Development and characterization of a differentiated thyroid cancer cell line resistant to VEGFR-targeted kinase

Crescent R Isham1, Brian C Netzel, Ayoko R Bossou

  • 1Division of Medical Oncology (C.R.I., A.R.B., K.C.B.), Department of Oncology, and Department of Laboratory Medicine and Pathology (B.C.N., D.M., K.W.C., S.K.B.), and the Endocrine Malignancies Disease Oriented Group (C.R.I., A.R.B., S.K.G., K.C.B.), Mayo Clinic, Rochester, Minnesota 55905.

Abstract

Insights

Acquired resistance to vascular endothelial growth factor-targeted kinase inhibitors in thyroid cancer cells was studied. A KRAS mutation led to resistance, suggesting new therapeutic strategies for drug-resistant thyroid cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Vascular endothelial growth factor (VEGF)-targeted kinase inhibitors show promise for radioiodine-refractory metastatic differentiated thyroid cancer.
  • Acquired drug resistance to these therapies is a significant clinical challenge, limiting treatment efficacy.

Purpose of the Study:

  • To investigate the mechanisms of acquired drug resistance in differentiated thyroid cancer.
  • To elucidate how prolonged exposure to pazopanib affects cancer cell behavior and genetic makeup.

Main Methods:

  • BHP2-7 human differentiated thyroid cancer cells were selected in vitro with pazopanib.
  • Resistant cells were subcloned and characterized for drug resistance profiles and genetic alterations.
  • In vivo xenograft growth was assessed to evaluate tumor aggressiveness.

Main Results:

  • Stable 2- to 4-fold pazopanib resistance developed, with increased in vivo xenograft growth.
  • Cross-resistance to sunitinib and sorafenib was observed, but not to MEK1/2 inhibition.
  • A novel activating KRAS codon 13 mutation was identified in resistant cells.

Conclusions:

  • In vitro selection can model acquired drug resistance seen in patients with thyroid cancer.
  • The KRAS mutation explains resistance to VEGF inhibitors and sensitivity to MEK inhibitors.
  • This model provides insights for developing preemptive strategies against drug resistance in thyroid cancer.