Ligtenberg M J, Siers M, Themmen A P, Hanselaar T G, Willemsen W, Brunner H G
Department of Human Genetics, University Hospital Nijmegen, The Netherlands.
J Clin Endocrinol Metab. 1999 Jun;84(6):2233-4. doi: 10.1210/jcem.84.6.5739.
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.
有人提出，卵巢颗粒细胞瘤可能是由于无对抗的过度刺激所致，这种过度刺激要么是由促性腺激素过度刺激引起，要么是由FSH受体基因、Gsα或Giα2等G蛋白亚基的激活突变引起。我们检测了卵巢颗粒细胞瘤中FSH受体基因的整个开放阅读框。此外，还对这些肿瘤进行了已知的致癌G蛋白突变Gsp和Gip2的评估。在所有23例卵巢颗粒细胞瘤中均得到正常结果。我们得出结论，FSH受体G蛋白信号通路的突变在这些肿瘤的发生中不发挥任何主要作用。
