Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although cancer in children is uncommon, it represents the second cause of death before the age of 15. One of the determinants in the development of malignancies in children may be formed by the parental occupational exposure to mutagenic or carcinogenic agents. In November 1988, the Department of Public Health of the Free University Brussels, started a case-control study to look for an association between parental occupational exposure and the development of cancer in their offspring. The cases are formed by all patients with leukemia, a brain tumors or a neuroblastoma treated in three pediatric hospitals in Brussels. For each case, two controls matched for age and sex, are recruited from the same hospitals. One control group is formed by all other cancer patients and a second group includes children hospitalized in the departments of surgery. The parents of the cases and the controls are interviewed about their occupations and occupational exposure in the past and the present. The occupational physicians are asked to supply a questionnaire about the occupational history of the employee. At the end of March 1990 the study will be closed. 20 parents of cases and 8 parents of control persons are already interviewed but we have no results yet.
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PMID:[Cancer in children--relationship with the occupational exposure to physical, chemical and/or biological agents of the parents?]. 261 May 49

We examined platelet aggregating activity (PAA) of 5 human leukemia cell lines (HL-60, ML-1, HPB-ALL, RPMI-1788, K562), human mature lymphocytes and 2 human neuroblastoma lines (NCG, GOTO). Although intact cell suspensions of all leukemia cells and mature lymphocytes did not induce platelet aggregation, all cells exhibited PAA in both heparinized and citrated platelet rich plasma (PRP) following neuraminidase treatment (2 units/ml). In contrast, NCG and GOTO cells with PAA in intact cell suspensions were not affected by neuraminidase. PAA of HL-60 cells pre-cultured in the presence of tunicamycin (0.1-1.0 microgram/ml) to inhibit glycosylation decreased after neuraminidase treatment. Neuraminidase treatment had no effect on procoagulant activity of any of the cells examined. There was no difference in total sialic acid contents between human leukemia and neuroblastoma cells. These results suggest the cell surface glycoconjugates on hematopoietic cells play a role in PAA, and that sialic acid prevents their interaction with platelets.
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PMID:Human leukemia cells and mature lymphocytes induce platelet aggregation after removal of cell surface sialic acid. 261 51

Deferoxamine (DFO) possesses antiproliferative activity against mitogen-stimulated lymphocytes, several tumor cell lines, and human leukemia and neuroblastoma cells. We have investigated its effects on the human myeloid leukemia lines HL-60, HEL, and U-937. In suspension culture, DFO causes a dose-dependent inhibition of proliferation of each cell line, with maximal inhibition observed at concentrations greater than 20 microM. These effects were prevented by cotreatment with iron salts and were at least partially reversible by removal of DFO from the culture system or addition of iron before 48 h of DFO exposure. Similar results were obtained in methylcellulose cultures of leukemic cells, with complete abolition of cell aggregates at day 7 in concentrations of 20 microM DFO or higher. DFO treatment caused a dose- and time-related decrease in DNA synthesis as measured by [3H]thymidine uptake, which was also reversed by treatment with iron salts. DFO caused slight reduction in RNA synthesis and did not affect protein synthesis. DFO caused significant antiproliferative effects on three myeloid leukemia cell lines, associated with inhibition of DNA synthesis, with in vitro effects observed at concentrations attainable in vivo. Evaluation of the antileukemic properties of DFO should continue.
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PMID:Antileukemic effects of deferoxamine on human myeloid leukemia cell lines. 237 80

The clinical and laboratory features of 6 children with arthritis or arthralgia as presenting manifestations of malignancy are described. 4 of the 6 had leukemia, 1 had a neuroblastoma and 1 had histiocytosis-X. The diagnosis of malignancy was made 2 days to 2.5 months after onset of symptoms. Although all patients presented with limp, the clinical courses suggested the need to consider leukemia and the other malignancies in the differential diagnosis.
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PMID:[Articular involvement as a presenting symptom of malignancy in childhood]. 280 63

Developments in the treatment of childhood cancer have been evaluated in patients who had been treated in the National Children's Hospital from 1965 to 1987. The total number of patients was 867, of which leukemia accounted for 376, malignant lymphoma 61, neuroblastoma 174, Wilms' tumor 55, yolk sac tumor 29, rhabdomyosarcoma 36 and hepatoblastoma 30. Patients were divided into three time intervals: the 1960s, 1970s and 1980s. A marked improvement in five-year survival was recognized in Wilms' tumor and yolk sac tumor, amounting to 80%, followed by rhabdomyosarcoma, acute lymphoblastic leukemia and malignant lymphoma. There was no improvement in patients with acute non-lymphoblastic leukemia, neuroblastoma and hepatoblastoma. Prognostic factors for neuroblastoma were further analyzed, and the age of onset and stage of disease were found to have remained constant for 23 years. Factors relating to the improvement of survival were discussed.
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PMID:Improvement in the treatment of childhood cancer: analysis of survival data from the National Children's Hospital (1965-1987). 284 93

Bone-marrow autotransplantation consists of the administration of extremely high doses of chemotherapy and/or radiation followed by "rescue" with autologous, cryopreserved, bone-marrow cells. This approach can produce responses unattainable with conventional doses of similar agents. Bone-marrow autotransplantation is increasingly being done. This report summarises data from 2570 patients receiving autotransplants at 43 centres worldwide for haematological malignancies and solid tumours; more than 50% of these transplants were done since 1984. Most transplants were performed for treatment of lymphoma, leukaemia, lung cancer, melanoma, neuroblastoma, and breast cancer. Preliminary analyses indicate favourable responses in some tumour types and provide a basis for future investigations.
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PMID:Bone-marrow autotransplantation in man. Report of an international cooperative study. 287 40

Several authors have reported an association between neuroblastoma and congenital heart disease; others contend that, unlike specific well-known associations between malignancy and congenital defects (Wilm's tumor and aniridia, leukemia and Down's syndrome), no real relationship exists. We present three cases of cyanotic congenital heart disease in which subclinical neuroblastoma was found. We speculate that abnormal neural crest cell migration and development may be a common link between cardiac malformations and congenital neuroblastoma.
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PMID:The association of congenital neuroblastoma and congenital heart disease. Is there a common embryologic basis? 292 25

Neuroblastoma was diagnosed in a child after a 20-month remission of a pre-B acute lymphoblastic leukemia (ALL). Clumps of atypical cells suggestive of neuroblastoma were seen in the bone marrow. They were positive for monoclonal antibody (MoAb) UJ13A (neuroblastoma cells) and negative for MoAb T29/33 (anti-leucocyte common antigen CD45) with immunocytochemical staining. A right paravertebral mass displacing the kidney was demonstrated by abdominal echotomography, and serum vanilmandelic acid was slightly increased. Despite specific chemotherapy against neuroblastoma and after a transient clinical improvement, the patient died 7 months later of disseminated disease. Immunocytochemical staining on cells frozen at diagnosis of leukemia with MoAb UJ13A and T29/33 was unable to demonstrate neuroblastoma cells and showed the pattern usually observed in leukemia (UJ13A- and T29/33+).
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PMID:Neuroblastoma during acute lymphoblastic leukemia in remission. 297 Aug 89

The expression of common acute lymphoblastic leukemia antigen (CALLA) on a human neuroblastoma cell line, SJ-N-CG, was demonstrated by indirect membrane immunofluorescence, complement-dependent cytotoxicity, and quantitative absorption, using two monoclonal antibodies (J-5 and BA-3) directed against CALLA. Immunoprecipitation of solubilized 125I-labeled membrane proteins from SJ-N-CG cells with J-5 antibody revealed a protein with a molecular weight of 100,000 as determined on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Morphological differentiation of SJ-N-CG cells could be induced in the presence of 2.0 mM dibutyryl adenosine 3'-5'-cyclic monophosphoric acid for 10 days of culture. Changes in cell surface membrane antigens associated with morphological differentiation were studied by indirect immunofluorescence and complement-dependent cytotoxicity using a panel of seven monoclonal antibodies. Increases in the antigens recognized by BA-2 (detecting leukemia-associated antigen), anti-Thy-1, and antibody 390 (Thy-1 antigen) were found in "differentiated cells," while those detected by BA-1 (B-cell-associated antigen) and J-5 (CALLA) were unchanged. In contrast, the antitransferrin receptor defined by B3/25 was inhibited, and expression of B7/21-defined la-like antigen was not induced. Kinetic studies on antigenic alterations showed that the expression of BA-2-defined antigen rose on Day 2 and remained at the same level until Day 10. The expression of CALLA was not changed from Days 2 to 10. The augmentation of Thy-1 antigen was noted on Day 4 and reached the maximum on Day 10. These results show that dibutyryl adenosine 3'-5'-cyclic monophosphoric acid is capable of inducing phenotypic changes in SJ-N-CG cells. The changes of expression of some antigens on exposure of cells to dibutyryl adenosine 3'-5'-cyclic monophosphoric acid may enable us to have a greater understanding of the differentiation of neuroblastoma to a more mature ganglioneuroblastoma phenotype.
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PMID:Altered expression of cell surface membrane antigens in a common acute lymphoblastic leukemia-associated antigen-expressing neuroblastoma cell line (SJ-N-CG) with morphological differentiation. 298 Nov 59

There is now clear evidence that cells cultured from human and animal tumours can be induced to differentiate in vitro by recognised hormones, regulatory peptides, polar solvents and cytotoxic drugs. Examples can be found from several different types of tumour with the bulk of the data deriving from neuroblastoma and myeloid leukaemia. There is no clear correlation of inducer with cell type, other than some specific peptides like MSH, and agents such as dimethyl sulphoxide and dexamethasone have wide ranging activity. Steroid hormone action may require interaction between different cell types, and the inability of tumours to differentiate in situ may implicate reduced cell-cell interaction, possibly due to degradation of extracellular matrix, or to alteration of the stromal phenotype by tumour-derived factors such as peptides or prostaglandins. When differentiation has been demonstrated, it has been possible, in some cases, to correlate increased differentiation with reduced malignancy by in vitro characterisation or tumorigenicity. Conditions which induce differentiation in rat mammary carcinoma and mouse myeloma also reduce tumour growth in vivo. Clinical trials have not provided any conclusive evidence for a therapeutic benefit so far, but relatively few trials have been carried out. There is clearly a need for further investigation both in vitro and in vivo to select optimal conditions and combinations of agents for clinical evaluation.
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PMID:Induction of differentiation in neoplastic cells. 298 18


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