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

Shahzya Chaudhury1,2, Caitríona O'Connor1, Ana Cañete1

  • 1Paul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.

Nature Communications
|December 13, 2018
PubMed

Insights

Acute myeloid leukaemia (AML) in children is often fatal, with relapse being a common cause of death. This study reveals that the age of the cell of origin significantly impacts AML development and characteristics, offering new therapeutic targets.

Area of Science:

  • Hematology
  • Pediatric Oncology
  • Cancer Biology

Background:

  • Acute myeloid leukaemia (AML) is a significant cause of cancer-related death in children.
  • Relapse is the primary cause of mortality in pediatric AML patients.
  • Understanding the biological differences in AML based on cell origin is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of cell-of-origin age in the development and characteristics of Acute Myeloid Leukaemia (AML).
  • To identify distinct biological pathways and prognostic markers in pediatric AML.
  • To establish in vivo murine models for studying pediatric AML and developing novel therapeutic strategies.

Main Methods:

  • In vivo modeling of AML in mice.
  • Transcriptional analysis of leukaemic cells.
  • Analysis of human pediatric AML patient samples.

Main Results:

  • AML development is discriminated by the age of the cell of origin: young cells can lead to myeloid, lymphoid, or mixed acute leukaemias, while adult cells exclusively produce AML with shorter latency.
  • Young AML cells do not remodel the bone marrow stroma, unlike adult AML cells.
  • Transcriptional analysis revealed upregulation of immune pathways in young AML, with human pediatric samples showing a similar immune cell interaction gene signature, highlighting RGS10 and FAM26F as prognostically significant.

Conclusions:

  • The age of the cell of origin is a critical factor in determining AML phenotype, latency, and stromal interaction.
  • Immune pathway dysregulation is a key feature of pediatric AML.
  • RGS10 and FAM26F are identified as potential prognostic markers for pediatric AML, paving the way for developing pediatric-specific therapeutic strategies.

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