Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pyrazofurin was administered to 17 patients with refractory acute myelogenous leukemia in 5-day courses every 2-3 weeks. Doses ranged from 30 to 60 mg/m2/day. Severe stomatitis and dermatitis occurred at doses effective in reducing the leukocyte count (45 mg/m2). Reduction of the dose to 30 mg/m2 resulted in less toxicity and less chemotherapeutic effect. These results indicate that at tolerable doses given as described, pyrazofurin had little antileukemic activity in acute myeologenous leukemia.
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PMID:Phase I study of pyrazofurin in refractory acute myelogenous leukemia. 15 46

Characterization of ribonucleic acid content of particles released from cultures of marrow cells of leukemic patients indicates the presence of RNA molecules of size and base sequence characteristic of oncornarviruses. Seventeen marrow samples obtained from leukemic patients in relapse or in a chronic phase of the disease yielded particles containing high-molecular-weight RNA with a sedimentation velocity (about 70 S) similar to that obtained for murine oncornavirus RNA. Eight of nine marrow samples from non-leukemic patients did not yield detectable high-molecular weight RNA. Among patients in firm hematological remission, three of three samples from patients with acute lymphoblastic leukemia and three of nine samples from patients with acute myeloblastic leukemia were positive for high-molecular-weight RNA. The base sequence of the RNA in particles was characterized by synthesizing complementary (3-H)DNA in an endogenous reaction and hybridizing to excess RNA from known oncornaviruses. Hybridization of 40-60% of input complementary DNA to simian sarcoma virus RNA was detected. No monology was detected with an avian oncornavirus (Rous sarcoma virus) while an intermediate level of homology (10-30%) was detected in hybridization to murine sarcoma virus (Kirsten) and murine leukemia viruses (Rauscher, Moloney, and Gross).
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PMID:Viral-related information in oncornavirus-lik particles isolated from cultures of marrow cells from leukemic patients in relapse and remission. 16 62

Herpesvirus saimiri (HVS) is an oncogenic virus for a variety of nonhuman primates. HVS does not produce overt disease upon inoculation in the natural host (squirrel monkey) but consistently induces neoplasms including lymphomas and lymphocytic leukemias in 4 other species of monkeys. Various drugs inhibit replication of HVS in vitro including cytosine arabinoside and adenine arabinoside. In addition, the lymphoma and leukemia induced in owl monkeys responds to vincristine and prednisolone, cyclophosphamide, cytosine arabinoside, and human interferon. Of the various chemical carcinogens studied, the antitumor agent procarbazine induces neoplasms in a variety of species including monkeys. Thus far this compound has induced acute myelogenous leukemia (AML), lymphoma, and hemangiosarcomas in macaques. We have induced primary liver tumors in macaques with several nitrosamines and aflatoxin B1 and these tumors produce alpha-fetoprotein (AFP) which can be assayed for both diagnosis and therapy. Thus far, therapy of hepatocellular carcinoma has been most successful with surgical resection; and the tumor mass and serum AFP have been less responsive to single agent chemotherapy. These nonhuman primate models are useful for an understanding of the cause, diagnosis, prevention, and treatment of the human disease.
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PMID:Nonhuman primate models for lymphoma, leukemia, and other neoplasms. 16 36

Sera from healthy humans contained naturally occurring antibody against group- or subgroup-specific antigen on the envelope of the following type C viruses isolated from primates: gibbon ape leukemia virus, simian (woolly monkey) sarcoma virus, baboon endogenous type C virus, and putative human type C viruses [HL23V isolated from blood cells of a patient with acute myelogenous leukemia (HL23) and HEL-12V from human embryonic diploid cells (CIH-32)]. Two sera also reacted with C57BL/6 mouse leukemia induced by Friend virus. These results were obtained by indirect immunoelectron microscopy with various virus-producing cells and by absorption tests using as targets gibbon lymphosarcoma cells that release gibbon ape leukemia virus. In a previous report, the presence of natural antibody in sera from healthy gibbon apes was demonstrated. When the specificities of the human and gibbon natural antibodies were compared, the human natural antibody reacted with two nonproducing culture cell lines of human lymphocytic leukemia (CEM-A and MOLT) and with human embryonic diploid (CIH-1(V-) cells [which became type C virus-producing CIH-32(V+) cells after many passages], but did not react with normal gibbon spleen monolayer cells. In contrast, gibbon natural antibody showed no reaction with CEM-A, MOLT, and CIH-1(V-) cells but reacted with gibbon spleen monolayer cells. Neither human nor gibbon natural antibody that was reactive with gibbon ape leukemia virus crossreacted with feline leukemia virus and mouse wild-type AKR leukemia virus. The gibbon lymphosarcoma cells releasing gibbon ape leukemia virus were used in a screening study of sera from healthy humans. Out of 72 sera screened by indirect immunoelectron microscopy using this system, 55 were positive (76%), i.e., 26 out of 35 males (74%) and 29 out of 37 females (78%). The highest incidence of antibody production was in 1- to 10-year-olds and 31- to 40-year-olds, with the adults exhibiting higher levels. Differences in incidence of natural antibody were not found to be sex-linked. These findings suggest that type C RNA viruses related to the gibbon ape leukemia virus and simian (woolly monkey) sarcoma virus family as well as the baboon endogenous type C virus family may be widespread in humans.
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PMID:Natural antibodies in sera from healthy humans to antigens on surfaces of type C RNA viruses and cells from primates. 18 53

A uniform system of classification and nomenclature of the acute leukaemias, at present lacking, should permit more accurate recording of the distribution of cases entered into clinical trials, and could provide a reference standard when newly developed cell-surface markers believed to characterize specific cell types are applied to cases of acute leukaemia. Proposals based on conventional morphological and cytochemical methods are offered following the study of peripheral blood and bone-marrow films from some 200 cases of acute leukaemia by a group of seven French, American and British haematologists. The slides were examined first independently, and then by the group working together. Two groups of acute leukaemia, 'lymphoblastic' and myeloid are further subdivided into three and six groups. Dysmyelopoietic syndromes that may be confused with acute myeloid leukaemia are also considered. Photomicrographs of each of the named conditions are presented.
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PMID:Proposals for the classification of the acute leukaemias. French-American-British (FAB) co-operative group. 18 40

B.M. cells of RLV-infected BALB/c mice can proliferate in methylcellulose in the absence of E.P., while normal B.M. cells cannot (12). Not only the more primitive BFU-E shows hormone-independency (18). This phenomenon is in favour of the view that the Rauscher virus induced erythroblastosis is a true neoplasia although transplantation experiments failed so far. The experiments in which transformation in vitro of B.M. cells by RLV is established (19) show that the CFU-E can serve as a target for the virus. Treatment of normal mice with CFA leads to a rapid increase in CFU-E in the bone marrow (18). Splenomegaly of RLV-infected mice is enhanced by CFA-treatment probably due to an increase in targets. Transfection with proviral DNA also can transform the CFU-E of BALB-c mice. This approach allows in vitro studies on the resistence of mouse strains to RLV in vitro. The studies are of interest for the human disease in two aspects. In vitro transformation assays are needed to study the oncogenic potential of putative human leukemia viruses. Furthermore the studies have yielded some new insight in the pathogenesis of virally induced erythroblastosis. This might serve as a model for e.g. acute myeloid leukemia in man.
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PMID:Hormone independent in vitro erythroid colony formation by mouse bone marrow cells. 18 23

Two cases of acute myeloblastic leukemia were observed in a young 22 year old woman, then two years later, in her brother aged 16 years. The elder brother had died previously probably from the same disease. The very rare families in which more than two members had the same type of leukemia show the possible intervention of a hereditary factor in leukemogenesis.
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PMID:[Familial leukemia]. 19 13

The effect of cyclophosphamide administration on survival of 4- to 7-week-old chickens as well as on induction of leukemia after avian myeloblastosis virus (AMV) injection was studied. The drug treatment alone did not cause any neoplastic effect in the birds during 4 months of observation. Immediate application of AMV to cyclophosphamide-pretreated age-resistant chickens induced acute myeloblastic leukemia in about 80 per cent of test animals. The sensitivity of chickens against AMV, induced by cyclophosphamide, had transient character only. When AMV was injected delayed, 3 or 10 days later, after the administration of the drug was completed, a rapid and pronounced increase of resistance was observed again.
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PMID:Cyclophosphamide induced sensitivity against avian RNA myeloblastosis virus in age-resistant hosts. 20 74

The level of cAMP was determined in isolated cells from bone marrow and peripheral blood of healthy subjects and patients with proliferative syndrome (acute and chronic myeloid leukaemia and chronic lymphatic leukaemia). In the investigations tritiated cAMP (3H-cAMP) was used and for binding of endogenous as well as exogenous cAMP protein isolated from bovine muscles was used. The mean cAMP level in peripheral blood granulocytes of healthy subjects was 27.90+/-3.82 pmol/10(7) cells and in normal lymphocytes it was from 11 to 18 pmol/10(7) cells. Much higher concentrations of cAMP: 56.4+/-16.25 and 52.7+/-11.02 pmol/10(7) cells were observed in myelocytes and metamyelocytes isolated from the bone marrow of healthy subjects. Lowering of cAMP concentration (below 4 pmol/10(7) cells) was observed in the lymphocytes of patients with chronic lymphatic leukaemia, while a higher cAMP concentration (above 90 pmol/10(7) cells) was found in the myeloblasts of patients with acute myeloid leukaemia.
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PMID:[Intracellular cAMP concentration in isolated cells of white blood cell series of peripheral blood and bone marrow in healthy subjects and patients with different proliferative syndromes]. 20 43

Collagenolytic activity in leukocytes and plasma concentration of hydroxyproline were estimated in 80 patients with leukemias and Hodgkin's disease and in 20 healthy individuals. An increase of both studied parameters was found in chronic myelocytic leukemia and Hodgkin's disease, and a decrease was shown in acute myelocytic leukemia and acute lymphatic leukemia. The results obtained imply that metabolic changes occur in leukemia leukocytes, and indicate the presence of disturbances in the metabolism of connective tissue in the studied disorders.
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PMID:Collagenolytic activity in leukocytes isolated from patients with leukemias and Hodgkin's disease. 21 37


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