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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new method was developed whereby close comparisons can be made between components of a computed tomography (CT) image and neuropathological findings. This was achieved by a combination of intravital (terminal) CT, postmortem CT, and whole brain sectioning of formalin-fixed tissue. The method was applied in seven cases of malignant supratentorial astrocytic gliomas (Kernohan Grades III and IV) and in one case of thalamic ependymoma. The glioblastoma-like parts of the astrocytic gliomas were usually correctly delineated by postcontrast CT, although there were exceptions to this rule. Tumor components consisting of diffusely growing malignant astrocytoma were difficult or impossible to delineate by CT. Necrotic areas within the tumors were accurately outlined by postcontrast CT. Peritumoral edema was correctly delineated by CT, but growth of diffuse astrocytoma or the presence of astrocytic gliosis within this edematous area seems difficult or impossible to evaluate by current CT techniques.
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PMID:Reliability of computed tomography in assessing histopathological features of malignant supratentorial gliomas. 627 55

The effects of mitogenic lectins Phytohemagglutinin (PHA), and Concanavalin A (Con A) on the growth rate of cells derived from glial tumors (astrocytoma, ependymoma, glioblastoma, medulloblastoma, and C6 rat glioma), neural crest tumors (neuroblastoma and schwannoma), and meningiomas were studied. The cell lines were of human and animal origin. The specificity of lectin binding to mitogenic receptors was evaluated using complementary monosaccharides. In all glial- and some neural-crest tumor-derived cell lines, there was a lectin concentration-dependent and cell density-dependent, biphasic growth rate response with stimulation at low and inhibition at high lectin concentrations. This response did not depend on the type of glial tumor, species of origin, or passage level in vitro. Although, in meningioma-derived cell lines, lectins did not induce a growth rate response, they caused morphological changes ("whorling"). Lectin stimulation in glial tumor-derived cell lines resembles that occurring in peripheral blood lymphocytes. Lectin-induced mitogenesis may lay the groundwork for the establishment of a model of glial cell proliferation, and that permits the evaluation of cell surface effects, intracellular mechanisms, and epigenetic factors in studies of tumors, neural development, and neuroimmunology.
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PMID:Mitogenic lectin receptors of nervous system tumors. Study of gliomas, neural crest tumors, and meningiomas in vitro using phytohemagglutinin and concanavalin A. 628 95

In a series of 26 consecutive autopsy cases of intracranial tumors of neuroectodermal origin, tumor seeding on the ventricular surface and in the subarachnoid space was studied. Five cases of glioblastoma multiforme, six of malignant astrocytoma, six of medulloblastoma, one mixed glioblastoma-fibrosarcoma, one unclassified glioma, and one ependymoma showed ventricular and/or subarachnoid seeding of tumor. The incidence of tumor seeding in our series (76.9%) is much higher than in other series. This discrepancy is probably due to the inclusion of a large number of very small tumor metastases that may have been overlooked in other series. In all cases where metastases were observed the primary tumor extended into the cerebrospinal fluid (CSF). Tumor seeding via the cerebrospinal pathway was more frequently associated with malignant tumors. The distribution of tumor metastases correlated with CSF flow and with the site of focal ependymal defects, which were present in normal brains but occurred more frequently and widely in hydrocephalus.
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PMID:Ventricular and subarachnoid seeding of intracranial tumors of neuroectodermal origin--a study of 26 consecutive autopsy cases with reference to focal ependymal defect. 630 22

An analysis of more than 18,000 primary central nervous system (CNS) tumors revealed only 18 cases (0.01%) in which dropped spinal metastases had caused the presenting symptoms. This group included 11 males and 7 females in whom there was no history of surgical intervention or irradiation. Primitive neuroectodermal tumors ( PNET , medulloblastoma), comprised the largest group (11 patients) followed by high-grade astrocytomas (anaplastic and glioblastoma) (5 patients). One case each of germinoma and ependymoma were also identified. The clinicopathologic data of these cases, and a brief review of the literature are presented.
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PMID:Spinal metastases. A rare mode of presentation of brain tumors. 632 8

In 80 specimens of human glioma the production of glial fibrillary acidic protein (GFAP) by tumour cells invading meninges or connective tissue was studied immuno-cytochemically by the PAP technique. In 38 of 55 cases of astrocytoma, glioblastoma, gliosarcoma, and oligoastrocytoma, GFAP immunoreactivity was greater in the invading cells as compared with the main part of the neoplasm. Fifty-eight percent of the astroglial tumours invading the leptomeninges, all astroglial tumours invading connective tissue and all gliosarcomas showed enhanced GFAP immuno-reactivity of tumour cells getting in contact with collagenous tissue, whereas meningeal infiltrates of 25 non-astroglial tumours (oligodendroglioma, ependymoma, medulloblastoma) remained GFAP-negative like the main part of the respective tumours. In the majority of astroglial tumours an increase of GFAP immunoreactivity was found also in perivascular cells of the main part of the tumour. It is concluded that glioma cells are capable of adapting their cytoskeleton to their micro-environment. Contact with dense collagenous tissue appears as an important factor able to induce an increased production of GFAP by adjacent glial cells.
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PMID:Production of glial fibrillary acidic protein (GFAP) by neoplastic cells: adaptation to the microenvironment. 639 Oct 69

In 1,491 autopsy cases with CNS tumors observed at the Pathological Institute of the Medical Academy of Erfurt in the period from 1953 to 1976 (54,946 autopsies) 72 cases (4.8%) with neurinomas were found. They comprise 67 solitary neurinomas, 1 bilateral acoustic neurinoma without other signs of neurofibromatosis, and 4 cases of neurofibromatosis with neurinomas of the CNS. Among the 68 cases with CNS neurinomas (neurofibromatoses excluded) 87% were acoustic neurinomas, 12% spinal tumors, and 1 case was located in the trigeminal nerve. In 60 (88%) of these 68 cases, the neurinoma was operated upon or clinically diagnosed, resp. The diameter of 18 (26%) neurinomas of the autopsy material was larger than 5 cm. Patients in the 6th decennium predominated in this series. The sex distribution revealed a preponderance of females over males (3:1). In 3 cases further CNS tumors (ependymoma, glioblastoma, meningioma) were found. Additionally, 3 cases had carcinomas of different localization (Table 5). Following tumors were seen in 9 cases of Morbus Recklinghausen with CNS involvement: 4 cases with multiple neurinomas, 3 meningiomas, 1 astrocytoma, 2 glioses and 1 angiomatous malformation (Table 6). Among 1,670 CNS tumors in biopsy material, 144 (8.6%) were neurinomas. 60% of them were located in the nervus acusticus, 40% spinally, mainly in the thoracic region. The 6th decennium was most affected, and females were more frequent than males (2:1) in our material. Nearly all CNS neurinomas were benign. Only 1 spinal tumors was classified as a malignant neurinoma. 2 of the 9 cases with Morbus Recklinghausen had malignant neurogenic tumors (neurofibrosarcomas).
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PMID:[Tumors of the central nervous system in biopsy and autopsy material. 7th communication: neurinomas and neurofibromatoses with CNS involvement]. 641 Jun 15

In normal conditions, neuron-specific enolase (NSE) is histochemically demonstrable only in neurons and cells of the amine precursor uptake and decarboxylation (APUD) system. This has been found not to be true for neoplastic cells. Several types of CNS tumors, including glioblastoma, astrocytoma, oligodendroglioma, ependymoma, medulloblastoma, pineocytoma , meningioma, and choroid plexus papilloma, focally stained positively for NSE. Reactive astrocytes were also frequently positive. In the peripheral nervous system, neuroblastoma, ganglioneuroma, and paraganglioma stained positively for NSE. A number of non-APUD tumors were focally positive. These included schwannoma, carcinoma and fibroadenoma of the breast, renal cell carcinoma, giant cell tumor of the tendon sheath, and chordoma. Caution should be exercised in relying on the immunohistochemical demonstration of NSE as a diagnostic marker in those tumors that do not belong to the APUD cell system. It seems of little value as evidence of differentiation in CNS tumors.
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PMID:Immunohistochemical demonstration of neuron-specific enolase in neoplasms of the CNS and other tissues. 654 18

In a follow up study of 38 patients with supratentrial malignant glioma verified histologically during the 3 years from 1979 to 1982, the same therapeutic method which was the postoperative synchronized radiation-immunochemotherapy was applied. And we investigated the relationships between the survival rate and the histological malignancy, the operative area, and age of admission. Total dose of 5000 to 6000 rad radiation was given after surgery. 0.02 mg/kg of VCR was administered intravenously on the first and the 29th day of radiation, and 2 mg/kg of ACNU was administered intravenously 24 hours after VCR administration. After synchronized radiotherapy, 2 mg/kg of ACNU was given every 6 weeks and 3 g of PS-K was given orally every day. Dose of PS-K was increased especially during the radiation and for 2 weeks after ACNU administration. This radioimmunochemotherapy was applied to 38 patients with malignant glioma, 25 cases of glioblastoma multiforme, 12 cases of malignant astrocytoma, one cases of malignant ependymoma, one case of malignant oligodendroglioma. A complete clinical course of all patients was observed. 18 of 38 cases are surviving. The survival rate of malignant gliomas was 71.2% for one year, 47.6% for 2 years, 34.8% for 3 years. The survival rate of glioblastoma was 56.3% for one year, 36.9% for 2 years, 12.3% for 3 years. The survival rate of the patients receiving macroscopically total removal was higher than that of the patients receiving subtotal removal. The survival rate of the younger patients (under 49 years old) was higher than that of the older patients (over 50 years old). Side effect of this therapy was myelosupression in 75.8%.
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PMID:[Evaluation of radiation immunochemotherapy in the treatment of malignant glioma. Combined use of ACNU, VCR and PS-K]. 658 94

We investigated the effects of local administration of interferon (IFN) on 13 patients with recurrent brain tumors. Histologic diagnoses were glioblastoma (eight patients), medulloblastoma (one), ependymoma (one), ependymoblastoma (one), pontine glioma (one), and astrocytoma (one). When tumor recurrence was evident local administration of IFN was started through an Ommaya reservoir, which was placed during repeat craniotomy. No tumor regressions were seen in the patients given weekly injections of IFN; however, in two of six patients given daily injections, a decrease of tumor volume and augmentation of natural killer activity were seen.
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PMID:Local administration of interferon for malignant brain tumors. 668 76

Interferon inducing activity, antitumor activity and toxicity of poly ICLC (poly IC stabilized with poly L-Lysine and carboxymethyl cellulose) in rodents were studied. SD strain rats were injected intravenously with poly IC or poly ICLC. Interferon in rat plasma was assayed by a plaque reduction method using stomatitis virus. The peak level of plasma interferon of the poly ICLC injection rat was as high as that of poly IC injection rat, and in the former, high level of plasma interferon persisted for 4-12 hours. Next, brain tumor-bearing rats were treated intravenously with poly ICLC and observed for death daily. Weekly treatment with 1 mg/kg of poly ICLC increased the mean survival time although no antitumor effect was observed with poly IC. The LD 50 value of poly IC was 33.5 mg/kg, and that of poly ICLC was 18.6 mg/kg and as to poly ICLC administration, no remarkable side effect was recognized below the dose of 1.5 mg/kg. In clinical trials, poly ICLC was given intravenously at the dose of 0.05-0.2 mg/kg to 9 patients with malignant brain tumor. (6 patients were glioblastoma, 1 was astrocytoma, and 2 were ependymoma.) In 2 patients, poly ICLC was administered once, in 2 patients twice, in 2 patients 3 times, and in 3 patients more than 5 times. The interval of each administration was 7 days. Poly ICLC induced high level of serum interferon (more than 100 reference unit/ml) in all patients and over 100 unit/ml of interferon was maintained for 24 hours. The highest interferon titer induced was 875 unit/ml. The most frequently encountered toxic reaction was fever, which occurred in all cases. The mean peak temperature elevation was 1.9 degrees C, which usually occurred 4-8 hours after drug administration. Modest hypotention was detected in one case. Leucopenia was detected in 3 cases. These abnormalities were all modest, and improved in a few days. As to the effect of poly ICLC, neurological improvement was recognized in 3 cases, and in one of them, remission on CT scan was also recognized.
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PMID:[Effect of interferon inducer (poly ICLC) in the treatment of malignant brain tumor (author's transl)]. 709 65


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