The presence of
eosinophilia in
acute myeloid leukemia (AML) suggests an underlying
core binding factor (CBF) lesion, a
platelet derived growth factor (PDGFR) translocation, or another rare translocation (such as ETV6-ABL1). Each of these cytogenetic entities carries unique diagnostic, prognostic, and therapeutic implications. CBF AML is most common and as such, its treatment is more clearly established, consisting of intensive
induction chemotherapy followed by
cytarabine based consolidation. Due in large part to its intrinsic chemo-sensitivity, CBF AML is associated with relatively high rates of remission and survival. PDGFR mediated AML is comparatively rare, and as such, diagnostic and treatment paradigms are not as well defined. Early identification of PDGFR translocations is essential, as they confer profound
imatinib sensitivity which may, in many instances, spare the need for
chemotherapy. Prompt recognition of such lesions requires a strong index of suspicion, and as such these diagnoses are often initially overlooked. Unfortunately, many cases of PDGFR associated AML, particularly those with other concurrent
cytogenetic abnormalities, demonstrate treatment emergent
imatinib resistance. Such patients continue to present a challenge, even with the advent of novel
tyrosine kinase inhibitors (TKIs). Patients with rare translocations such as ETV6-ABL1 are not well described however seem to follow an aggressive
clinical course, with limited response to
imatinib, and poor outcomes. This review examines the significance of
eosinophilia in the context of AML, with respect to its presentation, pathology, and cytogenetics, and with special attention to appropriate evaluation and treatment.