Phospho-mTOR is not upregulated in metastatic SDHB paragangliomas

Eur J Clin Invest. 2013 Sep;43(9):970-7. doi: 10.1111/eci.12127. Epub 2013 Jul 26.

Abstract

Background: Pheochromocytomas (PCCs)/paragangliomas (PGLs) are neuroendocrine tumours that may cause arrhythmia and death if untreated. Treatment for patients with metastatic tumours is lacking. As new PCC/PGL susceptibility genes are discovered that are associated with the mTOR pathway, treatment targets focusing on this pathway are being intensively explored.

Design: Twenty-one human PCC/PGLs were analysed from two tertiary care centres. Immunohistochemistry (IHC) analysis was performed for phospho-mTOR (pmTOR), phospho-S6K (pS6K), phosphoinositide 3-kinase (PI3K), phospho-4EBP1 (p4EBP1), HIF1α and MIB-1 in 6 metastatic SDHB PCC/PGLs, 15 nonmetastatic PCC/PGLs, (including 1 TMEM127 PCC and 1 nonmetastatic SDHB PGL) and 6 normal adrenal medullas. The product of the intensity of stain and percentage of cells stained was calculated as an H score.

Results: Using a two-sample t-test and paired t-test, pmTOR and pS6K had significantly higher H scores in nonmetastatic PCC/PGLs than in metastatic SDHB PCC/PGLs. HIF1α had significantly higher H scores in metastatic SDHB PCC/PGLs compared with nonmetastatic PCC/PGLs and normal adrenal medulla. No difference in H scores was seen with p4EBP1, PI3K and MIB-1 when comparing metastatic SDHB PCC/PGLs and nonmetastatic PCC/PGLs. Significantly higher difference in pS6K was seen in normal adrenal medullas compared to nonmetastatic PCC/PGLs and metastatic SDHB PCC/PGLs.

Conclusion: The present results suggest that the use of mTOR inhibitors alone for metastatic SDHB PCC/PGLs may not achieve good therapeutic efficacy in patients.

Keywords: Paraganglioma; SDHB; pmTOR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Adrenal Medulla / metabolism
  • Cell Cycle Proteins
  • Female
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • MAP Kinase Signaling System / physiology
  • Male
  • Mutation / genetics
  • Neoplasm Metastasis
  • Paraganglioma / drug therapy
  • Paraganglioma / genetics
  • Paraganglioma / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Phosphoproteins / metabolism
  • RNA-Binding Proteins / metabolism
  • Ribosomal Protein S6 Kinases / metabolism
  • Succinate Dehydrogenase / genetics*
  • TOR Serine-Threonine Kinases / antagonists & inhibitors
  • TOR Serine-Threonine Kinases / metabolism*
  • Ubiquitin-Protein Ligases / metabolism
  • Up-Regulation

Substances

  • Adaptor Proteins, Signal Transducing
  • Cell Cycle Proteins
  • EIF4EBP1 protein, human
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • PA2G4 protein, human
  • Phosphoproteins
  • RNA-Binding Proteins
  • SDHB protein, human
  • Succinate Dehydrogenase
  • MIB1 ligase, human
  • Ubiquitin-Protein Ligases
  • MTOR protein, human
  • Ribosomal Protein S6 Kinases
  • TOR Serine-Threonine Kinases