Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cultured cells of explants from 23 human gliomas (seven astrocytomas, eleven anaplastic astrocytomas, three ependymal tumors and two medulloblastomas) were studied to examine cell morphology and expression of glial fibrillary acidic protein (GFAP), vimentin, fibronectin, and N-myc oncoprotein. The most common antigenic phenotype consisted of cells that were GFAP-positive and fibronectin-positive. Both low and high grade astrocytomas retained GFAP expression after several passages in vitro. The establishment of glial tumors in vitro may not necessarily result in loss of GFAP expression early in passage nor is expression of GFAP and fibronectin mutually exclusive. N-myc oncoprotein was seen in only two specimens, one anaplastic astrocytoma and one ependymoma.
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PMID:Expression of glial fibrillary acidic protein, vimentin, fibronectin, and N-myc oncoprotein in primary human brain tumor cell explants. 166 98

The peroxidase anti-peroxidase technique was used for localization of glial fibrillary acidic protein (GFAP) and vimentin (VM) in 19 ependymal tumors in order to determine if a unique pattern of intermediate filament (IF) expression could be demonstrated. Cytokeratin (CK) immunoreactivity was examined in a subgroup of 7 tumors with papillary pattern. Nineteen non-ependymal neuroectodermal tumors were used as controls. Ependymomas, subependymomas and astrocytomas were positive for both IF. Oligodendrogliomas, oligodendroglial portions of mixed gliomas and the majority of medulloblastomas were negative for GFAP and VM. Areas of poor differentiation in all tumors demonstrated little expression of any IF. A composite ependymoma/choroid plexus papilloma showed the presence of GFAP, VM and CK in the papillomatous portion only. Four papillary ependymomas were negative for CK. This study emphasizes the parallel distribution of GFAP and VM in well differentiated ependymomas and other glial tumors and casts doubt upon the concept of VM as a marker for de-differentiation in neuroectodermal neoplasia.
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PMID:Immunocytochemical analysis of intermediate filaments in human ependymal tumors. 245 16

During the period from 1966 to 1996 the authors analyzed the clinicopathological characteristics of 46 cases of histologically verified primary brain tumors with symptomatic onset during the first 3 years of life. The patient group included 27 males and 19 females. There were 14 patients during the first year, 13 during the second year, and 19 during the third year. Supratentorial tumors (60.9%) were more common than infratentorial tumors. Histologically, neuroepithelial tumors predominated. The incidence of ependymal tumors, particularly malignant ones, and of neuronal/mixed neuronal-glial tumors was higher than in previous reports. Congenital brain tumors, those occurring within 2 months after birth, or tumors of dysplastic origin comprised 42.9% of the tumors that developed within 1 year of birth. At the onset, macrocephaly, failure to thrive, and seizures were prominent symptoms or signs in the younger patients. Focal neurological deficits and increased intracranial pressure predominated in the older patients. All but one patient underwent surgical treatment, and 17 patients received adjuvant therapy after surgery. The prognosis was mainly related to the histology of the malignancy. The outcome of medulloblastomas was poor. The quality of life of surviving patients was relatively good, 77.8% having better performance status (PS) than the Eastern Cooperative Oncology Group PS 2.
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PMID:Primary brain tumors in children under age 3 years. 987 57

Protein (lectin)-carbohydrate interaction is supposed to be relevant for tumor cell behavior. The aims of the present work are to investigate whether galectin-1 modulates migration/invasion features in human gliomas in vitro, whether it can be detected in human gliomas immunohistochemically, and whether its expression is attributable to certain glioma subgroups with respect to invasion and prognosis. For this purpose, we quantitatively determined (by computer-assisted microscopy) the immunohistochemical expression of galectin-1 in 220 gliomas, including 151 astrocytic, 38 oligodendroglial, and 31 ependymal tumors obtained from surgical resection. We also xenografted three human glioblastoma cell lines (the H4, U87, and U373 models) into the brains of nude mice in order to characterize the in vivo galectin-1 expression pattern in relation to tumor invasion of the normal brain parenchyma. In addition, we characterized the role in vitro of galectin-1 in U373 tumor astrocyte migration and kinetics. Our data reveal expression of galectin-1 in all human glioma types with no striking differences between astrocytic, oligodendroglial, and ependymal tumors. The level of galectin-1 expression correlated with the grade in the group of astrocytic tumors only. Furthermore, immunopositivity of high-grade astrocytic tumors from patients with short-term survival periods was stronger than that of tumors from patients with long-term survivals. In human glioblastoma xenografts, galectin-1 was preferentially expressed in the more invasive parts of these xenografts. In vitro experiments revealed that galectin-1 stimulates migration of U373 astrocytes.
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PMID:Galectin-1 is highly expressed in human gliomas with relevance for modulation of invasion of tumor astrocytes into the brain parenchyma. 1124 42

Complex and variable morphological phenotypes pose a major challenge to the histopathological classification of neuroepithelial tumors. This applies in particular for low-grade gliomas and glio-neuronal tumors. Recently, we and others have identified microtubule-associated protein-2 (MAP2) as an immunohistochemical marker expressed in the majority of glial tumors. Characteristic cell morphologies can be recognized by MAP2 immunoreactivity in different glioma entities, i.e., process sparse oligodendroglial versus densely ramified astrocytic elements. Here, we describe MAP2-immunoreactivity patterns in a large series of various neuroepithelial tumors and related neoplasms (n = 960). Immunohistochemical analysis led to the following conclusions: (1) specific pattern of MAP2-positive tumor cells can be identified in 95% of glial neoplasms; (2) ependymal tumors do not express MAP2 in their rosette-forming cell component; (3) tumors of the pineal gland as well as malignant embryonic tumors are also characterized by abundant MAP2 immunoreactivity; (4) virtually no MAP2 expression can be observed in the neoplastic glial component of glio-neuronal tumors, i.e. gangliogliomas; (5) malignant glial tumor variants (WHO grade III or IV) exhibit different and less specific MAP2 staining patterns compared to their benign counterparts (WHO grade I or II); (6) with the exception of melanomas and small cell lung cancers, MAP2 expression is very rare in metastatic and non-neuroepithelial tumors; (7) glial MAP2 expression was not detected in 56 non-neoplastic lesions. These data point towards MAP2 as valuable diagnostic tool for pattern recognition and differential diagnosis of low-grade neuroepithelial tumors.
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PMID:Microtubule-associated protein-2 immunoreactivity: a useful tool in the differential diagnosis of low-grade neuroepithelial tumors. 1514 46

We previously demonstrated that the developmentally regulated gene, SOX6, is strongly expressed in glioma cells and in the fetal brain, but only faintly in the normal adult brain. Recent studies have indicated that brain tumor cells may share antigens, signaling systems, and behavior with neural stem/progenitor cells. To test the validity of this proposition, we analyzed the expression of SOX6 in various human central nervous system (CNS) tumors. Immunohistochemical analysis revealed that astrocytic and oligodendroglial tumors expressed SOX6; neuronal-glial cell tumors (central neurocytoma) and embryonal tumors (medulloblastoma), which arise from multipotential stem cell precursors, also showed a high intensity of SOX6 staining. In contrast, ependymal tumors (ependymoma and subependymoma), meningioma, and schwannoma, which are all well differentiated tumors, showed either no staining or only faint staining for SOX6. These results suggest that SOX6 may be expressed in bipotential or multipotential cells capable of neuronal and glial differentiation, but not in fully differentiated cells. SOX6 may be a useful marker for the diagnosis of tumors arising from immature bipotential cells that may differentiate into neuronal and glial cells.
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PMID:Immunohistochemical analysis of SOX6 expression in human brain tumors. 1569 72

The expression of Wilms' tumor gene WT1 protein was investigated immunohistochemically in 73 glial tumors, including 60 astrocytic tumors, eight oligodendroglial tumors, and five ependymal tumors. WT1 protein was detected in 70 of the 73 glial tumors (95.9%) examined. Almost all glioblastomas, anaplastic astrocytomas, anaplastic ependymomas, and anaplastic oligodendrogliomas expressed high levels of WT1 protein. A significant (p < 0.001) correlation was found between WT1 protein expression and MIB-1 staining index. Histological examination found that WT1 protein was strongly expressed in the anaplastic portions and areas with perivascular proliferation and high cellularity, implying that WT1 gene might be important in glial tumor cell proliferation. WT1 gene is overexpressed in various types of solid tumors and WT1 protein is a target antigen for cancer immunotherapy. This study indicates that many malignant glial tumors are good candidates for cancer immunotherapy targeting WT1 protein and that WT1 protein expression could be used as a proliferation marker in glial tumors.
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PMID:Expression of WT1 protein and correlation with cellular proliferation in glial tumors. 1745 20

Ependymomas are well-characterized central nervous system (CNS) tumors that occur most often in children and young adults. Several other CNS tumor entities, including astroblastoma, chordoid glioma, papillary tumor of the pineal region, angiocentric glioma, and pilomyxoid astrocytoma, variably display histopathologic features of ependymal differentiation. The ependymal differentiation in some of these tumors is generally accepted, whereas in others, it is controversial. This article briefly reviews ependymal cell development and conventional ependymomas, the pathologic findings and clinical behavior of tumors with variable ependymal features, and the rationales for their inclusion with ependymomas or exclusion from a larger family of ependymal tumors. These issues are addressed in the context of early morphologic insights of Bailey and Cushing, Friede, and others; contemporary oncologic concepts; and recent relevant molecular and tumor stem cell studies.
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PMID:Central nervous system tumors with ependymal features: a broadened spectrum of primarily ependymal differentiation? 1834 9

Ependymomas are generally considered to be noninfiltrative tumors that have discrete borders with adjacent brain tissue. Most occur in the posterior fossa or spinal cord. Supratentorial ependymal tumors arise near the ventricular system or, more rarely, within the cerebral white matter or cortex. Presented here are 6 supratentorial ependymal tumors, 3 that primarily involve the cerebral cortex and 3 that extend into the cortex from the underlying white matter. By microscopy, all of these tumors locally infiltrate the cortex and/or white matter along small blood vessels and axonal fiber tracts. They also form other glioma secondary structures including perineuronal tumor cell satellitosis and subpial tumor cell mounds. The 3 cortical ependymal tumors show a spectrum of features ranging from conventional and clear-cell ependymoma-like patterns to more angiocentric glioma-like histology. Because ependymal tumors generally have a significantly better prognosis than other infiltrating gliomas, recognition of their capacity to infiltrate adjacent cortex and white matter is important to prevent the misdiagnosis of oligodendroglioma, astrocytoma, or infiltrating glioma, not otherwise specified. Cortical ependymomas and angiocentric gliomas may comprise a group of locally infiltrative ependymal tumors that are associated with an excellent prognosis after gross total surgical resection.
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PMID:Patterns of brain infiltration and secondary structure formation in supratentorial ependymal tumors. 1871 54

In diagnostic pathology thyroid transcription factor-1 (TTF-1) is used as a relatively specific and sensitive diagnostic marker of thyroid and lung adenocarcinomas and lung carcinoids but has also been demonstrated in minor proportions of carcinomas from other organs as well as nonepithelial neoplasms. Two antibody clones are widely used for TTF-1 demonstration, 8G7G3/1 and SPT24, the latter being the most sensitive. Few studies have addressed the occurrence of TTF-1 in central nervous system (CNS) tumors with highly divergent results, a major reason for which seems to be use of different clones. Based on multitissue blocks we analyzed the TTF-1 expression in a series of 155 CNS tumors comparing antibody clones 8G7G3/1 and SPT24 in optimized protocols on the Benchmark Ultra stainer. With clone SPT24 TTF-1 staining was observed in 13 cases (8%). Among astrodendroglial and oligodendroglial tumors, TTF-1 expression was found in 10 of 56 grades III to IV tumors (18%), as opposed to 0 of 47 grades I to II tumors (0%). The TTF-1 expression in positive tumors was generally weak to moderate and focal (mean histoscore 28, range: 2 to 120). TTF-1 positivity was inversely correlated to the expression of nestin. Among 52 other CNS tumors, TTF-1 expression was found in 1 of 3 central neurocytoma (the only CNS tumor with a moderate, diffuse staining), 1 of 18 ependymal tumors, and 1 of 5 choroid plexus tumors, whereas 4 pineal tumors, 11 meningiomas, 8 embryonal tumors, and 4 mixed neuronal-glial tumors all were negative. None of the 155 tumors stained with the 8G7G3/1 antibody clone. TTF-1 expression in primary brain tumors should be taken into consideration when interpreting brain tumors of uncertain origin.
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PMID:Thyroid transcription factor-1 in primary CNS tumors. 2132 40


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