Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 19-year-old man with telangiectatic osteosarcoma of the left proximal femur was started on a course of neoadjuvant chemotherapy consisting of intraarterial administration of cis-platinum. Within 72 hours of receiving the first intraarterial dose, the patient developed signs and symptoms of fat embolism syndrome (FES). A physical examination revealed cyanosis, tachycardia, and seizure activity. Laboratory studies demonstrated a pO2 of less than 65 mmHg, lipuria, and a drop in hematocrit of three percentage points. There was no clinical or roentgenographic evidence of pathologic fracture. Tumor necrosis secondary to intraarterial cis-platinum therapy in this patient with osteosarcoma may have caused a sudden release of free fatty acids and embolization of fat macroglobules that precipitated this episode of FES. FES in association with the intraarterial administration of cis-platinum seems not to have been previously reported.
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PMID:Fat embolism syndrome complicating intraarterial chemotherapy with cis-platinum. 232 45

Ifosfamide/mesna was given to 97 patients who had malignant solid tumors diagnosed before they were 21 years of age. Patients received 1.6 g/m2 ifosfamide daily x 5, given i.v. over 15 min, followed by 400 mg/m2 i.v. mesna at 15 min and 4 and 6 h after ifosfamide. Responses were noted in patients with osteosarcoma, Ewing's sarcoma, rhabdomyosarcoma and other soft-tissue sarcomas, rhabdoid tumor, neuroblastoma, Wilms' tumor, primitive neuroectodermal tumor, retinoblastoma, germ-cell tumors, and B-cell lymphoma. Toxicity included mild to moderate nausea and vomiting, transient, reversible myelosuppression, transient elevations of serum blood urea nitrogen (BUN) and creatinine and liver enzymes, infections, and self-limiting neurotoxicity characterized by changes in mental status, motor dysfunction, cranial nerve palsy, cerebellar dysfunction, and seizures. Neurotoxic symptoms were generally seen in patients who had previously received cisplatin. Ifosfamide is an important alkylating agent that should be combined with other agents in phase II and III trials. Alternate dose schedules should also be investigated.
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PMID:Ifosfamide in pediatric malignant solid tumors. 250 57

Ifosfamide was given to 61 patients with malignant solid tumors diagnosed before the age of 21 years. In this phase II study, all patients received 1.6 g/m2/day X 5 iv over 15 minutes followed by mesna at a dose of 400 mg/m2 iv at 15 minutes and 4 and 6 hours after ifosfamide. Responses were observed in five of 15 patients with osteosarcoma, two of ten with neuroblastoma, two of six with Wilms' tumor, two of five with rhabdomyosarcoma, four of eight with other soft tissue sarcomas, one of one with retinoblastoma, one of two with germ cell tumors, one of one with B-cell lymphoma, and one of one with a primitive neuroectodermal tumor. Fifty-nine of 61 patients had received prior alkylating agent therapy which included cyclophosphamide, cisplatin, mechlorethamine, melphalan, or dacarbazine. Fourteen of 19 responses developed in patients whose tumors were resistant to treatment with cyclophosphamide. A patient with malignant Schwannoma who had received no prior chemotherapy developed a complete response which lasted 12 months. A patient with brain metastases of osteosarcoma has had complete response for greater than 2 years. Complete response was also observed in a patient with B-cell lymphoma. Toxicity consisted of mild to moderate nausea and vomiting, transient reversible myelosuppression, occasional elevation of serum BUN or creatinine, and transient neurotoxicity characterized by somnolence, confusion, weakness, tremor, hallucinations, or seizures. We conclude that ifosfamide is an important alkylating agent without apparent complete cross-resistance with cyclophosphamide, and as such should be further investigated for determination of its activity in patients with pediatric neoplasms and considered for incorporation into phase II-III trials for certain tumors.
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PMID:Phase II trial of ifosfamide in children with malignant solid tumors. 310 34

During a 4-year period, 26 children with systemic malignancies suffered cerebrovascular accidents. These occurred in 17 patients with lymphoreticular malignancy and nine patients with solid tumors. They were the presenting signs of malignancy in three patients and were the direct cause of death in six. Cerebrovascular accidents were directly related to disseminated intravascular coagulation in eight patients, to chemotherapy in eight patients, to metastatic tumor in three patients, to thrombocytopenia in three patients, and to fungal meningitis in one patient. All patients with disseminated intravascular coagulation had leukemia and at times, cerebrovascular thrombosis predated systemic or laboratory evidence of disseminated intravascular coagulation. This review indicates that four major syndromes are apparent in children with cancer: vascular thrombosis associated with disseminated intravascular coagulation, acute arterial or sagittal sinus thrombosis secondary to L-asparaginase in children with leukemia, acute neurologic dysfunction in patients with osteogenic sarcoma treated with high-dose methotrexate, and obtundation, seizures, and focal neurologic deficits in patients with neuroblastoma metastatic to the torcular region. Although elevated WBC counts and thrombocytopenia occur frequently in children with cancer, in themselves they uncommonly result in strokes. It is concluded that cerebrovascular accidents are a relatively frequent cause of acute neurologic compromise in children with cancer and that certain types of malignancies and their treatment predispose patients to this complication.
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PMID:Cerebrovascular accidents in children with cancer. 386 Jul 96

The aim of this phase II study was to determine the efficacy of high-dose ifosfamide with moderate dose etoposide in childhood osteosarcoma. From January 1992 to January 1995, 27 children (15 male, 12 female) with relapsed or refractory evaluable osteosarcoma were included in a phase II study of two courses of ifosfamide 3g/m2/day and etoposide 75 mg/m2/day for 4 days. Median age was 14 years (7-19 years). All but one had received high-dose methotrexate and doxorubicin as first-line treatment. 22 patients had previously received ifosfamide. This regimen was given as first-line in 1 patient, second-line in 23 and third-line in 3. Evaluable disease was lung metastases in 21 patients, local relapse in 5 and adenopathy in 1. There were six complete responses, seven partial responses, three minor responses, six stable disease and five progressive disease (including one mixed response). Response rate was 48% (95% confidence interval, 29-67%). Duration of response was not available (10 responding patients had other treatments). Response rate was equivalent in the subgroup of 22 patients who had previously received ifosfamide (4 CR, 6 PR). Among 3 patients who received the phase II regimen as third-line chemotherapy, there was 1 PR. All but 4 patients had a well tolerated grade 4 neutropenia. Transient mild confusion or seizures were each observed once. 5 patients are alive 15-31 months after the beginning of chemotherapy. This combination of drugs at this dosage has tolerable toxicity, is efficient and deserves evaluation in phase III studies.
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PMID:Ifosfamide and etoposide in childhood osteosarcoma. A phase II study of the French Society of Paediatric Oncology. 913 94

We report the case of an 18 year-old woman treated for femoral osteogenic sarcoma who presented generalized seizures requiring sedation, tracheal intubation and artificial ventilation. CT brain scan showed diffuse hypodensities. Doppler studies showed an increased cerebral arterial resistance. Regional cerebral blood flow was decreased. A right carotid angiogram showed abnormalities consistent with diffuse cerebral arteritis. The patient slowly recovered and 6 weeks later, magnetic resonance imaging showed disseminated areas of hyposignal on T1 and hypersignal on T2 weighted images. We reviewed the different published cases of acute high dose methotrexate neurotoxicity and the different underlying mechanisms.
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PMID:[Neurologic toxicity of methotrexate in a patient with cerebral arteritis. Report of a case]. 984 41

A 15-year-old girl with homozygous sickle cell anemia (HbSS) and osteosarcoma is described. Delayed clearance of methotrexate (MTX) after the second course of high-dose MTX (HDMTX) led to the development of renal and hepatic toxicities. Rescue was accomplished with high-dose leucovorin, intravenous carboxypeptidase G2, and thymidine. Although the renal and hepatic abnormalities resolved, focal tonic-clonic seizures developed, accompanied by abnormal brain imaging. Four weeks after this episode, all clinical and biochemical abnormalities resolved. Preexistent end-organ damage associated with HbSS may compromise the ability to deliver high-dose chemotherapy with curative intent in patients with malignant disease.
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PMID:Delayed methotrexate clearance in a patient with sickle cell anemia and osteosarcoma. 1020 66

Enterovirus meningoencephalitis is rare but can be severe. Very few cases of these infections have been reported in pediatric oncology. We report the case of a 10-year-old boy with tibial osteosarcoma and lung metastases who developed enterovirus 71 meningoencephalitis during aplasia. Clinical features comprised fever, hypotension, vesicular rash, generalized seizures, and altered consciousness. Diagnosis was confirmed by polymerase chain reaction on samples of cerebrospinal fluid and skin vesicles. The patient received treatment with intravenous immunoglobulins with an excellent outcome with no cutaneous or neurologic sequelae. Immunoglobulin therapy could be considered in cases of invasive enteroviral infection with such severity in pediatric oncology.
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PMID:Enterovirus 71 meningoencephalitis during chemotherapy in a child with metastatic osteosarcoma. 1776 99

Primary meningeal osteosarcomas are rare tumors, with only 19 reported cases in the literature; only 4 of these, including the present case, are in pediatric patients. In this report, the authors present the case of an 8-year-old boy with a history of generalized tonic-clonic seizures who was found to harbor a meningeal osteosarcoma within the sylvian fissure. Initial working diagnoses included meningioma and glioma. After tumor enlargement and progressive symptoms, the patient underwent a large frontotemporal craniotomy and complete resection of the lesion, which recurred 6 and 12 months after the initial surgery and was surgically treated after each recurrence. The rarity of primary meningeal osteosarcomas can make their diagnosis difficult, and histopathological evaluation is mandatory for diagnosis. Because of their fast progression, they must be treated aggressively by means of surgery, chemotherapy, and radiotherapy.
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PMID:Primary meningeal osteosarcoma of the brain during childhood. Case report. 1837 10

Temporal lobe epilepsy is a common form of pharmacoresistant epilepsy, in which epileptogenic foci propagate to other regions of the brain from the area of the initial insult. The present study focused on epileptogenesis, that is, the development of the first foci inducing seizures in amygdala-kindled mice, a model of temporal lobe epilepsy, to find the molecular process promoting the formation of epileptogenic networks. The expression of growth hormone (GH) was up-regulated along neural circuits during the epileptogenesis, while there was no difference in the pituitary gland. The up-regulation was associated with increased phosphorylation/activation of signal transducer and activator of transcription 5 and expression of the Serum Response Element-regulated genes, FBJ osteosarcoma oncogene, early growth response 1, and Jun-B oncogene, suggesting that expression of GH leads to GH signaling in the hippocampus and cortex. Furthermore, the administration of the hormone into the hippocampus markedly enhanced the progression of kindling. The administration of an inhibitor of its secretion into the hippocampus elicited a delay in the progression. Our results demonstrate directly that regulation via growth hormone has a robust impact in epileptogenesis.
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PMID:Distinct role of growth hormone on epilepsy progression in a model of temporal lobe epilepsy. 1945 22


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