Skip to main content
. Author manuscript; available in PMC: 2022 May 2.
Published in final edited form as: Stem Cell Rev Rep. 2021 Aug 23;17(6):2059–2080. doi: 10.1007/s12015-021-10230-x

Figure 4. Almost all infant/neonatal leukemias and most of childhood leukemias originate from infant.

Figure 4.

Almost all primary genetic abnormalities can be detected in fetal HSCs/HPCs, suggesting a fetal stage of pre-leukemia development. The different peaks of leukemia onsets induced by distinct genetic abnormalities are determined by: 1) efficiency of leukemia induction capacity of the primary genetic abnormalities; 2) the occurrence time of the secondary genetic abnormalities. For examples, Gata1s or MLL-r alone is sufficient to induce TMD or ALL development respectively, explaining the early onset peaks of DS-TMD and ALL in neonatal and infant. Secondary genetic mutations are required for the leukemia onsets induced by other primary genetic abnormalities, explaining the latter onset peaks of childhood AMkL and ALL.