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Showing 1–12 of 12 results
Advanced filters: Author: "Sarah-Maria Fendt" Clear advanced filters

  • After earning a PhD in Molecular Systems Biology from ETH Zurich and studying cancer metabolism as a postdoctoral fellow at MIT, Sarah-Maria Fendt started an independent research group in 2013 in a joint appointment at the Flemish Institute for Biotechnology (VIB) and the University of Leuven (KU Leuven) in Belgium.

    • Sarah-Maria Fendt
    Comments & Opinion
    Nature Cell Biology
    Volume: 24, P: 1012

  • A cellular condition called oxidative stress can kill cancer cells. The finding that skin cancer cells evade such destruction using lipids acquired while passing through lymphatic vessels reveals a mechanism that boosts cancer spread.

    • Barbara M. Grüner
    • Sarah-Maria Fendt
    News & Views
    Nature
    Volume: 585, P: 36-37

  • Fendt and colleagues find that pre-metastatic niche formation and a high-fat diet increase palmitate availability in future organs of metastases and show that breast cancer cells use palmitate to generate acetyl-CoA, acetylate the NF-κB subunit p65 and induce pro-metastatic signaling.

    • Patricia Altea-Manzano
    • Ginevra Doglioni
    • Sarah-Maria Fendt
    Research
    Nature Cancer
    Volume: 4, P: 344-364

  • In this study, the serine biosynthetic enzyme PHGDH is shown to transition from the cytosol to the nucleus following nutrient stress. Nuclear PHGDH reduces local NAD+ availability needed for the PARylation of the transcription factor c-Jun. Consequently, c-Jun activity is reduced, contributing to sustained cancer cell proliferation.

    • Daniela Annibali
    • Sarah-Maria Fendt
    News & Views
    Nature Metabolism
    Volume: 3, P: 1284-1285

  • Demicco, Liu et al. discuss how metabolic adaptations in cancer contribute to tumour progression. These adaptations entail high spatial and temporal metabolic heterogeneity, based on local adaptations in different regions of the tumour microenvironment, as well as metabolic evolution over time as the tumour progresses and metastasizes.

    • Margherita Demicco
    • Xiao-Zheng Liu
    • Sarah-Maria Fendt
    Reviews
    Nature Metabolism
    Volume: 6, P: 18-38

  • Metastasizing cancer cells rewire their metabolism to support their malignant phenotypes. Here, the authors show that the acquisition of a metastatic phenotype in breast cancer cell lines results in increased proline catabolism and that inhibition of this pathway decreases lung metastasis formation in two mouse models.

    • Ilaria Elia
    • Dorien Broekaert
    • Sarah-Maria Fendt
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-11

  • This study identifies a crucial role for fatty acid oxidation (FAO) in endothelial cells during angiogenesis, and reveals that fatty-acid-derived carbons are used for the de novo synthesis of nucleotides, and hence FAO stimulates vessel sprouting by increasing endothelial cell proliferation.

    • Sandra Schoors
    • Ulrike Bruning
    • Peter Carmeliet
    Research
    Nature
    Volume: 520, P: 192-197

  • This Review describes the metabolic rewiring that occurs in cancer cells transitioning through the metastatic cascade and discusses the evidence for metabolically distinct features of primary tumours and metastases.

    • Gabriele Bergers
    • Sarah-Maria Fendt
    Reviews
    Nature Reviews Cancer
    Volume: 21, P: 162-180