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)

The pharmacokinetics of 8 g/m2 methotrexate (MTX) was compared following short (6 h) and long (24 h) infusions of the drug to 11 children with osteogenic sarcoma (OS; 42 infusion) and 28 children with acute lymphoblastic leukemia (ALL: 118 infusions), respectively. No difference was observed in the first-phase half-life, in systemic clearance or in the volume of distribution of the drug (P greater than 0.05). The concentration of MTX at the end of the infusion was approximately 4-fold higher when the drug was given over only 6 h. However, patients receiving 24-h infusions had approximately 9-fold higher levels by 24 h after the beginning of the infusion. The area under the data curve from start of the MTX infusion until the beginning of folinic acid rescue administration was significantly higher in patients with osteogenic sarcoma (6-h infusions), while the area under the log-data curve was significantly longer in the ALL group (24-h infusions) for the same period. The latter parameter is considered to be characteristic for the concentration-time-effect relationship. The longer duration of MTX administration (with delayed rescue) is thought to be more beneficial from the pharmacokinetic aspect. Patients with osteogenic sarcoma had significantly lower concentrations of MTX at the end of their last treatment with MTX than at the end of the first infusion. Patients developing MTX toxicity had shorter half-lives of MTX in the beta phase. It is suggested that cisplatin induced tubular loss of MTX and folinic acid is responsible for these observations. A wider application of clinical pharmacologic findings in the practice of the administration of cytostatics is indicated.
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PMID:Methotrexate administered by 6-h and 24-h infusion: a pharmacokinetic comparison. 326 Aug 32

Cerebral cortical sclerosis is an acquired condition that has rarely been described in cancer patients. We reviewed necropsy findings in all children with cancer who died at the Children's Hospital of Philadelphia during the 20 year period 1963-1982 and found cerebellar sclerosis in 14 children with cancer (12 with acute lymphoblastic leukemia, 1 each with neuroblastoma and osteogenic sarcoma). The lesions were focal (3), multifocal (9) or diffuse (2). They occurred more frequently in children with acute lymphoblastic leukemia who had received intravenous methotrexate therapy. Ten of these 12 children had also received whole brain irradiation. The pathogenesis of the cerebellar sclerosis is unknown, but it is possible that extrinsic cerebellar compression by tumor or chronically increased intracranial pressure may have played a role in 6, ischemia/hypoxia in 3, and methotrexate toxicity in 2. No clear associations could be ascertained in 3. Methotrexate may be a previously unrecognized cause of cerebellar cortical injury. In addition, oncologic treatment regimens that include other central nervous system-penetrating drugs and irradiation may sensitize cerebellar cortex and make it more susceptible to other cerebellar sclerosis-causative factors.
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PMID:Cerebellar sclerosis in pediatric cancer patients. 347 68

Body weight and lean body mass are different reflections of the nutritional status of patients receiving cancer chemotherapy. In the present study, the relation between lean body mass and body weight during cytostatic treatment was investigated in 3 groups of newly-diagnosed children and young adults with acute lymphocytic leukemia, osteosarcoma, or a small round cell sarcoma. Body weight and lean body mass were determined before and after an initial period of cytostatic treatment. Lean body mass was derived from total body water volume, which was assessed by deuterium oxide dilution. A significant dissociation between body weight and lean body mass was observed in leukemia patients (n = 8, P = 0.008, paired t-test), and in osteosarcoma patients (n = 13, P = 0.001). No dissociation was found in patients with a small round cell sarcoma (n = 8, P = 0.839). We conclude that during cancer chemotherapy periodic assessment of body weight may give a false picture of the preservation of lean body mass. Considering the course of body weight alone may prevent the establishment of a timely diagnosis of malnutrition, which is mandatory for optimal supportive care.
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PMID:Dissociation of body weight and lean body mass during cancer chemotherapy. 347 60

There has been a striking improvement in the overall numbers of children and adolescents who become disease-free and remain disease-free as a result of intensive therapy as defined today, for the following cancers: acute nonlymphocytic leukemia (ANLL), non-Hodgkin's lymphoma (NHL), poor risk acute lymphocytic leukemia (ALL), osteosarcoma, and Ewing's sarcoma. The therapy for each of these tumors, with the exception of osteosarcoma, consisted of combination chemotherapy with or without radiotherapy and was started as soon after diagnosis as possible. Aggressive therapy of osteosarcoma has consisted of surgical removal of lung metastases and chemotherapy. Intensive chemotherapy recently has included the use of high doses of certain drugs such as cytosine arabinoside (Ara-C), methotrexate, VP-16-213 and melphalan in the treatment of patients with tumors that are currently difficult to treat.
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PMID:Indications for and benefits of intensive therapies in treatment of childhood cancers. 352 34

Diaziquone (AZQ), a new lipid-soluble antitumor agent, was given by 15-30-minute infusion on a daily X 5 schedule to 47 children with refractory solid tumors and leukemia. The starting daily dose of 6 mg/m2 was escalated to 10 and 35 mg/m2 in patients with solid tumors and leukemia, respectively. In patients with solid tumors, myelosuppression was dose-limiting at a daily dose of 10 mg/m2. In patients with leukemia, prolonged pancytopenia and bone marrow hypoplasia were observed at daily doses greater than or equal to 25 mg/m2. At these higher doses, significant hyperbilirubinemia associated with sepsis was also seen. Corresponding increases of transaminases or alkaline phosphatase and significant hemolysis were not noted. The maximum tolerated dose for this daily dose schedule was 9 mg/m2 in children with solid tumors and 25 mg/m2 in children with relapsed leukemia. Responses to AZQ included stabilization of disease in osteosarcoma, neurofibrosarcoma, pinealoma, and ependymoma. A patient with juvenile chronic myelocytic leukemia in blast crisis converted back to the chronic phase. A patient with acute lymphoblastic leukemia had a substantial decrease in cerebrospinal fluid blast count. Bone marrow aplasia was achieved in children with acute lymphoblastic leukemia and acute nonlymphoblastic leukemia; however, remissions were not achieved. A phase II study of AZQ in children with refractory malignancies is now being performed by the Childrens Cancer Study Group.
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PMID:Phase I clinical evaluation of diaziquone in childhood cancer. 385 80

We have studied the incidence pattern of childhood cancers in Korea. Although the incidence of many tumors in Korea is similar to that in other countries, the incidence of acute myelogenous leukemia, non-Hodgkin's lymphoma and hepatoma is greater in Korean children. Yonsei Cancer Center commenced a study of multi-modality treatment of childhood cancers in July 1974. The most striking improvement of survival rate was seen in patients with acute lymphocytic leukemia (50% at 5 years), Wilms' tumor (65% at 5 years), neuroblastoma (45% at 2 years), osteogenic sarcoma (55% at 2 years) and malignant histiocytosis (20% at 5 years). This study is an attempt to create a basic framework providing the best possible treatment of childhood cancer in Korea. The data obtained in Korea are briefly compared with those in Japan and the United States.
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PMID:The present status of childhood cancer therapy in Korea. 609 45

Pretreatment serum samples obtained at diagnosis from 89 children with various pediatric malignancies were examined for circulating immune complexes (CIC) using the [125I]Clq binding assay. The study population consisted of 35 children with acute lymphocytic leukemia (ALL), 22 children with acute non-lymphocytic leukemia (ALL), 24 with neuroblastoma (NB), and eight with osteosarcoma (OS). Concomitant quantitation of immunoglobulins was performed in 55 patients, revealing normal values for age. Increased levels of CIC at diagnosis were found in 9%, 22%, 42%, and 50% of children with ALL, AML, NB, and OS, respectively. Except for a higher proportion of CIC-positive patients observed in stage IV NB (nine of 17) compared to stage I-III NB (one of seven), no correlation was observed between initial CIC level and presenting clinical features, response to treatment, prognosis, or presence of infection. Longitudinal sampling of six NB and two OS patients did not reveal a clear relationship between disease activity and quantity of CIC. For the pediatric malignancies studied, these data demonstrate minimal value in quantitating CIC as a means of assessing disease activity or predicting response to treatment and are in contrast to the apparently adverse effect of elevated pretreatment CIC on response to therapy and survival observed in adults with ALL, AML, and OS.
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PMID:Circulating immune complexes in childhood malignancies: a Pediatric Oncology Group study. 658 17

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

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

Acute lymphoblastic leukemia (ALL) was diagnosed in a 13-year-old girl who had been treated previously for osteosarcoma of the left distal femur (23 months after her first cancer onset and 12 months after the end of treatment). The patient started chemotherapy for ALL and achieved complete remission; she is in continuous complete remission 5 years after the diagnosis of secondary ALL and 7 years after the onset of osteosarcoma.
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PMID:Acute lymphoblastic leukemia in a girl treated for osteosarcoma. 762 77


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