Thyroid Gene Expression in Familial Nonautoimmune Hyperthyroidism Shows Common Characteristics with Hyperfunctioning Autonomous Adenomas | Zendy

Aline Hébrant | Zendy; Jacqueline Van Sande | Zendy; Pierre P. Roger | Zendy; Martine Patey | Zendy; Marc Klein | Zendy; Claire Bournaud | Zendy; Frédérique Savagner | Zendy; Jacques Leclère | Zendy; Jacques E. Dumont | Zendy; Wilma C.G. van Staveren | Zendy; Carine Maenhaut | Zendy

Open Access

Thyroid Gene Expression in Familial Nonautoimmune Hyperthyroidism Shows Common Characteristics with Hyperfunctioning Autonomous Adenomas

Author(s) -

Aline Hébrant,

Jacqueline Van Sande,

Pierre P. Roger,

Martine Patey,

Marc Klein,

Claire Bournaud,

Frédérique Savagner,

Jacques Leclère,

Jacques E. Dumont,

Wilma C.G. van Staveren,

Carine Maenhaut

Publication year - 2009

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2008-2191

Subject(s) - phenotype , biology , gene , thyroid , somatic cell , endocrinology , gene expression , medicine , mutation , microarray analysis techniques , receptor , cell , genetics , cancer research

Dominant activating mutations of the TSH receptor are the cause of familial nonautoimmune hyperthyroidism (FNAH) (inherited mutations affecting the whole gland since embryogenesis) and the majority of hyperfunctioning autonomous adenomas (AAs) (somatic mutations affecting only one cell later in the adulthood).

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