Abstract
Cancer metabolism has received a substantial amount of interest over the past decade. The advances in analytical tools have, along with the rapid progress of cancer genomics, generated an increasingly complex understanding of metabolic reprogramming in cancer. As numerous connections between oncogenic signalling pathways and metabolic activities emerge, the importance of metabolic reprogramming in cancer is being increasingly recognized. The identification of metabolic weaknesses of cancer cells has been used to create strategies for treating cancer, but there are still challenges to be faced in bringing the drugs that target cancer metabolism to the clinic.
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Change history
02 January 2013
Nature 491, 364–373 (2012); doi:10.1038/nature11706 We inadvertently omitted to cite reference 101, which should have been cited on page 267 at the end of the following sentence: “Recent evidence suggests that renal cyst formation after Fh1 deletion is independent of HIF, but involves activation of the NRF2 pathway by fumarate, and that activation of NRF2 may contribute to the development of fumarate-hydratase-deficient cancers51,101 .
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Acknowledgements
The authors thank C. Santos and S. Ros for their critical reading and feedback. A.S. is funded by Cancer Research UK and the EMBO Young Investigator Programme. A.L.H. is funded by Cancer Research UK, the Oxford Cancer Imaging Centre, the Breast Cancer Research Foundation and the Oxford NIHR Biomedical Research Centre.
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Schulze, A., Harris, A. How cancer metabolism is tuned for proliferation and vulnerable to disruption. Nature 491, 364–373 (2012). https://doi.org/10.1038/nature11706
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DOI: https://doi.org/10.1038/nature11706
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