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Intraoperative cytodiagnosis of progressive multifocal leucoencephalopathy

tin, CD10, CD117, CK7, CK20, EMA, CK8/18, HMB45, smooth muscle actin and E-cadherin. Besides CD10, and cytokeratin immunoexpression, the neoplastic cells also expressed E-cadherin, CD117 (focally) and EMA. Racemase was focally positive (Table 1). Contrary to what occurs in clear cell-type RCC, vimentin was not expressed in the neoplastic cells of this case. Immunohistochemical markers of CRCC (colloidal iron, CD117, EMA, CK7) were also absent or only very weakly expressed (Table 1). The cellular characteristics and the immunohistochemical profile allowed the exclusion of other renal tumours with eosinophilic/oncocytic features such as atypical angiomyolipoma and oncocytoma but did not provide any clue for a more accurate classification other than RCC, NOS (Table 1). Using FISH, no translocation involving the TFE3/ TFEB genes was detected, but several copy number changes, namely two to four copies of TFE3 (Xp11), PRCC (1q21), ASPL (17q25) and three to four copies of TFEB (6p11) were observed. Such genetic alterations have not been reported to date in any RCC to the best of our knowledge. Our results indirectly support the assumption of Schreiner et al. that the absence of typical features of any RCC subtype or, in other words, the extreme heterogeneity of RCC in the setting of TSC may reflect the variability of additional molecular events that eventually occur in cells already carrying a TSC1 or TSC2 mutation. Further molecular studies of RCC in TSC are necessary to find out whether our findings are merely by chance or indicate a way to make progress in the understanding of tumour pathogenesis.