The findings in the former patient suggest that either c-mos is not involved in the etiology of M2-ANLL or, alternatively, if c-mos is important in the pathogenesis of this disease, it must be activated by some mechanism other than transposition of this oncogene to an aberrant position.
Another protooncogene, c-mos, is also retained at the conserved junction, suggesting that one or both of these genes may play a role in the pathogenesis of acute myelogenous leukemia.
We isolated the 21q+ chromosome of this translocation in a somatic cell hybrid and showed that the c-mos oncogene had not been translocated to chromosome 21, ruling out the possibility that translocation of c-mos to chromosome 21 is necessary for development of AML-M2.