Practical prognostic score for predicting the extent of resection and neurological outcome of gliomas in the sensorimotor area

OBJECTIVE: In this prospective study, we assessed the utility of a novel prognostic score (PS) in guiding the surgical strategy of patients with sensorimotor area gliomas. PATIENTS AND METHODS: Form December 2012 to April 2016, we collected data from patients diagnosed with brain gliomas in the sensorimotor area. All the patients had intraoperatively confirmed contiguity or continuity with sensorimotor cortical and subcortical structures. Several clinical and radiological factors were analyzed to generate a PS for each patient (range 1-8). The end-points included the extent of resection (EOR) and neurological outcome (modified Rankin Score; mRS). We assessed the predictive power of the PS using different analyses. Crosstabs analyses and Fisher's exact test (Fet) were used to evaluate the possible predictive parameters, and for the classification of positive or negative outcomes for the chosen proxies; the significance threshold was set at p<0.05. RESULTS: Using independent t-tests, we compared the mRS at different time points (pre, post, and at 6 months) for 2 subgroups from the total sample using a cut-off PS value of 4. For the EOR, a PS value of ≥5 was predictive of successful outcome, a value of 4 indicated an uncertain outcome, and a value of ≤3 predicted a worse outcome. CONCLUSIONS: This PS value can be easily used in clinical settings to help predict the functional outcome and EOR in sensorimotor area tumors. Integration with information from fMRI, DTI, and TMS, along with MRI spectroscopy could further enhance the value of this P

Corrigendum to "Quantification of chloride channel 2 (CLCN2) gene isoforms in normal versus lesion- and epilepsy-associated brain tissue" [Biochim. Biophys. Acta 1772 (2007) 15-20] (DOI:10.1016/j.bbadis.2006.10.015)

SCOPUS: er.jinfo:eu-repo/semantics/publishe

A neuro-oncologic challenge: the case of a large, aggressive, malignant meningioma of the skull base with paranasal sinus involvement

Malignant meningiomas, rare tumors that account for approximately 1%-3% of all meningioma, have high recurrence, morbidity, and mortality rate and a particularly poor outcome. Surgical excision followed by adjuvant radiotherapy is the current approach for the treatment of these tumors

Second line treatment of recurrent glioblastoma with sunitinib: results of a phase II study and systematic review of literature

Second line treatment of recurrent or progressive glioblastoma multiforme (GBM) is not standardized. Anti-angiogenic strategies with tyrosine-kinase inhibitors have been tested with conflicting results. We tested the association of sunitinib (S) plus irinotecan (CPT-11) in a phase II trial in terms of response rate (RR) and 6-months progression-free survival (6-PFS). We also reviewed the clinical evidence from all the trials with S in this setting published to date and summarized it in a meta-analysis

The treatment of patients with 1-3 brain metastases: is there a place for whole brain radiotherapy alone, yet? A retrospective analysis

To evaluate the efficacy of whole brain radiotherapy (WBRT) with or without other treatments in patients (pts) with 1-3 brain metastases (BM)

EGFR amplified and overexpressing glioblastomas and association with better response to adjuvant metronomic temozolomide

Background: Lack of robust predictive biomarkers, other than MGMT promoter methylation, makes temozolomide responsiveness in newly diagnosed glioblastoma (GBM) patients difficult to predict. However, we identified patients with long-term survival (35 months) within a group of newly diagnosed GBM patients treated with standard or metronomic adjuvant temozolomide schedules. We thus investigated possible molecular profiles associated with longer survival following temozolomide treatment. Methods: We investigated the association of molecular features with progression-free (PFS) and overall survival (OS). Human-derived GBM cancer stem cells (CSCs) were used to investigate in vitro molecular mechanisms associated with temozolomide responsiveness. Surgically removed recurrences allowed investigation of molecular changes occurring during therapy in vivo. Statistical analyses included one-and two-way analysis of variance, Student's t test, Cox proportional hazards, and the Kaplan-Meier method. All statistical tests were two-sided. Results: No association was found between survival and gene classifiers associated with different molecular GBM subtypes in the standard-treated group, while in metronomic-treated patients robust association was found between EGFR amplification/overexpression and PFS and OS (OS, EGFR-high vs low: hazard ratiodeath = 0.22, 95% confidence interval = 0.09 to 0.55, P =. 001). The result for OS remained statistically significant after Bonferroni correction (P interaction <. 0005). Long-term survival following metronomic temozolomide was independent from MGMT and EGFRvIII status and was more pronounced in EGFR-overexpressing GBM patients with PTEN loss. In vitro findings confirmed a selective dose-and time-dependent decrease in survival of temozolomide-treated EGFR+ human-derived glioblastoma CSCs, which occurred through inhibition of NF-\u3baB transcriptional activity. In addition, reduction in EGFR-amplified cells, along with a statistically significant decrease in NF-\u3baB/p65 expression, were observed in specimens from recurrent metronomic-treated EGFR-overexpressing GBM patients. Conclusions: EGFR-amplified/overexpressing glioblastomas strongly benefit from metronomic temozolomide-based therapies

Quantification of chloride channel 2 (CLCN2) gene isoforms in normal versus lesion- and epilepsy-associated brain tissue.

The chloride channel 2 (CLCN2) gene codes for a protein organized in N- and C-terminal regions with regulatory functions and a transmembrane region which forms the ring of the pore. Mutations in the gene have previously been described in patients with idiopathic familial epilepsy. In this study we looked for new isoforms of CLCN2 and we estimated expression levels by real time PCR in brain tissue containing epileptic foci. Samples used in this study were first analyzed and selected to exclude mutations in the coding region of the gene. Four isoforms (skipping exons 3, 16, 22 and 6/7) were identified and quantified by Real Time PCR and compared with total expression of the gene. Expression of the region common to all CLCN2 isoforms was 50% less in epilepsy-associated brain tissue than in controls. The ratio of the various isoforms was slightly greater in epileptic than control tissue. The greatest difference was recorded in the temporal lobe for the isoform with skipped exon 22. Analysis of these isoforms in brain tissue containing epileptic foci suggests that CLCN2 could be implicated in epilepsy, even in the absence of mutations.Journal Articleinfo:eu-repo/semantics/publishe