Authors analyzed retrospectively the incidence of pituitary apoplexy in a series of 799 pituitary adenomas with respect to the long term follow-up of the patients. Focal vascular abnormalities in histological specimens of tumours, regarded as morphological suggestion of past apoplexy (haemorrhage, ischaemic infarction or necrosis), were established in 113 out of 783 surgical cases (14.4%). Acute clinical onset, justifying the clinical diagnosis of pituitary apoplexy, occurred in 39 patients only (5% of the whole series), 19 of them were subjected to urgent surgical decompression due to severe neurological deficit. The haemorrhagic character of apoplexy was established in most cases requiring immediate surgery. The detailed clinical picture of this condition and its management are discussed with respect to the long term prognosis. On this basis the authors suggest the necessity of surgical treatment in every case of pituitary apoplexy, taking into account not only neurological recovery, but also endocrine and oncological aspects of the disease. The observation that pituitary apoplexy may be a "marker" of tumour invasiveness (even in small, "enclosed" adenomas) is highlighted.

Objective Pituitary corticotroph adenomas commonly cause Cushing’s disease (CD) but part of these tumours are hormonally inactive (silent corticotroph adenomas, SCA). USP8 mutations are well-known driver mutations in corticotrophinomas. Differences in transcriptomic profiles between functioning and silent tumours or tumours with different USP8 status have not been investigated. Design and methods Forty-eight patients (28 CD, 20 SCA) were screened for USP8 mutations with Sanger sequencing. Twenty-four patients were included in transcriptomic profiling with Ampliseq Transcriptome Human Gene Expression Core Panel. The entire patients group was included in qRT-PCR analysis of selected genes expression. Immunohistochemistry was used for visualization of selected protein. Results We found USP8 mutation in 15 patients with CD and 4 SCAs. USP8 mutations determine molecular profile of the tumours as showed by hierarchical clustering and identification of 1648 genes differentially expressed in USP8-mutated and USP8-wild-type tumours. Mutations affect many molecular pathways as observed in Gene Set Enrichment analysis. USP8-mutated adenomas showed higher level of POMC, CDC25A, MAPK4 but lower level of CCND2, CDK6, CDKN1B than USP8-wt tumours. Eighty-seven genes differentially expressed between CD-related adenomas and SCAs were found, including those involved in cell signalling (GLI2, DLC1, TBX2, RASSF6), cell adhesion (GJA1, CDH6), ion transport (KCNN4, KCNJ5) and GABA signalling (GABBR2, GABRD). Conclusion USP8 mutations occur in functioning and silent corticotrophinomas. They have pleiotropic effect, not limited to EGFR signalling, and affect expression levels of many genes involved in different pathways. Expression of GABA-related genes GABBR2, GNAL, GABARD and KCNJ5 correspond to functional status of the tumours.

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MRI, ophthalmologic examination and plasma ACTH determination were the most valuable investigations for early diagnosis of Nelson's syndrome. Early neurosurgery offered the best outcome in our group of patients.

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Our results indicate that the IDH1 R132H mutation is a powerful prognostic marker in GBM treated with chemoradiation. The PCR-RFLP method allows for a fast, inexpensive, and sensitive mutation screening.

Fluorescence-guided resection of primary and recurrent MGs with 5-ALA improves control of the tumour resection. It enables the cytoreduction to be maximized but experience in neuro-oncological surgery is required to avoid serious, postoperative neurological deficits.

Meningiomas are among the most frequent intracranial tumors. Treatment involves surgical resection with optional subsequent radiotherapy for high-grade meningiomas or radiosurgery following incomplete tumor removal. At present, no pharmacological agents are used as treatment. The use of targeted therapies has been considered, and specific therapies, including anti-EGFR treatment, have been clinically tested. The experience from the treatment of various types of cancers shows that patient outcome depends on the mutational status of particular molecules, including epithelial growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (PIK3CA). Therefore, the aim of the present study was to assess the occurrence and potential use of these markers in patients with meningioma. In total, 55 formalin-fixed, paraffin-embedded meningioma samples were subjected to genomic sequencing of EGFR (exons 18–21), KRAS (exon 1), BRAF (exon 15) and PI3K (exons 9, 20). No mutations were identified in EGFR, KRAS or BRAF. Point mutations in PIK3CA were revealed in the samples of two patients with atypical and anaplastic meningiomas. Although these mutations appear to be rare, this result, along with previously reported findings, indicates that the PI3K/protein kinase B pathway may serve as a more reasonable molecular target for meningioma than EGFR.