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Showing 1–6 of 6 results
Advanced filters: Author: Daina Avizonis Clear advanced filters

  • Metabolic reprogramming is crucial in tumorigenesis, with alterations in glucose and fatty acid metabolism playing key roles. Here, the authors show that inhibiting fatty acid oxidation in HER2-driven breast cancers delays tumor growth and enhances the effectiveness of HER2-targeted therapies.

    • Ipshita Nandi
    • Linjia Ji
    • William J. Muller
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-20

  • Cancers with concomitant SMARCA4/2 deficiencies are often resistant to chemotherapies and confer a poor prognosis. Here, the authors identify a metabolic dependency of these tumours on glutamine as an energy source and, using multiple approaches, demonstrate the efficacy of therapeutically targeting this vulnerability.

    • Xianbing Zhu
    • Zheng Fu
    • Sidong Huang
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-16

  • Complex I inhibition induces oxidative stress leading to cancer cell cytotoxicity. Here, the authors show, in breast cancer models, that inflammatory mediators can potentiate complex I inhibitor phenformin cytotoxicity through STAT1-mediated downregulation of the reactive oxygen species scavenger NQO1.

    • Stephanie P. Totten
    • Young Kyuen Im
    • Josie Ursini-Siegel
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-20

  • β-cell dysfunction in diabetes is caused by glucose and inflammation toxicity. Here, Fu et al. show that β-cell glucose metabolism can be protective though pyruvate carboxylase–mediated shunting of arginine to ureagenesis and away from toxic nitric oxide production, thus suppressing inflammation.

    • Accalia Fu
    • Juan Carlos Alvarez-Perez
    • Nika N. Danial
    Research
    Nature Metabolism
    Volume: 2, P: 432-446

  • Metabolic reprogramming is a hallmark of pancreatic ductal adenocarcinoma (PDA). Here, the authors show that in PDA cells redox and central carbon metabolism are driven by an eIF4F dependent translation program, and combined targeting of eIF4A and glutaminase can impact PDA proliferation.

    • Karina Chan
    • Francis Robert
    • Iok In Christine Chio
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-16