Cases reported "Glioma"

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1/36. Solitary subependymal giant cell astrocytoma: case report.

    In this report, we describe a case of subependymal giant cell astrocytoma in a patient lacking clinical symptoms of tuberous sclerosis. The absence of any features of tuberous sclerosis initially dissuaded us from including subependymal giant cell astrocytoma in our differential diagnosis.
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2/36. Suprasellar chordoid glioma.

    Brat et al. (J Neuropathol Exp Neurol 57:288-290, 1998) reported eight cases of a new clinico-pathological entity, which occurs mainly in the third ventricle of middle-aged females, which they described as chordoid glioma of the third ventricle. We report a new case of a 41-year-old woman with a suprasellar chordoid glioma with histological, immunohistochemical and ultrastructural studies. We discuss the differential diagnosis between chordoma, chordoid meningioma, germinoma and pituitary adenoma. Histologically, the tumour showed cords and lobules of isomorphic epithelioid cells in a vacuolated matrix with prominent multifocal lymphoplasmacytic infiltrates in which some histiocytes and isolated Touton-type giant cells were seen; cells were immunoreactive for glial fibrillary acidic protein but negative for epithelial membrane antigen. Ultrastructural examination revealed abundant intermediate filament but no desmosomes, microvilli nor cilia were seen.
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3/36. Pleomorphic xanthoastrocytoma: report of a case with light and electron microscopy.

    A case of pleomorphic xanthoastrocytoma is reported with light and electron microscopic findings. This unusual tumor arose in a 15-year-old male. The tumor consisted predominantly of nests of xanthomatous cells and plump spindle cells surrounded by a prominent reticulin network. There was considerable cellular pleomorphism with abundant bizarre giant cells and multinucleated cells. Occasional mitoses were present. Electron microscopy and immunoperoxidase localization of glial fibrillary acidic protein (GFAP) confirmed the glial nature of the tumor. Recognition of this tumor is important. Despite its "m alignant" appearance, the tumor characteristically has a relatively good prognosis and should not be confused with high-grade gliomas or meningeal sarcomas, which require aggressive therapy.
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4/36. Fulminant blastomycosis with blastomycotic infection of a cerebral glioma. light microscopic and ultrastructural observations.

    Except for isolated case reports, blastomycosis has not been identified as a significant problem in immunosuppressed patients. We describe an unusual case with blastomycotic infection of a cerebral glioma in a 56-year-old man who underwent radiotherapy for his tumor and died of fulminant blastomycotic pneumonia. This is believed to be the first reported case of blastomyces dermatitidis infection of a cerebral glioma. The light microscopic and ultrastructural features of B. dermatitidis, the giant forms of which were encountered in our patient, are described, and thr role of immunosuppression due to steroid therapy in the pathogenesis of this fulminant infection are reviewed.
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5/36. Cellular whorls in brain tumors other than meningiomas.

    Cellular whorls with or without secondary calcification are generally regarded as reliable diagnostic criteria in the differential diagnosis of meningiomas. They may however occasionally occur in other primary and metastatic brain tumors. Five cases (metastatic laryngeal carcinoma, metastatic mammary carcinoma, metastatic melanoma, medulloblastoma, and giant cell glioblastoma) are presented to illustrate this phenomenon occurring in non-meningothelial brain tumors.
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6/36. Neonatal subependymal giant cell astrocytoma associated with tuberous sclerosis: MRI, CT, and ultrasound correlation.

    We describe a term newborn with tuberous sclerosis who presented with a neonatal brain tumor, diagnosed as a subependymal giant cell astrocytoma. We compare the various imaging modalities used in the diagnosis of this tumor.
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7/36. Giant cell glioblastoma: a work-up of 2 cases with long survival.

    Two patients, in whom visual disturbance (Case 1) and sudden hemiparalysis due to a hemorrhagic lesion (Case 2) had led to craniotomy and histological diagnosis of giant cell glioblastoma, each had an unexpectedly long survival period of 7 and 9 years, respectively. Radiologically, the tumours were well demarcated, but without any distinguishing features, by comparison with glioblastomas in general. The tumours, to a great extent, consisted of cells with large, bizarre multiple nuclei. The highly pleomorphic cells displayed strong cytoplasmic GFAP immunopositivity, which suggested an astroglial origin. Thus, these tumours were considered a variant of glioblastoma ("giant cell glioblastoma") with a more favourable prognosis than experienced by most patients with glioblastoma.
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8/36. The incidence of multifocal cerebral gliomas. A histologic study of large hemisphere sections.

    A series of 241 gliomas (astrocytomas, oligodendrogliomas, glioblastomas, and subependymal giant-cell astrocytomas) was studied. This represents all the gliomas examined post mortem over 25 years at one hospital. Two hundred and one cases (85%) were apparently solitary tumors; of the 40 cases with multiple tumor foci, 23 (9.5%) were true multicentric gliomas. After excluding cases in which there was concomitant disease (neurofibromatosis, tuberose sclerosis, or multiple sclerosis), 18 cases of multicentric tumor (7.5%) remained. Multicentric tumors with different histologic appearances accounted for 2.9% of the series. Celloidin-embedded whole brain sections proved invaluable for the detection of microscopic neoplastic foci and unsuspected diffuse spread. The estimated incidence of multiplicity in gliomas is higher than in most series, but the findings suggest that detection of multifocal neoplastic change in these tumors is directly related to the extent to which the brain is sampled, and that figures obtained in this study may well underestimate the true incidence.
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9/36. Myofibroblastic differentiation of a primary intracerebral sarcoma with gliomatous reaction.

    Microscopic examination of an intracerebral tumor removed from a 50 year-old man revealed a gliomatous rim surrounding a sarcoma. The sarcoma had central necrosis and vascular hyperplasia. Sarcomatous cellular elements consisted of medium-sized undifferentiated cells together with spindle cells associated with a loose collagenous matrix. Although grossly circumscribed, the sarcoma microscopically invaded the brain along an ill-defined border. Adjacent, and encompassed cerebral parenchyma had undergone gliomatous changes consisting of swollen body astrocytes with cellular and nuclear pleomorphism, hyperchromatism and cellularity, and the presence of multinucleated giant cells. The sarcomatous cells were unreactive to antibodies for carcinoembryonic antigen (CEA), keratin, glial fibrillary acidic protein (GFAP), S 100, actin and factor viii although the endothelium and muscularis of neovascular areas were positive for factor viii and actin respectively. The gliomatous rim and encompassed glial elements were strongly positive for GFAP. Ultrastructure of the spindle cell component, found only in the sarcoma, revealed well-formed myofibroblasts with dilated cisternae of rough endoplasmic reticulum (RER) and bundles of myofilaments with dense bodies. The medium-sized cells of the sarcoma were generally undifferentiated. However some of these cells had bundles of microfilaments with areas of condensation although these cells lacked the configuration and dilatations of the RER characteristic of myofibroblasts. Transitional cells between the mature and immature components also occurred. These findings suggest that this sarcoma originates from mesenchymal stem cells undergoing myofibroblastic differentiation.
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10/36. Does successful interferon treatment of tumor patients require life-long treatment?

    Case histories of 5 tumor patients treated with natural leukocyte interferon-alpha (IFN-alpha) are presented. One patient with juvenile laryngeal papillomatosis responded well to interferon treatment, but the disease recurred when therapy was withdrawn. Upon reinstitution of treatment, the patient once again responded well. Another patient with myelomatosis also responded well to interferon therapy and in this case, too, the tumor recurred when interferon treatment was withdrawn. Reinstitution of interferon therapy was, however, unsuccessful. One patient with generalized giant cell tumor of bone responded with regression after more than 5 years of interferon treatment. Another patient with pulmonary osteosarcoma metastases, having received irradiation and interferon combination therapy followed by sole interferon treatment, responded well with a lasting stationary radiogram after 6 years of interferon treatment. One patient with malignant glioma, showing signs of tumor growth during the first few months of interferon therapy, eventually responded, and became disease-free after 6 years. The latter 3 patients are continuously receiving interferon therapy although more than 5 years have elapsed since their interferon therapy was initiated. It is suggested that interferon therapy for malignant tumors be given for life (or to progression of disease) in responding patients. Such a concept entails biological implications for interferon therapy in general and for antitumor action of interferons in particular. Other possible clinical schedules should only be constructed within the framework of controlled clinical trials.
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