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)

Three cases of postirradiation osteosarcoma which presented in childhood are reported and the pertinent literature reviewed. The children had been treated in each instance before the age of 3 years for an astrocytoma, retinoblastoma, and neuroblastoma, respectively. An average latent interval of 9.5 years lapsed before the osteosarcomas were diagnosed. Two of the tumors occurred in unusual sites, the cervical vertebrae and maxilla but were within the fields of prior irradiation. The tumors were predominantly sclerotic and were high-grade osteosarcomas. Only one patient has remained free of disease after treatment. One tumor-related death has occurred and the third patient has had two wedge resections of pulmonary metatases.
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PMID:Postirradiation osteosarcoma in childhood. A clinicopathologic study of three cases and review of the literature. 693 66

A total of 114 children with solid tumors refractory to conventional therapy were evaluated for response and/or toxic effects after receiving cisplatin at doses of 3.0-4.5 mg/kg with aggressive hydration and mannitol diuresis every 3 weeks; a minimum of two courses was required for evaluation of response (110 patients). Objective responses were noted in 18 patients: rhabdomyosarcoma (three), Wilm's tumor (three), osteogenic sarcoma (three). Ewing's sarcoma (two), neuroblastoma (one), undifferentiated sarcoma (one), hepatoblastoma (one), ovarian teratoma (one), hepatocellular carcinoma (one), embryonal carcinoma of the mediastinum (one), and thymoma (one). Twenty-six patients had some evidence of renal toxicity. Asymptomatic hearing loss was commonly found when audiometry was performed (eight of 18 patients tested). Eight additional patients had symptomatic hearing problems--tinnitus or hearing loss. Myelosuppression was mild. Hypomagnesemia and/or hypocalcemia were common but only one patient had symptoms. Cisplatin, administered at a dose of 3.0 mg/kg with aggressive hydration and mannitol diuresis, is reasonably well-tolerated. Its role in the therapy for those tumors against which it shows activity remains to be determined.
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PMID:Phase II trail cisplatin in refractory childhood cancer: Children's Cancer Study Group Report. 694 56

Spinal cord compression is a rare but serious complication of malignant diseases in children. Epidural cord compression was noted in 81 patients within the past 17 years at this center. The complication developed at different times during the course of the primary disease. For 29 of our patients, cord dysfunction was one of the initial signs of cancer--Ewing sarcoma, neuroblastoma, Hodgkin disease, and malignant lymphoma. By contrast, for most of the patients with osteosarcoma and rhabdomyosarcoma, it appeared later in their clinical course. The treatment outcome of patients who were paraplegia with complete loss of sensory function for greater than or equal to 48 hours was poor. Only four of 22 in this group became ambulatory. Ten patients with osteosarcoma did not undergo laminectomies because they all had multiple metastases and terminal disease. Paraplegia developed in all ten. There was no difference in ambulatory rates among other patients, with or without laminectomies.
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PMID:Metastatic epidural tumors in children. 695 58

We have studied the repair of X-ray-induced, potentially lethal damage (PLD) in 9 human tumour lines derived from tumours of varying radiocurability. Cells derived from 3 tumours considered non-radiocurable (1 osteosarcoma, 2 melanoma) repaired significantly more X-ray PLD than cells from 3 tumours considered radiocurable (2 breast, 1 neuroblastoma). The remaining tumour lines were intermediate in their ability for repair, and included cells from another osteosarcoma, a hypernephroma and a glioblastoma. We conclude that the repair of X-ray PLD may be an important cellular determinant of clinical radiocurability.
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PMID:Cellular repair factors influencing radiocurability of human malignant tumours. 705 52

Cytostatics- and radiation-induced alterations of the parenchyma of the lung were investigated in 30 children with malignomas before, during and after therapy by means of lung perfusion scintigraphy. Before the tumour-therapy (2 children) lung-scintigrams were regular. 16 children (Hodgkin- and non Hodgkin-lymphoma, acute lymphocytic leukemia with mediastinal tumour, intrathoracal neuroblastoma and Ewing-sarcoma) received epidiaphragmatical radiation and cytostatics. All 35 lung-scintigrams of these patients (1-60 months after beginning of therapy) were abnormal. Within 6 months after radiation obstructions to perfusion could be demonstrated in ray-treated parenchyma of the lung only. Subsequent to 6 months after radiation, during cytostatics, disturbances of perfusion were diffusely spreading in the lung parenchyma. 12 children (acute lymphocytic leukemia, Histiocytosis X and osteogenic sarcoma) received cytostatics only. All 18 lung-scintigrams of these patients (1-55 months after beginning of therapy) were pathological. After cessation of therapy (radiochemotherapy or chemotherapy only) scintigraphically improvement of perfusion occurred in the majority of patients. Obviously the diffusely spreading obstructions to perfusion represent alterations during the early phase of their development induced by chemotherapy.
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PMID:[Lung-scintigraphy in the control of children with malignancies treated by radiochemotherapy (author's transl)]. 734 31

Elucidating the relevant genomic changes mediating development and evolution of prostate cancer is paramount for effective diagnosis and therapy. A putative dominant-acting nude mouse prostatic carcinoma tumor-inducing gene, PTI-1, has been cloned that is expressed in patient-derived human prostatic carcinomas but not in benign prostatic hypertrophy or normal prostate tissue. PTI-1 was detected by cotransfecting human prostate carcinoma DNA into CREF-Trans 6 cells, inducing tumors in nude mice, and isolating genes displaying increased expression in tumor-derived cells by using differential RNA display (DD). Screening a human prostatic carcinoma (LNCaP) cDNA library with a 214-bp DNA fragment found by DD permitted the cloning of a full-length 2.0-kb PTI-1 cDNA. Sequence analysis indicates that PTI-1 is a gene containing a 630-bp 5' sequence and a 3' sequence homologous to a truncated and mutated form of human elongation factor 1 alpha. In vitro translation demonstrates that the PTI-1 cDNA encodes a predominant approximately 46-kDa protein. Probing Northern blots with a DNA fragment corresponding to the 5' region of PTI-1 identifies multiple PTI-1 transcripts in RNAs from human carcinoma cell lines derived from the prostate, lung, breast, and colon. In contrast, PTI-1 RNA is not detected in human melanoma, neuroblastoma, osteosarcoma, normal cerebellum, or glioblastoma multiforme cell lines. By using a pair of primers recognizing a 280-bp region within the 630-bp 5' PTI-1 sequence, reverse transcription-PCR detects PTI-1 expression in patient-derived prostate carcinomas but not in normal prostate or benign hypertrophic prostate tissue. In contrast, reverse transcription-PCR detects prostate-specific antigen expression in all of the prostate tissues. These results indicate that PTI-1 may be a member of a class of oncogenes that could affect protein translation and contribute to carcinoma development in human prostate and other tissues. The approaches used, rapid expression cloning with the CREF-Trans 6 system and the DD strategy, should prove widely applicable for identifying and cloning additional human oncogenes.
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PMID:Identification of the human prostatic carcinoma oncogene PTI-1 by rapid expression cloning and differential RNA display. 754 76

The dramatic progress observed in the survival of children treated for cancer in the last two decades due to the use of aggressive chemotherapy and radiotherapy has brought an increased incidence of second malignant tumors. Five clinical cases of second malignant neoplasms after a period of six months to seventeen years after diagnosis are presented. The second tumors observed were: one patient with malignant fibrous histiocytoma of the orbit after treatment bilateral retinoblastoma; one patient with multifocal osteosarcoma after cerebelli medullo-blastoma; one patient with Ewing's sarcoma of the fibula after neuroblastoma of the adrenal gland; one case of carcinoma of the thyroid gland after osteosarcoma of the femur and one patient with acute lymphoblastic leukemia after been treated of osteosarcoma of the femur. The genetic, immunologic and therapeutic risk factors are reviewed and analyzed.
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PMID:[Second tumors in pediatric oncologic patients. Report of 5 cases]. 756 49

A phase I trial of a murine anti-ganglioside (GD2) monoclonal antibody (mAb) 14G2a was conducted in 14 neuroblastoma patients and 1 osteosarcoma patient to assess its safety, toxicity and pharmacokinetics in pediatric patients. The pharmacokinetics of mAb 14G2a were biphasic with a t alpha 1/2 of 2.8 +/- 2.8 h and a t beta 1/2 of 18.3 +/- 11.8 h. In general, t beta 1/2 was dose-dependent with a level of significance of P = 0.036, and it reached a plateau at doses of 250 mg/m2 or more. Overall the peak serum levels were dose-dependent at P < 0.001. However, they demonstrated an abrupt increase between doses of 100 mg/m2 and 250 mg/m2. The latter two suggest a saturable mechanism for mAb elimination. In addition, peak serum concentrations were observed earlier at higher mAb doses, which indicates the achievement of a steady state. The t beta 1/2 of mAb 14G2a in children appears to be shorter than in adults. Furthermore, 2 patients demonstrated a considerable decrease in t beta 1/2 following retreatment with 14G2a. This was paralleled by high human anti-(mouse Ig) antibody levels. This study represents the first comprehensive analysis of murine mAb pharmacokinetics in children and will be useful in the future design of mAb therapy.
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PMID:Pharmacokinetics of anti-ganglioside GD2 mAb 14G2a in a phase I trial in pediatric cancer patients. 764 Dec 17

The principles of cancer chemotherapy applied to adult patients today have been substantially derived from experience of cancer in children. Studies of pediatric solid tumors also provided the first evidence that chemotherapy combined with surgery and/or radiotherapy could markedly enhance the curative potential of these local modalities. Conceptual advances in cancer chemotherapy revealed the superiority of intermittent chemotherapy over continuous low-dose therapy with respect to tumor cell kill and the recovery of normal cells. Childrens' Cancer and Leukemia Study Group of Japan applied intensive intermittent chemotherapy for maintenance therapy for leukemia, malignant lymphoma and to adjuvant chemotherapy for solid tumors. Event-free survival rate in treatment of childhood cancer by the Department of Pediatrics, Aichi Medical University, has markedly improved: ALL, 70%; malignant lymphoma, 50%; ANLL, 33%; hepato-blastoma, 100%; osteosarcoma, 65%; neuroblastoma, 54%; and rhabdomyosarcoma, 51%. The 14% rate for brain tumors was the only exception. Current Phase I and II trials based on pharmacokinetics and pharmacodynamics in children were reviewed.
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PMID:[Current status in treatment of childhood cancer]. 766 60

2 mM Ascorbic acid has a potent cytotoxic effect on neuroblastoma, osteosarcoma, retinoblastoma, and rhabdomyosarcoma cells cultured in vitro. At a lower concentration (0.2 mM), ascorbic acid remains highly cytotoxic for neuroblastoma, osteosarcoma and retinoblastoma cells, but it has a stimulatory effect on the growth of rhabdomyosarcoma cells.
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PMID:Ascorbic acid is cytotoxic for pediatric tumor cells cultured in vitro. 770 4


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