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. 2021 Feb 17;12:637975. doi: 10.3389/fimmu.2021.637975

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Copyright © 2021 Jackson, Ling and Roy.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Developmental origins of ALL. Schematic representation of the main sites of early life B-lymphopoiesis (FL, fetal liver; FBM, fetal bone marrow; PBM, pediatric BM). Different fetal lymphoid progenitors could be the target cell for infant ALL (iALL), and childhood-ALL. While iALL can develop after just one intrauterine “hit” such as KMT2A gene rearrangement (KMT2A-r), childhood-ALL usually develops after a second postnatal hit. Fetal-specific gene expression programs are down regulated after birth. These programs might be key in providing a permissive cellular context for prenatal B-progenitor leukemia initiation in specific target cells as described above.