The consistent occurrence of trisomy 12 in different subtypes of sex cord-stromal tumours suggests a common mechanism of oncogenesis within this diverse group of neoplasms. To find supporting evidence that this was the case in human granulosa cell tumours, It has been investigated whether LOH of the INHA locus at 2qqter was evident in a series of 17 granulosa cell tumours. Neither point mutations exons analysed only , nor LOH of TP53 were evident in a series of 17 granulosa cell tumours, suggesting that they have a distinct molecular pathogenesis to that of epithelial ovarian tumours. Prognosis The prognosis of sex-cord-stromal tumours is good, as these tumours usually present when confined to a single ovary, and are responsive to chemotherapy. Note Involvement of the follicle stimulating hormone receptor, FSHR , gene in granulosa cell tumours has now been excluded. It was found that over-expression of TP53 was not characteristic of 19 ovarian granulosa cell tumours; whereas other workers found a correlation between expression of mutated TP53 with poor prognosis, which was supported by other findings.
These findings corroborate previous reports of the prevalence of trisomy 12 and 14 and monosomy 22 in granulosa cell tumours. Cyclin D2 CCND2 has been suggested as the candidate gene on 12p, and has been reported to demonstrate increased expression. Sertoli cell tumours contain Sertoli cells in a tubular arrangement. Mutations outside the hotspot exon were not excluded by their study, but are unlikely to be significant since an association between TP53 and granulosa cell tumour by immunohistochemistry was not demonstrated in th efirst study. Trans abdominal hysterectomy or bilateral salpingo-oophorectomy is appropriate for women beyond childbearing age, whereas unilateral oophorectomy is appropriate for younger women. For individuals with granulosa cell tumours, diffuse growth pattern, increased mitotic figures and cellular atypia correlate with poor prognosis. The prognosis of Sertoli-Leydig cell tumours is governed by the stage and differentiation of the tumour. Surgical intervention of patients with sex cord-stromal tumours is age dependent. Pelvic radiation has also been used for localised tumours. Individuals with completely resected granulosa cell tumours with normal DNA diploid content, have a much better prognosis than when residual tumour remains after laparotomy, and the DNA content is aneuploid. A role for the INK4 family of cyclin-dependent kinase inhibitors has also been suggested in granulosa cell tumours. Studies on the role of TP53 mutations in granulosa cell tumours have been contradictory. There is a paucity of data on treatment of advanced or recurrent stromal tumours due to their rarity, varied histology and indolence. Cytogenetics Molecular CGH and FISH analysis of an ovarian metastasising Sertoli-Leydig cell tumour demonstrated trisomy 8 as the sole anomaly, suggesting that the molecular pathogenesis of Sertoli-Leydig cell tumours differs from the other subtypes of sex cord-stromal tumours. It is characterised by sex cord cells in the form of a ring with nuclei orientated around a central hyalonized body. Cytogenetics Cytogenetics Morphological Trisomy 12 is a recurrent finding, often as the sole anomaly in benign sex cord-stromal tumours including fibromas, fibrothecomas, thecomas, granulosa cell tumours. Altered expression levels of the following genes have also been found in granulosa cell tumours: Numerical abnormalities of chromosome 12 can readily be demonstrated by interphase cytogenetics. Trisomy 12 and 14, and monosomy 22 are the characteristic recurrent cytogenetic aberrations in granulosa cell tumours. Neither point mutations exons analysed only , nor LOH of TP53 were evident in a series of 17 granulosa cell tumours, suggesting that they have a distinct molecular pathogenesis to that of epithelial ovarian tumours. However this supports the observation of elevated expression of inhibin which has been reported previously in these tumours. Monosomy 22 and trisomy 14 may be early events in the pathogenesis of adult granulosa cell tumour, and particularly adult granulosa-thecoma cell tumours. Knockout mouse models null for the INHA gene develop granulosa cell tumours suggesting that this gene may act as a tumour suppressor gene. No effective treatment is available for metastatic lipid cell tumours. Adult granulosa cell tumours usually develop in postmenopausal women, recur after longer time intervals, average of 5-years , and the average survival following recurrence is 5-years. In the low percentage of granulosa cell tumours showing aggressive behaviour, any organ can be affected by metastatic disease, although it is usually confined to the pelvis and abdomen.
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