Cellular metabolic changes are commonly observed in various cancers. How they directly influence cancer development is under investigation. Ayuna Hattori et al. show that the metabolic enzyme BCAT1 is upregulated in chronic myeloid leukemia, mediated by Musashi2. BCAT1 is shown to function by aminating branch-chain keto acids to BCAAs. Inhibition of BCAT1 leads to differentiation and impaired propagation of chronic myeloid leukaemia in mice. In humans, elevated BCAT1 expression is also associated with poorer outcome of the illness and therefore might be used alongside other biomarkers to help predict disease outcome in patients.
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