GFAPδ, the delta isoform of the glial fibrillary acidic protein, is mainly expressed in the subventricular zone of the brain, together with other neural stem cell markers like nestin. The authors of this paper were among the first that described in detail the expression of GFAPδ and its correlation with malignancy and invasiveness in cerebral astrocytoma. Later, several papers confirmed these findings, showing that the alternative splice variant GFAPδ is overexpressed in glioblastoma (CNS WHO grade 4) compared with lower grade gliomas. Other studies suggested that a high GFAPδ/α ratio is associated with a more malignant and invasive behavior of glioma cells. Moreover, the changing of GFAPδ/α ratio affects the expression of high-malignant genes. It is now suggested that discriminating between predominant GFAP isoforms, GFAPδ or GFAPα, is useful for assessing the malignancy state of astrocytoma, and may even contribute to the classification of gliomas. Therefore, the purpose of this paper is to review the literature with emphasize on the role of GFAPδ as a potential biomarker, and as a possible therapeutic target in glioblastoma.

Hydatidosis is a rare and serious parasitic disease caused by Echinococcus granulosus larvae, with central nervous system (CNS) involvement being a potentially fatal complication. We present a case of neurohydatidosis in a 55-year-old male farmer exhibiting symptoms of the left parietal syndrome. Imaging studies revealed six well-defined, non-enhancing cystic lesions in the left parietal lobe, and serological evaluation confirmed the presence of Echinococcus-specific IgG antibodies. A chest-abdomen-pelvis CT scan showed no additional hydatid cysts in other organs.The patient underwent microsurgical resection of all six cerebral parietal cysts without rupture, using Dowling's maneuver of hydrodissection with isotonic saline solution. Intraoperatively, the membrane of a previously ruptured seventh cyst was found and excised, and the remaining cavity was irrigated with hypertonic saline solution to prevent recurrence. The patient recovered well without any new neurological deficits or postoperative complications, and a histopathological examination confirmed the diagnosis. He was discharged with previous symptoms in remission and continued antihelminthic treatment with albendazole for 28 days.Cerebral cystic echinococcosis should be included in the differential diagnosis for patients with multiple cystic lesions in the brain. This case report highlights the unusual presentation of multiple cerebral hydatid cysts without the involvement of other parenchymal organs. Surgical resection using hydrodissection combined with antihelminthic therapy is an effective treatment approach for neurohydatidosis.

Symptomatic pontine cavernous malformations carry a high risk of recurrent bleeding, which may result in permanent neurological deficit. Such lesions require surgical management that can be challenging to the neurosurgeon due to their anatomical location and their proximity to delicate neural structures. An ideal surgical approach should provide maximal surgical resection with minimal morbidity. We present the case of a 48-year-old woman with a pontine cavernoma with repeated spontaneous intralesional hemorrhages, resected using a telovelar approach extended by a minimal incision of the inferior vermis, with good surgical outcome. The telovelar approach provided a good access to the lateral recesses and the foramen of Luschka, while the lower vermian incision provided a greater vertical working angle inside the ventricle.

Adult astrocytomas, particularly IDH1/IDH2-wildtype infiltrating astrocytic gliomas, represent a significant challenge for medical professionals. Despite recent progress in understanding tumor biology and the use of molecular biomarkers, therapeutic options have not significantly improved patient outcomes. Although targeted therapies, such as small-molecule tyrosine kinase inhibitors (TKIs), have shown benefits in other solid tumors, they have largely failed to improve survival in adult astrocytoma patients. Characterized by remarkable heterogeneity, these tumors develop robust drug resistance mechanisms. The molecular processes driving this resistance are complex and not yet fully understood. In this review, we briefly present the growth factor receptors (GFRs) and their signaling pathways in adult astrocytomas and discuss the known mechanisms of resistance to small-molecule tyrosine kinase inhibitors.

Glioblastoma (GBM) shows extensive epigenetic heterogeneity. In IDH-wildtype (IDH-WT) GBM, promoter DNA methylation may regulate lineage programs influencing tumor evolution and prognosis; here, we systematically profiled promoter-level methylation dynamics across longitudinal tumors. Genome-wide DNA methylation data were obtained from the publicly available Gene Expression Omnibus (GEO; GSE279073) dataset, comprising a longitudinal cohort of 226 IDH-wildtype glioblastomas profiled on the Illumina Infinium EPIC 850K array across primary and recurrent stages at the University of California, San Francisco. From 333 Gene Ontology gliogenesis-annotated genes (GO:0042063), a 48-gene promoter panel was derived, with ≥2 probes per gene. Promoter methylation was summarized as the median β-value and tested using one-sample Wilcoxon with FDR correction. Functional enrichment, longitudinal variation, and patient-level methylation burden were assessed. Validation analyses were performed using independent IDH-wildtype GBM datasets from The Cancer Genome Atlas (RNA-seq and 450K methylation; n = 347). Promoter hypomethylation predominated across all stages, with 25 genes consistently hypomethylated and 7 hypermethylated. Functional enrichment highlighted gliogenesis, glial cell differentiation, neurogenesis, and Notch-related signaling. In TCGA, promoter methylation inversely correlated with expression for 11 of 33 genes (FDR < 0.05). An Expression Score contrasting hypomethylated and hypermethylated genes was positively associated with improved overall survival, where higher scores predicted better outcome (HR = 0.87, p = 0.016; Q4 vs. Q1 HR = 0.68, p = 0.025), and a complementary Methylation Score showed that higher promoter hypermethylation predicted poorer outcome (HR = 1.73, p < 0.001). CNTN2 and TSPAN2 were adverse prognostic genes (FDR < 0.05). The Expression Score was highest in Proneural tumors and lowest in Mesenchymal tumors (p < 0.001), reflecting a proneural-like state associated with better prognosis. Promoter methylation within gliogenesis genes defines a stable yet prognostically informative epigenetic signature in IDH-WT GBM. Hypomethylation promotes transcriptional activation and a favorable outcome, whereas hypermethylation represses lineage programs and predicts poorer survival.