Age-specific biological and molecular profiling distinguishes paediatric from adult acute myeloid leukaemias

Shahzya Chaudhury, Caitríona O’Connor, Ana Cañete, Joana Bittencourt-Silvestre, Evgenia Sarrou, Áine Prendergast, Jarny Choi, Pamela Johnston, Christine A. Wells, Brenda Gibson and Karen Keeshan ()
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Shahzya Chaudhury: University of Glasgow
Caitríona O’Connor: University of Glasgow
Ana Cañete: University of Glasgow
Joana Bittencourt-Silvestre: University of Glasgow
Evgenia Sarrou: University of Glasgow
Áine Prendergast: University of Glasgow
Jarny Choi: The University of Melbourne
Pamela Johnston: University of Glasgow
Christine A. Wells: The University of Melbourne
Brenda Gibson: Royal Hospital for Children
Karen Keeshan: University of Glasgow

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Acute myeloid leukaemia (AML) affects children and adults of all ages. AML remains one of the major causes of death in children with cancer and for children with AML relapse is the most common cause of death. Here, by modelling AML in vivo we demonstrate that AML is discriminated by the age of the cell of origin. Young cells give rise to myeloid, lymphoid or mixed phenotype acute leukaemia, whereas adult cells give rise exclusively to AML, with a shorter latency. Unlike adult, young AML cells do not remodel the bone marrow stroma. Transcriptional analysis distinguishes young AML by the upregulation of immune pathways. Analysis of human paediatric AML samples recapitulates a paediatric immune cell interaction gene signature, highlighting two genes, RGS10 and FAM26F as prognostically significant. This work advances our understanding of paediatric AML biology, and provides murine models that offer the potential for developing paediatric specific therapeutic strategies.

Date: 2018
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DOI: 10.1038/s41467-018-07584-1

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