Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen patients were treated in a Phase I study of intracarotid carboplatin (200-400 mg/m2) in 5% dextrose and water infused over 15 to 30 minutes through a transfemoral catheter with a 0.2-micron inline filter. This study was done because intravenous carboplatin has less neurotoxicity than cisplatin and is active against brain tumors. Eleven men and four women ranging in age from 37 to 72 years (median, 59 years) were treated. The Eastern Cooperative Oncology Group performance status was 1 in 3, 2 in 4, and 3-4 in 8 patients. Eight patients had one to three previous chemotherapy regimens; previous radiotherapy had failed in 13 patients. The response of patients in the Phase I study follows: glioblastoma, 6 failed; not evaluated because of early death from pulmonary embolus, 1; recurrent Grade II and III glioma, 1 stable (minor response with neurologic improvement) and 2 failed; malignant oligodendroglioma, 1 failed; brain metastases from nonsmall cell lung cancer, 1 partial remission, 1 stable (minor response), and 1 failed; brain metastases from unknown primary, 1 stable (minor response with neurological improvement). Median survival was 9 weeks. Nausea was mild to moderate. One patient had granulocytopenia, and 2 had thrombocytopenia (mild). At 200 mg/m2 (2 patients), 1 had a focal seizure. At 300 mg/m2 (9 patients), 2 with abnormally small arteries had severe pain early in the treatment and posttreatment ipsilateral conjunctival edema, decreased vision, and cerebral edema (with partially reversible increased hemiparesis); 1 other had mild decrease in ipsilateral vision and 1 had transient aphasia on removal of the catheter (possibly the result of a vascular spasm).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of intracarotid administration of carboplatin. 131 64

A 24-year-old female was hospitalized for progressive headache and nausea. Computed tomography showed a mass lesion in the left lateral ventricle near the foramen of Monro. On light microscopy, this tumor morphologically resembled an oligodendroglioma. However, ultrastructural examination disclosed synapses and neuronal differentiation. Review of the literature revealed 21 cases of intraventricular neuronal tumors in adults that were diagnosed as central neurocytoma or differentiated neuroblastoma. Fourteen of the 21 patients were males and seven were females. Their ages ranged from 16 to 52 years and averaged 30.7 years. All of the tumors were located near the foramen of Monro and the clinical symptoms were primarily headache and nausea. The outcome was generally good. Surgical removal was the most effective treatment, whereas the effect of radiation therapy was unclear. The diagnosis requires demonstration of neuronal differentiation. Generally, the diagnosis is neurocytoma if the neuronal tissue is mature, with complete synapses, and neuroblastoma if it is immature. However, the criteria for differentiation between these two tumors are still controversial.
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PMID:[Central neurocytoma. Case report]. 248 96

We report a case of an oligodendroglioma associated with a cavernous angioma. The patient, a 20-year-old man with an 8-year history of epileptic seizures, presented an acute onset of headache, nausea, and vomiting. Computerized tomographic scan and angiogram revealed multiple vascular malformations in both hemispheres including a cystic hemorraghic lesion with a perifocal edema attributing to a mass effect. Repeated puncture of the cyst failed to give improvement of elevated intracranial pressure. At surgery, the cyst and the underlying lesion were excised and found to be oligodendrocyte-rich tissue with malformed vascular tissue. Final histological examination revealed an oligodendroglioma associated with a cavernous angioma. As concurrence of oligodendroglioma and vascular malformation is rare, this case raises a broad range of differential diagnoses such as reactive oligodendroglial gliosis due to a vascular malformation, unusual vascularity of an oligodendroglioma as well as other kinds of cerebral tumors or malformations. The diagnostic difficulties as well as the pathogenetic and pathological significance of the concurrence of an oligodendroglioma and cavernous angioma are discussed.
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PMID:Association of oligodendroglioma-like cell proliferation and angiomatous vasculature--coincidence or pathogenetically related lesions? 956 27

RMP-7, a nine amino acid peptide bradykinin agonist, increases the delivery of hydrophilic compounds across the blood-tumour barrier. In this dose ranging study, 14 patients with progressing malignant glioma (9 glioblastoma multiforme, 4 anaplastic astrocytoma, 1 anaplastic oligodendroglioma; age range 31-68 years, baseline Karnofsky range 60-90%, 5 having had prior chemotherapy) were treated with intravenous RMP-7 and carboplatin to assess the safety, tolerability, and side-effect profile of increasing doses of this combination. Carboplatin dosing was by target area under the curve (AUC) according to the Calvert protocol. Patients were allocated to one of five treatment regimes: cohort A (n = 2) received 50 ng/kg RMP-7 and target AUC 5 mg/ml/min carboplatin; cohort B (n = 3) 100 ng/kg RMP-7 + AUC 5; cohort C (n = 2) 100 ng/kg RMP-7 + AUC 7; cohort D (n = 2) 200 ng/kg RMP-7 + AUC 7; cohort E (n = 5) 300 ng/kg RMP-7 + AUC 7. Treatment was given once every 4 weeks with magnetic resonance imaging scans every 2 months. Patients received 37 cycles in total (median 2, range 1-7). The drug combination, as a cancer treatment, was tolerated in all groups. Effects possibly related to RMP-7 included flushing, nausea, headache and mild increase in heart rate, all transient. 3 patients in cohort E experienced grade 3/4 neutropenia and thrombocytopenia. These toxicities are consistent with known effects of carboplatin at this dose range. In cohort E (n = 5) 1 patient improved and another remained stable for > or = 6 months. In summary, the dose was escalated to the maximum dose of RMP-7 given to volunteers without additional related side-effects. The side-effects of the combination were consistent with giving the two drugs alone and would merit further study for efficacy.
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PMID:A phase I study of intravenous RMP-7 with carboplatin in patients with progression of malignant glioma. 989 73

KRN8602 (MX2) is a newly developed morpholino anthracycline that crosses the blood-brain barrier where it becomes distributed in brain tissue after intravenous administration. This morpholino anthracycline has been found to be effective against human glioma cells and the intracerebrally transplanted tumors in vivo, We performed a phase II trial using KRN8602 as a single agent in malignant glioma patients who had not received prior adjuvant therapy. The 13 patients (5 glioblastomas, 7 anaplastic astrocytomas and 1 malignant oligodendroglioma) enrolled received at least 1 cycle of KRN8602 at 35 mg/m2/day in 3-4 week intervals by intravenous bolus. Ten of these patients could be evaluated for response, and 13 for toxicity. Three patients (1 glioblastoma and 2 anaplastic astrocytomas) demonstrated a complete response (3/10, 30%). Concerning side effects, myelosuppression was moderately severe, with 30.7% of patients developing grade 3 leukopenia. Severe nausea/vomiting was observed in 69% of the patients, however, cardiotoxicity was not observed. The results indicate that KRN8602 demonstrated modest activity against malignant glioma with relatively severe, but manageable toxicity. Further assessment of the efficacy and toxicity of KRN8602 against malignant glioma may be worthwhile.
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PMID:Phase II trial of pre-irradiation KRN8602 (MX2) in malignant glioma patients. 1108 79

This phase II study in recurrent high-grade glioma evaluated the response rate, toxicities, and time to treatment failure of high-dose carboplatin modulated by a 24-h infusion of thymidine (75 g/m(2)). The trial was based on preclinical data and a prior phase I study ( J. Clin. Oncol. 17, 2922-2931, 1999); a phase II recurrent high-grade glioma study was initiated in July of 1998. Thymidine was given over 24 h; carboplatin was given over 20 min at hour 20 of the thymidine infusion. The starting dose of carboplatin had a value of 7 for the area under the curve (AUC), with allowance for dose escalation of 1 AUC unit per cycle if grade 2 toxicity was observed. Treatment cycles were repeated every 4 weeks. Accrual as of September 1999 was 45 patients [4 were unevaluable]: 76% with glioblastoma multiforme (GBM), 20% with anaplastic oligodendroglioma, 2% with mixed type, and 2% with anaplastic astrocytoma. Most patients had prior chemotherapy (78%). As observed in the earlier phase I study (in which carboplatin pharmacokinetics were unaltered by thymidine or antiseizure medications), thymidine was myeloprotective, resulting in a minimal need for dose reduction for patients having a >2 grade toxicity (in only 4% of the courses of treatment). Of 101 total courses, the number of courses (at the AUCs) was 3 (5), 4 (6), 58 (7), 20 (8), 11 (9), and 5 (10). Grade 3 nonhematologic toxicities included headache (4%), altered consciousness (3%), fatigue (1%), and nausea (3%). Responses included 2 partial (1 oligodendroglioma, 1 GBM; 5%); 3 minor (1 anaplastic astrocytoma, 2 GBM; 7.3%); 6 stable disease (14.6%); and 30 progressive disease (73.2%). For GBM patients, median survival was 23 weeks (with a 95% confidence interval of 20 to 50 weeks), and progression-free survival was 8 weeks (with a 95% confidence interval of 7-16 weeks). These results in GBM were comparable to other phase II GBM trials and thus do not represent a therapeutic advance in the treatment of GBM. Taken collectively, however, results are consistent with continued investigation of thymidine in combination with chemotherapeutic agents for high-grade glioma and other malignant diseases. The significant myeloprotection afforded by thymidine may have particular relevance to polychemotherapeutic regimens.
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PMID:A phase II trial of thymidine and carboplatin for recurrent malignant glioma: a North American Brain Tumor Consortium Study. 1191 2

To determine the efficacy and toxicity of a novel chemotherapeutic approach with topotecan, a camptothecin analog, for progressive or recurring anaplastic oligodendroglioma or mixed oligoastrocytoma.Patients from seven centers with recurrent or progressive disease were treated with topotecan, 1.5 mg/m(2) intravenously (i.v.), 30 min dailyx5 days every 3 weeks. Efficacy and toxicity were assessed clinically and radiologically. The study was planned to accrue up to 30 evaluable patients if there was at least one response among the first 15 patients treated. Sixteen eligible patients entered the study. No response was documented in 14 evaluable patients. Eleven patients had stable disease of a median of 3.8 months and three had progressive disease. Sixteen patients were evaluable for toxicity. The most significant toxic effect was myelosuppression. Grade 3 or 4 granulocytopenia was experienced by 15 of 16 patients and led to dose reduction in nearly half of the cycles delivered. Other adverse effects were fatigue, nausea, stomatitis, alopecia, and vomiting.Topotecan, delivered in the dailyx5 regimen, is relatively well tolerated. We could not demonstrate significant activity among the population studied to justify completing accrual to 30 patients. Topotecan did not demonstrate, with this small sample size, efficacy as a salvage chemotherapy monotherapy after exposure to procarbazine, CCNU and vincristine. Further trials with different agents in this indication are certainly warranted.
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PMID:A phase II study of topotecan in patients with anaplastic oligodendroglioma or anaplastic mixed oligoastrocytoma. 1458 16

Multiple metastatic brain tumors and multifocal primary brain tumors of a single histological type are well described in the literature. The concurrent presence of multiple primary brain tumors with different histological characteristics, however, is very rare. The authors describe the first known case in which an oligodendroglioma and a juvenile pilocytic astrocytoma (JPA) presented as synchronous primary brain tumors in the same patient. This 43-year-old man presented with a 2-month history of progressive headaches, nausea, and vomiting. Magnetic resonance imaging demonstrated an enhancing heterogeneous right medial cerebellar lesion and a larger calcified, nonenhancing, heterogeneous right frontal lesion with surrounding edema and a mass effect. The results of a metastatic workup were unremarkable. The patient underwent an initial right frontotemporal craniotomy and a subsequent suboccipital craniectomy 2 years later for resection of the posterior fossa lesion. Histological examination revealed the frontal and cerebellar lesions to be an oligodendroglioma and JPA, respectively. A molecular analysis detected a deletion of chromosome 1p36 in the oligodendroglioma, but not in the JPA. After the initial operation, the patient received follow-up care for his oligodendroglioma, but eventually required temozolomide for tumor progression. His condition remains stable both neurologically and according to imaging studies. The authors describe the first known case in which a low-grade oligodendroglioma and a JPA presented as synchronous primary brain tumors. They review the literature on multiple primary brain tumors with different histological characteristics and discuss potential mechanisms for the development of these lesions.
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PMID:Oligodendroglioma and juvenile pilocytic astrocytoma presenting as synchronous primary brain tumors. Case report with histological and molecular differentiation of the tumors and review of the literature. 1507 Jan 26

The authors report the case of a 2-year-old boy with a primary, diffuse leptomeningeal oligodendroglioma in which the deletion of chromosome arm lp was identified by performing a fluorescence in situ hybridization (FISH) analysis. This previously healthy child initially presented with malaise, anorexia, nausea, vomiting, and macrocephaly. Imaging studies confirmed the presence of hydrocephalus, and a ventriculoperitoneal shunt was placed. The postoperative course was complicated by emesis, continued weight loss, and numerous seizurelike episodes. A contrast-enhanced magnetic resonance imaging study performed approximately 10 weeks postoperatively showed diffuse leptomeningeal thickening and enhancement without evidence of an intraparenchymal mass lesion. A right frontal lobe brain biopsy revealed a hypercellular proliferation of small oligodendroglioma-like cells, which occupied the leptomeninges diffusely and spared the underlying cortical gray matter. The tumor cells displayed prominent perinuclear clearing and had evenly spaced, uniformly round nuclei. Occasional mitotic figures were observed. Background vessels were thin and delicate, and there was no evidence of necrosis. The tumor cells showed strong immunoreactivity for S100 protein; the results of immunohistochemical staining were negative for glial fibrillary acidic protein, vimentin, epithelial membrane antigen, NeuN, and synaptophysin. The deletion of lp was demonstrated by FISH analysis; lq, 19p, and 19q were intact. This appears to be the first reported case of a primary diffuse leptomeningeal oligodendroglioma in which a lp deletion was identified.
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PMID:Primary disseminated leptomeningeal oligodendroglioma with 1p deletion. Case report. 1718 79

The oral alkylating agent, temozolomide (Temodal: TMZ), is the only anticancer drug that has been shown in a phase III study to improve survival in glioblastoma (GBM) when administered with concomitant radiotherapy. Pharmacokinetic studies have documented relatively high concentrations of TMZ in brain tumors and cerebrospinal fluid (20-40% of the area under the plasma concentration curve), and other studies have demonstrated that TMZ is effective for treatment of various brain tumors, including recurrent and newly diagnosed glioma, primary CNS lymphoma, metastatic melanoma, and neuroblastoma. Molecular markers that predict a favorable response to TMZ plus concomitant radiotherapy include methylguanine methyltransferase (MGMT) promoter methylation patients with GBM and chromosome 1p/19q deletion in patients with anaplastic oligodendroglioma or low-grade glioma. Myelosuppression, nausea and constipation are relatively frequent in patients undergoing treatment with TMZ, and prophylaxis against Pneumocystis carinii pneumonia should be instituted. This article will summarize and discuss these issues as well as review ongoing and anticipated studies of TMZ in combination with other anti-cancer therapies.
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PMID:[Temozolomide: Temodal]. 1834 14


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