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)

A 3-year-old child diagnosed as having acute lymphatic leukemia (ALL), developed meningeal leukemia 36 months after the onset of the disease. He was twice subjected to cranial irradiation plus intrathecal methotrexate (i.t. MTX). Skull radiology showed bilateral gyriform calcification of both cerebral hemispheres. Hematological relapse was first detected 5 years after diagnosis and the child died 5 months later. The most striking findings of a right frontal lobe biopsy and the postmortem examination were wide calcium deposits located in the cortex and in the adjacent white matter. Intense demyelination as well as areas of neuron poverty were apparent in the necropsy but in the biopsy specimen. The possible interrelationship between such deposition and cranial irradiation and/or i.t. MTX suggests a new iatrogenic disorder.
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PMID:Intracerebral calcifications in childhood lymphoblastic leukemia. A new iatrogenic disease? 41 41

A 52-year-old man with mild diabetes and acute stem cell leukaemia developed an orbitofacial mucormycosis. Cultures showed the fungus to be Rhizopus oryzae. Vigorous treatment with amphotericin B and other bactericidal and bacteriostatic antibiotics for a concurrent sepsis failed to suppress the infections, and the patient died. On post-mortem examination characteristic haematoxylin-staining, broad, aseptate fungal hyphae were found in the right eye, orbit, and lung. A striking and unusual feature of this case is the presence of brightly birefringent crystals within the severely degenerated eye. These were found by histochemical staining and x-ray diffraction studies to be calcium salts of fatty acids, apparently liberated from necrotic adipose tissue of the orbit.
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PMID:Orbitofacial mucormycosis with unusual pathological features. 50 83

A review of CT scans of 7,081 patients demonstrated calcifications of the basal ganglia in 53. The calcifications were evident in the skull roentgenograms of only 4 patients out of 40 in whom both CT scans and plain roentgenograms were available, demonstrating the superior resolution of this new method. Seventy-five percent of the patients were older than 50 years of age. Of the younger patients, 5 had had prior cranial irradiation; 1 had received cranial irradiation and intrathecal methotrexate therapy for meningeal leukemia; and 2 others had deep-seated arteriovenous malformations. Serum concentrations of calcium and phosphorus were normal in all 46 patients in whom they were measured. We conclude that the detection of small calcifications of the basal ganglia in persons above 50 years of age is infrequently associated with either clinical signs of basal ganglia dysfunction or calcium and phosphorus abnormalities. Calcium deposition in these patients may be related to vascular changes associated with aging. In younger patients a specific pathogenetic factor or underlying process is infrequently found.
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PMID:Clinical correlations of CT scan-detected calcifications of the basal ganglia. 53 49

The pathogenesis of hypercalcemia and mode of action of glucocorticoid therapy was examined in a patient with lymphosarcoma cell leukemia. Circulating neoplastic cells were cultured in vitro and secreted a bone-resorbing factor. The bone-resorbing factor was partially purified with the use of a bioassay for bone resorption, and was found to be chromatographically and pharmacologically similar to osteoclast activiating factor (OAF), which is produced by normal mitogen-activated peripheral blood lymphocytes. Other factors which stimulate bone resorption, such as parathyroid hormone, prostaglandins and the vitamin D metabolites, were excluded by criteria which included dose-response curves, radioimmunoassays, extraction in organic solvents and failure of glucocorticoids to inhibit bone-resorbing activity. The patient's hypercalcemia responded rapidly to prednisone therapy. The effects of the bone-resorbing factor secreted by the neoplastic cells on bone cultures to which cortisol was added were examined. Cortisol inhibited bone resorption directly at low doses (10(-8) M), which suggests that prednisone may have lowered the serum calcium in this patient by direct inhibition of bone resorption.
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PMID:Pathogenesis of hypercalcemia in lymphosarcoma cell leukemia. Role of an osteoclast activating factor-like substance and a mechanism of action for glucocorticoid therapy. 70 20

The authors present the case of a child aged 7 years who suffered from relapsing acute lymphocytic leukemia. Treatment consisting mainly of oral and intrathecal methotrexate and x-ray therapy produced remission of the hematologic symptoms. Three years after the onset of the leukemia, mental deterioration gradually appeared. Radiography of the skull revealed diffuse bilateral calcium deposits in both cerebral and cerebellar hemispheres. Four years after the onset of the disease, a hematologic relapse occurred. Behavioral disorders became more severe and the child died after a period of seizures and unconsciousness. The main pathologic data obtained by the study of a brain biopsy and after a complete postmortem examination consisted of calcifications located bilaterally in the cerebral and cerebellar cortex. No signs of leukemia were present. Cerebral calcification is an extremely rare complication in the course of the therapy of lymphocytic leukemia. Its possible causes are discussed.
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PMID:Intracerebral calcifications appearing during the course of acute lymphocytic leukemia treated with methotrexate and X-rays. 105 35

Cortical calcifications, ween on X-ray in the brain of achild suffering from leukaemia, were submitted to morphological and chemical analysis. The morphology was studied by a combination of low teperature ashing and microscanning. The calcification principally affected axons and capillary walls and consisted of spherules amalgamated into hollow cylinders. The results of chemical analysis of the calcified material were compared and structure of both types of calcification were similar, but the Mn concentration washigher in case of Fahr's disease. X-ray diffraction showed that the calcification consisted of amorphous calcium phosphate and acid calcium orthophosphate, most probably precursors of hydroxyapatite..
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PMID:Brain calcification in a case of acute lymphoblastic leukaemia. 105 77

Ultrastructural histochemical evaluation of the surface of normal human blood and bone marrow cells exposed to the pyroantimonate-osmium (PAO) reaction indicated the selective binding of pyroantimonate to certain cations (calcium, magnesium, and possibly sodium) associated with the plasma membrane of neutrophilic leukocytes and their developmental forms. Other leukocytes and their precursors did not exhibit plasma membrane PAO reactivity. The extent of surface binding was related to cell maturity, with maximal labeling evident in the mid and late promyelocytes; decreased binding occurred with subsequent maturation while myeloblasts were nonreactive. This study was initiated to ascertain if histochemical surface modifications of neutrophilic cells occur in certain myeloproliferative disorders. In this regard, we have been able to demonstrate a distinctive defect in the plasma membrane PAO binding characteristics of the leukemic cells in chronic myelocytic leukemia (CML). Limited binding of pyroantimonate to the plasma membrane of the leukemic cell series in four patients with CML contrasted with that of the normal granulocytic cell series and the neutrophilic cells seen in myelomonocytic leukemia (two patients), myelofibrosis (one patient), and acute myelocytic leukemia (three patients). Comparison of surface PAO reactivity of neutrophilic cells in all stages of maturation in two patients with CML in blast crisis revealed that, in the patient with 30% circulating blast cells, PAO reactivity was identical to that noted in CML, while in the patient with 80% circulating blast forms, the PAO reactivity of the maturing neutrophilic cells more nearly resembled that observed in neutrophilic cells from normal individuals. Many neutrophilic cells from patients with myelofibrosis and myelomonocytic leukemia and from one patient in severe blast crisis had large surface deposits of pyroantimonate considered to reflect increased membrane-associated reactive cation.
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PMID:Ultrastructural histochemical alteration of the plasma membrane in chronic myelocytic leukemia. 106 Apr 72

A fraction of the unintegrated viral DNA that appears early after infection of mouse cells by Moloney leukemia virus is infectious. The infectivity could be deomonstrated by an XC plaque assay of the cells exposed to DNA co-precipitated with calcium phosphate. The number of plaques deriving from closed-circular, supercoiled DNA was proportional to the concentration of added DNA, indicating that a single DNA molecule of about 5.5 X 10(6) daltons carries all the viral information. Nonsupercoiled viral DNA is also infectious; these molecules appear to be largely double-stranded and 5 to 6 X 10(6) dalthons in mass.
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PMID:Infectious viral DNA of murine leukemia virus. 106 Oct 80

We studied a patient with acute myeloblastic leukemia, hypercalcemia, hypophosphatemia and inappropriately elevated serum parathyroid hormone levels to define the mechanism of the hypercalcemia. On six occasions during two years, hypercalcemia occurred in conjunction with relapses of leukmia. Each time, serum calcium decreased to normal levels in parallel with reduction of the leukemic mass. During two periods of hypercalcemia, immunoreactive parathyroid hormone values were abnormally high. In addition, hormone was detected in vitro after short-term incubation of the leukemic cells (after 24 hours, the patient's cells produced 129 pg of PTH per milliliter, whereas myeloblasts from a normocalcemic patient with leukemia produced only 33 pg). In freeze-thawing experiments, 39 pg of parathyroid hormone was released form 1 x 108 of the patient's myeloblasts; no hormone was released from the normocalcemia cells. These findings suggest that the hypercalcemia resulted from ectopic parathyroid hormone production by leukemic cells.
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PMID:Acute myelobalstic leukemia and hypercalcemia. A case of probable ectopic parathyroid hormone production. 106 24

Crosslinking HLA-DR molecules by monoclonal antibodies (moAbs) induces protein tyrosine phosphorylation and results in a secondary elevation of free cytoplasmic calcium concentrations in activated human T cells. Binding of bacterial superantigens or moAbs to DR molecules on activated T cells was recently reported to induce homotypic aggregation through activation of protein kinase C (PKC) and mediated by CD11a/CD54 (LFA-1/CAM-1) adhesion molecules. Here, we report that moAbs directed against framework DR, but neither DR1, 2- and DRw52- nor DQ- and DP-specific moABs induced homotypic aggregation of antigen- and alloantigen-activated T cells, antigen-specific CD4+ T-cell lines, a CD8+ T-cytotoxic cell line, and T-leukemia cells (HUT78). Protein tyrosine kinase (PTK) inhibitor herbimycin A partly blocked class-II-induced aggregation responses. In contrast, phorbol ester (PMA)-induced aggregation was essentially unaffected. A potent inhibitor of PKC, staurosporin, inhibited both moAb- and PMA-induced aggregation responses. The aggregation responses were completely inhibited by low temperatures, cytochalasins B and E, and partly inhibited by EDTA and CD18 moAbs, but unaffected by aphidicolin, mitomycin C, an adenylate cyclase inhibitor (2'5'-dideoxyadenosine), and moAbs against other adhesion molecules (CD2/CD58 [LFA-3], CD28/CD28 ligand B7, CD4, and CD44). In conclusion, HLA class-II-induced aggregation responses in activated T cells appear to involve PTK and PKC activation and to be mediated through CD11a-dependent and independent adhesion pathways.
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PMID:Signal transduction by HLA class II molecules in human T cells: induction of LFA-1-dependent and independent adhesion. 128 78


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