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)

Short term cultures of bovine leukemic lymphocytes release virus particles with biochemical properties of RNA oncogenic viruses. These particles, tentatively called Bovine Leukemia Virus (BLV) have a high molecular weight-reverse transcriptase complex and a density averaging 1.155 g/ml in sucrose solutions. Molecular hybridizations between BLV-3H cDNA and several viral RNAs show that BLV is not related to Mason-Pfizer Monkey Virus (MPMV) Simian Sarcoma Associated Virus (SSV-1) Feline Leukemia Virus (FeLV) or Avian Myeloblastosis Virus (AMV). Rauscher Leukemia Virus (RLV) exhibits a slight but reproducible relatednesse to BLV. The high preference of BLV reverse transcriptase for Mg++ as the divalent cation suggests that BLV might be an atypical mammalian leukemogenic type C virus. Hybridization studies using BLV 3H cDNA as a probe suggest that the DNA of bovine leukemic cells contains viral sequences that cannot be detected in normal bovine DNA.
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PMID:Bovine leukemia virus: an exogenous RNA oncogenic virus? 6 82

Two murine sarcoma viruses, the Kirsten and the Harvey, were isolated by passage of mouse type C leukemia viruses through rats. These sarcoma viruses have genomes containing portions of their parental type C mouse leukemia virus genomes, in stable association with specific rat cellular sequences that we find to be quite likely not those of a rat type C leukemia virus. To determine if these murine sarcoma viruses provide a model relevant to the events occurring in spontaneous tumors, we have hybridized DNA and RNA prepared from rat tumors and normal rat tissues to [3H]DNA prepared from the Kirsten murine sarcoma virus. We have also hybridized these rat tissue nucleic acids to [3H]DNA prepared from a respresentative endogenous rat type C leukemia virus, the WFU (Wistar-Furth). Sarcoma-viral rat cellular sequences and endogenous rat leukemia viral sequences were detected in the DNA of both tumor and normal tissues, with no evidence of either gene amplification or additional sequences being present in tumor DNA. Sarcoma-viral rat cellular sequences and endogenous rat leukemia viral sequences were detected at elevated concentrations in the RNA of many rat tumors and in specific groups of normal tissues.
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PMID:Rat sequences of the Kirsten and Harvey murine sarcoma virus genomes: nature, origin, and expression in rat tumor RNA. 17 19

The activity of MAO (EC 1.4.3.4) was measured in liver homogenates of mice with experimental tumours Sarcoma S-180 and Leukemia L-1210. The enzyme activity was determined by two methods: spectrophotometric--with benzylamine as a substrate and the second with the application of oxygen electrode and adrenaline as a substrate. An increase of the enzyme activity was observed in liver homogenates of mice with Sarcoma S-180 as compared with the controls. High activity of MAO with both substrates was also observed in Sarcoma ascites. In Leukemia L-1210 changes of activity in relation to adrenaline as a substrate were very small, but towards benzylamine the affinity of enzyme was higher (the increase of activity was about 50%).
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PMID:[The vehaviour of monoaminooxydase (MAO) activity in tumours. I. MAO activity measurement in experimental tumours (author's transl)]. 19 Sep 72

Cell lines of four mammalian species were each examined for the number of Moloney murine sarcoma virus (M-MSV) DNA copies in total cellular DNA after M-MSV transformation. Sarcoma-positive, leukemia-negative (S+L-) M-MSV-transformed cells were compared to M-MSV-transformed cells infected with a replicating leukemia virus. Both unfractionated M-MSV complementary DNA and complementary DNA representing the MSV-specific and the MSV-murine leukemia virus-common regions of the M-MSV genome were hybridized to total cellular DNA of various species. DNAs of mouse, cat, dog, and human S+L-cells contained from less than one to a few proviral M-MSV DNA copies per haploid genome. In contrast, helper virus-coinfected, M-MSV-producing cells of each species showed a 3- to 10-fold increase in M-MSV proviral DNA over that found in corresponding S+L- cells. MSV-specific and MSV-murine leukemia virus-common nucleotide sequences were each increased to a similar degree. A corresponding examination of cellular DNA of leukemia virus-infected normal or S+L- mammalian cells was performed to establish the resulting number of leukemia proviral DNA copies. The infection of normal or S+L- mammalian cells with several leukemia-type viruses that did not have nucleotide sequences closely related to the cell before infection resulted in the appearance of one to three corresponding leukemia proviral DNA copies.
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PMID:Effect of helper virus on the number of murine sarcoma virus DNA copies in infected mammalian cells. 19 57

The genomes of three independent isolates of feline sarcoma virus (FeSV) were compared by molecular hybridization techniques. Using complementary DNAs prepared from two strains, SM- and ST-FeSV, common complementary DNA'S were selected by sequential hybridization to FeSV and feline leukemia virus RNAs. These DNAs were shown to be highly related among the three independent sarcoma virus isolates. FeSV-specific complementary DNAs were prepared by selection for hybridization by the homologous FeSV RNA and against hybridization by fline leukemia virus RNA. Sarcoma virus-specific sequences of SM-FeSV were shown to differ from those of either ST- or GA-FeSV strains, whereas ST-FeSV-specific DNA shared extensive sequence homology with GA-FeSV. By molecular hybridization, each set of FeSV-specific sequences was demonstrated to be present in normal cat cellular DNA in approximately one copy per haploid genome and was conserved throughout Felidae. In contrast, FeSV-common sequences were present in multiple DNA copies and were found only in Mediterranean cats. The present results are consistent with the concept that each FeSV strain has arisen by a mechanism involving recombination between feline leukemia virus and cat cellular DNA sequences, the latter represented within the cat genome in a manner analogous to that of a cellular gene.
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PMID:Nature and distribution of feline sarcoma virus nucleotide sequences. 22 44

A murine model of immune responsiveness had been adapted to study anergic conditions associated with neoplasia. Marked anergy observed in mice bearing L1210 leukemia and P-388 lymphoma is contrasted to the minimal immune depression associated with B-16 melanotic melanoma and Sarcoma 180J. The ability of N,N-bis(2-chloroethyl)-N-nitrosourea chemotherapy to reduce tumor burden without prolonged suppression of delayed cutaneous hypersensitivity is compared to the profound suppression of the cutaneous response observed with Adriamycin cytoreductive therapy. The applications of our model are discussed in relation to tumor-associated anergy, new approaches to the evaluation of pharmaceuticals, and studies of combined chemoimmunotherapy regimens.
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PMID:Delayed cutaneous hypersensitivity to oxazolone in mice with tumors. 63 44

In an effort to better understand the epidemiology of cancer in Zaire, a retrospective review of biopsy-proven malignant tumors was undertaken. Of 188 biopsies taken from children aged 0-15 years over a 4.5 year period, 73 (39%) revealed malignancy. Fifty-six percent of patients with malignant tumors were boys. Lymphoma was the most common tumor (28 patients, 15 with Burkitt's Lymphoma). Sarcoma (15 patients), carcinoma (8 patients), Wilms' Tumor (6 patients), and retinoblastoma (5 patients) were also seen. Lymphomas were most heavily represented in the first 5 years of life, while sarcoma and carcinoma accounted for most of the malignancies in children after 10 years of age. Lymphomas and sarcomas are relatively more common in Zaire than in North America and Europe, while leukemia and central nervous system tumors are notably less common in Zaire. In view of current limitations on health care in rural Zaire, cancer care should be directed toward early diagnosis, quick referral for appropriate surgical care, and use of the limited arsenal of chemotherapy.
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PMID:Malignant tumors in children of northeastern Zaire. A comparison of distribution patterns. 230 7

Antitumor effects of Royal Jelly (RJ) were investigated employing the transplantable tumors of mouse advance leukemia L1210 and P388 strains and Ehrlich, Sarcoma-180 ascites and solid tumor strains. RJ was administered orally in a prophylactic-therapeutic (30 days before and 30 days after the transplantations of tumor cells) or a therapeutic (30 days after the transplantations of tumor cells) manner. Tumor cells were transplanted i.p. (ascites tumor) or s.c. (solid tumor). The daily dose of RJ was 0 (control), 10, 100, or 1000 mg/kg. In the case of the therapeutic experiments employing advance leukemia L1210 and P388 strains, which gave quite a short survival period of 8 approximately 9 days, RJ did not show any antitumor effect. In the case of the therapeutic RJ application employing the Sarcoma-180 ascites tumor, which gave a moderate survival period of 16 days, the increased life span was 9.3 approximately 19.3%; and with the Ehrlich ascites tumor (survival period of 22.1 days), the increased life span was 20.4% (RJ 10 mg/kg . day) and 17.6% (RJ 1,000 mg/kg . day), but no antitumor effect was observed at the dose of 100 mg/kg . day. In the case of the therapeutic experiment employing Ehrlich solid tumor, tumor growth inhibition was 25.3 approximately 54.8%, where as the use of the prophylactic-therapeutic regimen gave a tumor growth inhibition of 38.3 approximately 45.7%. In the case of the therapeutic RJ application employing Sarcoma-180 solid tumor, tumor growth inhibition was 45.1 approximately 59.7%, where as the prophylactic-therapeutic regimen gave a tumor growth inhibition of 49.1 approximately 56.1%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antitumor effects of royal jelly (RJ)]. 357 Jan 5

Antibacterial, antifungal and antitumor activity of 15 newly synthetized compounds were investigated in vitro. These compounds were mainly 1-[4-pyridyl]-pyridinium salts, dipyridyl sulphides and corresponding sulphones. Antitumor activity was evaluated in a model of leukemia L1210, P388, Sarcoma 180, Ehrlich carcinoma, NK-lymphoma and melanoma B16. None of the compounds investigated, even at the concentration of 100 micrograms/ml, appeared to influence Gram-negative bacteria. However, at the concentration as low as 1.0 microgram/ml, three of them (No. III, VI and VII) strongly inhibited the growth of Gram positive bacteria and fungi. The compounds did not prolong the survival time of Sarcoma 880 leukemia L1210 or P388--bearing mice. Few of the compounds examined exerted marked antitumor effect on Ehrlich carcinoma and NK-lymphoma--compounds No. I and XV inhibited the growth of these tumors by ca. 70%. The strongest inhibitory effect on melanoma B16 was observed with compound No. XV, the effect being dose-dependent.
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PMID:Biological properties of dipyridyl sulphides and related compounds. 408 10

Treatment of ascites and solid tumors in mice (Sarcoma-1 and Ehrlich ascites carcinoma) with bovine enterovirus-1 resulted in regression of the tumors without any pathological effect on the animals. Death of mice with lymphatic-leukemia L4946 was delayed after such treatment. The oncolytic specificity of the virus does not appear to involve the production of interferon, but requires specific adsorption of virus to the tumor cells. The specificity of killing extends to cells in culture, since viral-transformed cells and oncogenic cells are susceptible to the virus, in contrast to cells of untransformed lines and cells of primary cultures, which are resistant. The possibility of utilizing the specificity of nonvirulent viruses in therapeutic treatment of human cancers is considered.
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PMID:Viruses as an aid to cancer therapy: regression of solid and ascites tumors in rodents after treatment with bovine enterovirus. 432 92


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