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)

Chromosome banding patterns were obtained for 50 of 55 consecutive adult patients with acute nonlymphocytic leukemia during a 5-yr period. Twenty-two of the 50 cases were diagnosed as acute myelocytic leukemia (AML), 24 as acute myelomonocytic leukemia (AMMol), 2 as acute promyelocytic leukemia (APL), and 2 as erythroleukemia. Twenty-five patients had initial chromosome abnormalities during the course of the disease. The median survival of patients with normal chromosomes initially (group I) was 10 mo, whereas that of patients with abnormal chromosomes initially (group II) was 2 mo. Similar times were obtained for treated patients with AML and AMMol. However, when the AML patients were separated into those with and those without a chromosome abnormality, the median survival times were markedly different (2 mo versus 18 mo, respectively). Patients with AMMol demonstrated no difference in median survival times when subgrouped according to the presence or absence of chromosome abnormalities. The treated group II patients whose marrow samples had only abnormal metaphases had a poorer response (10% complete remission) and median survival (2 mo) than the group II patients who had at least one normal metaphase (42% complete remission with a median survival of 9 mo). The two cases of APL demonstrated a deletion of the long arm of No. 17 which occurred in the same region of the chromosome in each case. Both patients had similar clinical histories, with disseminated intravascular coagulation, and neither responded to therapy.
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PMID:Acute nonlymphocytic leukemia in adults: correlations with Q-banded chromosomes. 5 14

A histological stain described by Menzies in 1963 has been useful in detecting early evidence of erythroleukemia (Friend disease) in mouse hemopoietic tissues fixed in formaldehyde solution. With the use of this stain, one can distinguish erythroblastic leukemia cells from lymphoblastic leukemia cells.
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PMID:A histological stain for detecting Friend leukemic cells in fixed hemopoietic tissue. 6 94

The Friend erythroleukemia cell line T3-C12, which produces Friend murine leukemia virus (F-MuLV) and can be induced to synthesize hemoglobin by dimethyl sulfoxide (DMSO), was monitored for viral RNA-dependent DNA polymerase reverse transcriptase (RT) activity. The amount of viral 60-70S RNA released from DMSO-treated cells was unaffected or increased compared to that from control cells, while RT activity from treated cells was decreased. Accordingly, the specific activity in F-MuLV from DMSO-treated cells expressed as RT/70S RNA was decreased to 8% of the control activity. The 5-bromo-2'-deoxyuridine added to cultures containing DMSO reversed the differentiation process, and the F-MuLV thus treated did not exhibit the reduced RT activity normally observed in DMSO-treated virus. Cell-free F-MuLV incubated with and without DMSO showed the same RT activity, indicating that DMSO itself did not inhibit RT activity. However, when F-MuLV-containing pellets from control and DMSO-treated culture fluids were mixed, there was marked inhibition of the control RT activity, suggesting that RNase hybrid activity was stimulated or that an inhibitor was produced. Assays of F-MuLV-RNase hybrid released from control and DMSO-treated cells showed no difference in activity, indicating that a specific inhibitor of RT was produced or activated. Additions of certain nucleotide triphosphates to RT incubation mixtures did not result in any stimulation of RT activity in DMSO-treated F-MuLV, suggesting that phosphatase was not responsible for the observed inhibition. The results suggested that DMSO treatment of T3-C12 cells caused a reduction in viral RT activity by stimulating the production of an inhibitor, the nature of which is unknown.
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PMID:Viral reverse transcriptase suppression associated with erythroid differentiation of Friend leukemia cells. 6 77

The existence of a nonvirion tumor-associated cell surface antigen (TASA) on cells transformed with Friend (FLV) on Rauscher (RLV) leukemia virus has been difficult to demonstrate. Antisera raised against classically defined Friend- Moloney-Rauscher antigenic determinants have been shown to react with virus structural proteins coded for by genetic information contained in the lymphatic leukemia or helper (LLV) virus genome. The recent development of nontrans-formed fibroblast cell lines which contain the replication-defective spleen focus-forming virus (SFFV) genome, free of replicating LLV, has allowed investigation of an SFFV-specific antigen. We have applied the techniques of mixed tumor-lymphocyte culture stimulation followed by lymphocyte-mediated cytolysis assays to search for the cell surface expression of an antigen coded expressly by SFFV genetic information. SFFV nonproducer-immune, in vitro activated spleen cells were capable of effecting the lysis of SFFV-containing BALB/c 3T3 and Fischer rat epithelial, cloned cell lines. Normal BALB/c 3T3 and BALB/c 3T3 cells infected with three types of ecotropic LLV were unaffected. Syngeneic FLV and RLV-induced murine leukemia cells were also killed by SFFV nonproducer-immune lymphocytes. In addition, Kirsten sarcoma virus-transformed, replication-defective and replication-rescued BALB/c 3T3 fibroblasts were not susceptible to SFFV antigen-directed cytolysis. Antibody-dependent complement-mediated cytolysis assays using monospecific goat antisera confirmed that SFFV nonproducers lacked cell surface expression of virion structural proteins. These observations suggest that the antigen detected in LMC experiments was not coded for by genetic information contained in the helper component of FLV, and that it represents a true SFFV-specific cell surface antigen. Based upon the recent molecular evaluation of the SFFV genome as consisting of both xenotropic and ecotropic virus sequences, it appears reasonable that xenotropic genetic information may be responsible for expression of the SFFV- specific antigen. Since the replication-defective SFFV genome is also responsible for the malignant transformation associated with FLV-induced erythroleukemia, one might postulate that gene sequences capable of programming transformation may also code for the TASA detected in these studies.
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PMID:The detection of a spleen focus-forming virus neoantigen by lymphocyte-mediated cytolysis. 7 57

Previous studies have demonstrated that the Rauscher virus induces a biphasic erythroleukemia in DBA mice, and the regression of the disease is connected with the appearance of antibody-dependent cellular cytotoxicity. In the present work, attempts were made to reveal the mechanism leading to the lethal exacerbation of the leukemia. In the sera of leukemic mice soluble tumor-specific antigen could be demonstrated in the stages of early progression and regression but not in the stage of exacerbation. The antigen was present in form of immune complexes with free antibodies in excess. The emergence of a new population of leukemia cells has been observed during the stage of regression. On the surface of these cells the antigen receptor sites were masked by sialic acid which resulted in the loss of immunosensitivity and immunogenicity.
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PMID:Immune response to Rauscher virus-induced leukemia in DBA mice. II. Correlation between antigenic expression and pathogenesis. 7 84

It was demonstrated that the nonvirulent strain of Listeria monocytogenes isolated from vegetable matter prolonged significantly the survival time of mice inoculated with murine virus erythroleukemia. The most significant survival time was recorded when live listeriae were administered on the same day but into another site than the leukemia virus was.
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PMID:An attempt at immunotherapy of murine virus erythroleukemia. 10 89

Silica, an agent predominantly toxic for macrophages, inoculated i.v. to Friend leukemia virus (FLV)-infected mice, blocks the FLV-leukemosuppressive effects of chlorite-oxidized oxyamylose (COAM)-statolon treatment. FLV-infected, COAM-statolon-treated mice that have received silica and have failed to suppress FLV leukemia produced normal amounts of interferon, but did not make antibodies cytotoxic for FLV leukemic cells. Transfer of untreated spleen cells, splenic T cells, or thymocytes from mice with suppressed FLV erythroleukemia to FLV-infected mice treated with silica and COAM-statolon restores the humoral immune response to FLV antigens and results in leukemosuppression. Thus, T lymphocytes from mice with suppressed erythroleukemia participate in FLV leukemosuppression either directly as effector cells, or indirectly as helper cell in the production of antibodies to FLV antigens.
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PMID:Use of silica to identify host mechanisms involved in suppression of established Friend virus leukemia. 18 37

The genome of the Friend strain of the spleen focus-forming virus (SFFV) has been analyzed by molecular hybridization. SFFV is composed of genetic sequences homologous to Friend type C helper virus (F-MuLV) and SFFV-specific sequences not present in F-MuLV. These SFFV-specific sequences are present in both the Friend and Rauscher strains of murine erythroleukemia virus. The SFFV-specific sequences are partially homologous to three separate strains of mouse xenotropic virus but not to several cloned mouse ecotropic viruses. Thus, the Friend strain of SFFV appears to be a recombinant between a portion of the F-MuLV genome and RNA sequences that are highly related to murine xenotropic viruses. The implications of the acquisition of the xenotropic virus-related sequences are discussed in relation to the leukemogenicity of SFFV, and a model for the pathogenicity of other murine leukemia-inducing viruses is proposed.
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PMID:Friend strain of spleen focus-forming virus: a recombinant between mouse type C ecotropic viral sequences and sequences related to xenotropic virus. 19 58

Recent studies have indicated that both the replication-defective spleen focus-forming virus (SFFV) in the Friend virus complex and the helper-independent mink cell focus-inducing (MCF) viruses derived from AKR-murine leukemia virus (MuLV) are env gene recombinants between ecotropic virus and xenotropic virus. In an attempt to isolate additional env gene recombinants between Friend murine leukemia virus (F-MuLV) and xenotropic virus, we have inoculated cloned ecotropic F-MuLV into newborn NIH Swiss mice and analyzed MuLV released from preleukemic and leukemic spleens of infected mice. Two helper-independent MCF strains of F-MuLV have been isolated. Like the previously described AKR-MCF viruses, the Friend MCF viruses are env gene recombinants between an ecotropic virus (F-MuLV) and a mouse xenotropic virus, as shown by host range, interference pattern, and tryptic peptide analysis of the gp70s of these MuLV. Furthermore, RNA from the Friend MCF viruses hybridizes completely to cDNAsffv, a nucleic acid probe which detects that portion of SFFV which was not derived from P-MuLV. The ability to isolate replicating MCF viruses derived from F-MuLV FURTHER strengthens the parallels between the Friend erythroleukemia system and the AKR thymic leukemia system. Finally, the potential relationship of helper-independent env gene recombinants between F-MuLV and xenotropic virus to be highly leukemogenic SFFV is discussed.
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PMID:Helper-independent mink cell focus-inducing strains of Friend murine type-C virus: potential relationship to the origin of replication-defective spleen focus-forming virus. 21 4

Blood lymphocytes from 13 untreated acute leukemia patients, 3 pre-leukemias 3 immunoblastic lymphadenopathias and one infectious mononucleosis showed significantly lower spontaneous (SCMC) and antibody-dependent cellular cytotoxicity (ADCC) against 51Cr-labeled allogeneic melanoma cells of the IGR3 cell line than effector lymphocytes from 20 age- and sex matched control persons. While control lymphocytes exhibited the highest cytotoxic activity after depletion of mononuclear phagocytes (Fraction FFF), followed by the "Ficoll" purified Fraction F and defibrinated whole blood, the reverse was true for acute leukemias: here, the highest cytotoxicity was found in whole blood followed by the lymphocyte fractions F and FFF. Comparatively high cytotoxicity was found with two leukemia patients who had received blood transfusions the day before testing. During the course of an acute erythroleukemia chemotherapy drastically reduced SCMC and ADCC activities. A therapeutical splenectomy, on the other hand, did not affect cellular cytotoxicity in the case of a hairy cell leukemia. The angioimmunoblastic lymphadenopathies showed strikingly high percentages of EA- and EAC-rosettes forming cells and showed a marked increase of SCMC and ADCC activities after elimination of mononuclear phagocytes from the effector cell population.
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PMID:[Effector function of acute leukemias in "spontaneous" (SCMC) and antibody dependent cellular cytotoxicity-tests (ADCC) (author's transl)]. 28 Jul 29


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