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FLT3 inhibitor-induced neutrophilic dermatosis

Amir T Fathi1, Long Le, Robert P Hasserjian

  • 1Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA 02114, USA. afathi@partners.org.

Blood
|May 21, 2013
PubMed

Insights

FMS-like tyrosine kinase 3 (FLT3) inhibitors can cause skin issues in acute myeloid leukemia patients. These dermatoses result from FLT3-mutant myeloblasts differentiating into neutrophils, indicating a potential therapy-related syndrome.

Area of Science:

  • Hematology
  • Oncology
  • Dermatology

Background:

  • The FMS-like tyrosine kinase 3 (FLT3)-ITD mutation is a poor prognostic marker in acute myeloid leukemia (AML).
  • FLT3 inhibitors are a targeted therapy approach for AML with FLT3 mutations.
  • Recent studies indicate potent FLT3 inhibition can induce terminal differentiation in FLT3-mutant myeloblasts.

Observation:

  • Three AML patients treated with FLT3 inhibitors developed distinct skin nodules.
  • Dermatopathologic evaluation revealed deep dermal and subcutaneous neutrophilic infiltrates.
  • No myeloblasts were identified in the skin lesions.

Findings:

  • Genetic analysis (FLT3 and NPM1 mutational analysis, FISH) confirmed the neutrophils originated from FLT3-mutant myeloblasts.
  • FLT3-ITD and NPM1 mutations were found in two samples.
  • FLT3-ITD and 7q deletion were identified in the third sample.

Implications:

  • FLT3 inhibition can induce clinically apparent dermatoses.
  • These skin manifestations suggest a broader "syndrome" associated with FLT3-targeted therapy.
  • The findings highlight the impact of FLT3 inhibition on myeloid differentiation in AML.

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