No evidence for core-binding factor CBFß as a leukemia predisposing factor in chromosome 16q22-linked familial AML.

Acute myeloid leukemia (AML), as suggested by clinical data and murine leukemia models, arises through a multistep process involving more than one genetic alteration. Transcription factors play an important role in this process as they frequently show recurrent, somatically acquired, chromosomal abnormalities and point mutations. Familial cases of AML are best suited to define the initiating steps in leukemogenesis, and studies of familial AML have identified TF RUNX1 (AMLI, CBFA2) as the first known familial leukemia susceptibility gene.