OBJECTIVE Imposter syndrome (IS) occurs when high-achieving individuals have a pervasive sense of self-doubt combined with fear of being exposed as a fraud, despite objective measures of success. This is one of the main causes of burnout among professionals, threatening their mental health and general well-being. The prevalence and severity of IS among neurosurgery residents and young neurosurgeons has not been yet studied. The primary outcomes of this study were the prevalence and severity of IS. METHODS An anonymous cross-sectional survey including both a demographic questionnaire (Clance Imposter Phenomenon Survey) and compensatory mechanisms was distributed to young neurosurgeons and residents in neurosurgery in Italy. RESULTS A total of 103 responses were collected. The prevalence rate was 81.6%. Among the respondents with IS, 42.7% showed moderate signs, 27.2% frequent, and only 11.7% had an intense symptomatology. Level of education, female sex, and academic achievements were all identified as predictive factors of IS. CONCLUSIONS A total of 81.6% of respondents reported potentially significant levels. The implications of IS on both the outcomes in patients and the well-being of neurosurgeons should be evaluated in future studies.
Surgical management of Diffuse Low-Grade Gliomas (DLGGs) has radically changed in the last 20 years. Awake surgery (AS) in combination with Direct Electrical Stimulation (DES) and real-time neuropsychological testing (RTNT) permits continuous intraoperative feedback, thus allowing to increase the extent of resection (EOR). The aim of this study was to evaluate the impact of the technological advancements and integration of multidisciplinary techniques on EOR. Two hundred and eighty-eight patients affected by DLGG were enrolled. Cases were stratified according to the surgical protocol that changed over time: 1. DES; 2. DES plus functional MRI/DTI images fused on a NeuroNavigation system; 3. Protocol 2 plus RTNT. Patients belonging to Protocol 1 had a median EOR of 83% (28–100), while those belonging to Protocol 2 and 3 had a median EOR of 88% (34–100) and 98% (50–100) respectively (p = 0.0001). New transient deficits with Protocol 1, 2 and 3 were noted in 38.96%, 34.31% and 31,08% of cases, and permanent deficits in 6.49%, 3.65% and 2.7% respectively. The average follow-up period was 6.8 years. OS was influenced by molecular class (p = 0.028), EOR (p = 0.018) and preoperative tumor growing pattern (p = 0.004). Multimodal surgical approach can provide a safer and wider removal of DLGG with potential subsequent benefits on OS. Further studies are necessary to corroborate our findings.
Predictive factors for response to regorafenib in recurrent glioblastoma, IDH-wildtype, are scarcely recognized. The objective of this study was to identify molecular predictive factors for response to regorafenib using a clinically available platform. We analyzed a prospective cohort of 30 patients harboring recurrent glioblastoma, IDH-wildtype, and treated with regorafenib. Next-generation sequencing (NGS) analysis was performed on DNA extracted from paraffin-embedded tissues using a clinically available platform. Moreover, MGMT methylation and EGFRvIII expression analyses were performed. Six-month progression-free survival (PFS) was 30% and median overall survival (OS) was 7.5 months, in line with literature data. NGS analysis revealed a mutation in the EGFR pathway in 18% of cases and a mutation in the mitogen-activated protein-kinase (MAPK) pathway in 18% of cases. In the remaining cases, no mutations were detected. Patients carrying MAPK pathway mutation had a poor response to regorafenib treatment, with a significantly shorter PFS and a nonsignificantly shorter OS compared to EGFR-mutated patients (for PFS, 2.5 vs 4.5 months, p = 0.0061; for OS, 7 vs 9 months, p = 0.1076). Multivariate analysis confirmed that MAPK pathway mutations independently predicted a shorter PFS after regorafenib treatment (p = 0.0188). The negative prognostic role of MAPK pathway alteration was reinforced when we combined EGFR-mutated with EGFRvIII-positive cases. Recurrent glioblastoma tumors with an alteration in MAPK pathway could belong to the mesenchymal subtype and respond poorly to regorafenib treatment, while EGFR-altered cases have a better response to regorafenib. We thus provide a molecular selection criterion easy to implement in the clinical practice.
OBJECTIVE Glioma-associated stem cells (GASCs) have been indicated as possible players in supporting growth and recurrence in glioblastoma. However, their role in modulating immune response in the peritumoral area has not yet been described. In this study, the authors aimed to investigate programmed death-ligand 1 (PD-L1) differential expression at the protein level in GASCs derived from different tumor areas (core, periphery, and surrounding healthy brain). METHODS Tumor tissue samples were collected from patients who underwent surgery for a histopathologically confirmed diagnosis of glioblastoma. Sampling sites were confirmed via neuronavigation and categorized on 5-aminolevulinic acid (5-ALA) fluorescence as bright (ALA+), pale (ALA PALE), or negative (ALA−), which corresponds to the tumor mass, infiltrated peritumoral area, and healthy brain, respectively, during surgery. GASCs were first isolated from the 3 regions and analyzed; then Western blot analysis was used to evaluate the level of PD-L1 expression in the GASCs. RESULTS Overall, 7 patients were included in the study. For all patients, the mean values ± SD of PD-L1 expression in GASCs for ALA+, ALA PALE, and ALA− were 1.12 ± 1.14, 0.89 ± 0.63, and 0.57 ± 0.18, respectively. The differentially expressed values of PD-L1 in GASCs sampled from the 3 areas were found to be significant (p < 0.05) for 3 of the 7 patients: patient S470 (ALA+ vs ALA− and ALA PALE vs ALA−), patient S473 (ALA+ vs ALA PALE and ALA PALE vs ALA−), and patient S509 (ALA+ vs ALA−). CONCLUSIONS This analysis showed, for the first time, that GASCs expressed a constitutive level of PD-L1 and that PD-L1 expression in GASCs was not uniform among patients or within the same patient. GASC analysis combined with 5-ALA–guided sampling (from core to periphery) made it possible to highlight the role of the tumor microenvironment at the infiltrating margin, which might cause clinical resistance, opening interesting perspectives for the future.
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