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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 alpha or Gi alpha2. 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.

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

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