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

Serum from C57BL/6 (B6) mice hyperimmunized with NB-tropic Friend virus complex (FV) was cytotoxic for FV-induced erythroleukemic spleen cells and B6 Friend-murine leukemia virus (F-MuLV) lymphoma cells. Cytotoxic activity for erythroleukemia cells remained after repeated absorption of B6 anti-FV antiserum with Friend-Moloney-Rauscher MuLV lymphoma cells but was removed by absorption with erythroleukemia cells induced by FV or Rauscher Vrus. This serologic test system identified a previously unrecognized cell-surface antigen of mouse leukemia, designated Friend Erythroleukemia (FE) antigen to signify its appearance as a determinant of virally induced erythroleukemic differentiation. FE antigen was not detected on 15 transplanted or primary hematopoietic neoplasms, nor was it detected on cells infected with ecotropic, xenotropic, or dualtropic MuLV isolates in tissue culture. Two spleen focus-forming virus (SFFV) nonproducer cells of rats and one of mice express FE antigen in amounts comparable to primary erythroleukemia cells. Absorption tests with FE typing serum indicated that FE antigen was expressed on bone marrow and spleen but not thymus, lymph node, or peripheral blood of uninfected AKR, BALB/c, DBA, and SWR mice; all five tissues from B6 and C57L were negative. Quantitiative absorption tests indicated that the expression of FE antigen, though much lower than on erythroleukemic cells, was greatest on fetal liver, less on bone marrow, and lowest on spleen from BALB and SWR mice. Treatment of BALB/c or SWR fetal liver, bone marrow, spleen, thymus, or lymph node cells with FE typing serum did not result in significant lysis. These observations are consistent with the interpretation that FE antigen is expressed by a minor cell population present in fetal liver, bone marrow, and spleen. Expression of FE antigen, determined by absorption with bone marrow cells, cosegregated with inheritance of the Fv-2s allele in the 17 inbred, 7 recombinant inbred, and 4 congenic mouse strains tested. In summary, the FE antigenic system identifies a cell-surface determinant that has the properties of a SFFV-specified antigen and hematopoietic differentiation alloantigen controlled by the Fv-2 locus. The similarity of FE antigen to Abelson antigen may provide insight into the pathogenic properties of defective transforming MuLV.
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PMID:Friend erythroleukemia antigen. A viral antigen specified by spleen focus-forming virus and differentiation antigen controlled by the Fv-2 locus. 44 85

The results published in the period from 1973 to 1983 entitled "Cytogenetic findings in acute myeloic leukemias" (M 1 to M 6 of FAB classification) were compiled. In 50-60 per cent of those patients affected with acute myeloic leukemia a deviating karyotype could be detected. With a markedly higher frequency chromosomes 8 and 21 will take part in aberrations, with translocations (8; 21) having the main share with about 30-40 per cent. More than half the male bearers of translocation exhibits a loss of the Y-chromosome, a third of female patients a loss of the X-chromosome. Trisomy 8 and 9 as well as monosomy 7 appear in about 20 per cent. These aberrations can also be found in all other leukemic and preleukemic processes. Patients with karyotypic abnormalities in all their cells will have the slightest average survival time and the worst appeal to therapy. The sole appearance of monosomy 7 or Ph1-chromosome respectively seems to be an unfavourable sign from a prognostic point of view. Children with acute myeloic leukemia will possess an aberrant karyotype more frequently than adults, but they have a longer average life, boys are more frequently affected by this. Acute promyelocytic leukemia can be characterized cytogenetically in 94 per cent of the cases by translocation (15; 17). However, distinct geographical differences can be observed here, the causes of which have not been elucidated. About 40 per cent of the patients with acute myelo-monocytic leukemia developed aberrations. Further investigations will have to show whether the chromosome 11 really took part in it somewhat more frequently than merely at random. Chromosome anomalies have not a visible influence on the course of the disease. In 30-40 per cent of patients with a rarely occurring acute monocytic leukemia, an abnormal karyotype could be found. There was an incidence of 47 per cent for a specific translocation (9; 11) or a similar variant respectively. Erythroleukemia is characterized by a high instability of chromosomes and karyotypical variability, particularly in erythrocyte precursors and by an average survival time of one months. Megakaryoblastic and eosinophilic leukemia are very rare kinds of acute leukemias. The small number of publications allows no general statement to be made concerning karyotypical changes.
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PMID:[Cytogenetic findings in acute myelogenous leukemias (FAB M 1 to M 6)]. 241 78

We have studied the immunophenotypic and genotypic characteristic of acute nonlymphoblastic leukemias (ANLL) in infants aged less than one year. Sixty-four percent of cases (16/25) showed a myeloid or myelomonocytic differentiation pattern and 10 of these were classified as FAB M5 (7 M5a, 3 M5b). Only seven of the latter cases expressed the CD14 antigen. Acute megakaryocytic leukemia with a high number of glycoprotein IIb/IIIa or IIIa positive blasts were identified in five patients. Erythroleukemia with a high percentage of rather mature glycophorin A positive erythroblasts were diagnosed in two infants. Cytogenetic studies were successfully performed in all 20 cases investigated. Abnormalities involving chromosome 11 were present in 10 of 17 patients with an abnormal karyotype including five cases with a t(9;11)(p21;q23). Immunoglobulin (Ig) and T cell receptor (TCR) gene analyses were performed in 20 patients. A rearrangement of Ig heavy chain sequences was detected in five cases (20%), one of whom exhibited multiple rearranged fragments. Three of these patients showed additional TCR delta-chain gene rearrangements, while Ig kappa, TCR beta- as well as TCR gamma-chain genes showed a germline configuration in all cases analyzed. Our study confirms the high incidence of myelomonocytic and monoblastic subtypes in infants with ANLL, which are particularly closely associated with chromosome 11 abnormalities. However, we also observed an unexpected high frequency of megakaryoblastic leukemias as well as erythroleukemias. As previously reported for ALL in infants, ANLL of infancy shows a similar heterogeneity regarding phenotypic and genotypic features.
Leukemia 1989 Oct
PMID:Phenotypic and genotypic heterogeneity in infant acute leukemia. II. Acute nonlymphoblastic leukemia. 277 87

Erythroleukemia occurred in a BCF1 mouse after X-irradiation. This leukemia was maintained by leukemic cell transplantation successively without changes in the characters of leukemia. According to leukemic cell proliferation, peripheral blood leukemic cells increased in number, and anemia and granulocytopenia developed. Following leukemic cell infiltration, granuloid-committed stem cells (CFU-C) in bone marrow decreased but those in spleen increased. Neither leukemic cells nor leukemic cell-conditioned medium inhibited CFU-C culture in vitro. Effects of leukemic cells on hematopoiesis were discussed.
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PMID:Effects of leukemic cells on hematopoiesis in radiation-induced murine erythroleukemia. 679 74

Erythroleukemia cell lines HFL/d and HFL/b, derived from tumors induced in vivo in BALB/c (H-2d) and congenic BALB.B (H-2b) mice, respectively, by a polycythemia-inducing strain of Friend virus, produced both spleen focus-forming virus (SFFV) and its native NB-tropic helper virus (Friend murine leukemia virus [FMuLV]) during early-passage generations in culture. Eventually each line ceased production of both infectious viruses but retained its tumorigenic potential in syngeneic hosts. Virus-producer and -nonproducer clones of these cell lines were examined for expression of proteins encoded by the SFFV or FMuLV genomes. Lysates of labeled cells were treated with various antiviral sera, and the precipitates were examined by gel electrophoresis. Expression of the FMuLV env gene-encoded precursor protein, gPr84env, was observed in all producer and most nonproducer clones, but the FMuLV gag and pol gene products, Pr65gag and Pr200gag-pol, were uniformly undetectable in nonproducer clones. All HFL/d and HFL/b clones expressed appreciable amounts of the SFFV-encoded envelope protein, gp52, including one exceptional clone which had ceased to express any FMuLV-encoded proteins. The molecular weight of this SFFV-encoded envelope protein was consistently smaller in all HFL/b clones than in HFL/d clones, regardless of their producer or nonproducer status. The virus-nonproducer phenotype thus appears to be due to shutdown of expression of the 5' portion of the FMuLV genome in two independent cell lines.
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PMID:Viral protein expression in producer and nonproducer clones of friend erythroleukemia cell lines. 693 35

Erythroleukemia was observed in two unrelated cats infected with feline leukemia virus (FeLV) from the same household. Case 1, a 1-year-old neutered male cat developed erythroleukemia (M6) after a diagnosis of myelodysplastic syndrome (MDS-Er) on the criteria of FAB classification of acute leukemias. Case 2, a 1-year-old neutered female cat, which had close contact with Case 1, also developed erythroleukemia (M6Er). In both cases, marked proliferation of erythroid progenitor cells with disproportionally large numbers of immature forms was observed in the bone marrow. In Case 1, neoplastic proliferation of myeloid cells in the bone marrow was also noted at the terminal stage. Combination chemotherapy with daunomycin was partially effective for treatment of these erythroid neoplasias, but did not induce complete remission. Southern blot analysis using exogenous FeLV-specific probes indicated the clonal origin of these hematopoietic tumor cells. Furthermore, the erythroid and myeloid tumor cells in Case 1 were shown to be derived from independent transformed clones. A variant FeLV was shown to be integrated into the tumor cells in Case 1, while a full-length FeLV was found in both cases. Because these erythroid neoplastic diseases occurred in two unrelated cats kept in the same household and these diseases are rare, they may both have been associated with the same FeLV strain.
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PMID:Erythroleukemia in two cats naturally infected with feline leukemia virus in the same household. 749 33

Friend leukemia virus complex (FLV) consists of replication-defective, Friend spleen focus-forming virus (F-SFFV) and replication-competent, Friend murine leukemia virus (F-MuLV). We produced transgenic mice possessing F-SFFV gp55 gene and clarified that the gp55 glycoprotein encoded by F-SFFV env-related gene is, by itself, responsible for the initiation of erythroleukemia. The occurrence of erythroleukemia, however, is sporadic in these mice. Erythroleukemia cell lines established from these mice possessed mutations in the p53 allele. One had a temperature-sensitive mutant p53 allele, p53Val-135 and showed induction of apoptosis by expressing a wild-type p53 protein at 32 degrees C. Superinfection of the mice with Moloney murine leukemia virus (Mo-MuLV) conferred 100% induction of erythroleukemia, mutating p53 gene or activating Spfi-1 gene by insertional events. Activation of the JAK/STAT pathway, which is involved in cytokine signaling, was investigated in the gp55 signaling mediated by the erythropoietin receptor. JAK1 and STAT5 were constitutively tyrosine-phosphorylated but the DNA binding activity of STAT5 was not induced.
Leukemia 1997 Apr
PMID:Pathogenesis of Friend leukemia virus. 920 27

Erythroleukemia is an uncommon leukemia with heterogeneous morphologic and karyotypic features. Some cases might actually represent acute myeloid leukemia with a reactive erythroid hyperplasia. In this report, we described a 68-year-old woman with erythroleukemia and monosomy 7 and showed by fluorescence in situ hybridization that both myeloid and erythroid lineage were clonally involved and that both normal and abnormal erythroid populations coexisted, albeit indistinguishable by morphological examination. These findings may account for the variation in the erythropoietic activity observed in the clinical course of erythroleukemia.
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PMID:Abnormal erythropoiesis in erythroleukemia: a fluorescence in situ hybridization study. 972 40

Erythroleukemia is, within FAB classification, a proliferation of erythroblasts superior to 50% and of myeloblasts superior to 30%. The new WHO classification abolishes the frontier between RAEB-t with 20% and leukemia with 30% of blasts. AML6 variant is a new entity characterized by the proliferation of immature erythroblasts and the absence of non-erythroid blast cells. We analyzed 16 erythroleukemia, 5 RAEB-t and 2 AML6 variants to clarify their relationship. We suggest on survival, karyotype and cytologic characteristics that secondary erythroleukemia are the same entity as RAEB-t, confirming the WHO classification and that amongst de novo erythroleukemia, there is 'AML6 variant' with pure erythroid lineage proliferation.
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PMID:Erythroleukemia: a comparison between the previous FAB approach and the WHO classification. 1191 13

As its name suggests, tumor necrosis factor (TNF) is known to induce cytotoxicity in a wide variety of tumor cells and cell lines. However, its use as a chemotherapeutic drug has been limited by its deleterious side effects of systemic shock and widespread inflammatory responses. Some nonsteroidal antiinflammatory drugs, such as sodium salicylate, have been shown to have a chemopreventive role in certain forms of cancer. Here, we reveal that sodium salicylate selectively enhances the apoptotic effects of TNF in human erythroleukemia cells but does not affect primary human lymphocytes or monocytes. Sodium salicylate did not affect the intracellular distribution of TNF receptors (TNFRs) but stimulated cell surface TNFR2 shedding. Erythroleukemia cells were shown to possess markedly greater basal NF-kappaB responses and elevated Fas-associated protein with death domain-like IL-1 converting enzyme (FLIP) levels. Sodium salicylate achieved its effects by reducing the elevated NF-kappaB responsiveness and FLIP levels and restoring the apoptotic response of TNF rather than the proliferative/proinflammatory effects of the cytokine in these cancer cells. Inhibition of NF-kappaB or FLIP levels in human erythroleukemia cells by pharmacological or molecular-biological means also resulted in switching the character of these cells from a TNF-responsive proliferative phenotype into an apoptotic one. These findings expose that the enhanced proliferative nature of human leukemia cells is caused by elevated NF-kappaB and FLIP responses and basal levels, reversible by sodium salicylate to allow greater apoptotic responsiveness of cytotoxic stimuli such as TNF. Such findings provide insight into the molecular mechanisms by which human leukemia cells can switch from a proliferative into an apoptotic phenotype.
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PMID:Elevated NF-kappaB responses and FLIP levels in leukemic but not normal lymphocytes: reduction by salicylate allows TNF-induced apoptosis. 1764 62


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