Glioma accounts for the majority of human brain tumors. With prevailing treatment regimens, the patients have poor survival rates. In spite of current development in mainstream glioma therapy, a cure for glioma appears to be out of reach. The infiltrative nature of glioma and acquired resistance substancially restrict the therapeutic options. Better elucidation of the complicated pathobiology of glioma and proteogenomic characterization might eventually open novel avenues for the design of more sophisticated and effective combination regimens. This could be accomplished by individually tailoring progressive neuroimaging techniques, terminating DNA synthesis with prodrug-activating genes, silencing gliomagenesis genes (gene therapy), targeting miRNA oncogenic activity (miRNAmRNA interaction), combining Hedgehog-Gli/Akt inhibitors with stem cell therapy, employing tumor lysates as antigen sources for efficient depletion of tumor-specific cancer stem cells by cytotoxic T lymphocytes (dendritic cell vaccination), adoptive transfer of chimeric antigen receptor-modified T cells, and combining immune checkpoint inhibitors with conventional therapeutic modalities. Thus, the present review captures the latest trends associated with the molecular mechanisms involved in glial tumorigenesis as well as the limitations of surgery, radiation and chemotherapy. In this article we also critically discuss the next generation molecular therapeutic strategies and their mechanisms for the successful treatment of glioma.

Glioblastoma multiforme (GBM) occurs rarely in children. Relatively few studies have been performed on molecular properties of pediatric GBMs. Our objective in this study was to evaluate the genetic alterations in pediatric GBM (age < or = 18 years) with special reference to p53, p16, and p27 protein expression, alterations of the epidermal growth factor receptor (EGFR), and deletion of the phosphate and tensin homolog gene (PTEN). Thirty cases of childhood GBMs reported between January 2002 and June 2007 were selected, and slides stained with hematoxylin and eosin were reviewed. Immunohistochemical staining was performed for EGFR, p53, p16, and p27, and tumor proliferation was assessed by calculating the MIB-1 labeling index (LI). Fluorescence in situ hybridization analysis was performed to evaluate for EGFR amplification and PTEN deletion. Histopathological features and MIB-1 LI were similar to adult GBMs. p53 protein expression was observed in 63%. Although EGFR protein overexpression was noted in 23% of cases, corresponding amplification of the EGFR gene was rare (5.5%). Deletion of the PTEN gene was also equally rare (5.5%). One case showed polysomy (chromosomal gains) of chromosomes 7 and 10. Loss of p16 and p27 immunoexpression was observed in 68% and 54% of cases, respectively. In pediatric de novo/primary GBMs, deletion of PTEN and EGFR amplification are rare, while p53 alterations are more frequent compared to primary adult GBMs. Frequency of loss of p16 and p27 immunoexpression is similar to their adult counterparts. This suggests that pediatric malignant gliomas are distinctly different from adult GBMs, highlighting the need for identification of molecular targets that may be adopted for future novel therapeutic strategies.

Being the second largest series to date, it adds significant valuable contribution to this topic. Poor prognostic factors were age >8 years, females, large defects (>7 cm), severe head injury at initial trauma, defects crossing midline and delayed repair (>8 months). Delayed onset seizures and new onset/progression of pre-existing deficits can be indirect markers of evolution. Surgical repair with water-tight dural closure is the standard treatment. Emphasis on early treatment is highlighted which is probably beneficial in improving neurological deficits. Good-to-excellent outcomes are noted in majority, even in cases with delayed presentations.

Formation and expansion of SAC is not completely understood. Myelography, CT myelography and cinematic MRI can demonstrate the location of the communication site between the spinal subarachnoid space and the cyst cavity. The usual management of SAC is excision of the cyst with closure of the dural defect in extradural cysts, while in case of intradural cysts, especially the ones located anterior to the cord, fenestration of the cyst is usually performed.

A 40-year-old male presented with mid-thoracic backache and progressive, ascending, spastic, paraparesis for one year. Magnetic resonance imaging demonstrated an extraosseous, extradural mass, without any bone invasion at the T2-T4 vertebral levels, located dorsal to the thecal sac. The spinal cord was compressed ventrally. The lesion was totally excised after a T2-T4 laminectomy. Histopathological examination revealed a cavernous hemangioma. The authors reported this case and reviewed the literature, to explain why extraosseous, extradural, cavernous hemangiomas should be considered in the differential diagnosis of extradural thoracic compressive myelopathy.