The majority of pediatric malignancies are either germline related, in utero (de novo mutation/SV, potentially caused or facilitated by maternal environmental exposures), or a reverse lottery winner. There simply isn't enough time for somatic mutation to cause the sort of devastating fallout that you see in DIPG or infant leukemias. (Furthermore, even the point mutations seen in pediatric cases are characteristic and rare or absent in adults; some structural variants are also observed in adults, but they are much rarer and accompanied by fewer cooperating events)
>"There simply isn't enough time for somatic mutation to cause the sort of devastating fallout that you see in DIPG or infant leukemias."
This depends on the error + division rates (along with number of cells) in that tissue at that age though. From my research there not really such data available on any of those terms. Also, the errors need not be somatic mutation. For example, chromosomal missegregation may be much more common and potent since it can mess up the expression of many genes at once:
I'm just saying there are a number of other assumptions being made here, and if we get rid of the standard ones the Armitage-Doll model is capable of fitting the data surprisingly well.
