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颗粒细胞瘤的分子发病机制

Molecular pathogenesis of granulosa cell tumours.

作者信息

Fuller Peter J, Chu Simon, Fikret Sonay, Burger Henry G

机构信息

Prince Henry's Institute of Medical Research, PO Box 5152, Clayton, Vic. 3168, Australia.

出版信息

Mol Cell Endocrinol. 2002 May 31;191(1):89-96. doi: 10.1016/s0303-7207(02)00059-x.

DOI:10.1016/s0303-7207(02)00059-x
PMID:12044922
Abstract

Granulosa cell tumours (GCT) of the ovary arise from granulosa cells of the ovary on morphological, biochemical and molecular criteria. In order to understand the molecular pathogenesis of these tumours better we have sought to define their molecular phenotype, to identify activating mutations of the FSH-signalling pathway, to characterise their estrogen receptor expression and to explore the hypothesis that GCT may be resistant to inhibin. The pattern of gene expression observed in GCT suggests a phenotype which is similar to that of late preovulatory granulosa cells which would be consistent with activation of the FSH receptor signalling pathway, however, there is no evidence for activating mutations of either the FSH receptor or the associated trimeric G-proteins. Estrogen receptor beta is abundantly expressed in GCT. The various subunits and isoforms of the activin-inhibin receptor are expressed in GCT. These observations provide a basis for future studies of GCT, including further characterisation of signalling pathways known to be important in the regulation of granulosa cell growth and differentiation.

摘要

卵巢颗粒细胞瘤(GCT)根据形态学、生物化学和分子标准,起源于卵巢的颗粒细胞。为了更好地理解这些肿瘤的分子发病机制,我们试图确定其分子表型,识别促卵泡激素(FSH)信号通路的激活突变,表征其雌激素受体表达,并探讨GCT可能对抑制素耐药的假说。在GCT中观察到的基因表达模式表明其表型与排卵前晚期颗粒细胞相似,这与FSH受体信号通路的激活一致,然而,没有证据表明FSH受体或相关三聚体G蛋白存在激活突变。雌激素受体β在GCT中大量表达。激活素-抑制素受体的各种亚基和异构体在GCT中表达。这些观察结果为GCT的未来研究提供了基础,包括进一步表征已知在颗粒细胞生长和分化调节中起重要作用的信号通路。

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