Cases reported "Brain Neoplasms"

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1/111. Progressive multifocal leukoencephalopathy (PML) and cerebral toxoplasmosis in an adult patient, with no symptoms of underlying immunosuppressing illness.

    We present a case of the coincidence of progressive multifocal leukoencephalopathy (PML) and central nervous system (CNS) toxoplasmosis in an adult patient, without a detectable cause of cell-mediated immunity impairment. The proper diagnosis was made postmortem on the basis of histological changes typical of both pathological processes. PML was characterized by the presence of subcortical focal demyelination, containing enlarged, densely basophilic oligodendrocyte nuclei, often with intranuclear inclusion, and bizarre astrocytes, mimicking neoplastic cells. PML was confirmed by detecting numerous papova virus particles in oligo- and astroglial nuclei by thin-section electron microscopy. Cerebral toxoplasmosis was characterized by the presence of multiple well-circumscribed necrotizing abscesses. Numerous toxoplasma gondii (T. gondii) cysts and free, non-encysted protozoan parasites were found among the inflammatory infiltrates. The diagnosis of cerebral toxoplasmosis was further confirmed by immunocytochemistry. In order to detect putative immunosuppressive background underlying both pathological processes, hiv infection was taken into consideration, however, no histopathological changes indicative of AIDS either in the CNS or in the peripheral organs were eventually found. Moreover no hiv provirus genome was identified in the formalin-fixed, paraffin embedded brain tissue by the polymerase chain reaction (PCR). Current view on the selected aspects of the pathogenesis of both disorders were discussed.
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2/111. Graphic analysis of microscopic tumor cell infiltration, proliferative potential, and vascular endothelial growth factor expression in an autopsy brain with glioblastoma.

    BACKGROUND: Growth of brain tumors requires tumor-cell attachment to adjacent structures, degradation of surrounding matrixes, migration of tumor cells, proliferation of vasculature, and tumor cell proliferation. Comparison of the findings on neuroimaging, degrees and patterns of tumor invasion, regional tumor cell viability detected by Ki-67 immunohistochemistry, and regional vascular endothelial growth factor (VEGF) expression in whole-brain specimen of glioblastoma therefore is of great interest, and will facilitate study of the host reaction against the glioblastoma. methods: We graphically analyzed microscopic tumor-cell infiltration, regional differences in Ki-67 labeling indices (LI), and immunohistochemical expression of VEGF in an autopsy brain with glioblastoma. RESULTS: glioblastoma cells infiltrated the brain far beyond the gross limits of the tumor and the areas with high signal intensity on T2-weighted magnetic resonance images. A wide range of histologic malignancy was apparent from hematoxylin-eosin staining and the Ki-67 labeling indices. VEGF was highly expressed in normal astrocytes located outside the tumor. CONCLUSION: Graphic analysis of histologic and immunohistochemical patterns is a useful method of investigating the mechanisms of glioma growth, tumor cell infiltration in the brain, and the host reaction of the brain against neoplasms.
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3/111. A case history of glioma progression.

    Low-grade diffuse astrocytomas have an intrinsic tendency for malignant progression but the factors determining the kinetics of this process are still poorly understood. We report here the case of a male patient who developed a fibrillary astrocytoma at the age of 33 years and who underwent six surgical interventions over a period of 17 years without radiotherapy or chemotherapy. The first three biopsies spanned a period of 11 years and led to the diagnosis of low-grade, diffuse astrocytoma (WHO grade II), with a growth fraction (MIB-1 labeling index) of 2.3-3.7%. The fourth to sixth biopsies showed histological features of anaplastic astrocytoma (WHO grade III), with growth fractions between 5.0 and 10.5%. The fraction of gemistocytic neoplastic astrocytes also increased, from 0.3% in the first biopsy to 17.5% in the last biopsy and preceded the increase in proliferative activity and transition to anaplastic astrocytoma. The fraction of tumor cells immunoreactive to BCL-2 increased from 0.3% to 8.2%. A p53 mutation in codon 273 (CGT-->TGT, Arg-->Cys) was identified in the first biopsy and persisted throughout the course of the disease. However, the fraction of cells with p53 protein accumulation increased significantly during progression, from 3.2% in the first biopsy to 13.7% in the last. The absence of additional genetic alterations (PTEN mutations, loss of chromosome 10 and 19q) may be responsible for the slow progression and lack of glioblastoma features even after a 17-year disease duration.
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4/111. Primary malignant lymphoma of brain. A review of four cases diagnosed by means of CT-guided stereotactic biopsy.

    In a series of 66 CT-guided stereotactic biopsies (SB) of the brain performed in 1995-1998, four were found to be the primary non-Hodgkin's lymphomas (PCNSL). All cases were studied with immunohistochemistry (broad panel of antibodies; reactions performed mainly on cytological smears) and with the use of an electron microscopy. In an immunophenotyping all cases were positive for leukocyte common antigen (LCA) and 3/4 showed B-cell phenotype. Since the PCNSL are typically located in central, periventricular region of brain and the surgical removal does not bring any benefit, the stereotactic biopsy is a method of choice to make a definite diagnosis that opens the chances for implementation of chemo- and radiotherapy. The diagnostic difficulties that are derivatives of an extremely small amount of the available biopsy material were discussed and the role of the immunophenotyping and of the electron microscopy for avoiding the possible diagnostic mistakes was stressed. Cytological smears stained with H&E and the smears and histological slides with immunohistochemical reaction against glial fibrillary acidic protein (GFAP) showing sometimes extremely dense network of astrocytes mingled with neoplastic lymphoma cells are especially interesting and seem to suggest the involvement of astroglia in the pathogenesis of PCNSL.
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5/111. gliosarcoma: a case with unusual epithelial feature.

    Astrocytic tumors, particularly gliosarcoma, may contain epithelial features in the form of trabecular, adenoid, papillary arrangement, and squamous metaplasia. A case of gliosarcoma with unusual epithelial feature is described. The patient was a 60-year-old male with frequent seizures. The mass was 4 cm and in the left frontal lobe. Trabecular or rarely adenoid arrangement of neoplastic astrocytes was present in the mucinous stroma, and there was a distinctive transition between the trabecular area and typical anaplastic astrocytoma. The tumor cells in the trabecular area showed positive immunostain for glial fibrillary acidic protein, but did not react with various kinds of cytokeratin. The sarcomatous area was undifferentiated and was not labeled by factor-VIII, desmin, and anti-smooth muscle actin. Occurrence and histogenesis of epithelial features in gliosarcoma are reviewed. The importance to recognize the existence of epithelial feature in malignant astrocytic tumor is emphasized.
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6/111. glioblastoma multiforme with epithelial appearance: a case report.

    A case of glioblastoma multiforme with epithelial appearance, which was difficult to diagnose at first operation, is described. microscopy revealed small, darkly staining anaplastic cells which were densely packed. In some areas, these cells were arranged in a tubular, gland-like pattern mimicking a poorly differentiated epithelial neoplasm. Immunostaining of glial fibrirally acidic protein (GFAP) was negative in the densely compact anaplastic areas and within the epithelial patterns, except for a small number of cells in one area. Further pathological study at the second and third operations indicated that the tumor consisted of neoplastic astrocytes and had characteristic features of glioblastoma multiforme, including necrosis, pseudopalisading, and endothelial proliferation. Many of the tumor cells were GFAP-positive. This rare case of glioblastoma multiforme was compared with cases reported in the literature.
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7/111. Cerebellar astrocytoma associated with von hippel-lindau disease: case report with molecular findings.

    We describe the rare occurrence of a cerebellar astrocytoma developing in a patient with the von hippel-lindau disease. This tumour possessed well-differentiated fibrillated astrocytes and moderate vascular proliferation. Tumour cells were uniformly GFAP positive and negative for lipids. This tumour showed an A to C mutation at nucleotide 675 at the splicing donor site of exon 2 of the VHL gene and a concurrent loss of heterozygosity of the 3p25 locus, a site of allelic deletions reported in some astrocytomas. Allelic loci at 17q11, a site of common loss in pilocytic astrocytoma, however, were retained in this tumour. This case illustrates that astrocytomas are rarely found in the von hippel-lindau disease and they may contain genetic changes common to both haemangioblastomas and some astrocytomas.
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8/111. A case of an unclassified tumor closely resembling dysembryoplastic neuroepithelial tumor with rapid growth.

    We describe a rare case of a tumor resembling dysembryoplastic neuroepithelial tumor. A 3-year-old girl had a generalized convulsion as the initial symptom, without other neurological deficits. Computed tomography showed a hypodense lesion with calcific hyperdensity in the left frontal lobe associated with deformity of the overlying calvarium. Four months later, she had a second seizure, and computed tomographic scan showed that the lesion had increased in size. Subtotal removal of the tumor was performed, and the postoperative course was uneventful without radiation therapy. Histological examination revealed a cortical lesion in which an oligodendrocyte-like area and an astrocyte-like area with cytological atypia were observed. Although the clinical course and the radiological findings closely resembled those of dysembryoplastic neuroepithelial tumor, specific glioneuronal elements were not found histologically. Daumas-Duport reported a complex form of dysembryoplastic neuroepithelial tumor that contained glial nodules in addition to a specific glioneuronal element. The histological findings of the glial nodules in this case were quite similar to those she described. We conclude that this could be an unclassified tumor closely resembling dysembryoplastic neuroepithelial tumor without a specific glioneuronal element.
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9/111. Expression and localization of scatter factor/hepatocyte growth factor in human astrocytomas.

    Scatter factor/hepatocyte growth factor (SF/HGF) is a pleiotropic cytokine that has been implicated in glioma invasion and angiogenesis. The SF/HGF receptor, MET, has been found to be expressed in neoplastic astrocytes as well as in endothelial cells of the tumor vasculature. Both SF/HGF and MET expression have also been described to correlate with the malignancy grade of human gliomas. However, most glioblastoma cell lines lack SF/HGF expression, raising the question of the cellular origin of SF/HGF in vivo. Using in situ hybridization, we analyzed glioblastomas, anaplastic astrocytomas, diffuse astrocytomas, pilocytic astrocytomas, and normal brain for the expression of SF/HGF mRNA. We detected strong SF/HGF expression by the majority of the tumor cells and by vascular endothelial cells in all glioblastoma specimens analyzed. Combined use of in situ hybridization with fluorescence immunohistochemistry confirmed the astrocytic origin of the SF/HGF-expressiong cells. In contrast, CD68-immunoreactive microglia/macrophages, as well as vascular smooth muscle cells reactive to alpha-smooth muscle actin, lacked SF/HGF expression. In anaplastic, diffuse, and pilocytic astrocytomas, SF/HGF expression was confined to a subset of tumor cells, and signals were less intense than in glioblastomas. In addition, we detected SF/HGF mRNA in cortical neurons. SF/HGF expression was not up regulated around necroses or at tumor margins. MET immunoreactivity was observed in GFAP-expressing astrocytic tumor cells and endothelial cells as well as in a subset of microglia/macrophages. We conclude that in vivo, both autocrine and paracrine stimulation of tumor cells and endothelium through the SF/HGF-MET system are likely to contribute to tumor invasion and angiogenesis. Lack of SF/HGF expression by most cultured glioblastoma cells is not representative of the in vivo situation and most likely represents a culture artifact.
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10/111. Mixed conventional and desmoplastic infantile ganglioglioma: an autopsied case with 6-year follow-up.

    We describe a case of desmoplastic infantile ganglioglioma (DIG) arising in the ventral diencephalon of a 3-1/2-month-old boy. On biopsy, the tumor featured a desmoplastic, S-100 protein and GFAP immunoreactive stromal element, as well as a variable spectrum of ganglion cells. Electron microscopy demonstrated astrocytes, and morphologically fibroblasts, as well as neurons containing 120-nm dense core granules. In addition, tubular structures composed of tightly apposed cells with features of astrocytes and of Schwann-like cells were also noted. Devoid of fibroblasts, the tubular structures were surrounded by a single basal lamina. At autopsy 6 years later, the multinodular, cystic mass had replaced the diencephalon, extended into both temporal lobes as well as the optic nerves, and showed marked leptomeningeal involvement. Microscopically, superficial portions of the tumor consisted of typical DIG, whereas deep, nondesmoplastic portions exhibited pattern variation ranging from pilocytic astrocytoma to ganglioglioma and gangliocytoma. There was also a minor element of small, 'primitive-appearing' neuroepithelial cells. Dysplastic ganglion cells variously reactive for neurofilament protein and synaptophysin were present throughout the tumor. Our study not only confirms DIG as a variant of ganglioglioma, one capable of slow growth, infiltration, and fatal progression but suggests that its differentiating potential includes elements of both the central and peripheral nervous systems. If so, their derivation may be from multipotential cells of the neural plate.
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