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Oncogenic mutations in the thyrotropin receptor of autonomously functioning thyroid nodules in the Japanese

V Vanvooren1, S Uchino, L Duprez

  • 1Institute of Interdisciplinary Research, University of Brussels, Campus Erasme, Route de Lennik 808, B-1070 Brussels, Belgium. vvvooren@ulb.ac.be

Abstract

Insights

Activating mutations in the thyrotropin receptor (TSHR) and G(alpha)s were investigated in Japanese autonomously functioning thyroid nodules (AFTNs). Four TSHR mutations and one G(alpha)s mutation were identified, suggesting their role in AFTN development.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Genetics

Background:

  • Activating mutations in the thyrotropin receptor (TSHR) are common in European autonomously functioning thyroid nodules (AFTNs).
  • The prevalence and role of these mutations in Japanese AFTNs remain less understood.
  • Previous studies identified only one TSHR mutation in Japanese AFTNs.

Purpose of the Study:

  • To determine the frequency of activating mutations in the TSHR and G(alpha)s genes in Japanese AFTNs.
  • To compare mutation prevalence between Japanese and European AFTN patients.
  • To investigate potential alternative genetic causes for AFTNs lacking TSHR/G(alpha)s mutations.

Main Methods:

  • Genomic DNA was extracted from 10 Japanese AFTN tissue samples.
  • The TSHR and G(alpha)s genes were amplified and sequenced.
  • Sequence analysis identified specific mutations within these genes.

Main Results:

  • Four distinct mutations were identified in the TSHR gene (T632A, I486M, M453T, L512R).
  • One mutation (R201H) in the G(alpha)s gene was found in a sample negative for TSHR mutations.
  • When considering solitary nodules, the mutation proportion (70%) matched that observed in European patients.

Conclusions:

  • Activating mutations in TSHR and G(alpha)s contribute to the development of Japanese AFTNs.
  • The findings support a similar genetic basis for AFTNs in Japanese and European populations, particularly in solitary nodules.
  • Other genetic factors likely contribute to the pathogenesis of AFTNs in multinodular goiters.

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