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Background: Glioblastoma (GBM) is the most common primary, malignant brain tumor in adults and has a poor prognosis. The median progression-free survival (mPFS) of newly diagnosed GBM is approximately 6 months. The recurrence rate approaches 100%, and the case-fatality ratio approaches one. Half the patients die within 8 months of recurrence, and 5-year survival is less than 10%. Advances in treatment options are urgently needed. We report on the efficacy and safety of a therapeutic vaccine (SITOIGANAP: Epitopoietic Research Corporation) administered to 21 patients with recurrent GBM (rGBM) under a Right-to-Try/Expanded Access program. SITOIGANAP is composed of both autologous and allogeneic tumor cells and lysates. Methods: Twenty-one patients with rGBM received SITOIGANAP on 28-day cycles in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), cyclophosphamide, bevacizumab, and an anti-programmed cell death protein-1 (anti-PD-1) monoclonal antibody (either nivolumab or pembrolizumab). Results: The mPFS was 9.14 months, and the median overall survival (mOS) was 19.63 months from protocol entry. Currently, 14 patients (67%) are at least 6 months past their first SITOIGANAP cycle; 10 patients (48%) have received at least six cycles and have a mOS of 30.64 months and 1-year survival of 90%. The enrollment and end-of-study CD3+/CD4+ T-lymphocyte counts strongly correlate with OS. Conclusions: The addition of SITOIGANAP/GM-CSF/cyclophosphamide to bevacizumab and an anti-PD-1 monoclonal antibody resulted in a significant survival benefit compared to historic control values in rGBM with minimal toxicity compared to current therapy.
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BACKGROUND: This study sought to present a very rare case of a posttraumatic midbrain lesion producing a debilitating constellation of symptoms identified as Benedikt's syndrome. METHODS: A 20-year-old woman with traumatic brain injury presented with ipsilateral internal and external ophthalmoplegia, and contralateral hemiataxia, proprioception disturbances, hypertonicity, slight hemiparesis, and hyperactive tendon reflexes. A bibliographic search was performed in PubMed. RESULTS: Neuroimaging revealed a left midbrain lesion at the level of the superior colliculi. In the literature, virtually all Benedikt's syndrome cases, which are rare anyway, are due to midbrain infarcts (basilar or posterior cerebral artery branches). There is only one case from 1963, reported as a posttraumatic Benedikt-type dyskinesia (French language). The historical evolution of the anatomopathologic correlations of the syndrome is also discussed. CONCLUSIONS: Benedikt's syndrome is a very rare condition, usually of vascular etiology. Our case is just the second one of traumatic pathogenesis ever reported, the first in the English language literature.