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 statistically significant seasonality by month of birth, which differed for children diagnosed as having acute lymphatic leukemia in the under 2, 2-3 and 4-9-year age groups, was observed in urban counties of upstate New York. This suggested that the mothers of patients diagnosed in these three age groups might have been exposed to leukemogenic factors during different trimesters, but with each trimester consisting of the same specific group of months. Since a similar birth-month seasonality was not observed in rural regions, it seemed likely that leukemogenic factors might operate with a greater regularity in urban areas. Using these observations and reported trends for acute leukemia in the United States and New York State (excluding New York City), an effort was made to determine whether varicella, influenza, rubeola or rubella had similar epidemiologic features. Only varicella manifested both the urban-rural differences in seasonality and concomitant variations in time trends that were comparable to reported mortality trends for acute leukemia. Rank correlation coefficients for varicella and lymphatic leukemia incidence rates by month were also statistically significant when leukemia cases diagnosed in the three age groups and born in urban countries, were placed in the month of their appropriate trimesters. A retrospective search of varicella case records identified 63 instances of this viral disease complicating pregnancy. Three children resulting from these pregnancies subsequently developed acute lymphatic leukemia.
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PMID:Childhood lymphatic leukemia: prenatal seasonality and possible association with congenital varicella. 106 32

Simian antisera to human leukemia cells were able to distinguish antigens specific for lymphocytic types of leukemia from those expressed on certain myeloid leukemia cells. In this investigation, cells from acute myelomonocytic leukemia patients (AMML) were examined for their membrane-associated leukemia antigens. Simian antisera to both lymphocytic and myelogenous leukemia cells lysed cells from AMML donors. Monkey antisera to AMML cells, by direct microcytotoxicity testing, were cytotoxic for cells from all AMML patients, as well as for cells of certain patients with myeloid leukemia. Cells from patients with lymphatic leukemia were nonreactive. However, absorption studies indicated an antigen present on cells from patients with chronic lymphocytic leukemia which cross-reacted with AMML cell antigens. Sequential analyses of the serologic reactivity of cells from AMML patients undergoing chemotherapy corresponded with the clinical course of the patient, even though there was little correlation between the percentage of blast cells present and the per cent cytotoxicity with the antisera. At certain times a higher percentage of seropositive cells could be detected over that seen on morphological evaluation. The estimation of leukemic cells by serologic means could aid in the diagnosis and management of AMML patients during chemotherapy.
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PMID:Human acute myelomonocytic leukemia: serologic studies with simian antisera. 106 71

The lymphoblastic leukemia ERLD, induced by radiation in a C57BL/6 mouse, was established in culture. Three cell lines, ERLD/Y3, ERLD/T ERLD/Two, have been in culture for nearly three years. Their isolation and growth depended upon the presence of 2-mercaptoethanol, glutamine, and asparagine in the medium. The cell lines, except ERLD/T, possess the TL antigen, a characteristic of ERLD and of other murine leukemia cells in vivo and of normal thymus cells of certain mouse strains, but not of C57BL/6. A distinctive submetacentric marker chromosome is also common to ERLD and the derived cell lines. The successful establishment of ERLD in culture provides a malignant thymocyte-related cell system for studies in nutrition and immunobiology.
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PMID:Radiation-induced murine leukemia ERLD in cell culture. 106 84

BALB/c mice infected with Rowson-Parr virus, a lymphatic leukemia virus isolated from the Friend complex, undergo a rapid depression of antibody response. Spleen cells from these mice in culture show a similar deficit in the response to stimulation with sheep red cells and inhibit the reactivity of normal splenocytes. In an attempt to reverse this immunosuppression, near normal responses were obtained in vitro from infected splenocytes by increasing antigen dose, by adding E. coli lipopolysaccharide, or, more effectively, by cocultivating with small numbers of unfractionated or T cell-depleted peritoneal exudate cells (PC), whereas other manipulations proved ineffective. PC did not prevent the inhibition of normal splenocytes by infected spleen cells, but exhibited substantial restorative activity in vivo. In similar experiments, the immunosuppression exerted by the entire Friend complex could be reversed by PC in vitro but not in vivo. These results indicate that a functional deficit of macrophages may be partially responsible for the immunological impairment induced by leukemia viruses and suggest rational approaches to evaluate the relevance of this impairment to oncogenesis.
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PMID:Reversal of immunosuppression induced by murine leukemia viruses. 107 70

AKR mice are genetically destined to develop Gross (RNA) virus-induced lymphatic leukemia. Leukemic AKR mice treated with combination vincristine, cyclophosphamide (Cytoxan), and 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea sustained a 180% increase of life-span. Combination chemotherapy plus immunization with neuraminidase-treated allogeneic (Gross virus-induced) G2G leukemic cells intradermally resulted in 35% of animals surviving beyond 150 days without evidence of the disease. It is significant that allogeneic E2G leukemic cells as immunogen were as effective in prolonging the life-span of the immunized leukemic AKR mice as were syngeneic leukemic thymocytes. Virazole (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide), an antiviral compound, alone showed no apparent antitumor effect. However, in experiments in which the clinically diagnosed leukemic AKR mice received a combination of cytoreductive therapy [vincristine plus prednisone or, more effectively, vincristine, Cytoxan plus 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea, followed by Virazole], there was a noticeable reduction of the viral titer, a delay in the reappearance of viable clonogenic cells, and an increase in the survival time for the leukemic AKR mice as compared to those receiving cytoreductive therapy alone. The effectiveness of purified mouse interferon in AKR mice was also examined. The decrease in the viral titer of animals that received interferon treatment was markedly greater than of those receiving a combination of cytoreductive therapy with Virazole or immunotherapy. The administration of mouse interferon had a direct effect on the appearance of the spontaneous leukemia in AKR mice. The median life-span of the control animals was 36 weeks, whereas 45% of the AKR mice treated with five doses of 5 X 10(4) units of interferon are still alive at 54 weeks of age. Thus, interferon not only reduces the Gross murine leukemia virus titer in the chronically infected AKR mice but also significantly delays the appearance of the primary lymphoma.
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PMID:Treatment of spontaneous leukemia in AKR mice with chemotherapy, immunotherapy, or interferon. 108 96

The in vivo biologic activities of a clonal isolate of the Rauscher strain of murine leukemia virus and several conditional lethal mutants with impaired replicative functions at the non-permissive temperature were investigated. The parental virus induced a rapidly developing lymphoid leukemia in a high percentage of NIH Swiss mice inoculated as newborns. Mice inoculated in parallel with temperature-sensitive mutant viruses showed no evidence of disease. The implications of these findings with regard to the requirements for type-C virus replication to permit oncogenic transformation of lymphoid cells in vivo are discussed.
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PMID:Temperature-sensitive mutants of murine leukemia virus. V. Impaired leukemogenic activity in vivo. 109 42

Mixtures of friend virus (CFV) and the regressing strain of friend virus (RFV) induce leukemia which regresses. The dominance of the regressing phenotype is solely a function of a threshold dose of RFV. The minimum amount of RFV which induced regression of CFV leukemia is below the titer for induction of friend disease, but does correlate ith the titer of lymphocytic leukemia (helper) activity in the these stocks.
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PMID:Spontaneous regression of friend virus induced leukemia: coinfection with regressing and conventional strains of virus. 110 26

Exposure of NIH Swiss mouse embryo fibroblasts (MEF) to infectious Friend virus (FV) complex [containing defective spleen focus-forming virus (SFFV) and endogenous NB-tropic leukemia-inducing helper virus (LLV-F)] resulted in the productive infection of these cells by both SFFV and LLV-F. Stocks of SFFV derived after extensive growth in this Swiss MEF cell culture system are fully leukemogenic in adult mice for the induction of erythroleukemia and spleen foci. In addition, in vitro-derived LLV-F, when isolated free of SFFV, is fully leukemogenic for the induction of lymphatic leukemia when inoculated into susceptible newborn BALB/c mice. The host range of in vitro-derived FV complex (i.e., FV-TC) for focus formation in vivo is NB-tropic. Unlike in vivo-derived FV complex, FV-TC does not suppress the responsiveness of murine thymocytes to concanavalin A (Con A) in vitro. Rather, FV-TC acts as a mitogen to nonspecifically stimulate the proliferation of BALB/c thymocytes. The mitogenicity of in vitro-derived FV complex is directly associated with the presence of type-C virus particles, is a heat-labile and UV-sensitive property of the virus, and may be primarily due to LLV since equivalent amounts of LLV with or without SFFV present are equally mitogenic. One in vivo passage of FV-TC resulted in the total loss of this mitogenic property with the reappearance of full immunosuppressive properties. This result demonstrates a clear association between in vivo growth of FV and its ability to suppress mouse thymocytes, and suggests that FV complex (SFFV-LLV) is not inherently immunosuppressive for these cells. While the mechanism of this interconversion between immunostimulatory and fully suppressive virus is unknown, both virus markers appear to be dependent upon the presence of infectious FV.
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PMID:Continuous replication of Friend virus complex (spleen focus-forming virus-lymphatic leukemia-inducing virus) in mouse embryo fibroblasts. Retention of leukemogenicity and loss of immunosuppressive properties. 117 91

From May 1985 to June 1990, 94 newly diagnosed cases of acute myelogenous leukemia (AML) were treated at the Institut Gustave-Roussy, of which four (4.3%) demonstrated mixed cell lineage. All these cases were morphologically and cytochemically considered as myelogenous leukemias according to the FAB classification. Immunophenotyping revealed in all four cases that the blast population had T-lymphoid (CD2, CD5, CD7 and cytoplasmic CD3) markers. In three of these cases, blast cells co-expressed myelogenous CD13 and CD33 markers. Cytogenetic analysis of the blast cells revealed a normal karyotype in all cases. The response to therapy has been poor. The two patients initially treated with a regimen usually used for AML did not achieve complete remission. By contrast, in three cases, complete remission was obtained with a drug combination used for lymphoblastic leukemia (in one case after failure of first line AML regimen). Only one patient remained disease-free for more than 18 months. We conclude that this form of leukemia is a distinct biological and clinical entity and may benefit form alternative therapy.
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PMID:Acute myelogenous leukemia with T-cell features. 130 36

We recently reported the isolation of the K-sam complementary DNA (cDNA), which was amplified preferentially in poorly differentiated types of stomach cancer and codes for one of the heparin-binding growth factor or fibroblast growth factor (FGF) receptor families. The K-sam-related gene, N-sam (NCC-IT-cell-derived sam), was isolated by screening of the cDNA libraries of human immature teratoma cells, NCC-IT. Sequence analysis of the N-sam cDNAs showed that N-sam encodes a human FGF receptor, the FLG protein. N-sam was expressed in lymphocytic leukemia/lymphoma cells, predominantly in the thymic T-cell phenotype. In a T-cell leukemia line, MOLT3, N-sam mRNA expression was markedly enhanced by 12-O-tetradecanoylphorbol-13-acetate treatment and was also up-regulated by basic FGF exposure. These results indicate that N-sam expression is regulated during T-cell ontogeny and modulated by its putative ligand exposure. The results also suggested that interaction between immature T-cell and marrow or thymic interstitial cells might be mediated by N-sam and basic FGF stored in the extracellular matrix of stromal cells.
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PMID:K-sam-related gene, N-sam, encodes fibroblast growth factor receptor and is expressed in T-lymphocytic tumors. 131 50


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