AMMs, as defined by 2000 WHO, are biologically heterogeneous. Recurrence-free survival can be further stratified by location and histological parameters, especially mitotic count, brain invasion, and Ki67 labeling index. Not only brain invasion, but also the presence or absence of brain tissue in surgical specimens should be reported, because the absence of brain invasion, when brain tissue is identified, provides very important positive prognostic information.

Glioblastoma multiforme is the most frequent primary malignancy of the central nervous system. Despite remarkable progress towards an understanding of tumor biology, there is no efficient treatment and patient outcome remains poor. Here, we present a unique anti-proteomic approach for selection of nanobodies specific for overexpressed glioblastoma proteins. A phage-displayed nanobody library was enriched in protein extracts from NCH644 and NCH421K glioblastoma cell lines. Differential ELISA screenings revealed seven nanobodies that target the following antigens: the ACTB/NUCL complex, VIM, NAP1L1, TUFM, DPYSL2, CRMP1, and ALYREF. Western blots showed highest protein up-regulation for ALYREF, CRMP1, and VIM. Moreover, bioinformatic analysis with the OncoFinder software against the complete “Cancer Genome Atlas” brain tumor gene expression dataset suggests the involvement of different proteins in the WNT and ATM pathways, and in Aurora B, Sem3A, and E-cadherin signaling. We demonstrate the potential use of NAP1L1, NUCL, CRMP1, ACTB, and VIM for differentiation between glioblastoma and lower grade gliomas, with DPYSL2 as a promising “glioma versus reference” biomarker. A small scale validation study confirmed significant changes in mRNA expression levels of VIM, DPYSL2, ACTB and TRIM28. This work helps to fill the information gap in this field by defining novel differences in biochemical profiles between gliomas and reference samples. Thus, selected genes can be used to distinguish glioblastoma from lower grade gliomas, and from reference samples. These findings should be valuable for glioblastoma patients once they are validated on a larger sample size.

BackgroundThe purpose of this randomised, single-centre study was to prospectively investigate the impact of anaesthetic techniques for craniotomy on the release of cytokines IL-6, IL-8, IL-10, and to determine whether intravenous anaesthesia compared to inhalational anaesthesia attenuates the inflammatory response.MethodsThe study enroled 40 patients undergoing craniotomy, allocated into two equal groups to receive either sevoflurane (n = 20) or propofol (n = 20) in conjunction with remifentanil and rocuronium. The lungs were ventilated mechanically to maintain normocapnia. Remifentanil infusion was adjusted according to the degree of surgical manipulation and increased when mean arterial pressure and the heart rate increased by more than 30 % from baseline. The depth of anaesthesia was adjusted to maintain a bispectral index (BIS) of 40–60. Invasive haemodynamic monitoring was used. Serum levels of IL-6, IL-8 and IL-10 were measured before surgery and anaesthesia, during tumour removal, at the end of surgery, and at 24 and 48 h after surgery. Postoperative complications (pain, vomiting, changes in blood pressure, infection and pulmonary, cardiovascular and neurological events) were monitored during the first 15 days after surgery.ResultsCompared with patients anaesthetised with sevoflurane, patients who received propofol had higher levels of IL-10 (p = 0.0001) and lower IL-6/IL-10 concentration ratio during and at the end of surgery (p = 0.0001). Both groups showed only a minor response of IL- 8 during and at the end of the surgery (p = 0.57).ConclusionsPatients who received propofol had higher levels of IL-10 during surgery. Neither sevoflurane nor propofol had any significant impact on the occurrence of postoperative complications. Our findings should incite future studies to prove a potential medically important anti-inflammatory role of propofol in neuroanaesthesia.Clinical trial registrationIdentified as NCT02229201 at www.clinicaltrials.gov

IntroductionMeningiomas are intracranial brain tumours that frequently recur. Recurrence rates up to 20% in 20 years for benign meningiomas, up to 80% for atypical meningiomas and up to 100% for malignant meningiomas, have been reported. The most important prognostic factors for meningioma recurrence are meningioma grade, meningioma invasiveness and radicality of neurosurgical resection. The aim of our study was to evaluate the differences in antigenic expression on the surface of meningioma cells between recurrent and non-recurrent meningiomas.Methods19 recurrent meningiomas and 35 non-recurrent meningiomas were compared regarding the expression of MIB-1 antigen, progesterone receptors, cathepsin B and cathepsin L, using immunohistochemistry.ResultsMIB-1 antigen expression was higher in the recurrent meningioma group (p=0.001). No difference in progesterone receptor status between recurrent and non-recurrent meningiomas was confirmed. Immunohistochemical intensity scores for cathepsin B (p= 0.007) and cathepsin L (p<0.001) were both higher in the recurrent than in the non-recurrent meningioma group.ConslusionsMIB-1 antigen expression is higher in recurrent compared to non-recurrent meningiomas. There is no difference in expression of progesterone receptors between recurrent and non-recurrent meningiomas. Cathepsins B and L are expressed more in recurrent meningiomas.