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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 2 493-496
Copyright © 1997 by The Endocrine Society

Endocrinological Oncology

G Protein and Thyrotropin Receptor Mutations in Thyroid Neoplasia1

Christopher Esapa, Sally Foster, Sarah Johnson, J. Larry Jameson, Patricia Kendall-Taylor and Philip E. Harris

Department of Medicine (C.E., P.E.H.), King’s College School of Medicine and Dentistry, London SE5 9PJ, United Kingdom; Departments of Medicine (S.F., P.K.-T.) and Pathology (S.J.), Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, United Kingdom; and Division of Endocrinology (J.L.J.), Northwestern University Medical School, Chicago, Illinois 60611

The cAMP pathway plays a central role in thyroid follicular cell growth and function. Mutations of the TSH receptor (TSHR) or G proteins (gsp) that activate adenylyl cyclase have been identified in autonomously functioning thyroid nodules. Gsp mutations have been identified also in other forms of thyroid neoplasia, but their reported prevalence has been extremely variable. We have studied the prevalence of gsp mutations and activating mutations of Gi2{alpha} (gip) in a series of 66 benign and 34 malignant thyroid tumors. Thirty-six tumors were from Boston and 64 from the UK. In addition, we examined the 64 UK tumors for mutations of the TSHR gene. DNA extracted from fresh-frozen or paraffin-embedded tissue was amplified by PCR and examined for mutations using oligonucleotide-specific hybridization and single-strand conformation polymorphism analysis. No G protein gene mutations were identified in the Boston tumors. One gsp mutation, R201C, in a Hürthle cell adenoma and 1 gip mutation, R179C, in a follicular adenoma were demonstrated in tumors from the UK. Oligonucleotide-specific hybridization and single-strand conformation polymorphism analysis of the UK tumors did not demonstrate any mutations of the TSHR gene. Eleven normal thyroid tissue samples were wild-type for Gs{alpha}, Gi2{alpha}, and the TSHR gene.




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