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Recurrent EZH1 mutations are a second hit in autonomous thyroid adenomas.

Davide Calebiro, Elisa S Grassi, Markus Eszlinger

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    Summary

    A novel hot-spot mutation in the enhancer of zeste homolog 1 (EZH1) gene is the second most frequent cause of autonomous thyroid adenomas (ATAs). This EZH1 mutation cooperates with cAMP pathway alterations to drive thyroid cell hyperproliferation.

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    Area of Science:

    • Endocrinology
    • Molecular Biology
    • Genetics

    Background:

    • Autonomous thyroid adenomas (ATAs) frequently cause hyperthyroidism.
    • Mutations in TSHR and GNAS account for ~70% of ATAs, but the pathogenesis of remaining cases is unknown.

    Purpose of the Study:

    • To identify novel genetic alterations in ATAs.
    • To elucidate the pathogenesis of ATAs with unknown genetic causes.

    Main Methods:

    • Whole-exome sequencing of 19 ATAs.
    • Targeted screening of EZH1 mutations in an independent cohort.
    • Functional studies assessing histone trimethylation and cell proliferation.

    Main Results:

    • A recurrent hot-spot mutation (p.Gln571Arg) in EZH1 was identified in 27% of ATAs.
    • EZH1 mutations were associated with alterations in cAMP pathway genes (TSHR, GNAS, ADCY9).
    • The p.Gln571Arg EZH1 mutation increased histone H3 trimethylation and thyroid cell proliferation.

    Conclusions:

    • EZH1 mutations are the second most frequent genetic alteration in ATAs.
    • A two-hit model involving cAMP pathway activation and EZH1 mutations is proposed for ATA pathogenesis.
    • Constitutive cAMP pathway activation and EZH1 mutations cooperate to induce thyroid cell hyperproliferation.