Haem oxygenase is synthetically lethal with the tumour suppressor fumarate hydratase

Christian Frezza, Liang Zheng, Ori Folger, Kartik N. Rajagopalan, Elaine D. MacKenzie, Livnat Jerby, Massimo Micaroni, Barbara Chaneton, Julie Adam, Ann Hedley, Gabriela Kalna, Ian P. M. Tomlinson, Patrick J. Pollard, Dave G. Watson, Ralph J. Deberardinis, Tomer Shlomi, Eytan Ruppin and Eyal Gottlieb ()
Additional contact information
Christian Frezza: Cancer Research UK, Beatson Institute for Cancer Research
Liang Zheng: Cancer Research UK, Beatson Institute for Cancer Research
Ori Folger: The Blavatnik School of Computer Science, Tel Aviv University
Kartik N. Rajagopalan: University of Texas–Southwestern Medical Center at Dallas
Elaine D. MacKenzie: Cancer Research UK, Beatson Institute for Cancer Research
Livnat Jerby: The Blavatnik School of Computer Science, Tel Aviv University
Massimo Micaroni: The University of Queensland, Institute for Molecular Bioscience, St Lucia
Barbara Chaneton: Cancer Research UK, Beatson Institute for Cancer Research
Julie Adam: Henry Wellcome Building for Molecular Physiology, University of Oxford, Roosevelt Drive
Ann Hedley: Cancer Research UK, Beatson Institute for Cancer Research
Gabriela Kalna: Cancer Research UK, Beatson Institute for Cancer Research
Ian P. M. Tomlinson: Molecular and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, University of Oxford
Patrick J. Pollard: Henry Wellcome Building for Molecular Physiology, University of Oxford, Roosevelt Drive
Dave G. Watson: Strathclyde Institute of Pharmaceutical and Biomedical Sciences, University of Strathclyde
Ralph J. Deberardinis: University of Texas–Southwestern Medical Center at Dallas
Tomer Shlomi: Technion, Israel Institute of Technology
Eytan Ruppin: The Blavatnik School of Computer Science, Tel Aviv University
Eyal Gottlieb: Cancer Research UK, Beatson Institute for Cancer Research

Nature, 2011, vol. 477, issue 7363, 225-228

Abstract: Drug targets for kidney cancer Inherited mutations in fumarate hydratase (FH), an enzyme in the tricarboxylic acid cycle — which links many of the metabolic reactions in aerobic cellular respiration — can lead to malignancies including kidney cancer. Frezza et al. now observe a metabolic pathway in FH-deficient cells that converts glutamine into bilirubin through the synthesis and degradation of haem. This renders FH-deficient cells sensitive to inhibition of haem oxygenase, a key enzyme in this pathway. Haem oxygenase might therefore be a therapeutic target in patients with tumours associated with FH loss.

Date: 2011
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DOI: 10.1038/nature10363

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