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Analysis of Mutations in Genes of the Follicle-Stimulating Hormone Receptor Signaling Pathway in Ovarian Granulosa Cell Tumors¹

Departments of Human Genetics (M.J.L., M.S., H.G.B.), Pathology (M.J.L., T.G.H.), and Gynaecology (W.W.), University Hospital Nijmegen, 6525 GA Nijmegen, the Netherlands; and Department Endocrinology and Reproduction (A.P.N.T.), Erasmus University, 3015 GE Rotterdam, the Netherlands

Address all correspondence and requests for reprints to: Han. G. Brunner, Department of Human Genetics-417, 6525 GA Nijmegen, the Netherlands. E-mail: h.brunner{at}antrg.azn.nl

It has been suggested that ovarian granulosa cell tumors may result from unopposed hyperstimulation, either by excessive gonadotropin stimulation, by activating mutations of the FSH receptor gene, or of the G protein subunits, Gs or Gi2. We have examined the entire open reading frame of the FSH receptor gene in ovarian granulosa cell tumors. In addition, these tumors were evaluated for the known oncogenic G protein mutations Gsp and Gip2. Normal results were obtained in all 23 ovarian granulosa cell tumors. We conclude that mutations of the FSH receptor G protein signaling pathway do not play any major role in the genesis of these tumors.

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