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)

The immunohistochemical distribution of alpha and beta subunits of S-100 protein (S-100 alpha, S-100 beta, respectively) in 138 cases of human brain tumors was investigated by the avidin-biotin immunoperoxidase method. Brain tumors can be divided into four groups: group 1 [S-100 alpha (+) and/or S-100 beta (+)]; astrocytoma, glioblastoma, ependymoma, subependymoma, oligodendroglioma, choroid plexus papilloma, gangliocytoma, meningioma, chordoma, malignant melanoma. Group 2 [S-100 alpha (+) and S-100 beta (-)]; pineoblastoma, pituitary adenoma, craniopharyngioma, rhabdomyosarcoma. Group 3 [S-100 alpha (-) and S-100 beta (+)]; acoustic Schwannoma. Group 4 [S-100 alpha (-) and S-100 beta (-)]; medulloblastoma malignant lymphoma, germinoma. The S-100 beta immunoreactivity pattern in brain tumors was similar to those obtained using conventional anti-S-100 protein sera. In the first group of brain tumors both the number of positively stained tumor cells and the staining intensity were generally greater for S-100 beta than for S-100 alpha with a few exceptions including one gemistocytic astrocytoma, one subependymoma, one malignant melanoma, and some cases of glioblastomas. As to the relationship between malignancy and S-100 protein in glioma, S-100 beta immunoreactivity decreased according to degree of malignancy, while that of S-100 alpha varied, suggesting a heterogeneity of tumor cells in glioblastomas. Immunostaining for S-100 alpha and S-100 beta might become a useful diagnostic procedure in brain tumors and may give us more detailed and precise data of S-100 protein in brain tumors.
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PMID:Immunohistochemical study on the distribution of alpha and beta subunits of S-100 protein in brain tumors. 188 40

100 tumours of the human nervous system were investigated by means of immunohistochemistry in order to determine the expression of epidermal growth factor receptor (EGFr) and the proliferative activity as evaluated by demonstration of the proliferation-associated Ki-67 antigen. Epidermal growth factyr receptor immunoreactivity was present in 79% (23/29) of the high-grade malignant gliomas examined but in only 9% (2/22) of the low-grade gliomas. Besides the gliomas, EGFr-expression was detectable in smaller amounts in most (13/15) meningiomas, in one anaplastic neurinoma and in individual tumour cells of one medulloblastoma. In addition, EGFr-expression was found in 50% (6/12) of metastatic carcinomas. Seven of eight medulloblastomas, two cerebral primitive neuroectodermal tumours (PNETs), three benign neurinomas, one ganglioneuroma, one metastatic intracerebral malignant melanoma, three spinal plasmacytomas and one immunocytoma showed no detectable EGFr-expression. Our results indicate that (1) the expression of EGFr in human tumours of the nervous system depends on the histological tumour type and (2) in the glioma group is related to the grade of malignancy. A close correlation between EGFr-expression and proliferative activity as evaluated by Ki-67 staining could not, however, be established.
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PMID:Epidermal growth factor receptor expression and growth fraction in human tumours of the nervous system. 256

MAb were derived from mice immunized with cells of the human neuroblastoma line IMR-32. Five hybridomas were selected according to their selective binding to human cell lines, tumors and normal tissues. One of them, CE7, reacted with all sympatho-adrenomedullary cells (neuroblastoma, ganglioneuroblastoma, ganglioneuroma, pheochromocytoma, adrenal medulla, sympathetic ganglion cells). Weak cross-reactivities were observed with melanocytes and with some human melanoma and glioma cell lines. The antigen recognized by CE7 was markedly expressed on neuroblastoma tumors of all histological grades, independently of the adrenergic or cholinergic nature of these cells. MAb derived from clones AD2, BC1, BC4 and CB10 bound variably to some, but not to all, neuroblastoma cells. By using these MAb, 3 phenotypes of neuroblastoma lines could be distinguished. The binding profiles of these types, however, showed no correlation with origin of the cell lines or stage of the disease.
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PMID:Production and characterization of monoclonal antibodies against human neuroblastoma. 394 22

Fifty-two patients were examined both with computed tomography using a different third generation scanner and by magnetic resonance imaging (MRI) at half Tesla field strength (Philips Gyroscan 5 S). Excellent contrast and spatial resolution as well as initial comparative results of normal anatomy and also selected clinical cases were demonstrated with the spin-echo (SE) and/or inversion recovery (IR) technique. The clinical material included a residual prolactinoma after transphenoidal surgery, follow-up of a recurrent partly calcified solid and cystic intra-/supra-sellar craniopharyngioma, low-grade glioma under stereotactic-like conditions, suspected pinealoma, recurrent astrocytoma (II-III) and ganglioneuroma at the posterior aspect of the middle and/or lower brain stem, small scar after lower brain stem infarction, stenosing degenerative disease of the cervical spine and multicystic lesion with an underlying benign ependymoma of the cervical spinal cord. MRI--although duplicating some CT results--provided better two- or three-dimensional anatomical detail as well as display of relevant vessels without need of contrast agent. It also gave more specific information in suprasellar tumours containing fat, afforded uniquely specific diagnosis in a bleeding venous malformation of the midbrain and defined more sensitively extra-/intra-axial lesions of the brain stem and cervical spinal cord. Small bony structures (erosions) and punctate calcifications may be missed by MRI. Although ferromagnetic material distorts the MR image, compared with CT, it is not impaired by non-ferromagnetic clips. This is an advantage with respect to postoperative control examinations.
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PMID:Initial experience with MR-imaging of intracranial midline-lesions and lesions of the cervical spine at half Tesla. 609 24

Ganglioglioma, together with its counterparts-ganglioneuroma and gangliocytoma are relatively uncommon neoplasms of the brain composed of neoplastic neurons (ganglion and ganglioid cells) and glial cells. We report here a case of ganglioglioma studied by electron microscopy. The case was further characterized by peculiar chromosomal alterations, 46,XX[6]/43,XX[1], der(1)t(1;5)(q21;q12), der(8;13)(q10;q10),-9,i(10)(q10). Routine light microscopy revealed mixed neuro-glial tumor composed of pilocytic astrocytes with abundant Rosenthal fibers and relatively numerous ganglion cells. The latter were immunoreactive with antibodies (Abs) against synaptophysin and neurofilament protein (NFP). Anti-NFP Abs also immunostained numerous distorted axons embedded in the tumor mass. Some of these showed bullous swellings and thus were analogous to dystrophic neurites or spheroids. Ganglion cells were characterized by abundant intracytoplasmic dense-core vesicles, absence of intermediate filaments and numerous microtubules. Occasionally a close apposition of ganglion cells and Rosenthal fibers were seen. Dense-cored vesicles were pleomorphic and ranged in diameter from small synaptic vesicles to large lysosome-like neurosecretory granules. The former occasionally formed characteristic dumbbell shapes. Neoplastic astrocytes were identical to those of other glial tumors of astrocytic lineage; numerous Rosenthal fibers were frequently seen.
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PMID:The immunohistochemistry and ultrastructure of ganglioglioma with chromosomal alterations: a case report. 870 69

Heterotopic neural tumors are rare in the skin; however, when encountered, they often pose a diagnostic problem. While the clinicopathologic features of most neuroaxis abnormalities are well-documented in the neuropathologic literature, their significance in cutaneous pathology as well as the associated nonneural dermatopathologic findings have not received enough attention. This report offers a comprehensive review of the most common cutaneous neural heterotopic abnormalities and their related tumors. The clinicopathologic features of the following entities along with their histogenetic considerations are discussed: classical and rudimentary meningocele, primary cutaneous meningioma, heterotopic brain tissue (nasal glioma), peripheral primitive neuroectodermal tumor, metastatic neuroblastoma, and ganglioneuroma. Familiarity with the associated dermatopathologic changes and with the differential diagnosis should assist in arriving at the correct diagnosis even without special training in dermatopathology or neuropathology.
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PMID:Cutaneous neural heterotopias and related tumors relevant for the dermatopathologist. 883 15

The role of inflammatory reactions in brain tumors is still unclear. In particular, there is little information about the participation of the microglia/macrophage cell system. We therefore investigated 72 surgical biopsy samples of brain tumors (astrocytoma, glioblastoma, oligodendroglioma, ependymoma, medulloblastoma, cerebral lymphoma, gangliocytoma, neurocytoma and germinoma) and the brains of eight cases with malignant gliomas that came to autopsy, using immunohistochemical markers for the monocyte/macrophage lineage (Ki-M1P, HLA-DR, KP1, My4, My7, Ki-M1, Ki-M6, EBM 11). These markers allowed us to characterize four subtypes of the microglia/macrophage cell system: ramified microglia, ameboid microglia, perivascular microglia and brain macrophages. Among the different tumors, glioblastomas and anaplastic gliomas showed the largest number of mixed cell populations, which consisted of macro-phages and ramified and ameboid microglia. In glial tumors of low malignancy fewer, predominantly ameboid, microglia were found. Neuronal tumors showed only a mild increase of microglia. Cerebral lymphomas contained macrophages diffusely distributed within the tumor center, while activated microglia were prominent at the border zone and in the adjacent brain tissue. The autopsy cases were used to study the morphometric distribution of microglia/macrophages. There was a significant increase of microglia/macrophages within the tumor, but no differences were seen between central and peripheral tumor areas. The non-neoplastic gray and white matter contained more microglial cells than controls. We conclude that the distribution pattern of ameboid and ramified microglial cells and macrophages is distinct in most of the investigated tumor types, underlining the complex immunological function of the microglia/macrophage cell system.
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PMID:Distribution and characterization of microglia/macrophages in human brain tumors. 887 Aug 31

OBJECTIVE Mutations in the isocitrate dehydrogenase (IDH) genes are of proven diagnostic and prognostic significance for cerebral gliomas. The objective of this study was to evaluate the clinical feasibility of using a recently described method for determining IDH mutation status by using magnetic resonance spectroscopy (MRS) to detect the presence of 2-hydroxyglutarate (2HG), the metabolic product of the mutant IDH enzyme. METHODS By extending imaging time by 6 minutes, the authors were able to include a point-resolved spectroscopy (PRESS) MRS sequence in their routine glioma imaging protocol. In 30 of 35 patients for whom this revised protocol was used the lesions were subsequently diagnosed histologically as gliomas. Of the remaining 5 patients, 1 had a gangliocytoma, 1 had a primary CNS lymphoma, and 3 had nonneoplastic lesions. Immunohistochemistry and/or polymerase chain reaction were used to detect the presence of IDH mutations in the glioma tissue resected. RESULTS In vivo MRS for 2HG correctly identified the IDH mutational status in 88.6% of patients. The sensitivity and specificity was 89.5% and 81.3%, respectively, when using 2 mM 2HG as threshold to discriminate IDH-mutated from wildtype tumors. Two glioblastomas that had elevated 2HG levels did not have detectable IDH mutations, and in 2 IDH-mutated gliomas 2HG was not reliably detectable. CONCLUSIONS The noninvasive determination of the IDH mutation status of a presumed glioma by means of MRS may be incorporated into a routine diagnostic imaging protocol and can be used to obtain additional information for patient care.
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PMID:Noninvasive assessment of isocitrate dehydrogenase mutation status in cerebral gliomas by magnetic resonance spectroscopy in a clinical setting. 2829 40