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Functioning and nonfunctioning thyroid adenomas involve different molecular pathogenetic mechanisms.

M Tonacchera1, P Vitti, P Agretti

  • 1Dipartimento di Endocrinologia e Metabolismo, Ortopedia e Traumatologia, Medicina del Lavoro, Università di Pisa, Italy. mtonacchera@hot-mail.com

The Journal of Clinical Endocrinology and Metabolism
|November 24, 1999
PubMed
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Activating mutations in the thyroid-stimulating hormone receptor (TShR) drive growth in most hyperfunctioning thyroid adenomas. Nonfunctioning adenomas lack these TShR or Gs alpha mutations, suggesting different molecular pathways in thyroid nodule development.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • The molecular mechanisms underlying follicular thyroid cell growth in thyroid nodules remain unclear.
  • Gain-of-function mutations in the thyroid-stimulating hormone receptor (TShR) or Gs alpha genes can promote TSh-independent neoplastic cell growth.

Purpose of the Study:

  • To investigate somatic mutations in the TShR and Gs alpha genes in hyperfunctioning and nonfunctioning follicular thyroid adenomas.
  • To elucidate the distinct molecular pathways involved in the pathogenesis of different thyroid nodule types.

Main Methods:

  • Direct sequencing of TShR exons 9 and 10 and analysis of Gs alpha codons 201 and 227 in genomic DNA from surgical specimens.
  • Histopathological examination of thyroid nodules to confirm diagnoses of follicular adenoma and identify any malignant transformations.

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Main Results:

  • Activating TShR mutations were identified in 12 of 15 hyperfunctioning follicular thyroid adenomas.
  • One hyperfunctioning adenoma harbored a Gs alpha gene mutation at codon 227.
  • No TShR or Gs alpha gene mutations were detected in nonfunctioning thyroid nodules, including those with features of malignancy.

Conclusions:

  • Hyperfunctioning and nonfunctioning follicular thyroid adenomas exhibit different molecular pathogenesis.
  • Activation of the cAMP cascade via TShR or Gs alpha mutations is a key mechanism in hyperfunctioning adenomas.
  • Other oncogenes are likely involved in the development of nonfunctioning follicular adenomas.