The first oncogene discovered as the
direct etiological basis of a malignancy, the BCR/ABL1
translocation in chronic myeloid leukemia (CML), results
in dysregulated tyrosinase activity, which can be treated
using the tyrosine kinase inhibitor Imatinib [10,11]. The
t (15; 17) chromosomal translocation in promyelocytic
leukemia (APML, AML-M3) functions in a similar way,
generating the novel fusion protein PML/RARa, and
ATRA (all-trans retinoic acid) offers an effective therapy for APML by specifically suppressing oncogenic
activities of the PML/RARa fusion protein [12,13]. The
FISH assay is considered the gold standard for detecting these chromosomal translocations and it therefore
plays a crucial role in selecting a targeted therapy for
various leukemias.