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)

The streptovaricin complex (SvCx) and rifamycin SV derivatives display potent antiviral activity against the polycythemic strain of Friend leukemia virus (FV-P), as measured by a reduction in the number of spleen foci produced in mice. Such reductions may be explained by inactivation of functions of (i) the spleen focus-forming virus (SFFV), (ii) its "helper" murine leukemia virus (MuLV), or (iii) both viruses normally present in FV-P. We noted that preincubation of FV-P with fractionation products of SvCx, or derivatives of rifamycin SV, at low concentrations (3 to 5 mug/ml) reduces the number of spleen foci 80 to 97%, whereas titers of MuLV (from the same inoculum) remain unaffected (MuLV titers were measured by XC, S(+)L(-), and "helper activity" assays). Our findings indicate a remarkable biological selectivity of ansamycins, as well as nonansamycin components of SvCx, against the transforming and defective spleen focus-forming virus as compared to MuLV. Thus, the drugs might be useful in distinguishing other types of oncornaviruses.
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PMID:Differential susceptibility of spleen focus-forming virus and murine leukemia viruses to ansamycin antibiotics. 1 86

A molecular hybridization technique has been used to quantitatively measure the nucleotide sequence relationships of selected mammalian RNA tumor viruses. Reciprocal cross-hybridization tests were done in which a given radioactively labeled, viral genomic RNA species was annealed with an excess of unlabeled, complementary DNA product synthesized in endogenously instructed reverse transcriptase reactions. Hybrid formation was measured with pancreatic RNase A. Three representative mammalian RNA tumor virus groups were examined: murine viruses, simian viruses, and feline viruses. The results of reciprocal cross-hybridization testing have revealed that the murine viruses consist of four distinctly related subgroups: (i) the Friend leukemia virus/Rauscher leukemia virus subgroup, (ii) the Gross leukemia virus subgroup, (iii) the Moloney sarcoma virus subgroup, and (iv) the Kirsten sarcoma virus subgroup. Simian sarcoma virus, the only simian virus examined, appeared to share limited interspecies sequence relationships with members of the other virus groups and in particular with Kirsten sarcoma virus. Of the two members of the feline virus group tested, Rickard feline sarcoma virus and RD-114, each was placed in a separate, unrelated subgroup. Rickard feline sarcoma virus exhibited limited sequence relatedness with members of the other virus groups, whereas RD-114 exhibited none.
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PMID:Quantitative nucleotide sequence relationships of mammalian RNA tumor viruses. 4 42

Inhibition of DNA polymerase from oncorna viruses by a new class of macromolecular inhibitors is reported. The macromolecule, designated as mercaptopolycytidylic acid (MPC), is a chemically modified polycytidylic acid containing 5-SH cytidylic bases in the polymerase. Partially thiolated polycytidylic acids (MPC I-III, containing 1.7%, 3.5%, and 8.6% 5-mercaptocytidylate units, respectively) inhibited the DNA-polymerase of Friend leukemia virus (FVL) in the endogenic reaction as well as in the presence of poly rA-(dT)14 or poly (dA-dT) templates; the inhibitory activities were directly related to the percent of tholation. In a bacterial DNA polymerase (E coli-K12 with denatured calf thymus DNA as template) MPCI-III showed no activity. Biological experiments showed that MPC III inhibits the leukemogenic potential of cell-free spleen extracts from FVL-infected mice to about 60%, measured on the basis of spleen weight. The enzymatic and animal experiments have led us to carry out preliminary clinical trials in some cases of Children leukemia. These cases, resistent to the known therapeutic regimes (combination chemotherapy), responded well when treated with MPC along, or in combination with poly I. The experiments indicate that the development of modified polynucleotids with structural similarities to functional templates may be of potential use in the future chemotherapy of leukemia.
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PMID:[Inhibition of viral reverse transcriptase and leukemogenesis by modified nucleic acids (author's transl)]. 4 86

Friend leukemia cells growing in suspension culture are thought to represent a population of primitive erythroid cells which have undergone malignant transformation. We have found that when growing in vivo or in plasma clots in vitro, these suspension culture cells can exhibit morphologic and enzymatic properties which are characteristic of primitive granulocytic cells. The microenvironment in which the tumor cells grow plays a major role in determining the direction of differentiation of these leukemia cells. Hence it appears likely that the Friend cell is in fact a neoplastic pluripotent hematopoietic stem cell.
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PMID:Granulocyte differentiation by Friend leukemia cells. 5 19

Cell-mediated immune reactions appear to play an important role in resistance against growth of leukemia cells in mice. Possible mechanisms for in vivo protection in two tumor systems are discussed. These tumor models, which are a Friend leukemia virus-induced transplantable tumor, FBL-3, and primary murine sarcoma virus (MSV) -induced tumors, are strongly antigenic; under some conditions, tumors regress completely. In mice with regressing FBL-3 tumors, cell-mediated cytotoxicity was measured by release of [125I]iododeoxyuridine. The response was biphasic, with an initial peak at 10 days and a 2nd peak after 30 days. A boost in reactivity could be elicited by later challenge with tumor cells. All of the reactivity was dependent on T-cells, being eliminated by treatment with anti-theta plus complement. The specificity of the reactions was not completely defined, but it was consistent with Friend type-specific antigen plus broader, common antigens. In mice with regressing MSV tumors, strong cell-mediated cytotoxicity, measured mainly by release of 51Cr, was seen against RBL-5, a Rauscher virus-induced leukemia. A single peak of response occurred at about 14 days after virus inoculation. Upon later challenge with RBL-5 cells, a vigorous and rapid secondary response was elicited, mainly in the region of tumor challenge. This cytotoxic reactivity and in vivo resistance to leukemia.lso was completely dependent on T-cells. In addition, macrophage-mediated inhibition of leukemia cell growth in vitro was seen in this system at the time of peak tumor development. The 51Cr release cytotoxicity was specific and directed primarily against an antigen, MEV-SA1, associated with mouse endogenous C-type viruses. The macrophage-induced growth inhibition appeared to be nonspecific. In both the FBL-3 and MSV tumor systems, protection against tumor growth could be adoptively transferred by immune lymphoid cells. In addition to induction of cell-mediated immunity by tumor cell or virus inoculation, cell-mediated cytotoxic reactivity was found to occur naturally in most young mice. This natural killer activity was quite distinct from the experimentally elicited reactions, being mediated by N-cells, a subpopulation of lymphoid cells with no clearly identifiable cell surface markers. The natural cytotoxicity was also directed against antigenic specificities different from those recognized by the MSV-immune cells. The central issue in all of these studies has been to determine the relationships between the in vitro-detected cell-mediated reactivity and in vivo resistance to leukemia.
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PMID:Cell-mediated immunity to leukemia virus- and tumor-associated antigens in mice. 5 23

The cytolytic reactivity of a complex goat anti-feline leukemia virus (FeLV) antiserum for mouse cells (Eveline) releasing large quantities of Friend leukemia virus (FLV) was analyzed by the sensitive [14C]nicotinamide release microcytotoxicity assay. Whereas this interspecies killing reactivity could be blocked by absorption of the goat anti-FeLV serum with a preparation of disrupted FLV, absorption with purified FLV gp71, the major envelope glycoprotein, had no effect. Subsequent serum absorptions with the individual FLV structural polypeptides revealed that the lysis of the Eveline cells by the goat anti-FeLV serum is mediated by antibodies recognizing the interspecies determinant of p30, the major internal capsid protein. The expression of this internal viral component at the surface of virus-producing cells is discussed further. The results also demonstrated that removal of approximately 70% of the carbohydrate portion of gp71 with a preparation of glycosidases did not affect the integrity of its interspecies determinant; these results are in agreement with an earlier study (Bolgnesi et al., 1975) that examined primarily the group- and type-specific sites.
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PMID:Interspecies determinants of Friend leukemia virus antigens involved in cytolysis of virus-pfoducing cells. 6 23

Cell membranes of Moloney lymphoma cells (YAC, of strain A origin) were solubilized by NP40. The antigenicity of the solubilized protein fraction was assayed by inhibition of the corresponding cytotoxic reaction against YAC target cells. The Moloney leukemia virus (MLV)-determined cell surface antigen (MCSA) was detected with mouse antisera, produced by the repeated inoculation of heavily irradiated YAC cells into syngeneic mice. Virion proteins gp71, p30, p15, p12 and p10 were identified with goat or rabbit antisera against purified Rauscher and Friend leukemia virus proteins. MCSA was found to bind to Con-A--Sepharose and was eluted by mannoside together with H-2A AND GP71. In contrast, p30, p12, p10 and part of p15 and p15(E), were not retained on the column and could be separated from MCSA. Passage of the glycoprotein fraction through Sephadex G-200 led to the separation of MCSA activity from gp71 and H-2A. MCSA eluted between the immunoglobulin (IgG) and the bovine serum albumin (BSA) size markers. MCSA could be also separated from the known viral proteins and from H-2 by velocity centrifugation in sucrose gradients. It sedimented with approximately 6.6 S ahead of gp71 (4.4 S) and H-2 (3.2 S). It is suggested that MCSA may be a glycoprotein with an approximate molecular weight of 110,000 and distinct from the known viral proteins gp71, p30, p15(E), p12, p10 and from H-2.
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PMID:Separation of the Moloney leukemia virus-determined cell surface antigen (MCSA) from known virion proteins associated with the cell membrane. 7 Dec 77

The expression of murine leukemia virus structural polypeptides on the surface of cells producing exogenous Friend leukemia virus, endogenous ecotropic AKR and xenotropic BALB/c virus was investigated. Antisera to Friend virus gp71, p30, p15E, p12 and p10 were employed in a complement-dependent chromium release assay and to immunoprecipitate lactoperoxidase iodinated surface polypeptides prior to analysis in polyacrylamide gel electrophoresis. With the latter technique gag-gene encoded proteins and their precursors were not discovered on the viral and cellular surface membranes. Only env-gene encoded polypeptides gp85, gp71, and p15E were detectable. p15E is embedded into the lipid membrane. gp85 is formed by disulfide linkage of p15E to surface-exposed gp71. The ratio of gp71 to gp85 is variable and apparently determined by the host cell. Antibodies of strong cytotoxicity are those against type- and group-specific epitopes of gp71 as well as type-specific epitopes of p12.
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PMID:Surface expression of murine leukemia virus structural polypeptides on host cells and the virion. 8 Nov 84

Fv-1 gene-mediated host restriction of Friend leukemia virus replication was investigated in terms of coat protein synthesis. By using the assay of pseudotype formation with vesicular stomatitis virus. it was shown that under restricting growth conditions the availablity of leukemia virus coat protein for pseudotype formation was decreased. These studies appear to eliminate a pure assembly defect as the mechanism of Fv-1 host restriction.
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PMID:Host restriction of Friend Leukemia virus coat protein synthesis. 17 69

Specific rabbit antisera to the major glycoproteins of Friend leukemia virus (gp71) and the mouse mammary tumor virus (gp52) were utilized to study the surfaces of C3H-, DBA-, BALB/c-, and C57BL-transformed and normal cells by immunoelectron microscopy. Antiserum to gp71 showed reactivity with all of the mouse cells tested regardless of strain, virus production, or state of transformation. In cells producing murine leukemia virus, budding viruses and other areas of the cell surface were consistently labeled with gp71 antiserum. A gp52-like antigen was likewise detected on both cell surfaces and virions of C3H and DBA cells producing the mammary tumor virus. Budding virions with surface spikes but with crescent-shaped nucleoids in C3H/HeJ cells were labeled specifically with gp52 antiserum. The antigen localized with anti-gp52 serum was detected in low concentration on the surface of nonvirus-producing cultures of a C57BL/6 sarcoma induced by the Schmidt-Ruppin D strain of Rous avian sarcoma virus (SRD-2), a BALB/c bone marrow culture (JLS-V9), and a normal BALB/c fibroblast culture (BALB/cF). Other cell cultures transformed by either C-type virus or methylcholanthrene failed to demonstrate gp52 antigen. Both gp52- and gp71-like antigens were found to be expressed simultaneously in C3H/HeJ, C3H-MT, DBA-MT, SRD-2 (transformed) and BALB/cF, JLS-V9, and C3H-1 (normal) cultures. Expression of gp52 antigen in the absence of gp71 was not detected in any of the cultures examined. These findings demonstrate the ubiquitous expression of gp71 in a wide variety of normal and transformed mouse cells while gp52 tends to be expressed predominantly in cells from mice with high mammary tumor incidence (C3H) and DBA), but only to a minor extent in cells from low mammary tumor incidence strains (BALB/c and C57BL).
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PMID:Detection of the major glycoproteins of Friend leukemia virus (gp71) and the murine mammary tumor virus (gp52) on the surface of mouse cells. 18 44


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