Discontinuation of sorafenib can lead to the emergence of FLT3-ITD-positive acute myeloid leukemia

J Oncol Pharm Pract. 2019 Dec;25(8):2010-2015. doi: 10.1177/1078155218816768. Epub 2018 Dec 4.

Abstract

A 69-year-old woman who had been diagnosed with unresectable papillary thyroid cancer was referred to our hospital. We initially treated her with sorafenib, but she subsequently developed erythema multiforme, which was suspected to be a drug rush due to sorafenib; therefore, sorafenib was discontinued. At the time of discontinuation, immature blast cells were detected in her peripheral blood. Approximately two weeks later, her skin rash improved substantially, but the proportion of blasts in the peripheral blood increased. We performed a bone marrow examination, and she was diagnosed with FLT3-ITD-positive acute myeloid leukemia. FLT3-ITD expression is found in 20-25% of AML and is a known independent poor prognostic factor. To overcome the poor prognosis associated with FLT3-ITD, molecular drugs targeting FLT3-ITD are attracting much attention. Sorafenib, a multi-kinase inhibitor, also has an effect on FLT3-ITD. Although primary disease flares after tyrosine kinase inhibitor discontinuation have been reported, this is the first report to describe discontinuation of sorafenib treatment as a potential trigger of FLT3-ITD-positive acute myeloid leukemia in papillary thyroid cancer.

Keywords: FLT3-ITD positive acute myeloid leukemia; erythema multiforme; leukemic proliferation; papillary thyroid cancer; sorafenib.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Female
  • Humans
  • Leukemia, Myeloid, Acute / etiology*
  • Mutation
  • Protein Kinase Inhibitors / administration & dosage*
  • Sorafenib / administration & dosage*
  • fms-Like Tyrosine Kinase 3 / genetics

Substances

  • Protein Kinase Inhibitors
  • Sorafenib
  • FLT3 protein, human
  • fms-Like Tyrosine Kinase 3