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)

Blood volume was measured using 125iodinated human serum albumin in 27 children with acute lymphoblastic leukemia, and in 7 children with various types of leukemia. Total blood volume was normal in patients without marked enlargement of spleen and liver, and increased progressively as spleen and liver size increased. The hypervolemia was entirely due to expansion of plasma volume. In the children with marked hepatosplenomegaly, only hematocrit (but not red cell mass) was below the normal range in most cases. Both hematocrit and red cell mass were subnormal in the majority of patients without considerably enlarged spleen and liver. Therefore, anemia in children with marked hepatosplenomegaly may be partly caused by hemodilution of red blood cells in expanded plasma volume.
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PMID:Blood volume of children with leukemia. 27 98

Malignant myelosclerosis has been described as a rare form of acute myeloproliferative disorder characterised by minimal or absent splenomegaly, cytopenias, circulating myeloblasts and diffuse marrow fibrosis, but distinction between this entity and acute myeloblastic leukaemia with marrow fibrosis is difficult. This report describes a 50-year-old man who presented with features similar to those of malignant myelosclerosis but ther terminal stage was characterised by generalised lymphadenopathy, bone tenderness, marked leucocytosis and myeloblastaemia. Post mortem examination showed multiple chloromata consisting of myeloblasts. These findings suggest that malignant myelosclerosis may be but a variant of acute myeloblastic leukaemia and probably should be treated similarly. A possible association between diagnostic medical irradiation and this acute myeloproliferative disorder is discussed.
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PMID:Acute myeloblastic leukaemia with marrow fibrosis (malignant myelosclerosis): acute leukaemia or malignant myelosclerosis? 27 42

SN11841 [4'-(9-acridinylamino)-methanesulfon-m-aniside] is an antitumor compound discovered by B.F. Cain. The LD50 for BALB/c mice with single intraperitoneal dosage is approximately 25 mg/kg. RLV-(Rauscher leukemia virus)-induced splenomegaly, a disease indicator in BALB/c mice, is inhibited at SN11841 doses not causing acute mortality. The life span of RLV-infected mice increases at some SN11841 doses. SN11841 does not have direct, or virolytic effects on RLV under conditions approximating those of antiviral effectiveness. SN11841 is cytotoxic for cells in tissue culture, as measured by inhibition of growth rate or vital dye uptake. At nontoxic concentrations SN11841 has no effect on RLV infectivity for murine cells, as determined by XC-cell induced syncytium formation. SN11841 has antiviral activity against vaccinia virus in tissue culture but is inactive against herpes simplex (Type 1), vesicular stomatitis, encephalomyocarditis, or reoviruses. SN11841 apparently does not act by inducing interferon. SN11841 is chemically labile, particularly in the presence of sulfhydryl compounds, but the degradation products resulting from prolonged storage in media are neither cytotoxic nor antiviral.
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PMID:Antiviral activities of 4'-(9-acridinylamino)-methanesulfon-M-aniside (SN11841). 28 Jan 45

A limited number of biologically active materials were examined for their relative ability to selectively inhibit the replication of Gross or Rauscher murine leukemia virus (MLV) in Swiss mouse embryo cells by means of the UV-XC plaque-reduction assay. Among the compounds demonstrating significant antiviral activity against Gross MLV in vitro were 1-(4-fluorobenzyloxy) adenosine (FBAR), polyadenylic acid [poly(A)], the carbocyclic analogue of 6-methylthiopurine ribonucleoside (C-MeMPR), 3-(2,4-dinitrophenylhydrazonemethyl)rifamycin SV (AF/DNFI), and phosphonoacetic acid (PAA). Five compounds that exhibited significant antiviral activity against MLV in vitro were tested for similar activity against Rauscher MLV in vivo. Three of these selected compounds, pyrazofurin (pyrazomycin), ribavirin (Virazole), and 9-beta-D-arabinofuranosyladenine (ara-A), produced a significant (50%-100%) inhibition of virus-induced splenomegaly development in mice, whereas the other two candidate inhibitors, 3-deazauridine (deazaUR) and rifamycin SV, the other two candidate inhibitors, 3-deazauridine (deazaUR) and rifamycin SV, failed to demonstrate any in vivo activity in this 21-day leukemogenesis assay. The administration of an inhibitor of adenosine deaminase (Co-vidarabine) in combination with ara-A resulted in an enhanced antiviral response in both infected cell cultures and animals. Co-vidarabine also increased the potency of ara-AMP against Gross MLV in vitro, indicating the probable dephosphorylation of the compound to ara-A and its subsequent deamination to ara-H in this system.
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PMID:Selective inhibition of RNA tumor virus replication in vitro and evaluation of candidate antiviral agents in vivo. 28 Jan 46

Four cases of lymphocytic leukaemia were distinguished from CLL by surface marker analysis. CLL cells have relatively little SIg and have the mouse erythrocyte receptor. Cells in these cases had denser Slg and lacked the mouse erythrocyte receptor. The group presented a fairly uniform picture with onset in sixth or seventh decade, very high lymphocyte counts, splenomegaly (gross in three), heavy infiltration of marrow, relative resistance to chemotherapy and response to splenectomy. The lymphocytes were somewhat larger than those usually found in CLL and histological examination showed a quasi-nodular pattern in lymph nodes with diffuse infiltration of the spleen. Difficulties of classification are discussed. The addition of surface marker analysis to clinical and morphological parameters allows these cases of B-lymphocytic leukaemia (mouse erythrocyte-negative B leukaemia) to be distinguished clearly from chronic lymphocytic leukaemia. The mouse erythrocyte receptor is particularly useful in making this distinction.
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PMID:B cell leukaemia distinguished from chronic lymphocytic leukaemia by surface markers. 28 76

Male BALB/c mice that received prophylactic iv treatment with pyran had significantly enhanced splenomegaly, an increased number of splenic foci induced by the spleen focus forming virus (SFFV) in the Friend murine leukemia virus (F-MuLV) complex, and a slightly decreased mean survival time as compared with untreated controls infected with F-MuLV. A corresponding increase in the lymphatic leukemia virus component of the F-MuLV complex was not observed, which suggests that the enhancement of the disease was due primarily to a selective increase in the SFFV component of the F-MuLV complex. That the enhancement was related to an increased number of target cells for SFFV was substantiated by data concerning erythropoiesis in iv pyran-treated animals. Increases in splenic hematocrits and in uptake of 59Fe in the spleens of animals treated iv with pyran provided quantitative evidence for the histologic finding of increased erythroid precursors in the spleens.
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PMID:Enhancement of erythroid target cells for Friend murine leukemia virus by intravenous pyran treatment. 28 1

This report discusses the case of a 60-year-old man who presented in 1969 with thrombocytopenia and mild marrow hypoplasia. A diagnosis of paroxysmal nocturnal haemoglobinuria (PNH), was established. The subsequent course included episodes of overt intravascular haemolysis. Thrombocytopenia reverted on several occasions during Oxymetholone therapy. The terminal phase of the illness was marked by the development of a leukocytosis and densely hypercellular bone marrow with splenomegaly. The features were those of a myeloproliferative disorder, although frank leukaemia did not develop.
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PMID:A case of paroxysmal nocturnal haemoglobinuria terminating in a myeloproliferative syndrome. 28 62

The initial clinical and laboratory data of 25 patients with acquired idiopathic sideroblastic anemia (AISA) were analyzed. Criteria for accepting the diagnosis were hyperferremia, ringed marrow sideroblasts, ineffective erythropoiesis, and exclusion of associated hematologic disorders. The findings of a mean age at onset of 70 years, increased mean corpuscular volume, relative neutropenia; and occasional splenomegaly at diagnosis corresponded with previous reports. During the followup for a median period of 32 months, 6 patients (25%) transformed to acute myelogenous or myelomonocytic leukemia after widely variable intervals. The initial data base of these patients was compared to that of the remaining 19 patients in order to isolate predictive features. Only a lesser degree of hyperferremia (P less than 0.001) made the group going on to leukemia distinctive. The median survival of these patients was 20 months. The median survival of 19 patients not developing leukemia was 72 months for males and 42 months for females. Hemochromatosis was diagnosed in four patients and was a primary or associated cause of death in three. Analysis of the transfusion history suggested that intrinsic iron leading was a major factor in these patients. We conclude that leukemic transformation in AISA is a common, poorly predictable event which required lengthy followup for detection. Hemochromatosis in AISA occurs frequently and shortens the median survival.
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PMID:Leukemia in patients with acquired idiopathic sideroblastic anemia: an evaluation of prognostic indicators. 29 23

Two children who presented initially with a lymphoid malignancy were noted to develop recurrences with myeloid features late in the course of their disease. In both cases, evidence of lymphoid differentiation was present in the myelogenous cells that were Ph1 chromosome negative. The first patient had acute myelogenous leukemia and developed a recurrence with morphologic features of acute myelogenous leukemia. Terminal transferase was present in the myelogenous blasts. The second patient initially had a diffuse lymphoblastic non-Hodgkin lymphoma. During the course of her illness she developed a myeloproliferative disorder characterized by basophilic meningitis, splenomegaly, and hypereosinophilia. Lymphocyte T-cell (E-rosette) markers were present on the eosinophils. These observations lend further support to the hypothesis of varying lymphoid and myeloid differentiation in certain cases of leukemia.
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PMID:Myelogenous leukemia evolving during the course of lymphoid malignancy in children. 29 24

The authors report on 16 cases of either subacute (SMML) or chronic (CMML) myelomonocytic leukemia as well as chronic monocytic leukemia (CMoL). All these cases were oligoblastic and, according to their clinical course, they could be termed as smouldering leukemias. The chronic types affected mainly males. The diagnostic cytomorphological and cytochemical criteria are discussed. Erythro- and thrombocytopoiesis were distinctly less impaired than in acute leukemias (AL). The leucocyte count in the peripheral blood of the SMML cases was within the normal range. Hepato- and splenomegaly were markedly increased as compared to AL. According to our materials leukemic skin infiltrations were less frequent in CMoL, CMML and SMML than in acute monocytic leukemias. In each of the three types of leukemia discussed monocytic leukemic cells could be readily identified by cytochemical tests and usually showed fairly normal maturation. In accordance with these observations lysozyme levels in urine and serum usually were strongly increased. The patients in the CMML and CMoL groups showed a mean survival of more than 13 months (2 out of 7 are still alive), whereas the SMML patients survived an average of 8 months. Deaths were frequently due to advanced age rather than to leukemia. In other cases a terminal accumulation of blasts marked a transition to acute leukemia. During the smouldering phase of the disease no beneficial effect of combined chemotherapy could be noted. Supportive and symptomatic therapy might improve length and quality of survival.
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PMID:[Subacute and chronic monocytic leukemia: diagnostic and clinical problems]. 29 89


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