Toward the manufacture of red blood cells?

pressed from trisomic chromosomes,6 it is possible that cooperation among several Hsa21’s is responsible for cT21 effects, as has also been suggested for explanation of other phenotypes of DS.7 Similarly to the leukemias of DS, sporadic childhood leukemias are initiated in utero. Somatic structural or numerical chromosomal aberrations acquired in fetal hematopoietic progenitors initiate the growth of a preleukemic clone.8 Thus, the relevance of studies, such as the 2 reported by Tunstall-Pedoe and Chou and their colleagues, extends beyond DS. They are important for the general understanding of how normal fetal hematopoietic development is diverted toward leukemia. Conflict-of-interest disclosure: The author declares no competing financial interests. ■ REFERENCES