Neurosurgery
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Brachytherapy with temporary implants may prolong survival in patients with recurrent glioblastoma multiforme (GBM), but it is associated with relatively high costs and morbidity. This study reports the time to progression and survival after permanent implantation of iodine-125 seeds for recurrent GBM and examines factors predictive of outcome. ⋯ Permanent iodine-125 implants for recurrent GBM result in survival comparable with that described in previous reports on temporary implants, but with less morbidity. Results are most favorable for patients who are younger than 60 years, and who undergo gross total resection. Despite this aggressive treatment, most patients die as a consequence of locally recurrent disease.
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Patients with third ventricular colloid cysts typically are diagnosed when they develop symptoms related to cerebrospinal fluid (CSF) obstruction at the foramen of Monro. However, the clinical and neuroimaging characteristics related to symptom development are poorly understood. ⋯ The patient and neuroimaging characteristics of the different patient classes support a theory on the natural history of colloid cysts. Patients with third ventricular colloid cysts become symptomatic when the tumor enlarges rapidly, causing CSF obstruction, ventriculomegaly, and increased intracranial pressure. Some cysts enlarge more gradually, however, allowing the patient to accommodate the enlarging mass without disruption of CSF flow, and the patient remains asymptomatic. In these cases, if the cyst stops growing, the patient can maintain a steady state between CSF production and absorption and may not require neurosurgical intervention.
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Human gliomas are known to be immunosuppressive. Recent reports have suggested novel strategies to overcome this immunosuppression, including immunogene therapy. We examined expression of 10 immunologically important molecules by human gliomas in vitro, and we discuss the implications for immunogene therapy. ⋯ Class I MHC and Fas expression suggests that human glioma cells may be susceptible to Class I MHC-dependent cytotoxic T cell recognition and Fas-mediated killing. Unfortunately, transforming growth factor beta2 and prostaglandin E2 probably impair T cell activation, and IL-6 may shift immunity to less effective humoral (T helper 2) responses. Proinflammatory gene expression (B7-2, granulocyte-macrophage colony-stimulating factor, and/or IL-12) is lacking. Together, these results suggest that modifying glioma cells via proinflammatory gene transfer or immunoinhibitory gene suppression might stimulate immune responses that are effective against unmodified tumors.