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The KRAS-BCAA-BCAT2 axis in PDAC development

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Understanding the metabolic rewiring of pancreatic ductal adenocarcinoma is an emerging strategy for identifying cancer-associated liabilities and improving treatment. A new study now elucidates the function of the transaminase BCAT2 in the early stages of tumor development, providing insights that could stimulate novel therapeutic strategies.

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Fig. 1: KRAS mutation boosts BCAA metabolism, which promotes PanIN development.

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Authors and Affiliations

  1. University of Glasgow Institute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, Glasgow, UK

    Mattia Falcone & Oliver D. K. Maddocks

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  1. Mattia Falcone
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  2. Oliver D. K. Maddocks
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Correspondence to Oliver D. K. Maddocks.

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Competing interests

O.D.K.M. contributed to the CRUK Cancer Research Technology’s filing of UK Patent Application no. 1609441.9, and is a founder and shareholder of Faeth Therapeutics.

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Falcone, M., Maddocks, O.D.K. The KRAS-BCAA-BCAT2 axis in PDAC development. Nat Cell Biol 22, 139–140 (2020). https://doi.org/10.1038/s41556-020-0467-2

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