VEGF, VEGFR3, and PDGFRB protein expression is influenced by RAS mutations in medullary thyroid carcinoma

Thyroid. 2014 Aug;24(8):1251-5. doi: 10.1089/thy.2013.0579. Epub 2014 Jun 3.

Abstract

Background: Tyrosine kinase inhibitors (TKIs) have achieved remarkable clinical results in medullary thyroid carcinoma (MTC) patients. However, the considerable variability in patient response to treatment with TKIs remains largely unexplained. There is evidence that it could be due, at least in part, to alterations in genes associated with the disease via their effect on the expression of TKI targets. The objective of this study was to evaluate the influence of RAS mutations on the expression levels in MTC tumors of eight key TKI target proteins.

Methods: We assessed by immunohistochemistry the expression of EGFR, KIT, MET, PDGFRB, VEGF, VEGFR1, VEGFR2, and VEGFR3 in a series of 84 primary MTC tumors that had previously been molecularly characterized, including 14 RAS-positive, 18 RET(M918T)-positive, and 24 RET(C634)-positive tumors, as well as 15 wild-type tumors with no mutations in the RET or RAS genes.

Results: In contrast to RET-positive tumors, RAS-positive tumors expressed neither PDGFRB nor MET (p=0.0060 and 0.047, respectively). Similarly, fewer RAS-positive than RET-related tumors expressed VEGFR3 (p=0.00062). Finally, wild-type tumors expressed VEGF more often than both RAS- and RET-positive tumors (p=0.0082 and 0.011, respectively).

Conclusions: This is the first study identifying that the expression of TKI targets differs according to the presence of RAS mutations in MTC. This information could potentially be used to select the most beneficial TKI treatment for these patients.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Neuroendocrine
  • DNA Mutational Analysis
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Immunohistochemistry
  • Mutation
  • Proto-Oncogene Proteins c-ret / metabolism
  • Receptor, Platelet-Derived Growth Factor beta / metabolism*
  • Thyroid Neoplasms / metabolism*
  • Treatment Outcome
  • Vascular Endothelial Growth Factor A / metabolism*
  • Vascular Endothelial Growth Factor Receptor-3 / metabolism*
  • ras Proteins / genetics*

Substances

  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • FLT4 protein, human
  • Proto-Oncogene Proteins c-ret
  • RET protein, human
  • Receptor, Platelet-Derived Growth Factor beta
  • Vascular Endothelial Growth Factor Receptor-3
  • ras Proteins

Supplementary concepts

  • Thyroid cancer, medullary