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Radiation necrosis (RN) occurs in 5% to 25% of patients with brain metastases treated with stereotactic radiosurgery. RN must be distinguished from recurrent tumor to determine appropriate treatment. Stereotactic biopsy remains the gold standard for identifying RN. Initial treatment of RN often involves management of edema using corticosteroids, antiangiogenic therapies, and hyperbaric oxygen therapy. For refractory symptoms, surgical resection can be considered. Minimally invasive stereotactic laser ablation has the benefit of providing tissue diagnosis and treating RN or recurrent tumor with similar efficacy. Laser ablation should be considered for lesions in need of intervention where the diagnosis requires tissue confirmation.

Malignant astrocytomas constitute the most aggressive and common primary tumors of the central nervous system. The standard treatment protocol for these tumors involves maximum safe surgical resection with adjuvant chemoradiotherapy. Despite numerous advances in surgical techniques and adjuncts, as well as the ongoing renaissance in the genetic and molecular characterization of these tumors, malignant astrocytomas continue to be associated with poor prognosis, with median overall survival averaging 15 months for grade IV astrocytomas after standard-of-care treatment. In this article, the goals, principles, techniques, prognostic factors, and modern outcomes of malignant astrocytoma surgery are reviewed. Particular attention is paid to contemporary methods of neuronavigation and functional mapping, the prognostic significance of the extent of resection, surgically delivered adjunctive therapies, and future avenues of research.

In this cadaveric study, a computer-assisted image guidance system was tested for accuracy of thoracic pedicle screw placement.

RNA interference–based spherical nucleic acid nanoconjugates are a potentially safe and brain-penetrant approach for glioblastoma treatment.

ABSTRACTGlioblastoma (GBM) promotes immunosuppression through upregulation of PD-L1 and regulatory T cell (Treg) expansion, but the association of these suppressive factors has not been well elucidated. Here, we investigate a role of PD-L1 in expanding Tregs and the value of targeting the PD-1 receptor to inhibit Treg expansion. Quantitative RNA sequencing data from The Cancer Genome Atlas were evaluated for an association between CD274 and FOXP3 transcript expressions and impact of FOXP3 on clinical outcomes. Peripheral leukocytes from patients with newly diagnosed GBM were profiled for PD-L1+myeloid expressions and Treg abundance. Healthy lymphocytes were assessed for impact of recombinant PD-L1 on expansion of the inducible Treg (iTreg) population. iTreg function was evaluated by the capacity to suppress effector T cell proliferation. Specificity of responses were confirmed by pharmacologic inhibition of the PD-1 receptor. Increased PD-L1 mRNA expression in GBM corresponded to increased FOXP3 mRNA (p= 0.028). FOXP3 elevation had a negative impact on overall survival (HR = 2.0; p< 0.001). Peripheral PD-L1 positivity was associated with an increased Treg fraction (p= 0.008). Lymphocyte activation with PD-L1 co-stimulation resulted in greater iTreg expansion compared to activation alone (18.3% vs. 6.5%; p< 0.001) and improved preservation of the Treg phenotype. Suppressive capacity on naïve T cell proliferation was sustained. Nivolumab inhibited PD-L1-induced Treg expansion (p< 0.001). These results suggest that PD-L1 may expand and maintain immunosuppressive Tregs, which are associated with decreased survival in glioma patients. Blockade of the PD-L1/PD-1 axis may reduce Treg expansion and further improve T cell function beyond the direct impact on effector cells.