Eosinophilia in acute myeloid leukemia: Overlooked and underexamined

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13 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)23-31
Number of pages9
JournalBlood Reviews
Volume36
DOIs
StatePublished - Jul 2019

Keywords

  • Acute myeloid leukemia (AML)
  • Core binding factor (CBF)
  • ETV6-ABL1
  • Eosinophilia
  • Imatinib
  • PDGFRa
  • PDGFRb

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