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 rabbit antiserum raised by repeated immunization with BALB/c fetuses obtained at 10-14 days of gestation was used to search for oncofetal antigens (OFA) in murine sarcomas which had previously been characterized for the expression of endogenous murine leukemia virus (MuLV). Iodinated protein A from staphylococcus aureus (IPA) was used to quantitate binding of the antiserum to cultured tumor or fetal cells or to saline extracts of tumors and fetuses. Use of the "antigen" extracts facilitated the assay: the extracts bound to plastic and served as targets for the binding assay, eliminating the need to establish tumors in culture. After absorbtion in vitro and in vivo with adult tissues the rabbit antiserum bound to day 10-14 fetal cells and extract but not to endogenous MuLV (BALB virus 1). The antiserum bound equally well to MuLV-negative and MuLV-positive sublines of MCA-induced sarcomas 1420 and 1414 but not to Moloney sarcoma cells and MCA-induced sarcoma 1386. Thus, the absorbed antiserum detects a class of common cross-reacting antigens which are serologically distinct from MuLV-associated antigens.
Int J Cancer 1978 Sep 15
PMID:Expression of oncofetal antigens on murine sarcomas characterized for expression of endogenous MuLV. 8 Nov 87

We reported earlier that core preparations of Rauscher murine leukemia virus, when separated on an isopycnic sucrose gradient, did not contain detectable levels of RNase H activity, while retaining high levels of reverse transcriptase activity. We reexamined this phenomenon, and the earlier observation was found to be reproducible. However, when doubly banded preparations of viral cores were solubilized and reverse transcriptase was isolated by ion-exchange chromatography, a coincident peak of a nuclease activity with the specificity of RNase H was observed, which indicated that RNase H was selectively inhibited in the core fractions. By direct activity measurements using the purified reverse transcriptase-RNase H from cores, this endogenous inhibitor has been identified as the viral RNA. Viral 70S RNA strongly inhibited RNase H activity purified either from whole virions or from prefractionated cores. Other RNAs tested that had inhibitory effects were yeast tRNA, polyadenylic acid, and polyguanylic acid. Polyuridylic acid and polyadenylic acid were moderately inhibitory, and polycytidylic acid did not inhibit the RNase H. A rabbit anti-reverse transcriptase immunoglobulin G inhibited both the reverse transcriptase and RNase H activities of the enzyme purified from cores. These data provide a rational explanation for the failure to detect RNase H activity in core preparations of Rauscher murine leukemia virus. Furthermore, these data are consistent with the idea that the RNase H and reverse transcriptase activities purified from cores reside on the same protein molecule. Possible biological implications of the observed inhibition of RNase H by RNA is discussed.
J Virol 1978 Sep
PMID:Inhibition by RNA of RNase H activity associated with reverse transcriptase in Rauscher murine leukemia virus cores. 8 12

The RNase H activity associated with purified avian myeloblastosis virus and Rauscher murine leukemia virus DNA polymerases is inhibited by homopolymeric RNA molecules, although the efficiency of inhibition by each homopolymer appears enzyme specific. Formation of duplex RNA molecules abolished the inhibitory activity. In contrast to these results, DNA polymerase-independent RNase H activities, such as the RNase H-II from Rauscher murine leukemia virus and calf thymus RNase H, were unaffected by the addition of exogenous RNA molecules to reaction mixtures. These results support the concept (M. J. Modak and S. L. Marcus, J. Virol. 22:253--256, 1977) that the catalytic site of DNA polymerase-associated RNase H activity may be that which is also involved in template binding. Naturally occurring RNA molecules of oncornaviral, procaryotic, or eucaryotic origin also proved to be efficient inhibitors of avian myeloblastosis virus DNA polymerase-associated RNase H activity. In contrast to this result, naturally occurring RNA molecules, at concentrations which inhibited the avian myeloblastosis virus enzyme, did not inhibit Rauscher murine leukemia virus DNA polymerase-catalyzed RNase H activity. This finding represents a new biochemical distinction between the two reverse transcriptases, and may be indicative of differences in the relative affinities of these enzymes for natural RNA molecules.
J Virol 1978 Sep
PMID:Reverse transcriptase-associated RNase H activity. II. Inhibition by natural and synthetic RNA. 8 13

RNase H of a temperature-sensitive mutant of Rauscher murine leukemia virus is thermolabile, establishing this activity as a virus-coded function of the mammalian type C virus reverse transcriptase.
J Virol 1978 Sep
PMID:Mammalian retrovirus-associated RNase H is virus coded. 8 14

We have analyzed normal rat kidney cells nonproductively infected with the Friend strain of spleen focus-forming virus (SFFV) for the presence of murine leukemia virus-specific type C viral proteins. SFFV was found to code for the p15 and p12 proteins of Friend-murine leukemia virus as determined by immunological typing of their antigenic determinants. Molecular-size analysis of p15 and p12 proteins in SFFV nonproductively infected normal rat kidney cells indicated that these proteins are translated as parts of polyprotein molecules. The apparent molecular weights of the polypeptides bearing p12 antigenic determinants revealed the presence of translational products of the SFFV genome that could not be accounted for by know type C virus helper structural proteins.
J Virol 1978 Sep
PMID:Analysis of translational products of Friend strain of spleen focus-forming virus. 8 15

The expression of immune response-associated (Ia) antigens on the surface of mouse strain GR (H-2dx) ascites leukemia (GRSL) cell lines was studied by cytotoxic tests, immunofluorescence, and immunoprecipitation assays. Ia expression varied among the three GRSL cells lines (GRSL 2, GRSL 14, and GRSL 15) studied by cytotoxic assay. GRSL 14 cells showed the strongest expression of Ia antigens among these three cell lines. A time-course study of tumor growth in mice revealed that Ia antigens on the tumor cells demonstrated the strongest expression 10 days after injection of GRSL cells into GR mice, and that subsequently it decreased until the death of the animal. Cells treated with neuraminidase exhibited more readily detectable Ia antigens, expecially in the late stages of leukemia, which suggested that Ia antigens had been masked by sialic acid. Immunoprecipitation studies revealed that Ia molecules on the leukemia cell had the same molecular weight as those on the normal lymphocytes. Immunofluorescence studies disclosed that Ia antigens were distributed diffusely on the surface of the tumor cells.
Transplantation 1978 Sep
PMID:Immune response-associated antigens on mouse leukemia cells. I. Detection of Ia antigens on GRSL cells. 8 49

Noninbred Sprague-Dawley rat embryo cell clones predictably undergo transformation after 20-30 in vitro passages following spontaneous release of endogenous rat leukemia virus (RaLV). In the presence of RaLV-specific antiserum, virus production and infectivity were reduced and transformation was delayed from 6 to 25 weeks. Transformation was not associated with an increased expression of Kirsten murine sarcoma virus-related src gene RNA.
J Natl Cancer Inst 1979 Sep
PMID:Inhibition of spontaneous transformation of rat embryo cells releasing endogenous type C virus by virus-specific antiserum. 8 11

An RNA-directed DNA polymerase was purified from a cell line derived from a radiation-induced lymphoma in NIH Swiss mice which produced non-infectious type C virus particles. The enzyme was isolated from a high speed particulate fraction which bands at a density of 1.16--1.19 g/ml in a sucrose gradient, and purified by successive chromatography on DEAE-cellulose, phosphocellulose and hydroxyapatite. The purified DNA polymerase has a molecular weight of 68 000, a pH optimum of 7.5, a KCl optimum of 50 mM, and a Mn2+ optimum of 0.25 mM. It prefers (dT)15 . (A)n to (dT)15 . (dA)n as the primer template and transcribes the poly(C) strand of (dG)15 .(C)n and (dG)15 . (OMeC)n. It transcribes heteropolymeric regions of avian myeloblastosis virus 70 S RNA, and is inhibited by antiserum to Rauscher murine leukemia virus DNA polymerase. Comparison of the properties of DNA polymerase purified from radiation-induced lymphoma cells with the DNA polymerase purified from non-defective murine type C RNA tumor viruses shows that the mouse lymphoma enzyme is both biochemically and immunologically related to murine leukemia virus DNA polymerases.
Biochim Biophys Acta 1979 Sep 27
PMID:Characterization of an RNA-directed DNA-polymerase from a cell line derived from a radiation-induced lymphoma in mice. 9 May 22

15 patients with acute myeloblastic leukaemia (AML) in remission were given immunotherapy and 17 similar patients were given immunotherapy plus chemotherapy with the drugs used to induce remission. Median remission length was 245 days for both groups and median survival was 465 days for patients given chemoimmunotherapy and 476 days for patients given only immunotherapy. The failure of remission chemotherapy in AML cannot be attributed to induced resistance because the same drugs induced a second remission in 60% of the patients. From laboratory studies with human AML cells it is suggested that in AML the residual leukaemic cells mature after induction chemotherapy and are then refractory to further drug treatment. Relapse occurs when the leukaemic population proliferates and the environment permits dedifferentiation into frank blast cells.
Lancet 1979 Sep 29
PMID:The nature of remission in acute myeloblastic leukaemia. 9 Jul 62

A discrete, 600-nucleotide-long plus-strand DNA has been identified among the products of reverse transcription by virions of Moloney murine leukemia virus. Its polarity was shown by hybridization to minus-strand DNA. It appears to be copied from the right end of minus-strand DNA because (i) its restriction endonuclease cleavage pattern corresponds to the redundant 600-base segment found at either end of the ultimate double-stranded reverse transcription products, (ii) its synthesis is actinomycin D sensitive, and (iii) its synthesis begins during the first hour of a reverse transcription reaction when only the right-hand end of minus-strand DNA is available as template. We therefore call this DNA plus-strong-stop DNA by analogy with the minus-strong-stop DNA copied from the left end of the viral RNA. Both strong-stop DNAs are made early during in vitro reactions and decline in concentration later, consistent with postulated roles as initiators of long minus- and plus-strand DNA. Unlike minus-strong-stop DNA, plus-strong-stop DNA remains as a double-stranded nucleic acid after its synthesis, as shown by S1 nuclease resistance. A primer to initiate plus-strong-stop DNA synthesis has not been identified; the product found thus far has no detectable RNA attached to it.
Proc Natl Acad Sci U S A 1979 Sep
PMID:Synthesis of a 600-nucleotide-long plus-strand DNA by virions of Moloney murine leukemia virus. 9 28


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