Nature Communications (Nov 2021)

A human fetal liver-derived infant MLL-AF4 acute lymphoblastic leukemia model reveals a distinct fetal gene expression program

  • Siobhan Rice,
  • Thomas Jackson,
  • Nicholas T. Crump,
  • Nicholas Fordham,
  • Natalina Elliott,
  • Sorcha O’Byrne,
  • Maria del Mar Lara Fanego,
  • Dilys Addy,
  • Trisevgeni Crabb,
  • Carryl Dryden,
  • Sarah Inglott,
  • Dariusz Ladon,
  • Gary Wright,
  • Jack Bartram,
  • Philip Ancliff,
  • Adam J. Mead,
  • Christina Halsey,
  • Irene Roberts,
  • Thomas A. Milne,
  • Anindita Roy

DOI
https://doi.org/10.1038/s41467-021-27270-z
Journal volume & issue
Vol. 12, no. 1
pp. 1 – 13

Abstract

Read online

It is unknown why infant acute lymphoblastic leukemia (ALL) produced by MLL rearrangements leads to worse outcomes than childhood ALL. Here the authors develop a CRISPR-Cas9-induced human xenograft model of MLL-AF4 infant-ALL that faithfully replicates the disease and reveals that fetal-specific genes are potential infant-ALL drivers.