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)

We are giving a report about the results of treatment of children (0 till 15 years old), who were from January 1, 1971 till December 31, 1985 with a neuroblastoma, a nephroblastoma or an osteosarcoma hospitalized in the Clinic of Paediatrics of the University at Rostock or in the Children's Clinic of the District Hospital at Schwerin. All together there were 65 cases with such a diagnosis. There is a summarizing life table analysis.
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PMID:[Neuroblastoma, nephroblastoma and osteosarcoma in patients at 2 pediatric oncologic centers. A 15-year report]. 217 15

Survival rates were analysed for a population-based series of over 15,000 childhood cancers registered in Great Britain during 1971-85. There were highly significant improvements (P less than 0.001 for trend) in survival for many major diagnostic groups. Between 1971-73 and 1983-85 the actuarial 5-year survival rates increased from 37% to 70% for acute lymphoblastic leukaemia, from 4% to 26% for acute non-lymphoblastic leukaemia, from 76% to 88% for Hodgkin's disease, from 22% to 70% for non-Hodgkin's lymphoma, from 61% to 72% for astrocytoma, from 24% to 42% for medulloblastoma, from 15% to 43% for neuroblastoma, from 58% to 79% for Wilms' tumour, from 17% to 54% for osteosarcoma, from 26% to 61% for rhabdomyosarcoma, from 59% to 94% for malignant testicular germ-cell tumours and from 43% to 77% for malignant ovarian germ-cell tumours. These increases in population-based survival rates reflect the substantial advances in treatment of a wide range of childhood cancers since 1970. The two principal diagnostic groups for which there was no evidence of any trend were retinoblastoma, which already had an excellent prognosis with a 5-year survival rate of over 85%, and Ewing's sarcoma, for which the survival rate remained below 45%.
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PMID:Trends in survival for childhood cancer in Britain diagnosed 1971-85. 217 43

Seventy-two children with recurrent, progressive, or metastatic lymphomas and other solid tumors, exclusive of primary central nervous system (CNS) tumors, were treated with aziridinylbenzoquinone (AZQ, diaziquone) at 9 mg/m2/day by 30-min intravenous infusion for 5 days every 3 weeks. Fifty-four patients were evaluable for response. Three partial responses occurred, two in patients with recurrent Hodgkin's disease and one in a patient with intraocular retinoblastoma. Sufficient numbers of patients with osteosarcoma, neuroblastoma, and Wilms' tumor were evaluable to demonstrate inactivity of this dosing regimen in these tumor types. Numbers of evaluable patients for other tumor types were insufficient to conclusively demonstrate inactivity. Myelosuppression, which was profound and prolonged, was observed. As administered in this study, AZQ has marginal activity and severe myelotoxicity in children with solid tumors.
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PMID:A phase II study of diaziquone in children with recurrent or progressive solid tumors. Report from the Childrens Cancer Study Group. 224 Apr 75

The curing chance of cancer disseminated to the lungs depends on the global curing chance of that specific tumor, the extent and distribution of its systemic spread and the availability of additional treatment modalities besides surgery. Of all tumors occurring in childhood and adolescence only osteosarcoma, Wilms tumor and Ewing's sarcoma preferentially disseminate to the lungs and such are the most promising candidates for successful treatment. In osteosarcoma with pulmonary dissemination surgical removal of the metastases is indispensable. In Wilms tumor chemoradiotherapy may replace or be used as an adjunct to surgery while in Ewing's sarcoma with primary pulmonary metastases chemoradiotherapy is the treatment of choice. Although metachronous lung metastases may still cured in osteosarcoma and Wilms tumor, they tend to be fatal however in Ewing's sarcoma. A small chance of success itself should not contraindicate metastasectomy but only the actual technically impossible intervention or the definite demonstration of tumor progression no longer controllable of different location. However, even palliative metastasectomy may be indicated in an individual patient.
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PMID:Surgical treatment of pulmonary metastases in childhood. 243 85

Between 1972 and June 1983, 21 children (mean age 9 years, range 20 months to 16.5 years) were operated on for pulmonary metastatic disease. Primary malignant tumors were Wilms-tumor (7 patients), osteogenic sarcoma (7 patients), Ewing's sarcoma (4 patients), hepatoblastoma (2 patients), and rhabdomyosarcoma (1 patient). The surgical intervention was part of a therapeutic pediatric oncological concept with curative purpose including chemotherapy and/or radiation in different combinations. Ten out of these 21 children survived disease-free 3 years and more after pulmonary metastasectomy. An aggressive surgical approach towards pulmonary metastatic disease in children thus appears to be justified.
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PMID:Long-term results following surgical removal of pulmonary metastases in children with malignomas. 243 86

A total of 22 patients with different solid tumours refractory to previous chemotherapy were treated between May 1985 and December 1986 (osteosarcoma, 7; Wilms' tumour, 6; rhabdomyosarcoma, 2; Ewing's sarcoma, 2; non-Hodgkin's lymphoma, 2; retinoblastoma, 1; cavum lymphoepithelioma, 1; dyktioma, 1). Patients were aged between 3 and 20 years (mean, 10.6 years). There was a 3.4:1 male-to-female ratio. The treatment consisted of ifosfamide given i.v. as a single agent at a dose of 3,000 mg/m2 over 1 h on days 1 and 2. Mesna was given as a uroprotector at 600 mg/m2 every 4 h, up to a total of 13 doses. The courses were repeated every 3 weeks. Every patient except those with osteosarcoma had previously received cyclophosphamide. There were 3 (13.6%) complete responses (CRs) in 2 osteosarcomas and 1 abdominal non-Hodgkin's lymphoma, lasting 12, 8 and 2 months, respectively; 4 (18.2%) partial responses (PRs) in 2 Wilms' tumours, 1 Ewing's sarcoma and 1 abdominal non-Hodgkin's lymphoma; 4 absences of remission (ARs); and 11 (50%) cases of progressive disease (PD). In all, 81 courses were given, and the toxicities found were leukopenia (less than 2,000 leukocytes) in 15 courses, thrombocytopenia in 3, microhaematuria in 7, neurotoxicity in 8, fever in 8 and hypertension in 2. The overall response rate (31.8%) was encouraging and the toxicity, acceptable and reversible. These results demonstrate that ifosfamide should be considered for introduction into phase III protocols for the treatment of solid malignancies in children.
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PMID:Phase II study of ifosfamide as a single drug for relapsed paediatric patients. 250 55

The pharmacokinetics of alkylating activity were studied in 17 children treated i.v. with ifosfamide (IF) at 3 g/m2 as a 1-h infusion for 2 consecutive days every 3 weeks, with mesna as a uroprotector. Two patients were treated for a newly diagnosed rhabdomyosarcoma according to the current SIOP (International Society of Pediatric Oncology) protocol. The other 15 patients were treated in a phase II study and presented with one of the following malignancies in relapse: neuroblastoma (7), osteosarcoma (3), soft tissue sarcoma (2), Wilms' tumor (1), non-Hodgkin's lymphoma (1), and acute lymphoblastic leukemia (1). Plasma alkylating activity levels determined by using 4(4'-nitro-benzyl)-pyridine showed considerable inter-individual and intercyclic variations and decreased biphasically, with mean alpha and beta half-lives of 60 min and 6-7 h, respectively. Probably as a result of liver mixed-function oxidase induction, on the 2nd day of treatment the terminal half-lives were shorter, the plasma exposures were lower, and the mean plasma clearances were higher. Renal excretion was almost complete after 24 h, accounting for a mean of 19% of the injected dose. The CSF alkylating activity levels, obtained in four children, were always lower than the plasma levels and ranged from 8 to 51 micrograms/ml, with a mean CSF/plasma ratio of 0.53 +/- 0.23 during the first 12 h. We conclude that IF alkylating activity was biphasically cleared from the plasma, with significant interindividual and intercyclic variability, that the renal contribution to the clearance was low, and that high levels of CSF alkylating activity could possibly contribute to the CNS toxic side effects observed in pediatric patients treated with high-dose IF/mesna.
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PMID:Alkylating activity in serum, urine, and CSF following high-dose ifosfamide in children. 250 56

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

The technique of somatic cell hybridization has established the phenomenon of tumour suppression and provided evidence for a genetic basis for suppression. Further refinements aimed at eventually identifying 'tumour suppressor' genes include the use of monochromosome transfer via microcell hybridization. The application of this technique to the study of tumour suppression in tumorigenic HeLa cell x fibroblast hybrids, Wilms' tumour, retinoblastoma and osteosarcoma cells is described. The issue of whether tumour suppression involves a direct effect on expression of activated oncogenes is discussed. Transformation of normal human cells in culture by activated cellular oncogenes is an extremely rare event. This may be due to a relatively greater genomic stability of human cells compared to rodent cells. We describe the use of a spontaneously immortalized human keratinocyte cell line, HaCaT, for studies of the effects of introduction of activated c-Ha-ras oncogene into these cells, with particular reference to tumorigenic conversion.
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PMID:A genetic basis for tumour suppression. 254 19

Using a somatic cell hybridization technique, four murine monoclonal antibodies (three immunoglobulin M and one immunoglobulin G3) were produced against a human neuroblastoma cell surface glycolipid antigen. They reacted strongly with all human neuroblastoma tumor-containing specimens and six of eight human neuroblastoma cell lines. More than 98% of each neuroblastoma cell population possessed this surface antigen, and in the presence of complement, 100% of them were killed. While melanoma and osteogenic sarcoma carried this antigen, leukemia and most Ewing's and Wilms' tumors did not. There was no cross-reaction with 30 normal or remission bone marrow samples and none with normal human tissues other than neurons in vitro. This antigen was neuraminidase sensitive, separable on thin-layer chromatogram, and did not modulate after combining with the monoclonal antibodies. These antibodies could detect less than 0.1% tumor cells deliberately seeded in the bone marrow samples. Because of their unique properties, these monoclonal antibodies may have diagnostic and therapeutic potentials.
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PMID:Monoclonal antibodies to a glycolipid antigen on human neuroblastoma cells. 258 Jun 25


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