EV(I1)olution of AML DNA methylation.

not conclusive, it suggests an alternative model of TEL-AML1 leukemogenesis (see figure, Model B). In this model, the initiating event (TEL-AML1 fusion) is as rare as the disease itself, implying that a high proportion (perhaps 100%) of babies born with a detectable TEL-AML1 fusion are destined to develop TEL-AML1 ALL. Could newborn screening for TEL-AML1 be considered in this scenario? Assuming a sensitive and specific clinical test could be developed, the problem of what to do with the small number of babies with positive screens would remain. How would one determine whether treating TEL-AML1 newborns during the preleukemic phase could prevent the development of ALL? Or whether using intensive surveillance to detect the development of ALL very early in the disease process could translate into improved outcomes? These important questions can only be answered with more research in this fascinating aspect of leukemia biology. Conflict-of-interest disclosure: The author declares no competing financial interests. ■