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)

Eflornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase, and mitoguazone (MGBG), a competitive inhibitor of S-adenosylmethionine decarboxylase, were evaluated in a phase I-II study for patients with primary recurrent malignant brain tumors. All patients had failed prior radiation therapy and most had also failed prior chemotherapy. Two dose schedules were used, with the second schedule (Group II) a modification of the first schedule (Group I). The Group II schedule, with different dose levels, was better tolerated than the Group I schedule. Gastrointestinal and myelotoxicity were dose-limiting in most patients, and tinnitus was dose-limiting in two patients. Nineteen of 33 evaluable patients had anaplastic gliomas, in whom response was observed in 21%, stable disease in 53%, and immediate progression after one course of therapy in 26%. Of six patients with glioblastoma multiforme, two had brief stabilization of disease. An additional patient with brainstem glioma and ependymoma also had disease stabilization. Four patients with medulloblastoma, a spinal cord mixed glioma, and one with oligodendroglioma failed DFMO-MGBG. Based on this study, we believe that a combination of DFMO and MGBG is well-tolerated and deserves further evaluation for patients with anaplastic gliomas, particularly those that appear to be biologically slow growing.
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PMID:Phase I-II study of eflornithine and mitoguazone combined in the treatment of recurrent primary brain tumors. 310 81

Three human glioma cell lines (TE-671 medulloblastoma, U-87 MG glioblastoma, and U-373 MG glioblastoma) were transplanted to the quadrigeminal cistern of the brain in 37 newborn Sprague-Dawley rats and to the subcutaneous space in 30 of their siblings. Two of the three gliomas (the TE-671 medulloblastoma and the U-87 MG glioblastoma) grew both intracranially and subcutaneously. The U-373 MG glioblastoma did not grow in either site. The resulting tumors expressed unique morphological features characteristic of their tissue of origin. The newborn rat represents a model for the heterologous transplantation of human gliomas, providing a biological window for the study of these lesions.
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PMID:Heterotransplantation of malignant human gliomas in neonatal rats. 319 98

The derivation of an IgG1k monoclonal antibody (HSAN 1.2) recognizing a cell membrane determinant on human neuroblastoma cells is reported. The determinant was found on all 17 cultured human neuroblastoma cells that were tested, but the density of the antigen varied widely on different cell lines. The antibody also bound to fresh and cultured Wilm's tumor cells, retinoblastoma cells, and one of two Ewing's sarcoma cell lines tested, it did not bind to mouse neuroblastoma cells, normal fibroblasts, blood, or bone marrow. Tumor cells that did not stain with HSAN 1.2 included glioma, medulloblastoma, melanoma, rhabdomyosarcoma, mesenchymoma, leukemia, and lymphoma cells. The distribution of the HSAN 1.2 antigen in normal tissues was confined to brain and newborn kidney. As few as 0.1% tumor cells in bone marrow aspirates were detectable by fluorescein-conjugated HSAN 1.2 antibody and flow cytometry. This antibody should be useful for the discrimination of neuroblastoma from other pediatric malignancies, for the detection of tumor cells in metastatic sites such as bone marrow, and for selective removal of neuroblastoma cells from marrow harvested for autologous transplantation.
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PMID:Monoclonal antibody recognizing a human neuroblastoma-associated antigen. 332 7

Twelve neonatal brain tumors, presenting within 60 days of birth, constituted 3.3% of pediatric brain tumors. Three-fourths were supratentorial. Two-thirds were benign. Forty-two percent were choroid plexus papilloma. Twenty-five percent were teratoma. Eight percent each were hypothalamic glioma, gliosarcoma, medulloblastoma, and primitive neuroectodermal tumor. Clinical symptoms were nonspecific. Signs of herniation were absent in all 12 patients. Forty-two percent of these patients died 1 day to 8 months after diagnosis. Ultrasound, CT, and magnetic resonance have all proved useful for displaying these lesions suitably for surgery.
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PMID:Neonatal brain tumors: CT and MR findings. 333 47

Recent studies have shown that the calcium channel blockers, when combined with standard anticancer drugs, help overcome resistance that often develops to those drugs. Little is known about the effects of the calcium channel blockers themselves on tumor cells. We have studied the effects of one calcium channel blocker, verapamil, on human tumor cell lines in vitro. Our results show a reversible, antiproliferative action of verapamil on human medulloblastoma, pinealoblastoma, glioma, and neuroblastoma tumor lines established from pediatric patients. Growth rates are inhibited 10 to 100% by 10 to 100 microM verapamil with 50% inhibition occurring between 25 and 50 microM verapamil. No cell line proliferates in 100 microM verapamil, yet washing the cells after 72 h of incubation with 100 microM verapamil results in resumed cell growth. Growth inhibition is accompanied by dose-dependent decreases in DNA, RNA, and protein synthesis which occur within minutes after addition of verapamil. DNA flow cytometry on propidium iodide-stained nuclei shows that, after incubation for 48 h with 100 microM verapamil, the medulloblastoma and neuroblastoma tumor lines as well as normal, human foreskin and lung fibroblast cell lines are reversibly blocked throughout the cell cycle with slight increases in G1. Verapamil appears to have no effect on nucleic acid precursors or on calcium influx or efflux in human medulloblastoma cells.
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PMID:Antiproliferative effect of verapamil alone on brain tumor cells in vitro. 337 5

Sixty consecutive evaluable children with recurrent primary tumors of the central nervous system were treated with a regimen of vincristine, nitrogen mustard, procarbazine, and prednisone over a 12-year period. Tumor types included medulloblastoma (19), brain-stem glioma (16), astrocytoma (13), and a miscellaneous glioma (12). Responses and sustained survivals were achieved. Responses were highly dependent on tumor type. Disease progression was halted in 73% of the children with medulloblastoma, and three have survived in complete remission for more than 10 years from the start of therapy with vincristine, nitrogen mustard, procarbazine, and prednisone. Two of four patients with anaplastic glioma, are long-term survivors. In contrast, less than one third of children with brain-stem gliomas responded. Toxicity consisted mainly of neutropenia, thrombocytopenia, infections, and rarely a procarbazine rash.
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PMID:Salvage chemotherapy for recurrent primary brain tumors in children. 341 10

In this paper, 374 cases of intracranial tumor were studied retrospectively. The incidence of glioma (45.6%) was the highest, next was meningioma (19%) and pituitary tumor (12.3%). Astrocytoma comprised 73.5% of glioma. 75% of medulloblastoma and 54% of ependymoma occurred under 20 years of age, whereas 71.8% of meningioma, 44% of astrocytoma and 47.4% of metastatic tumor occurred between 21 to 50. The ratio of male and female was 1.69:1 except 0.8:1 of meningioma. 73.8% of all the lesions was located above the tentorium of cerebellum, the rest under it. Ninety one cases were followed. The 5 year survival rate was 25.3% (23/91). According to Kernohan's classification, the authors believe that astrocytoma can be divided into four grades, which is of great use in clinical diagnosis and prognosis. The other gliomas are only divided into benign and malignant. The results of surgery are related to tumor type and differentiation. Pituitary adenoma, meningioma, neurilemmoma and astrocytoma grades I and II have a good result by operation, while medulloblastoma, astrocytoma grades III and IV and metastatic cancer have a higher mortality.
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PMID:[Clinicopathologic study of 374 cases of intracranial tumors]. 344 63

For the determination of their possible utility as tumors markers, 2 neural-associated isozymes, neuron-specific enolase [(NSE) EC 4.2.1.11] and creatine kinase BB [(CK-BB) EC 2.7.3.2], were quantitated by radioimmunoassay in human neuroectodermal-derived cell lines, primary brain tumors, and sera and cerebrospinal fluid (CSF) from brain tumor patients. The NSE content of neuroblastoma cell lines was more than sixfold that of the glioma and medulloblastoma lines; the CK-BB content of neuroblastoma and medulloblastoma lines was fourfold to nineteen-fold that of the glioma and other lines. Expression of NSE in neuroblastoma cell lines was not related to time in culture and was cell line specific. NSE in ex vivo medulloblastomas was raised six to ten times that in astrocytomas and gliomas, although no significant differences were noted for the CK-BB content. Serum and CSF NSE levels were markedly raised above control values in 10 of 29 and 6 of 10 cases of astrocytoma, respectively. Raised CK-BB levels in serum (greater than 10 ng/ml) and CSF (greater than 12 ng/ml) were found in 9 of 18 and 2 of 10 patients, respectively. These data suggest that NSE is preferentially expressed by neuroblastoma lines and medulloblastomas and that NSE and CK-BB may have clinical utility as markers for prognosis, diagnosis, and monitoring of response to therapy.
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PMID:Differential expression of neural isozymes by human medulloblastomas and gliomas and neuroectodermal cell lines. 346 6

Racial patterns of childhood brain cancer by histologic type were studied using data from the Third National Cancer Survey and the Surveillance, Epidemiology, and End Results Program. Incidence rates for whites of all types combined and of astrocytic glioma and medulloblastoma were slightly higher than those for blacks. Proportionately more black than white cases of astrocytic glioma were diagnosed between the ages of 5-9 years; this difference corresponded to twofold-higher rates at ages of 0-4 and 10-14 years and similar rates at ages of 5-9 years among whites compared to rates among nonwhites. A real difference in age-incidence curves rather than diagnostic delay among blacks appeared to explain the differences. For medulloblastoma, the male-female rate ratio differed between whites (1.7) and blacks (1.0). Time trend analyses revealed statistically significant increases in medulloblastoma and glioma not otherwise specified (NOS) for incidences among blacks. The rate of microscopic confirmation was significantly higher among whites than among blacks, a difference apparently not explained by differences in the accessibility of tumors for biopsy. For avoidance of biased comparisons, differences in rates of microscopic confirmation and time trends for glioma NOS should be considered in studies of racial patterns of childhood brain cancer incidence by histologic type.
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PMID:Racial patterns of childhood brain cancer by histologic type. 347 96

Carboplatin, a cisplatin analogue, was administered as an intravenous (IV) one-hour infusion in a 4-consecutive weekly dose schedule to 44 patients with recurrent childhood brain tumors. Twenty-four patients were registered on our phase I, and 20 on our phase II studies. The maximum tolerable dose derived from our phase I study was 210 mg/m2/wk in patients with solid tumors, and the recommended dose for subsequent pediatric phase II studies was 175 mg/m2/wk. This dose was administered to 14 patients in the phase I and all 20 patients in the phase II study. Nine of 36 (25%) evaluable patients in the combined studies experienced objective responses for a median duration of 10+ months. Seven of nine responders had received prior cisplatin. Disease-specific response rates were as follows: medulloblastoma, six of 14 (43%) with three complete (CR) and three partial responses (PR); pineoblastoma, one of one (PR); germinoma, one of two (CR); and brainstem glioma, one of eight (13%) (PR). Carboplatin had mild emetic effects but no significant auditory or renal toxicity. Thrombocytopenia (less than 49,000) was encountered in nine of 28 (32%) evaluable trials at a dose of 175 mg/m2/wk. Because of its low potential for auditory, renal, and emetic toxicity, ease of administration, and high disease-specific activity, carboplatin deserves further study in multiagent phase II and III trials, especially in chemotherapy-sensitive diseases such as medulloblastoma.
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PMID:Carboplatin and recurrent childhood brain tumors. 354 20


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