Salutary Response to Targeted Therapy in Anaplastic Thyroid Cancer

J Investig Med High Impact Case Rep. 2019 Jan-Dec:7:2324709619890942. doi: 10.1177/2324709619890942.

Abstract

Context. Anaplastic thyroid cancer (ATC) is an aggressive tumor with a median survival of 3 to 9 months, a 1-year survival of less than 10% and without definitive therapies. Recently, in BRAF V600E mutated ATCs, new targeted therapy using a combination of a BRAF inhibitor, dabrafenib (Dab), with a mitogen-activated extracellular protein kinase (MEK) inhibitor, trametinib (Tram), has shown significant promise. Case Description. We report a case of aggressive ATC with 5 sequence mutations: BRAF V600E (mutation fraction [MF] 34%), TERT E441del (MF 37%), RET N579K (MF 55%), EZH2 D154E (MF 60%), and CDK4 S259L (MF 48%). The patient had a dramatic response to the Dab/Tram combination with near complete resolution of his lung, bone, hepatic, and splenic lesions soon after starting therapy. Unfortunately, intolerable side effects (grade 2-3) on this regimen required tapering and discontinuation of the treatment. He had a quick resurgence of disease after stopping the combination therapy. The patient died approximately 3 months after discontinuing Dab/Tram. Autopsy revealed an atrophic thyroid gland with microscopic subcapsular focus of well-differentiated papillary thyroid carcinoma. There was extensive lymphatic spread of the tumor throughout bilateral lungs with fibrosis. No other metastatic site was identified. Conclusion. We report a unique case of ATC with 2 new mutations of EZH2 D154E and CDK S529L. This case exemplifies the significant promise Dab/Tram therapy holds, the potential side effects that limit their use, and autopsy findings status post use of this combination therapy.

Keywords: BRAF V600E; BRAF inhibitor; CDK4 mutation; EZH2 mutation; anaplastic thyroid cancer; mitogen-activated extracellular protein kinase inhibitor (MEK inhibitor); targeted therapy.

Publication types

  • Case Reports

MeSH terms

  • Aged
  • Autopsy
  • CDC2 Protein Kinase / antagonists & inhibitors
  • CDC2 Protein Kinase / genetics*
  • Enhancer of Zeste Homolog 2 Protein / antagonists & inhibitors
  • Enhancer of Zeste Homolog 2 Protein / genetics*
  • Fatal Outcome
  • Humans
  • Imidazoles
  • Male
  • Molecular Targeted Therapy*
  • Mutation
  • Oximes
  • Positron Emission Tomography Computed Tomography
  • Protein Kinase Inhibitors / therapeutic use
  • Proto-Oncogene Proteins B-raf / antagonists & inhibitors
  • Proto-Oncogene Proteins B-raf / genetics*
  • Pyridones
  • Pyrimidinones
  • Thyroid Carcinoma, Anaplastic / drug therapy
  • Thyroid Carcinoma, Anaplastic / genetics*
  • Thyroid Neoplasms / drug therapy
  • Thyroid Neoplasms / genetics*

Substances

  • Imidazoles
  • Oximes
  • Protein Kinase Inhibitors
  • Pyridones
  • Pyrimidinones
  • trametinib
  • EZH2 protein, human
  • Enhancer of Zeste Homolog 2 Protein
  • BRAF protein, human
  • Proto-Oncogene Proteins B-raf
  • CDC2 Protein Kinase
  • CDK1 protein, human
  • dabrafenib