11 October 2016
Molecular causes underlying acute myeloid leukaemia have been decoded for the first time by Canadian researchers.
A joint research paper, published in the latest edition of Nature Communications, reveals the effect of enzyme mutations when these cancers develop and the discovery could lead to personalized treatments.
Conducted by researchers Frederick Antoine Mallette, of the Maisonneuve-Rosemont Hospital Research Centre and the University of Montreal, and Marc-Étienne Huot, of Laval University, the findings shine a light on understanding the effect of IDH1/2 mutations in cancer by demonstrating their role in activating the pathways involved in cell proliferation and survival.
Scientists were already aware that there is a mutation phenomenon involving the metabolic enzymes isocitrate dehydrogenases 1 and 2 (IDH1/2) in various forms of brain cancer, including gliomas and glioblastomas, and in acute myeloid leukaemia.
However, there was a lack of understanding as to how the mutated forms of IDH1/2 contribute to cancer formation, the researchers say.
Research conducted by master’s student Mélissa Carbonneau has helped to better understand the effect of IDH1/2 mutations in cancer.
“With the identification of the molecular modes of action that contribute to cancer in patients carrying IDH1/2 mutations, it is now possible to consider personalised treatment to potentially improve therapeutic response,” said Dr Mallette.
Tumber A, Hulea L, Bergeman J et al. The oncometabolite 2-hydroxyglutarate activates the mTOR signalling pathway. Nature Communications September 2016; doi: 10.1038/ncomms12700
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