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)

Brainstem acoustic evoked potentials (BAEPs) were measured in 14 children with different type of posterior fossa tumours several times during the clinical course, in order to assess the value of this simple and non-invasive method in the diagnosis and follow-up of posterior fossa tumours in childhood. Eight children had midline medulloblastoma, three children had lateral astrocytoma, three had intrinsic brainstem glioma. Different BAEP patterns could be detected in different tumour's type: bilateral symmetrical or slightly asymmetrical I-V. IPL prolongation in midline medulloblastomas, unilateral or markedly asymmetrical I.-V. IPL prolongation or wave V. depression on the contralateral side in lateral astrocytomas, and severely distorted asymmetrical waveform in intrinsic brainstem gliomas. The BAEPs were abnormal earlier than CT scan in a case of craniospinal astrocytoma. BAEPs were useful in the follow-up: the effect of the preoperative chemotherapy or the progression of the inoperable tumours could be as well documented by this method, as by the CT scan. BAEPs proved effective in the assessment of postoperative neurological complications: bilateral symmetrical IPL prolongation and wave V. depression with clinical signs of increased intracranial pressure occurred in a case of postoperative occlusive hydrocephalus, unilateral IPL prolongation occurred during irradiation or chemotherapy after medulloblastoma removal as signs of cerebral oedema.
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PMID:Value of brainstem acoustic evoked potentials in posterior fossa tumours in childhood. 186 81

Cortically homografted C6 glioma-astrocytoma cells both invade the rat host brain as a mass and migrate as individual cells. In contrast, fetal astrocytes derived from homografted whole pieces of fetal cortex migrate only as individual cells throughout the brain of the rat but are not capable of invasion. Our experiment explored the migratory capacity (over 7 days) of cultured purified fetal astrocytes and C6 cells after seeding 10(6) cells on a hydrated artificial basement membrane wafer (Matrigel). The artificial basement membrane wafer was not a suitable substrate for the growth of cultured fetal astrocytes. In contrast, C6 cells migrated as individual cells from the surface of the wafer into the substrate. Individual C6 cells migrated 1.8 mm in the first 4 days and then ceased migration. The C6 cells were observed at the base of a digestion tube that extended from and was open to the surface of the wafer. At 3 days, micropockets were observed to form around each C6 cell at the base of each tube. By 7 days, the majority of pockets observed were large and contained several C6 cells. These multiple cell groups appeared to be progenitors of tumor masses. These data indicate that C6 glioma-astrocytoma cells, which in vivo appear to be a model for glioblastoma multiforme, primarily migrate as individual cells through artificial basement membrane and secondarily form tumor masses. Progenitor tumor masses form by coalescence of individual C6 cell micropockets or the division of a single cell in an individual micropocket.
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PMID:C6 glioma-astrocytoma cell and fetal astrocyte migration into artificial basement membrane: a permissive substrate for neural tumors but not fetal astrocytes. 187 42

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

A patient with parieto-occipital cortical calcification characteristic of Sturge-Weber-Dimitri disease (SWDD) is of interest in that she lacked the facial portwine lesion and almost all other features of the disease. She subsequently developed an astrocytoma in the underlying white matter. Although the absence of the facial lesion in SWDD has previously been described, there has been no report of a glioma developing in such a patient. The association of SWDD and astrocytoma in this case most likely has been fortuitous.
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PMID:Sturge-Weber-Dimitri disease? In association with an astrocytoma. 188 25

This audit of clinical management confirmed the poor prognosis for patients (n = 80) aged over 60 years with a diagnosis of supratentorial glioma. The median survival time after diagnosis was 9 weeks following steroids and 7 weeks after biopsy and steroids. Cytoreductive surgery and radiotherapy improved median survival time by a maximum of 16 weeks, but there was significant morbidity in some patients undergoing craniotomy. Although 92% of the biopsied lesions were either glioblastoma or anaplastic astrocytoma, the median survival of these patients was similar to the 8% of patients confirmed as having intermediate grade astrocytoma. Patients presenting with minimal functional deficit (WHO grade I or II) had longer median survival times than those presenting in poor condition (WHO grade III or IV). In this series there was no relationship between management undertaken and clinical status of the patient. The 9% of the cohort that survived 1 year were treated in a variety of ways. This audit, together with results from other studies, suggests that a prospective clinical trial of different management regimes in elderly patients with supratentorial gliomas is needed. Since median survival time in the most intensively treated patients will be around 6 months, treatment evaluation must consider the quality of life provided.
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PMID:Management of patients aged over 60 years with supratentorial glioma: lessons from an audit. 189 54

Sixteen patients with recurrent childhood brain tumors were treated with intravenous cisplatin, cytosine arabinoside and etoposide (PAE), daily for three days every three to four weeks. Objective responses were observed in 6 of 15 evaluable patients and an additional six patients had stable disease for greater than 6 months. The tumor-specific response rate for astrocytoma/glioma was 3 of 7 and for medulloblastoma was 2 of 4. The mean progression-free interval was 11.0 months and the hazard rate for progression was 0.085 per patient-month of observation. The most common toxicities were neutropenia and thrombocytopenia. Clinically significant ototoxicity was identified in 7 patients. The activity of PAE chemotherapy for recurrent childhood brain tumors warrants further investigation.
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PMID:Cisplatin, ara-C and etoposide (PAE) in the treatment of recurrent childhood brain tumors. 191 47

Two kinds of novel neural trophic factors were currently detected in von Recklinghausen neurofibroma (NF1) extracts. One of the two was a growth factor, neuroblastoma growth factor (Mr less than 5 kDa), which promotes the proliferation of human neuroblastoma cell and survival and neurite-extension of rat cortical neurons, but differently from nerve growth factor (NGF) or NGF-like factors. The other one was a glial growth inhibitor (Mr = 100 kDa), which suppresses the growth of glioma cell lines, astrocytoma, glioblastoma, oligodendroglioma and Schwannoma. These factors do not appear to be previously identified cytokines or growth factors such as interleukins, granulocyte colony-stimulating factor, NGF and fibroblast growth factor. There was also detectable ciliary neurotrophic factor-like activity in the extracts. The primary cause of high contents of these factors in NF1 is not known, but may relate to fundamental mechanisms controlling growth and differentiation of neurons and glias during development of nervous system.
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PMID:von Recklinghausen neurofibroma produces neuronal and glial growth-modulating factors. 193 68

Neuraxis radiation therapy (RT) for primary intracranial tumors is associated with major late effects if administered to very young children. To control residual tumor and to delay RT, we treated eight young children (median age 6.5 months) with primary central nervous system (CNS) tumors using combination chemotherapy: cisplatin, 20 mg/M2/day plus VP-16, 75 mg/M2/day i.v. for 5 days, given q. 3-6 weeks for 8 cycles. The tumors were medulloblastoma (one), malignant ependymoma (two), primitive neuroectodermal tumor PNET (two), malignant glioma (two), astrocytoma (one). Six had measurable disease; three had positive cerebrospinal fluid (CSF) cytopathology. All patients with measurable tumor had initial objective responses (three) complete response [CR], one partial response [PR], two minor response [MR], including cytopathology (three CR of three) and metastatic deposits (two CR of two). One patient relapsed during chemotherapy. Median time to disease progression was 17.5 months; median survival was 34 months. Three patients, none of whom received RT, have prolonged progression-free intervals of 47-67 months to date. Neurodevelopmental progress continued during and after chemotherapy. Chemotherapy toxicity was mild. Median neutrophil nadir was 312/mm3, platelets 72,000. Fever during neutropenia occurred in six of 61 courses. Moderate high-frequency auditory losses were detected in three patients, and mild renal injury (GFR less than 70 ml/min) was detected in two of seven evaluable children. This pilot study demonstrates the apparent efficacy and mild toxicity of 5 day courses of cisplatin plus VP-16, with delayed RT, in young children with CNS neoplasms. A POG treatment protocol that incorporates cisplatin plus VP-16 is evaluating primary chemotherapy with delayed radiotherapy in larger numbers of pediatric brain tumor patients.
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PMID:Efficacy of postoperative chemotherapy using cisplatin plus etoposide in young children with brain tumors. 199 Feb 53

The cooperative study on the beta-interferon (IFN) therapy for glioblastoma and malignant astrocytoma reported the response rate as 14.0%. Continuing study resulted the response rate of 24.0% to low grade astrocytoma and 20.0% to medulloblastoma. Totally, effectiveness of 19.2% to gliomas was confirmed in 120 evaluated cases. A randomized study was conducted on combination therapy with beta-interferon and chemoradiotherapy. The response rate of 41.2% (21/51) in the group treated with IFN, ACNU and Radiation was significantly higher than the rate of 19.6% (10/51) in the group treated with ACNU and radiation only. Application of IFN to a maintenance therapy is also on going. Adoptive immunotherapy has been developed as potential therapeutic method of malignant glioma. Lymphokine activated killer cells (LAK) and Tumor infiltrating lymphocytes (TIL) are put to clinical use. Clinical application of human monoclonal antibody (MAb) CLN-IgG was conducted to recurrent malignant glioma. 131I labeled MAb was administered intratumorously and the specific incorporation was confirmed by gamma-scintigraphy. Concomitant administration of interferon enhanced the efficacy of the therapy. This radio-immunotherapy holds future promise as a new therapeutic approach to gliomas.
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PMID:[Advances of BRM therapy of malignant brain tumors]. 199 12

The antitumor effect of alkyl-lysophospholipid (ALP) was studied on a continuous glioma cell line (GaMg) as well as on tumor spheroids obtained from three different primary brain tumor biopsies. GaMg monolayer growth was reduced by 50% after treatment with 30 microM ALP; cells accumulated in the G2M phase of the cell cycle as determined by flow-cytometric analyses. Tumor spheroid growth was reduced by 25 and 44% during treatment with 10 and 30 microM ALP, respectively. These drug concentrations also caused a severe destruction of spheroids. No effect on growth or morphology was seen in spheroids treated with 0.1 and 1.0 microM ALP. ALP caused a dose-dependent inhibition of invasion by GaMg tumor spheroids into brain aggregates. After 168 h of 1.0 microM ALP treatment, the volume of the intact brain aggregate was 90% larger than that in the untreated co-cultures. To further investigate the efficacy of ALP as an anti-invasive drug, co-cultures were performed with specimens obtained from three primary brain tumors: a highly invasive glioblastoma multiforme, an anaplastic astrocytoma, and an astrocytoma. Treatment of spheroids from the most invasive tumor with ALP caused a 7-fold preservation of normal brain tissue relative to control co-cultures. Moreover, the sensitivity of primary glioma spheroids to the anti-invasive effect of ALP seemed to be associated with the aggressiveness of the tumor; spheroids from the more malignant specimen (glioblastoma multiforme) were more sensitive than those from the less aggressive tumors. The anti-invasive effect seen with nontoxic concentrations of ALP may prove valuable in the treatment of malignant gliomas.
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PMID:Effect of alkyl-lysophospholipid on glioblastoma cell invasion into fetal rat brain tissue in vitro. 199 62


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