Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fenestrae were found in freeze-fractured cisternae of the Golgi apparatus and endoplasmic reticulum of glioblastoma, oligodendroglioma, ependymoma, medulloblastoma, medulloepithelioma, meningioma, cerebellar sarcoma, hemangioblastoma, and chromophobe adenoma. They were about 200--400 A in diameter and often diffusely distributed or concentrated in groups in Golgi cisternae, while they were around 300--600 A in size and scattered in distribution in cisternae of endoplasmic reticulum. They appeared as conical protrusions or circular broken-off necks of face A and as circular holes on face B in tangential fractures, and as several constrictions of cisternae in cross fractures.
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PMID:Fenestrae in golgi and endoplasmic reticulum cisternae of human brain tumours. 16 55

A 21-year-old man with nasopharyngeal tumor was first admitted to the Nagoya University Hospital on April 15, 1972. He had difficulty in speaking and swallowing, and developed double vision prior to admission. A soft and yellow tumor was found in the nasopharynx and revealed typical features of chordoma. The patient underwent Co60 irradiation after the operation. On January 25, 1973, the patient developed double vision of severe degree. Microscopic examination of the specimen which was obtained at the time of the second operation in February 9, 1973, disclosed a coexistence (collision) of chordoma and hemangioblastoma. The two different tumors were situated in juxtaposition on histological examination. Co60 irradiation was added during his second hospitalization. Three months after the second operation, he developed symptoms of meningitis and was hospitalized for the third time on June 3, 1973, at which time the tumor tissue extended through the right frontal and middle fossa. The third operation was done with frontal craniotomy and tumor was partially removed. The histological diagnosis was hemangioblastoma. Postoperatively the patient went downhill and died on September 19, 1973. The report of a collision tumor of intracranial chordoma and hemangioblastoma is not found in the previous literature. There have been many theories as to the origin of collision tumor. Some investigators have proposed that the existence of hyperplastic blood vessels within the glioblastoma is responsible for the collision tumor of sarcoma and glioblastoma. Since the advent of radiotherapy, several examples of sarcoma have been discovered at postmortem examination in patient irradiated for treatment of cerebral neoplasm, both gliogeneous and nongliogenous, suggesting a possible relationship between the tumor and the radiation therapy. In our case, the chordoma showed neither hyperplastic blood vessels nor malignant pattern on histological examination. It was suspected that post-operative radiation induced the hemangioblastoma. The etiology was discussed from the review of literature.
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PMID:[Intracranial collision tumor--A case report (author's transl)]. 103 89

Calcineurin is one of the calmodulin binding proteins and a Ca2+-dependent and calmodulin-stimulated phosphoprotein phosphatase. We used antisera to the calcineurin as a cell-type-specific marker in order to identify neuronal cells in the rat brain and human neoplasms. In normal rat brain slices, basal ganglia were stained macroscopically, and other areas such as cerebral cortex, corpus callosum, cerebellar cortex, granular layer and pyramidal tract of the spinal cord were lightly identified as well. Under the light microscope, it was found that only the neuronal cells were stained, and astrocytes, oligodendrocytes, ependymal cells and vessels were not. Intracellular distribution of the staining showed various patterns and staining intensity of varying degree. Using the PAP method, localization of the calcineurin in formalin-fixed, paraffin-embedded tissues were studied in 65 human intracranial neoplasms, and in 11 human extracranial neoplasms. The neuronal elements of neuroblastoma, ganglioglioma, ganglioneuroma and retinoblastoma were clearly stained. In contrast, glioblastoma, astrocytoma, oligodendroglioma, ependymoma, meningioma, neurinoma, pituitary adenoma, craniopharyngioma, hemangioblastoma, hamartoma, lymphoma and mesenchymal tumor were all negative. Two cases out of 5 medulloblastomas were stained, but others were not. Although positive tumors disclosed various staining patterns and intensities, these results indicated that calcineurin could be a new neuronal marker in human brain tumors.
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PMID:Calcineurin as a neuronal marker of human brain tumors. 242 51

In this article the authors deal with the morphology of primary tumors of the central nervous system and its coverings. The discussion includes astrocytoma variants/glioblastoma, ependymoma and its variants, subependymoma, choroid plexus papilloma and carcinoma, embryonal CNS tumors, neuronal neoplasms, meningioma, dural hemangiopericytoma (angioblastic mengioma), and hemangioblastoma.
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PMID:Central nervous system tumors. 303 Jun 12

The proliferation rate of 40 intracranial neoplasms (30 gliomas, 1 hemangioblastoma, 3 meningiomas, 1 neurinoma and 5 brain metastases) was investigated using the monoclonal antibody Ki-67. In eleven of the gliomas recurrences could be observed, and two of them recurred for second time. In total the Ki-67 labelling indices of 53 specimens were investigated. The Ki-67 nuclear antigen was demonstrated in frozen sections by application of the appropriate monoclonal antibodies according to a modified alkaline phosphatase-antialkaline phosphatase (APAAP) technique. The proliferation rate was evaluated by cell count calculation of the staining index. Ki-67-labelled glioma cells varied from 0.2 percent in one meningioma (WHO-grade I) to 9.1 percent in one glioblastoma. In ten glioma recurrences, higher Ki-67 staining indices could be observed than in their primaries, even when the histological grading did not change substantially. In a cerebellar hemangioblastoma, a trigeminal neurinoma and two endotheliomatous meningiomas the fraction of stained nuclei was less than one percent; however, one recurrent transitional meningioma without any histological sign of malignancy showed a staining index of 2.4 percent. The staining indices of five brain metastases of different malignancies ranged from 1.5 percent in a malignant melanoma to 6.1 percent in bronchial carcinoma. In the majority of the cases examined, the percentage of Ki-67 labelled cells was in accordance with the histologic grade of the neoplasm. In general, there was a direct relationship between the number of stained nuclei and the frequency of mitoses (mitotic index) evaluated in hematoxylin-eosin stained frozen sections. Interestingly, the frequency of mitosis and stained nuclei were higher in tumor recurrences than in the primaries. The results of this study imply that immunohistological labelling of the proliferating cell fraction should become an important additional criterion to predict the biological behaviour of human nervous system neoplasms.
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PMID:Relationship between Ki-67 positive cells, growth rate and histological type of human intracranial tumors. 305 45

To determine whether glial growth factor (GGF)-like activity is associated with human Schwann cell tumors, we tested extracts from these tumors for their ability to stimulate the proliferation of rat Schwann cells in culture. Extracts from 3 of 3 bilateral acoustic neuromas and from 5 of 7 unilateral acoustic neuromas demonstrated dose-dependent stimulation similar to that of partially purified bovine pituitary GGF. One neurofibroma also contained high levels of GGF-like activity, one demonstrated an intermediate level, and three showed low or no activity. Minimal activity was found in one neurofibrosarcoma and in one trigeminal schwannoma. Non-Schwann cell tumors studied included 3 meningiomas, 2 pituitary adenomas, 1 cerebellar astrocytoma, 1 glioblastoma, 1 hemangioblastoma, and 2 metastatic brain tumors. The cerebellar hemangioblastoma demonstrated high GGF-like activity; the others showed little or no activity. Normal tissues used as control specimens included brain, peripheral nerve, muscle, and fat. Some activity was noted in one nerve biopsy; all others showed minimal or no GGF-like activity. High-performance liquid chromatography demonstrated that the GGF-like activity from two acoustic neuromas eluted in a single peak close to that of bovine pituitary GGF. We conclude that acoustic neuromas contain a factor that is closely related to bovine pituitary GGF and that this factor may have a role in the abnormal proliferation of Schwann cells in these tumors.
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PMID:Glial growth factor-like activity in Schwann cell tumors. 376 16

Clinical and pathomorphological findings in 2 stillborn and 15 lifeborn children with primary intracranial tumors are reported. All infants died within the first year of life and the tumors were confirmed histologically. In 6 children the tumors (3 intracranial teratomas, 1 glioblastoma, 1 hemangioblastoma, 1 choroid plexus papilloma) were present at birth. All 6 were born with pathologically enlarged heads. Another child exhibited symptoms of brain tumor at the age of three weeks. The tumor was probably present at birth as well. In the remaining infants the signs and symptoms of tumor development became evident some months after birth. These tumors might have occurred postnatally. In a girl aged 9 months, a nephroblastoma of the right kidney and a malignant cerebral tumor, probably a glioma, were present. An incidental coexistence of both tumors is considered, however, a common etiology cannot be excluded. 8 of the 17 intracranial tumors were supratentorially situated. This supports the view that the proportion of supratentorial tumors is higher in early life than in older children.
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PMID:[Primary intracranial tumors as cause of death in the fetus and infant]. 632 94

In recent years, considerable interest has been directed towards the role of neurotransmitters in various types of brain dysfunctions. There are increasing experimental and clinical evidences that disturbances in the metabolism of central monoamine play an important role in the pathogenesis of brain diseases. Brain tumors are thought to affect and change the neurotransmitter function of the surrounding cerebral tissues. In this study, we tried to analyze and accumulate data about tissue concentrations of biogenic amines in brain tumors and their distribution. Samples from thirty-four intracranial tumors removed at operations were studied. The concentrations in tumor tissues were measured by high performance liquid chromatography systems which were equipped with electrochemical detection (LCEC) and were particularly well suited for the separation and the measurement of the concentration of norepinephrine (NE), dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites; homovanillic acid (HVA), 5-hydroxyindolacetic acid (5-HIAA) and 3-methyoxy-4-hydroxyphenylethyleneglycol (MHPG) in brain tissues. NE levels were under 3ng/g in twenty-five of thirty cases. DA levels were not detected in more than half of the cases. 5-HT levels varied from 0 ng/g to 166.4 ng/g. HVA levels were detected in one glioblastoma, one metastatic tumor, one meningioma and one hemangioblastoma. 5HIAA levels were not detected in most cases except for two meningiomas and one malignant lymphoma. Distribution of tissue concentrations of biogenic amines and their metabolites in four demarcated brain tumors was studied. Samples for determination of tissue concentrations were taken from tumor tissue at central, middle, and peripheral or adjacent portion from the edge of tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tissue concentrations of biogenic amines in brain tumors and their distribution]. 648 88

Cytoplasmic estrogen receptor (ER) and progesterone receptor (PR) proteins were measured by a dextran-coated charcoal absorption technique in 19 intracranial tumors (10 meningiomas, two acoustic neurinomas, two glioblastomas, one primary tumor of neuroectodermal origin, one hemangioblastoma, one metastasis of carcinoma, one chordoma, and one pituitary adenoma). Positive PR values (greater than or equal to 10 fmol/mg of protein) were found in nine meningiomas (90% of these tumors), in the chordoma, in one glioblastoma, and in the hemangioblastoma, whereas positive ER values were recorded only in the pituitary adenoma and in one glioblastoma. Evidence of PR in meningiomas might explain their predominance in women. A possible pharmacological therapy, based on these findings, is discussed.
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PMID:Estrogen and progesterone receptors in intracranial tumors. 650 43

A series of 16 cases of intracerebral hemorrhage associated with brain tumors are described. The literature is reviewed and the incidence of these cases is reported to be low, but we had clinically encountered these cases more commonly than reported, since CT was introduced to the neurosurgical field as a diagnostic aid. The presenting symptoms were those of spontaneous intracerebral hemorrhage or brain tumor. The intracerebral hemorrhage associated with brain tumor may mask the cause of bleeding and confuse the diagnosis. The majority of the tumor causing the intracerebral hemorrhage are highly malignant as glioblastoma or metastatic brain tumor, but there are some benign tumors such as pituitary adenoma, hemangioblastoma, benign astrocytoma and meningioma, which would have good survival rates if discovered early. The mechanisms of massive hemorrhage with brain tumor are not clear. From pathological findings of our cases and other reports, the mechanism seems to be due to the vascular endothelial proliferation with subsequent obliteration of the lung of the vessel. Thin walled, poorly formed vessels in tumor may also become distorted with growth of the tumor and these may easily rupture and bleed. Necrosis with subsequent loss of vessel support may be a factor in production of hemorrhage. Radiation therapy may be a predisposing factor. Children are rarely involved in these cases. The prognosis in the majority of cases would seen to be poor, since the majority of the tumor are highly malignant and most such patients are seen by the neurosurgeon some time after the hemorrhage has accomplished its fatal mischief.
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PMID:[Intracerebral hemorrhage in brain tumors (author's transl)]. 744 24


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