Abstract
In up to 30% of acute myeloid leukemia (AML), chromosomal translocations disrupt one of the core binding factor (CBF) genes most frequently by the t(8;21)(q22;q22). Although patients with CBF leukemia generally have a higher complete remission rate and disease-free survival as compared to those with a normal karyotype or other chromosomal aberrations, additional distinct mutations in genes involved in signal-transduction pathways, particularly in receptor tyrosine kinases (RTKs), herald a higher relapse rate (see below).
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