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)

A second instance in which a carcinoma metastatic to the brain has induced the formation of a sarcoma in the associated cerebral blood vessels, is reported. This is analogous to the more common gliosarcoma, a tumor in which a primary glioma, most often anaplastic astrocytoma (glioblastoma multiforme), has induced the formation of a similar sarcoma, with both neoplastic tissues in the same tumor mass. The formation of the sarcoma is attributed to a neoplastic change in the markedly hyperplastic endothelial cells of the cerebral blood vessels that are very commonly found with anaplastic astrocytomas and are often found in relation to metastatic carcinoma. The progression of hyperplasia to neoplasia has long been considered of oncogenetic significance, and in this specific circumstance, appears to be due to some factor or substance which passes from the carcinoma cells to the cerebral vessels.
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PMID:Sarcoma arising in metastatic carcinoma in the brain. A second instance. 647 39

Ten (23%) patients out of 43 with malignant glioma developed meningeal gliomatosis during the follow up period of at least one year. The duration between the first surgery and diagnosis of meningeal gliomatosis ranged from one to 78 weeks (median 45 weeks). In younger age group less than 20 years old, 5 (56%) out of 9 patients had meningeal gliomatosis, and on the contrary the incidence was lower in older age group above 20 years old (5 of 34, 15%). Seven (22%) out of 32 male and 3 (27%) out of 11 female patients developed meningeal gliomatosis. The primary tumor location were frontal lobe in 4 cases (including one bifrontal tumor), temporal in 2, parieto-occipital in 1, thalamus in 1, midbrain in 1, and cerebellar hemisphere in 1, respectively. Histologically, 7 tumors were anaplastic astrocytoma, and 3 were glioblastoma. The characteristic neurological findings observed during the course of meningeal gliomatosis were abnormal mental status (80%), cranial nerve palsies (50%), paraplegia (60%), stiff neck (80%), seizure (50%), and respiratory disturbance (80%), CSF cytology was positive in all 9 patients tested. CT scan demonstrated hydrocephalus (70%), and diffuse contrast enhancement of ventricular wall (60%) and basal cistern (10%). In 2 cases, block and irregular filling defect were seen by myelography. Six patients were treated by irradiation to the whole brain and/or spine, and 5, by intrathecal chemotherapy with methotrexate, cytosine arabinoside and bleomycin. However, all patients died of the tumor one to 46 weeks (median 18 weeks) after the diagnosis of meningeal gliomatosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of meningeal gliomatosis]. 649 23

Regional blood-to-tissue transport, expressed as a unidirectional transfer rate constant (K), was measured in experimental brain tumors using alpha-aminoisobutyric acid (AIB) labeled with carbon 14 and quantitative autoradiography. A total of sixteen oligodendrogliomas, four mixed gliomas, three astrocytomas, two diffuse gliomatosis, one anaplastic astrocytoma, one ependymoma and four malignant schwannomas were studied in 9 rats. The mean Ks for all glioma classifications were similar, averaging 2.6 +/- 0.4 (standard error of the mean) ml . kg-1 . min-1, and were only slightly higher than those for nontumorous parietal cortex (2.1 ml . kg-1 . min-1), corpus callosum (0.9 ml . kg-1 . min-1), and a comparable region of brain tissue in the contralateral hemisphere (1.3 ml . kg-1 . min-1). Values of K varied minimally in the intracerebral gliomas and were marginally correlated with tumor cell morphology in only two tumors. In some (but not all) of the larger gliomas, increased vascularity, with or without endothelial proliferation, was associated with a 3- to 15-fold increase in K. Regional K values in malignant schwannomas were highly variable (4 to 207 ml . kg-1 . min-1) and generally were not correlated with specific histological features of the tumor, except in some regions with increased vascularity. Estimates of the average fractional extraction of AIB by the intracranial gliomas and malignant schwannomas were 0.01 and 0.2, respectively; average fractional extractions for nontumorous brain were approximately 0.003.
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PMID:Regional blood-to-tissue transport in ethylnitrosourea-induced brain tumors. 662 37

Antineoplaston (Ap), a new antitumor agent, was clinically tested for effects on malignant brain tumors. The materials were 3 cases of glioblastoma (G,B), 2 cases of anaplastic astrocytoma, 1 case of pontine glioma, 2 cases of metastatic brain tumor and 1 case of medulloblastoma. All patients underwent radiochemotherapy and surgical resection of the tumors except the cases of pontine glioma, metastatic brain tumor and anaplastic astrocytoma. For gliomas, radiochemotherapy was used with Hu-IFN-beta. Ap was administered at a dose of 7-10 g/day in combination with remission maintenance therapy of gliomas. Complete response was obtained in one anaplastic astrocytoma. Partial response was obtained in 2 cases, a pontine glioma and a metastatic brain tumor. No change was observed in 2 cases, an anaplastic astrocytoma and a multiple brain metastasis. Progression of the disease was observed in 4 cases, 3 glioblastomas and 1 medulloblastoma, which showed continuous increase in tumor size. The effects of Ap on malignant brain tumors were considered due to synergy, since it was administered with other drugs and acceleration of tumor cellular differentiation. Ap is useful as an approach to remission maintenance therapy for brain tumors.
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PMID:The effect of Antineoplaston, a new antitumor agent on malignant brain tumors. 747 50

The secretion of transforming growth factor-beta (TGF-beta), a growth inhibitory factor with immunosuppressive properties, was investigated in one glioblastoma cell line and seven surgically resected malignant glioma cells. Cultured cells from surgically resected tumors were examined immunohistochemically for glial fibrillary acidic protein (GFAP) and S-100 protein. The levels of TGF-beta 1 and TGF-beta 2 in culture supernatants from malignant glioma cells were determined by a specific bioassay using anti-TGF-beta 1 and anti-TGF-beta 2 antibodies. Two glioblastoma cell lines were cultured in the presence of TGF-beta 1 or TGF-beta 2 to assess the effect of TGF-beta on the growth of glioblastoma cells. Cultured cells from surgically resected tumors were positive for both GFAP and S-100 protein. Both active and latent forms of TGF-beta 1 and TGF-beta 2 were detected in the culture supernatants from malignant gliomas, except in one patient with anaplastic astrocytoma which secreted only latent forms of TGF-beta 1 and TGF-beta 2. There was no statistical difference in the levels of TGF-beta 1 and TGF-beta 2 in glioblastomas and anaplastic astrocytomas. Neither TGF-beta 1 nor TGF-beta 2 affected the growth of glioblastoma cells. These findings suggest that most malignant glioma cells secrete both TGF-beta 1 and TGF-beta 2, can convert TGF-beta from a latent to active form, and may suppress cytokine secretion by activated lymphocytes in vivo as well as in vitro.
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PMID:Secretion of transforming growth factor-beta 1 and -beta 2 by malignant glioma cells. 747 84

Tenascin, an extracellular matrix glycoprotein, has been reported to be expressed predominantly on glioma tissue in the CNS, both in a cell associated and an excreted form. Recently, a highly sensitive sandwich type enzyme immunoassay for quantitative determination of tenascin was developed. In the present study, the amount of tenascin in CSF was measured. An increase of tenascin in CSF (> 100 ng/ml) was found in patients with an astrocytic tumour. The concentration was significantly higher (> 300 ng/ml) in high grade astrocytoma (anaplastic astrocytoma and glioblastoma) and a further increase (> 1000 ng/ml) was found in cases of CSF dissemination of high grade astrocytoma. On the other hand, tenascin concentrations were less than 100 ng/ml in non-astrocytic tumours and non-neoplastic neurological diseases, except meningeal dissemination of tumour cells, meningeal stimulation by infection, and subarachnoid haemorrhage. In cases of treated astrocytomas in remission, tenascin was negligible (< 100 ng/ml) in the CSF. The measurement of tenascin in CSF is useful for differential diagnosis of brain tumours and monitoring of astrocytic tumours.
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PMID:Tenascin in cerebrospinal fluid is a useful biomarker for the diagnosis of brain tumour. 752 4

Induction of angiogenesis is essential for the continued growth of solid tumors, and one critical component of tumor-induced angiogenesis involves the stimulation of microvascular cells to migrate into the growing mass. We have developed a convenient model system utilizing dual co-culture chambers to study cellular chemotaxis induced by glioma cells in vitro. In this system, rat C6 glioma cells induced migration of fibroblasts and brain capillary endothelial cells. The migratory response was directly related to the number of C6 cells serving as stimulus in the lower chamber. Similar migratory responses were induced by C6 cell conditioned medium in a concentration dependent fashion. Medium conditioned by cultured human anaplastic astrocytoma cells was also found to contain potent chemotactic factor(s). This system may ultimately be employed in the identification of particular glioma cell population(s) and secreted factor(s) responsible for the chemoattraction of microvascular cells.
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PMID:Glioma-stimulated chemoattraction of endothelial cells and fibroblasts in vitro: a model for the study of glioma-induced angiogenesis. 753 66

Proteases and their inhibitors have been shown to play roles in tumor invasion and metastasis in a number of experimental models. Recently, relative increases in the amounts of urokinase type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) in tumor samples have been correlated with poorer, pathological grade, shorter disease-free interval, and shorter survival. To date, all studies investigating the prognostic significance of proteases and their inhibitors have been limited to extracranial cancer. In this article, we review the literature and present our data on the prognostic significance of proteases in human brain tumors. High levels of uPA were seen in malignant glioma and metastatic tumors (n = 82), whereas normal levels of uPA were found in low-grade gliomas. Analysis with magnetic resonance imaging (MRI) demonstrated a significant correlation between high levels of uPA and necrosis and edema (n = 50; P < 0.05). Similarly, patients with high levels of uPA had shorter survival than did patients with low levels of uPA. Tissue-type plasminogen activator (tPA), which was virtually absent in glioblastoma multiforme (GBM), colon lung, and breast metastasis, was found in normal quantities in anaplastic astrocytoma (AA), low-grade glioma (LGG), and meningioma. Melanoma had significantly more tPA activity than normal brain did. A reverse correlation was found between tPA and MRI findings of necrosis, enhancement, and edema. Similarly, patients with no detectable tPA activity had shorter survival than did patients with detectable tPA activity. We conclude that high levels of uPA and absent tPA activity correlate with histologically malignant brain tumors, aggressive characteristics, and shorter survival.
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PMID:Prognostic significance of proteolytic enzymes in human brain tumors. 753 61

Gangliogliomas are generally low grade neoplasms composed of mixtures of neoplastic glial and neuronal elements whose origin and exact nature are still controversial. We studied a series of 60 intracranial gangliogliomas looking for coexistent cortical architectural abnormalities (cortical dysplasia, microdysgenesis) and to determine if tumor behavior correlates with MIB1 (marker of cellular proliferation) labeling. The patients included 34 males and 26 females who ranged in age from 6 months to 55 years (mean 20 years). Thirty-eight tumors (63%) were located in the temporal lobe and 6 (10%) in the frontal lobe. Fifty-four patients (90%) presented with seizures (most with intractable epilepsy) and the duration of seizures ranged from 1 to 38 years (mean 14 years). In all cases, the predominant glioma component resembled a low grade fibrillary astrocytoma. In 14 tumors (23%), an oligodendroglial component was present. In one case, the glial component resembled an anaplastic astrocytoma. The tumors were characterized variously by perivascular chronic inflammation (N = 45, 75%), vascular proliferation (N = 36, 60%), granular bodies (N = 54, 90%), binucleated neurons (N = 36, 60%), calcification (N = 28, 47%), and cystic degeneration (N = 26, 43%). Meningeal involvement by tumor was observed in five (8%) cases. In 38 patients, sufficient tissue was resected to evaluate for the presence of concomitant cortical architectural abnormalities. Cortical architectural abnormalities were identified near to but clearly separate from the tumor in 19 (50%) patients. Only four patients including the anaplastic tumor died with tumor progression. MIB1 indices (positive tumor cells/1,000 tumor cells counted) in 54 cases ranged from 0 to 10.2 (mean 1.1 +/- 1.0).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cortical architectural abnormalities and MIB1 immunoreactivity in gangliogliomas: a study of 60 patients with intracranial tumors. 754 47

Sixty-four adult patients with malignant glioma entered into a Phase II study on the use of accelerated hyperfractionated radiation therapy. Histology included anaplastic astrocytoma (AA) in 15 patients and glioblastoma multiforme (GBM) in 49 patients. Treatment consisted of radiation therapy doses of 66 Gy in 44 fractions in 22 treatment days in 4.5 weeks, fractions of 1.5 Gy, b.i.d. 1,3-bis(2-chlorethyl)-1-nitrosourea (BCNU) 80 mg/m2 and hydroxyurea 800 mg/m2 were both given on treatment days 1, 6, 11, 16, and 21 during the irradiation course. Median survival time for all 64 patients is 61 weeks (range; 12-163 weeks) from the date of starting irradiation. Median time to tumor progression (MTP) for GBM patients is 31 weeks, and 1-year and 3-year progression-free survival (PFS) are 16% and 0%, respectively, while MTP for AA patients is not attained yet, and 1-year and 3-year PFS are 100% and 73%, respectively. On univariate analysis of prognostic factors for GBM patients, younger age, total or subtotal tumor removal, and frontal tumor location are associated with a better prognosis. A multivariate analysis confirmed the importance of the extent of surgery and tumor site and revealed the interfraction interval (4.5-5.0 hours vs 5.5-6.0 hours, p = .041) as an important prognostic factor. Acute and late toxicity is not increased. Longer follow-up and more patients are needed to evaluate tumor control and toxicity in AA patients.
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PMID:Accelerated hyperfractionated radiation therapy for malignant glioma. A phase II study. 757 67


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