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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Near-infrared emission (1170-1475 nm) was studied from L1210 leukemia cells incubated with polyporphyrin (fractionated hematoporphyrin derivative), suspended in deuterium oxide buffer, and then exposed to light. Following pulsed laser excitation, the near-infrared emission decayed in two phases. The first phase of the emission (0-2 microseconds) was principally due to polyporphyrin fluorescence. The second phase of the emission (20-90 microseconds) was due mainly to singlet oxygen. Evidence supporting the assignment of the second phase emission to singlet oxygen included a spectral analysis showing a peak near 1270 nm and reductions in the second phase emission caused by the singlet oxygen quenchers, histidine, carnosine, and water. The second phase emission decayed in a biexponential manner with lifetimes of 4.5 +/- 0.5 and 49 +/- 4 microseconds. Most of the singlet oxygen in the second phase emission was likely due to singlet oxygen that was generated near the surface of the L1210 leukemia cells and then diffused into the deuterium oxide buffer. Direct measurements of singlet oxygen phosphorescence at 1270 nm may prove to be a useful analytical technique for studying photochemical generation of singlet oxygen in cultured cells.
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PMID:Direct observation of singlet oxygen phosphorescence at 1270 nm from L1210 leukemia cells exposed to polyporphyrin and light. 183 32

To search for genes that can collaborate with myc in lymphomagenesis, we exploited retroviral insertional mutagenesis in E mu-myc transgenic mice. Moloney murine leukemia virus accelerated development of B lymphoid tumors. Three quarters contained a provirus within the known pim-1 or pim-2 loci, new loci bmi-1 and emi-1, or combinations of these. bmi-1 insertions predominated, occurring in half the tumors, and resulted in elevated bmi-1 mRNA levels. Significantly, the bmi-1 gene, which is expressed in diverse normal cells, encodes a Cys/His metal-binding motif (C3HC4) that resembles those in several DNA-binding proteins and defines a new category of zinc finger gene. Thus, myc-induced lymphomagenesis can entail the concerted action of several genes, including the presumptive nuclear regulator bmi-1.
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PMID:Novel zinc finger gene implicated as myc collaborator by retrovirally accelerated lymphomagenesis in E mu-myc transgenic mice. 182 28

Nucleocapsid proteins of retroviruses are small basic, nucleic acid-binding proteins with either one or two "Cys-His" boxes, which have been shown to be involved in genomic RNA dimerization, encapsidation, and replication primer tRNA annealing to the initiation site for reverse transcription. The nucleocapsid (NC) protein of Moloney murine leukemia virus (MoMuLV NCp10) is made up of 56 residues with one Cys-His motif. The Zn(2+)-binding affinities and induced conformational changes of NCp10 were investigated by following the fluorescence of Trp 35 located in the Cys-His domain. At pH 7.5, NCp10 was shown to bind Zn2+ at a 1 : 1 ratio with a very high apparent binding constant of 1.2 (+/- 0.3).10(13)M-1. A similar apparent binding constant was obtained for a 19-residue peptide encompassing the Cys-His box, designated the "zinc finger motif," indicating that it contains most if not all the information to bind Zn2+ tightly. Changing Trp 35 to Phe in the peptide did not affect the Zn2+ affinity, indicating that Trp 35 is not crucial for Zn2+ binding. On the contrary, replacing Cys 29 by Ser, the chemical modification or oxidation of the three Cys sharply reduced Zn2+ affinity, confirming the essential role of Cys in Zn2+ binding. In addition, fluorescence and energy transfer data suggested that Zn2+ binding modifies the Trp 35 environment but not its solvent exposure, and increases the average distance between Tyr 28 and Trp 35 by about 2 A. These data suggest that Zn2+ binding to retroviral NC protein is biologically relevant.
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PMID:Investigation of zinc-binding affinities of Moloney murine leukemia virus nucleocapsid protein and its related zinc finger and modified peptides. 191 45

A 57-year-old man was diagnosed to have essential thrombocythemia (ET) in July 1977. He was doing well with continual medication of carboquone but was hospitalized because of slight unconsciousness and gait disturbance in May, 1988. His laboratory data were as follows: WBC count 81,600/microliters with 55% of blasts with cytoplasmic blebs, Hb 10.2 g/dl, and platelet count 2.6 x 10(4)/microliters. Bone marrow aspiration revealed hypercellular marrow with 72.8% blasts. Chromosomal analysis showed tetraploidy with 7p+ and 19p+. Cytochemistry of blasts showed the positivity for platelet peroxidase and CDw 41. The diagnosis of acute megakaryoblastic leukemia was made. Meningeal leukemia was also suspected by the cerebrospinal fluid data, and cytarabine was intrathecally injected. Then the percent of blasts of peripheral blood gradually decreased and the data of cerebrospinal fluid improved. However, several days later the patient became comatose probably due to cerebral bleeding, and died. In this case, two possibilities were considered (1) that a blastic transformation to acute leukemia from ET, and (2) that a secondary leukemia developed as a result of the chemotherapy, independently of ET. Since there was no evidence of myelodysplastic syndrome, it was concluded that this case represented a blastic transformation of ET.
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PMID:[Acute megakaryoblastic leukemia developing 11 years after diagnosis of essential thrombocythemia]. 194 27

A 3-year-old boy was referred to our hospital in September 1985, because of pancytopenia. His bone marrow was normocellular with 18% blasts, which had Auer rod and were positive for peroxidase staining. A diagnosis of refractory anemia with excess blasts in transformation was made according to FAB criteria. Chromosome analysis of bone marrow cells showed normal male karyotype. He attained complete remission with aclarubicin and BH-AC and continued it until August 1987 when pancytopenia and hypoplastic bone marrow developed. Chromosome analysis of bone marrow cells showed normal male karyotype and gene analysis revealed germ-line configuration of breakpoint cluster region (bcr). Overt leukemia developed in May 1988 when his WBC count increased to 60, 600/microliters with 91% blasts, which were negative for peroxidase staining, positive for anti-Ia and CDw 41 by cell surface analysis, and positive for ultrastructurally demonstrable platelet peroxidase. A diagnosis of megakaryocytic leukemia was made. Chromosome analysis of bone marrow cells showed 46, XY, t(9;22) (q34;q11) and gene analysis revealed rearrangement of bcr. He died in November 1988. Our results and review of literature suggest that late appearing ph1 chromosome and rearrangement of bcr may occur in a variety of hematologic malignancies and influence the course of disease.
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PMID:[Myelodysplastic syndrome in a child which developed into megakaryocytic leukemia with late appearing Ph1 chromosome and rearrangement of breakpoint cluster region]. 221 96

A 28-year-old male was admitted to our hospital because of hepatosplenomegaly and granular lymphocytosis. His peripheral leukocyte count was 3,000/microliters with 43% of granular lymphocytes (GL). These GLs were immunologically phenotyped as CD2+CD3-CD4-CD8-CD16+CD56+HLA-DR+ and were found that TcR genes coding beta and gamma chains were not rearranged. Chromosomal analysis of his GLs stimulated with IL-2 showed 47 XY, +8. This patient was diagnosed as a granular lymphocyte leukemia of natural killer cell type. Blood chemistry showed elevation of serum GOT, GPT and LDH values. The fever persisted until administration of prednisolone was initiated. But 40 days after, high fever appeared again and the liver and spleen were extremely enlarged. Combined chemotherapy was then started but resulted in no effects. He died of hepatic failure on the 77th day from admission. 47 XY, +8, that has been reported in acute non-lymphocytic leukemia and myelodysplastic syndrome, may be related to the pathogenesis in some cases of granular lymphocyte leukemia.
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PMID:[Granular lymphocyte leukemia of natural killer cell type; association with 47 XY, +8 by interleukin 2 (IL-2)-stimulated chromosomal analysis]. 225 62

We report a case of nosocomial fatal varicella infection in a 13-year-old boy with acute lymphoblastic leukemia complicated with staphylococcal scalded skin syndrome. His underlying leukemia, immunosuppressive drugs, disseminated varicella, S. aureus colonization, and acute renal insufficiency were all contributing factors that were pathogenetically linked in the development of his generalized SSSS.
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PMID:Concomitant disseminated varicella and generalized staphylococcal scalded skin syndrome in a leukemic patient. 228 Feb 6

Methotrexate (MTX) is frequently used as an antifolics agent in many malignant neoplasms such as leukemia, lymphoma and osteosarcoma. The major side effects of MTX are liver and renal damages, bone marrow suppression and so on. But careful management and citrovorum factor rescue could decrease the incidence and degree of these side effects. In this report, we described a patient with non-Hodgkin's lymphoma who developed and died of fulminant hepatic failure soon after the administration of intermediate dose MTX. Serological tests for HB virus were not changed throughout, and lymphocyte stimulation test for MTX was strongly positive. His autopsy revealed no inflammatory cell infiltration into the liver, but marked biliary congestion which is a distinctive feature of drug induced hepatitis. From above results, it was suggested that nature of this fulminant hepatic failure was an allergic reaction to MTX. There is no previous report which is concerning about MTX and fetal drug related hepatic failure.
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PMID:[Fulminant hepatic failure induced by intermediate dose methotrexate in a case of non-Hodgkin's lymphoma]. 228 73

The acute leukemias have been considered to represent a clonal expansion of a malignant transformed hematopoietic progenitor cell with adherence to either the myeloid or lymphoid lineage--"lineage fidelity." Lineage fidelity has been challenged by the demonstration of lineage switching or mixed-lineage leukemias. We describe a 7 year old male who presented with undifferentiated acute leukemia and nasopharyngeal and cervical masses. His blasts had the morphologic appearance of myeloblasts (FAB M1) and were positive solely for the myeloid antigen CD15. He entered a complete remission (CR) with acute nonlymphocytic leukemia therapy. At first relapse he had evidence of mixed-lineage leukemia with B-cell lymphoid and myeloid phenotypes. He again relapsed from a second CR with Burkitt-cell leukemia. Cytogenetic findings showed a consistent 14q+, 17p+ abnormality in the blasts and nasopharyngeal mass. The t(8;14) associated with Burkitt's lymphoma was found in the mass tissue only following passage in the nude mouse. Our patient demonstrates that limitations still exist in our ability to classify acute leukemia. That leukemic transformation occurred in a multipotential progenitor cell leading to undifferentiated leukemia at diagnosis and/or that chemotherapy can influence the genetic programs of leukemic cells leading to the evidence of mixed-lineage leukemia and lineage switching is supported.
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PMID:Undifferentiated acute leukemia and lineage infidelity (difficulties in classification and management). 229 88

A 77-year-old man was diagnosed as having acute myelomonocytic leukemia (M4) with increased ringed sideroblasts in the bone marrow (BM) in October, 1979. Complete remission was achieved and ringed sideroblasts disappeared after two courses of CMP (cytarabine, 6-mercaptopurine, prednisolone) therapy. Following remission, there was no increase of blasts during the course of the disease, but monocytosis and dysmyelopoiesis persisted for about seven years. The monocytosis was controlled by 6-mercaptopurine. In June, 1986, however, monocytosis in peripheral blood (PB) and BM developed again, and there was severe pancytopenia and reappearance of ringed sideroblasts without increase of blasts. The patient died of pneumonia on September, 1986. Postmortem examination revealed hypercellular marrow with a few blasts, leukemic cell infiltration into spleen, liver and lymph nodes, ad lung cancer. His clinical and hematological features after remission of acute leukemia accorded with those of CMMoL. The dysmyelopoiesis observed in this case in not induced by anti-leukemic agents, but originated from the same clone as the initial AMMoL, and his disease was thought to be CMMoL converted from blastic crisis to chronic phase.
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PMID:[Long survival of a patient presented with blastic crisis of chronic myelomonocytic leukemia]. 231 5


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