2-positive breast tumor growth in the brain, demonstrating that differences in nutrient availability across metastatic sites can result in targetable metabolic dependencies. More... »

PAGES

414-428

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  • Journal

    TITLE

    Nature Cancer

    ISSUE

    4

    VOLUME

    2

    Author Affiliations

  • Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
  • Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA
  • Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA
  • Novartis Institutes for BioMedical Research, Cambridge, MA, USA
  • Institut de Chimie & Biologie des Membranes & des Nano-objets, CNRS UMR 5248, Bordeaux, France
  • Department of Neuroscience, Cell Biology, and Anatomy, University of Texas Medical Branch, Galveston, TX, USA
  • Department of Pathology, Brigham and Women’s Hospital, Boston, MA, USA
  • Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA
  • Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden
  • Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
  • University of Michigan, Ann Arbor, MI, USA
  • Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA
  • Weill Cornell Medicine and New York Presbyterian Hospital, New York, NY, USA
  • Division of Signal Transduction, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
  • Lewis Sigler Institute, Princeton University, Princeton, NJ, USA
  • Center for Discovery and Innovation, Hackensack Meridian Health, Nutley, NJ, USA
  • Dana-Farber Cancer Institute, Boston, MA, USA
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s43018-021-00183-y

    DOI

    http://dx.doi.org/10.1038/s43018-021-00183-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1136852057

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/34179825


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