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Objective To establish a maximum tolerated dose of superselective intraarterial cerebral infusion (SIACI) of Cetuximab after osmotic disruption of the blood–brain barrier (BBB) with mannitol, and examine safety of the procedure in patients with recurrent malignant glioma. Methods  A total of 15 patients with recurrent malignant glioma were included in the current study. The starting dose of Cetuximab was 100 mg/m 2 and dose escalation was done to 250 mg/m 2 . All patients were observed for 28 days post-infusion for any side effects. Results  There was no dose-limiting toxicity from a single dose of SIACI of Cetuximab up to 250 mg/m 2 after osmotic BBB disruption with mannitol. A tolerable rash was seen in 2 patients, anaphylaxis in 1 patient, isolated seizure in 1 patient, and seizure and cerebral edema in 1 patient. Discussion  SIACI of mannitol followed by Cetuximab (up to 250 mg/m 2 ) for recurrent malignant glioma is safe and well tolerated. A Phase I/II trial is currently underway to determine the efficacy of SIACI of cetuximab in patients with high-grade glioma.

Leptomeningeal metastasis, also known as neoplastic meningitis, carcinomatous meningitis, and meningeal carcinomatosis, occurs when cancer cells gain access to cerebrospinal fluid pathways, travel to multiple sites within the central nervous system, settle, and grow. This disease has become an increasingly important late complication in oncology as patients survive longer, develop more brain metastases, and newer chemotherapies fail to penetrate the blood-brain barrier. The hallmark of clinical presentation is a cancer patient who complains of focal neurologic dysfunction and is found to have multifocal signs on neurologic examination. The clinical course is relentlessly progressive; treatment is limited and cures are the subject of case reports. This article reviews the clinical course of leptomeningeal metastasis and addresses recent developments in its pathophysiology, diagnosis, and treatment.

Purpose To assess the frequency of chromosomes 1p and 19q deletions in gliomas and to correlate 1p deletion with prognosis in patients with grade 2 and grade 3 gliomas independently of histologic subtype. Methods We retrospectively evaluated 208 patients with WHO grade 2 and 3 gliomas who had 1p/19q molecular studies performed between 2000 and 2004. DNA was extracted from tumor tissue and germline material and evaluated by PCR using microsatellite markers for each chromosome. Results There were 113 men and 95 women with a median age at diagnosis of 40. Thirty-eight patients had a low-grade astrocytoma (A2), 58 low-grade oligodendroglioma (O2), 31 low-grade oligoastrocytoma (OA2), 21 anaplastic astrocytoma (A3), 37 anaplastic oligodendroglioma (O3), and 23 had an anaplastic oligoastrocytoma (OA3). Chromosome 1p analysis was performed in all patients and showed deletions in 105 patients (76% of O2, 42% of OA2, 21% of A2, 89% of O3, 17% of AO3, and 14% of A3). Chromosome 19q studies were performed in 118 patients and showed deletions in 46 (56% of O2, 45% of OA2, 27% of A2, 76% of O3, 11% of OA3 and 0% of A3). On multivariate analyses, chromosome 1p was a prognostic factor for prolonged PFS (HR = 1.75, P  = 0.03) and OS (HR = 3.59, P  = 0.02) in grade 2 gliomas but not for grade 3 (HR = 0.81, P  = 0.7 for PFS; HR = 1.31, P =  0.7 for OS). Conclusion Chromosome 1p deletion is a significant positive prognostic marker in diffuse, grade 2 gliomas regardless of histologic subtype.

Primary central nervous system lymphoma (PCNSL) is a rare intracranial tumor, with an annual incidence of six per million population. Anaplastic variant of primary CNS diffuse large B-cell lymphoma is less common; to our knowledge, there is only one other case report in the world literature. We describe a 71 year old immunocompetent female without significant past medical history who presented with confusion and a homogeneously enhancing midline mass. The patient underwent craniotomy for tumor biopsy, followed by high-dose methotrexate-based chemotherapy despite a remarkably low performance status. Histologically, this tumor was composed of undifferentiated polymorphic tumor cells, multi-nucleated giant cells, extensive necrosis, and conspicuous mitotic activity, mimicking undifferentiated metastatic tumors. Immunohistochemical stains demonstrated immunopositivity of tumor cells for CD20, MUM-1, and BCL-6, and negative staining for CD3, CD10, and CD30. The clinical course, diagnostic workup, pathologic correlates, and treatment outcomes are described.

From basic science to clinical care, to epidemiological disease patters, The Neurology of AIDS is the only complete textbook available on AIDS neurology and the only one comprehensive enough to stand alone in each segment of study in brain disorders affected by the human immunodeficiency virus.

The recombinant antibody fragment Fab GLN 495 recognizes an epitope shared by members of the neuron-associated Hu protein family (including HuC, HuD, and HelNI). This novel reagent labels the nuclei of neurons throughout the peripheral and central neuraxes and has been shown to recognize pulmonary small cell carcinomas and central nervous system (CNS) tumors of mature neuronal phenotype or neuronogenic differentiating capacity. Using this Fab fragment, we have undertaken a systematic survey of normal human tissues and an assessment of 554 non-CNS tumor samples for immunohistochemical evidence of Hu expression. Adrenomedullary cells, pancreatic islet cells, paraganglial chief cells, isolated adenohypophyseal cells, and spermatogonia were the only nonneuronal normal tissue elements to bind Fab GLN 495. In addition to labeling all 10 small cell carcinomas studied (six of which were extrapulmonary in origin), this recombinant anti-Hu Fab proved immunoreactive with neuroblastomas (four/four), esthesioneuroblastomas (one/one), typical (three/four) and atypical (one/four) pulmonary carcinoids, pancreatic islet cell tumors (two/six), large-cell neuroendocrine carcinoma of lung (one/four), Merkel cell tumors (two/three), medullary carcinomas of the thyroid (four/six), pheochromocytomas (two/four) and paragangliomas (four/four). Nonneural/neuroendocrine tumor labeling was restricted to the neuronal and immature neuroepithelial components of teratomas, to extraskeletal myxoid chondrosarcomas (three/four) and to small subsets of cells within examples of renal rhabdoid tumor (one/four), desmoplastic small cell tumor (one/four), alveolar rhabdomyosarcoma (two/four), Ewing sarcoma/PNET (two/nine), and Wilms tumor (one/four). Immunoreactivity was principally nuclear, with variable cytoplasmic labeling. Our findings support the largely restricted expression of Hu by neural/neuroendocrine neoplasms, suggest a potential role for Fab GLN 495 in the identification of small cell carcinomas irrespective of primary site, and support a recent proposal that at least some extraskeletal myxoid “chondrosarcomas” actually represent neuroendocrine tumors of soft parts.

Intracranial mass lesions are common in HIV infected individuals, especially those with the AIDS. These mass lesions may have infectious or neoplastic etiologies. This chapter focuses on neoplastic lesions, though in some cases the distinction between neoplasms and other lesions is blurred because neoplasia can be closely associated with infectious agents (e.g., Epstein Barr Virus). Primary central nervous system lymphomas (PCNSL), gliomas, and leiomyosarcomas all occur with increased frequency in the HIVpositive population and are discussed. Of these conditions, primary central nervous system lymphomas, an AIDSdefining illness, is the most common and developed in greatest detail.