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 nonconditional mutant of B-tropic murine leukemia virus (MuLV), defective in polymerase, has been isolated by cloning chronically infected cells. The cell clone containing the mutant produced virus particles which were noninfectious. However, superinfection of the cells by replication-competent XC-negative viruses resulted in the rescue of virus capable of forming plaques in a modified XC test, termed the "complementation plaque assay" (A. Rein and R. H. Bassin, J. Virol. 28:656-660, 1978). Analysis of the noninfectious virions produced without superinfection demonstrated that they contained only 2 to 5% of the wild-type level of reverse transcriptase activity. Purification of this activity indicated that it was associated with a smaller molecule than that produced by wild-type virus. Cells producing the mutant virions did not contain the gag-pol precursor, Pr180gag-pol; however the cells contained proteins of 147K and 114K daltons precipitable with anti-pol serum. All of the normal structural proteins as well as 70S genomic RNA could be detected in the mutant particles. An interference test indicated that a functional ecotropic glycoprotein was synthesized by the mutant. These results indicate that the mutant has a unique defect in the pol gene.
J Virol 1979 Sep
PMID:Mutant of B-tropic murine leukemia virus synthesizing an altered polymerase molecule. 9 71

Antisera reactive with the Abelson murine leukemia virus (A-MuLV)-specified P120 (anti-AbT sera) were produced in C57L/J mice. Of many strains tested, only C57L/J reproducibly rejected syngenic A-MuLV-induced tumor cells; after multiple immunizations their sera would immunoprecipitate both P120 and Moloney-MuLV (M-MuLV) proteins. Using labeled A-MuLV-induced nonproducer cells, only P120 could be detected by anti-AbT sera, suggesting that it may be the only A-MuLV-specified protein. Reactivity of anti-AbT sera with P120 was not blocked by M-MuLV virion proteins, implying that the sera recognize a portion of P120 that is not homologous to any M-MuLV product. Anti-AbT sera stained the surface of live, A-MuLV-transformed nonproducer cells in a two-stage immunofluorescence assay, and such staining was not blocked by M-MuLV protein. Also, intact A-MuLV-transformed cells absorbed much of the reactivity of certain anti-AbT sera for P120. Thus a portion of P120 appears to be exposed on the surface of transformed cells. P120 lacks detectable carbohydrate, is not affected by endoglycosidase H, and cannot be labeled by lactoperoxidase-catalyzed iodination. Thus P120 is an unusual surface protein.
J Virol 1979 Sep
PMID:Preparation of syngeneic tumor regressor serum reactive with the unique determinants of the Abelson murine leukemia virus-encoded P120 protein at the cell surface. 9 72

Plasma membranes were isolated from the leukemia cell line ASL1w and extracted with detergent (DOC). DOC solubilized more TL activity than could be detected on isolated membranes. However, extraction of membranes with LDS or EDTA solubilized only 17% and 4%, respectively, of the activity. This indicated that TL was not loosely associated with the membrane but rather was integrated into the lipid bilayer. At low concentrations of DOC (0.05%), TL was found to be largely aggregated and was also prone to autolysis. Neither aggregation nor autolysis was observed at a higher DOC concentration (0.5%). The apparent molecular weight of TL in 0.5% DOC was determined by Sephadex G-200 chromatography to be about 65,000-70,000. Digestion of a 0.5% DOC extract of TL with either papain or trypsin produced a fragment of TL of about 35,000 molecular weight. These fragments were similar in size to a fragment produced by autolysis. These data suggested that a region of the TL molecule was very prone to proteolytic attack. The 35,000 molecular weight proteolytic fragments bound specifically to lentil lectin affinity columns, which indicated that they retained at least part of the carbohydrate present on the native molecule.
Tissue Antigens 1979 Sep
PMID:Some structural properties of thymus leukemia antigen (TL) solubilized with detergent. 9 17

The antigenicity of tumor-associated antigen (TAA) was compared between 3-methylcholanthrene-induced rat fibrosarcoma KMT-17 and Friend murine leukemia virus-infected KMT-17 (FV-KMT-17) cells. The antigenicity was classified into immunosensitivity and immunogenicity, and studied from the viewpoint of humoral immunity. The immunosensitivity to anti TAA antibodies increased by artificial infection of KMT-17 cells with Friend virus. The results suggested that an increase of lateral mobility of TAA on the cell surface contributes to the increase of immunosensitivity. Concerning the immunogenicity of TAA, an augmentation of anti-TAA antibody formation was demonstrated when FV-KMT-17 cells were used as the immunogen. In this case, a physical association between TAA and virus-associated antigen (VAA) was suggested to be very important to increase the immunogenicity of TAA.
Hokkaido Igaku Zasshi 1979 Sep
PMID:Topographical distribution and association of tumor--associated antigens and their role in antigenicity in rat tumor cells. 9 61

Terminal deoxynucleotidyl transferase (T.D.T.) has been measured in the cells of 112 leukaemia patients whose cells were characterised by membrane markers as well as by standard haematological and cytochemical criteria. The concentration of enzyme ranged from 0.1 to 1.4 units/10(8) cells in the bone-marrows of 20 patients with normal marrow or benign marrow hyperplasia. The enzyme level was raised in 30 of 31 patients with untreated acute lymphoblastic leukaemia (A.L.L.) whose cells reacted positively with an anti-A.L.L. serum (range 0.9-197, mean 59, units/10(8) cells) and in all 9 patients with thymic A.L.L. (Thy-A.L.L.) (range 1.5-95, mean 36, units/10(8) cells). All but 1 of 17 patients with acute myeloblastic leukaemia gave negative results (range 0-1.5, mean 0.60, units/10(8) cells), and T.D.T. was also normal in all 7 bone-marrow samples from patients with chronic granulocytic leukaemia (C.G.L.) in the chronic phase. The T.D.T. assay gave a clear distinction between 11 patients with C.G.L. in lymphoid transformation, anti-A.L.L.-serum positive (range 15-226, mean 83, units/10(8) cells), and 12 patients with C.G.L. in myeloblastic transformation, anti-A.L.L.-serum negative (range 0-1.9, mean 0.7, units/10(8) cells). Among 17 patients with otherwise unclassifiable acute leukaemia, 10 gave raised values (range 1.6-113 units/10(8) cells) and 7 gave normal values. It is concluded that the assay of T.D.T. in the peripheral blood or bone-marrow of patients with acute leukaemia is of value in differentiating lymphoid (including non-T non-B and Thy-A.L.L.) from myeloid leukaemia.
Lancet 1977 Sep 10
PMID:Terminal deoxynucleotidyl-transferase levels and membrane phenotypes in diagnosis of acute leukaemia. 9 30

It was shown previously, that an antiserum directed against highly purified fractions of migration inhibitory factor inhibits delayed hypersensitivity reactions in vivo and in vitro. Using radiolabeling techniques we determined that the anti-lymphokine serum reacted primarily with three lymphocyte activation products (m.w. 60,000, 45,000, and 30,000) all of which had a similar isoelectric point of 5.2. The cellular origin of this material was investigated. It was found that activated B cells, B leukemia cells (L2C), and growing fibroblasts produced material of a similar m.w. as analyzed on SDS-PAGE. No cross-reaction was found with radiolabeled products of activated murine and human lymph node cells and of SV 40-infected African green monkey kidney cells. The isoelectric point of the reactive material from B cells, leukemia cells, and fibroblasts was determined at 5.2. In addition to material with pI 5.2, lymph node cells also produced material with pI 3.5 to 4.5, which focused at pH 5.0 to 5.4. After neuraminidase treatment macrophage migration inhibitory activity in fibroblast culture supernatants could be absorbed specifically to insolubilized anti-lymphokine antibody. These findings suggests that lymphoid and nonlymphoid cells are capable of producing molecules whose physicochemical and functional properties appear to be identical.
J Immunol 1978 Sep
PMID:Antibodies to guinea pig lymphokines. VII. Reactivity with products of lymphoid and nonlymphoid cells. 9 76

Seventy-eight patients with Hodgkin's disease were treated with radiation therapy between July 1966 and July 1976 (30 Stage I, 28 Stage II, 20 Stage III). The mean follow-up period is greater than 5 years. 90% of Stage I, 86% of Stage II, 65% of Stage III, and 82% (64/78) of all patients are NED after radiotherapy alone. Since laparotomy option (1970) 89% (50/56) of patients are NED. Fourteen patients were failures. Chemotherapy "rescued" 6 of 14. Seven have died, 1 is alive with disease, and 1 died of leukemia. Absolute survival is 90% (70/78). Failures were more frequent in patients with unfavorable histological types (9/14), and Stage III disease, primarily IIIS+ or B category (7/14). Sites of failures were mainly extranodal, primarily lung (10/14) and bone (2/14), and are consistent with hematogenous dissemination. Laparotomy performed in 41 patients identified unsuspected splenic involvement in 9 cases (22%), but was a distinct failure in confirming most "small node" positive lymphangiograms. Two patients developed acute myelocytic leukemia, both while NED 5 years posttherapy. One patient had also received adjunctive MOPP. There has been no impairment in the quality of survival that could be directly attributed to radiotherapy.
Cancer 1978 Sep
PMID:Hodgkin's disease: radiotherapeutic management at a cancer oriented community hospital. 10 Jan 96

A set of intraveous injections of 7,8,12-trimethylbenz[a]anthracene consistently elicited leukemia in more than 75% of young adult Long-Evans female rats. There was a profound reduction in the incidence of leukemia in companion groups of rats fed small amounts (1--10 mg) of Sudan III or Sudan IV prior to each injection of the carcinogenic hydrocarbon. Repeated feedings of 1 mg of Sudan III induced cumulative increases in the concentration of menadione reductase (EC 1.6.99.2) in liver, whereas protein concentration was unchanged. A single feeding of 1 mg of Sudan III prevented fatal toxicity in all members of large groups of rats injected with massive doses of 7,12-dimethylbenz[a]anthracene, but 50% of the survivors developed leukemia; unprotected rats succumbed in 1--3 days. Sudan III was not carcinogenic under the experimental conditions.
Proc Natl Acad Sci U S A 1978 Sep
PMID:Azo dyes prevent hydrocarbon-induced leukemia in the rat. 10 Jul 87

When NIH/3T3 mouse fibroblasts were infected with the Moloney strain of murine leukemia virus, part of the viral genome RNA molecules were detected in polyribosomes of the infected cells early in the infectious cycle. The binding appears to be specific, since we could demonstrate the release of viral RNA from polyribosomes with EDTA. Moreover, when infection occurred in the presence of cycloheximide, most viral RNA molecules were detected in the free cytoplasm. Size analysis on polyribosomal viral RNA molecules indicated that two size class molecules, 38S and 23S, are present in polyribosomes at 3 h after infection. Analysis of the polyriboadenylate [poly(rA)] content of viral RNA extracted from infected polyribosomes demonstrated that such molecules bind with greatest abundance at 3 h after infection, as has been detected with total viral RNA. No molecules lacking poly(rA) stretches could be detected in polyribosomes. Furthermore, when a similar analysis was performed on unbound molecules present in the free cytoplasm, identical results were obtained. We conclude that no selection towards poly(rA)-containing viral molecules is evident on binding to polyribosomes. These findings suggest that the incoming viral genome of the Moloney strain of murine leukemia virus may serve as a messenger for the synthesis of one or more virus-specific proteins early after infection of mouse fibroblasts.
J Virol 1979 Sep
PMID:Viral genome RNA serves as messenger early in the infectious cycle of murine leukemia virus. 11 18

A 13-year-old boy with acute myelogenous leukemia resistant to conventional chemotherapy received a bone marrow transplant from his HL-A-identical, mixed lymphocyte culture-reactive sister. The recipient was prepared for transplantation with cyclophosphamide and total body irradiation. Despite cytogenetic evidence of engraftment, graft-versus-host disease was not observed. The patient died 38 days post-transplantation of Gram-negative bacteremia sepsis and recurrent leukemia of recipient origin.
Transplantation 1975 Sep
PMID:Bone marrow transplantation between mixed lymphocyte culture-reactive individuals. 12 39


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