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Sarcomatoid carcinoma of the prostate: ERG fluorescence in‐situ hybridization confirms epithelial origin

mutations), with a read depth of 1220. The discovery of somatic mutations associated with particular lesions and clinical phenotypes, such as Ollier disease, has improved our understanding of the pathogenesis of disease. For example, somatic mutations in IDH1 and IDH2 occur in gliomas and acute myeloid leukaemia (AML), and the observation that some of these patients also develop multiple enchondromas led to the discovery that IDH1/2 mutations also occur in conventional central and periosteal cartilaginous neoplasms, with a frequency of 56%. In view of the occasional occurrence of SCSTs in individuals with Ollier disease, and our previous finding of an IDH1 mutation in an ovarian fibroma in such a patient, we screened a cohort of ovarian SCSTs for IDH1 and IDH2 mutations. However, unlike the association of IDH mutations with Ollier disease and sporadic cartilaginous lesions, gliomas and AML, no mutations in IDH1 or IDH2 were detected in our cohort of SCSTs. Although we only analysed the DNA from one block it is unlikely that tumour heterogeneity accounts for the failure to detect the mutations, as these genetic variants appear to be ‘driver mutations’ in other tumours in which these mutations are detected. Ovarian SCSTs account for approximately 5% of ovarian neoplasms and 7% of malignancies. At a molecular level, SCSTs are a heterogeneous group of neoplasms that has yet to be characterized fully. However, there have been some recent significant developments in our understanding of the pathogenesis of SCSTs, namely that FOXL2 mutations occur in more than 95% of adult granulosa cell tumours but not in other SCSTs, and that Sertoli–Leydig cell tumours harbour DICER1 missense mutations. Targeted NGS is a technology which is highly sensitive and also a timeand cost-efficient approach to screen for known mutations. However, a more comprehensive NGS approach using exome or whole-genome sequencing is more likely to accelerate our understanding of the pathogenesis of ovarian SCSTs.