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. 2020 Jan 4;39(1):161–171. doi: 10.1007/s10555-019-09841-1

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Timeline of ALL development. The initiating lesions (green) occur in utero and lead to a state of preleukemia after birth. Exposure to infection leads to a dysregulated immune response in a small fraction (about 0.2–1%) of preleukemic children. Most preleukemic children remain healthy [6, 7]. The children develop ALL by acquiring secondary mutations, eventually leading to clonal expansion. In the case of KMT2A rearrangements (KMT2A-r, right), it is not completely clear whether the KMT2A-r are sufficient for ALL development (right dashed arrow). It is also possible that the KMT2A-r directly trigger secondary mutations (central dashed arrow). One case of a healthy KMT2A-r carrier has been reported [13], leading to the possibility of a preleukemic state for those cases (left dashed arrow). The given median ages of ALL onset are 2–5 years of age for B cell precursor subtypes (BCP, left) and < 1 year of age for pro-B cell subtype (pro-B, right)