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 cloned mouse DNA fragment containing an endogenous "virus-like" DNA (VL30 DNA) sequence was identified by virtue of its ability to hybridize to the virus-like RNA component of mixed-pseudotype AKR-murine leukemia virus virions, its lack of detectable sequence homology with cloned AKR-murine leukemia virus DNA, and its hybridization to a 5.6 kilobase pair (30S) cellular polyadenylic acid [poly(A)]-containing RNA species. Restriction enzyme mapping of the cloned mouse fragment revealed the presence of a 5- to 6-kilobase pair VL30 DNA segment flanked by non-VL30 segments of approximately 7 and 0.3 kilobase pairs. Southern blot analysis of VL30 DNA sequence organization in the DNA of two nontransformed mouse cell lines (AKR-2B, C3H/10T 1/2) and two chemically transformed derivatives (AKR-MCA, C3H/MCA-58) revealed 15 to 20 bands organized in an apparent strain-specific pattern. Within a given strain, however, no differences were detectable between the nontransformed cells and their chemically transformed counterparts. The expression of VL30 genes in the above cell lines was assayed by hybridization of 32P-labeled poly(A)-containing polysomal RNA to several internal restriction fragments derived from the cloned VL30 DNA sequence. The level of VL30 RNA was enhanced approximately 10-fold in both chemically transformed cell lines as compared to the nontransformed cell lines (under normal growth conditions). In addition, nontransformed AKR-2B cells maintained in the presence of purified epidermal growth factor exhibited similarly enhanced levels of VL30 RNA sequences in polysomal RNA. Since these cells displayed several growth characteristics of transformed cells but, in an epidermal growth factor-dependent and completely reversible fashion, these data suggest that the expression of VL30 genes is not simply incidental to chemically transformed cells but may be related to alterations in growth control.
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PMID:Organization and expression of endogenous virus-like (VL30) DNA sequences in nontransformed and chemically transformed mouse embryo cells in culture. 627 81

We characterized mink cell focus-forming murine leukemia viruses that were isolated from C3H/MCA-5 cells after induction with 5-iododeoxyuridine in culture. Mink lung epithelial cells malignantly transformed in vitro by induced virus were the source of four molecular clones of mink cell focus-forming virus. CI-1, CI-2, CI-3, and CI-4. Three clones, CI-1, CI-2, and CI-3, had full-length mink cell focus-forming viral genomes, one of which (CI-3) was infectious. In addition, we obtained a defective viral genome (CI-4) which had a deletion in the envelope gene. A comparison between the envelope genes of CI-4 and those of spleen focus-forming virus by heteroduplex mapping showed close homology in the substitution region and defined the deletion as being identical to the p15E deletion of spleen focus-forming virus. The recombinant mink cell focus-forming genomes are not endogenous in C3H/MCA-5 cells and therefore must have been formed in culture after induction by 5-iododeoxyuridine. CI-3, the infectious clone of mink cell focus-forming murine leukemia virus, was dualtropic, and mink cells infected with CI-3 were altered in their response to epidermal growth factor. In the presence of epidermal growth factor at 10 ng/ml, uninfected mink cells retained their epithelial morphology in monolayer culture and did not form colonies in soft agar. In contrast, CI-3 virus-infected mink cells grew with fibroblastic morphology in monolayer culture and showed an increased growth rate in soft agar in the presence of epidermal growth factor.
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PMID:Genome structure of mink cell focus-forming murine leukemia virus in epithelial mink lung cells transformed vitro by iododeoxyuridine-induced C3H/MuLV cells. 630 Apr 31

A new acute transforming type C retrovirus was isolated from mice inoculated with a virus stock obtained by iododeoxyuridine induction of methylcholanthrene-transformed C3H/10T1/2 mouse cells. This virus, designated 3611-MSV, transforms embryo fibroblasts and epithelial cells in culture and induces fibrosarcomas in vivo. 3611-MSV is replication defective, requiring a type C helper virus for propagation both in vitro and in vivo. By using endpoint transmission of 3611-MSV to MMCE C17 mouse and FRE 3A rat cells, several nonproductively transformed clonal cell lines have been derived. Pseudotype virus stocks obtained from such clones transform cells in vitro, are highly oncogenic in vivo, and exhibit host range and serological properties that are characteristic of their helper virus component. Analysis of viral antigen expression in 3611-MSV-transformed cells has led to the demonstration of a 90,000-molecular-weight (Mr) polyprotein and a 75,000-Mr probable cleavage product, both containing the amino-terminal murine leukemia virus gag gene proteins p15 and p12. In contrast to gene products of many previously described mammalian transforming viruses, 3611-MSV-encoded polyproteins lack detectable protein kinase activity, and 3611-MSV-transformed cells resemble chemically transformed cell line C3H/MCA-5, from which 3611-MuLV was originally derived, in that they do not exhibit elevated levels of phosphotyrosine. By using molecular hybridization the 3611-MSV transforming gene was found to be distinct from previously described mammalian cellular oncogenic sequences, including c-ras, c-abl, c-fes, c-fms, c-sis, and c-mos.
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PMID:New mammalian transforming retrovirus: demonstration of a polyprotein gene product. 630 Apr 62

The mink cell focus-forming (MCF) class of recombinant murine leukemia viruses (CI-1 to 4) were isolated from iododeoxyuridine-induced C3H/MCA 5 cells in culture and molecularly cloned. These genomes included infectious (CI-3) and defective (CI-4) recombinants. A total of 2,408 nucleotides of CI-3 virus DNA, including the MCF envelope gene, were sequenced and compared with ecotropic, dual-tropic, and xenotropic sequences. The extent of recombinational exchange in CI-3 was from 145 nucleotides 3' of the splice acceptor site for the envelope mRNA to nucleotide 1,722, between the end of gp70 and the beginning of Prp15E. Thus, the entire gp70 sequence of the endogenous nonecotropic parent was present in this recombinant. The nature and location of the recombinant junctions were consistent with a mechanism involving DNA exchange during reverse transcription. Comparison of the substituted sequence in CI-3 with that of Moloney MCF virus suggests a very close relationship, if not identity, between the endogenous dual-tropic proviruses from which they were derived. A nonidentity of xenotropic and MCF gp70s was observed, suggesting that xenotropic murine leukemia viruses are not the nonecotropic parent of the env gene of MCF murine leukemia viruses. The replication-defective virus CI-4 had a 684-nucleotide deletion present in the env gene, eliminating the hydrophobic regions within the gp70 carboxy end and the p15E amino end. This sequence was bordered by an 11-nucleotide direct repeat in CI-3 viral DNA.
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PMID:Envelope gene sequence of two in vitro-generated mink cell focus-forming murine leukemia viruses which contain the entire gp70 sequence of the endogenous nonecotropic parent. 631 52

In A-Jax mice, the appearance of MCA-induced sarcomas in delayed by Vitamin A application. Continuous uptake of drinking water containing 0.05% of a retinol palmitate emulsion leads to a significant inhibition. Administration of ethylnitrosourea (ENU) to pregnant Swiss mice on the 17th day of gravidity results in the formation of lymphoblastoid leukemias from the beginning of the 12th week after birth, 90% of the animals dying within 25 weeks. In this case, continuous addition of 0.1% retinol palmitate emulsion to drinking water leads to a dramatic reduction of the tumor risk to about 50%. By additional administration of proteolytic enzymes of animal and plant origin this risk can be further reduced. The lung adenomas developing to 100% in the animals are not influenced by this treatment. Vitamin A, added to drinking water, exerts a strong inhibitory effect on transplacentally induced leukemia.
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PMID:Experimental cancer prophylaxis. 635 37

Culture supernatants of spleen or thymus cells from BALB/c mice bearing transplanted, syngeneic, methylcholanthrene-induced sarcomas suppress T lymphocyte-mediated lysis of cells from the tumor borne by the donor of the spleen or thymus cells. On this basis, we hybridized thymus cells from mice bearing sarcoma MCA-1490 with cells from the T lymphoma BW5147. The hybrids (hybridomas) formed were tested for production of factors that could suppress T lymphocyte-mediated lysis of MCA-1490 cells. One hybridoma, and a clone derived from it, produced factors that suppressed the lysis of MCA-1490 cells in vitro. In addition, these factors enhanced the growth of MCA-1490 in immune mice and prevented the destruction of MCA-1490 cells by immune lymphocytes in tumor neutralization (Winn) assays. In vitro lysis of cells from another MCA-induced sarcoma by immune lymphocytes was not suppressed. The suppressor factors did not affect the proliferative response of BALB/c lymphocytes to mitogens or the generation of a cytotoxic response to C57BL/6 alloantigens. Neither did they inhibit the generation of primary or secondary cytotoxic responses to murine leukemia virus-related antigens present on a BALB/c lymphoma line, LSTRA. Although our findings suggest that these suppressor factors are specific for MCA-1490, their specificity for antigens restricted to this tumor needs further definition.
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PMID:T-T hybridoma product specifically suppresses tumor immunity. 644 19

The effect of Lactobacillus casei YIT 9018 (LC 9018) on the growth of transplantable allogeneic and syngeneic mouse tumors was studied. Intraperitoneal treatment of LC 9018 caused a significant prolongation of the life span of ICR mice inoculated with sarcoma-180 intraperitoneally and BDF1 mice inoculated with L1210 leukemia intraperitoneally. Intravenous injection of LC 9018 markedly inhibited the growth of subcutaneously inoculated sarcoma-180. This organism was also effective against methylcholanthrene-induced syngeneic MCA K-1 tumor in BALB/c mice. The antitumor activity of LC 9018 was reduced by treatment with carrageenan, an anti-macrophage agent, and was also observed in T-cell deficient athymic nude mice. These results suggested that the antitumor activity of LC 9018 may be macrophage-dependent.
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PMID:Antitumor activity of Lactobacillus casei in mice. 679 51

Based on the fact that human cancer patients excrete increased amounts of various modified nucleosides and bases in their urine, we investigated whether the same phenomenon takes place in mice bearing experimentally induced tumors. We did indeed find that mice with MCA-induced skin tumors and mice exhibiting leukemia after X-ray irradiation excrete severalfold higher levels of modified nucleosides and bases than do untreated control mice. Comparison of the time course of altered urinary excretion of these RNA catabolites with the appearance of a recognizable tumor after MCA application revealed that the onset of the altered excretion rate of these compounds precedes tumor diagnosis. At present, the time-course studies in our mice exposed to a single X-ray dose to induce lymphoblastic leukemia seem to indicate a similar situation. Mice exhibiting preleukemic histological features already excrete increased amounts of various modified nucleosides and bases. Confirmation of our results by analysis of further irradiation-exposed mice in our present detailed time-course studies and of tumors experimentally induced in other organs of mice and other species will be taken as a basis for developing an in vivo test for carcinogenicity. Furthermore, the results could provide a foundation for the setting up of a noninvasive, early screening method for cancer in human beings.
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PMID:Increasing urinary levels of modified nucleosides and bases during tumor development in mice. 684 99

Murine oncovirus antigens represent excellent targets for immune recognition, and virus-associated tumors are generally susceptible to various immunotherapy protocols. Virus-negative tumors, however, are nonimmunogenic and refractory to immunologic control. Therefore, the feasibility of the introduction of antigens onto non-virus-expressing tumors in situ in inbred C57BL/6J mice by systemic administration of nononcogenic murine retroviruses was investigated. Two classes of murine fibrosarcomas were studied: a 3-methylcholanthrene-induced fibrosarcoma syngeneic to C57BL/6 mice (MCA-FS) and a Harvey murine sarcoma virus-transformed, nonproducer fibrosarcoma syngeneic to C57BL/6 mice (H-NP). Both were found to be devoid of infectious ecotropic murine leukemia virus (MuLV) or MuLV antigens. A single dose of Friend murine leukemia virus (F-MuLV) was used to superinfect MCA-FS- and H-NP-induced tumors in vivo and converted these tumors to a highly productive, virus-positive state. In vivo superinfected tumors were indistinguishable from their preinfected counterparts by competition radioimmunoassays for the virion's major envelope glycoprotein, gp71, and its group-specific antigen, p30, and by assays for infectious virus. Analysis of virus from tumor extracts proved that the antigenic specificity of the superinfected tumor was provided by F-MuLV administered systemically to the animals. Finally, an immunoperoxidase technique, applied to tumor cross sections, demonstrated the uniform appearance of viral antigens in the superinfected tumors.
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PMID:In vivo antigenic modification of tumor cells. I. Introduction of murine leukemia virus antigens on non-virus-producing murine sarcomas. 694 81

Murine leukemia viruses were previously demonstrated to be able to infect efficiently non-virus-expressing tumors in vivo. In the present study the infectivity and tissue distribution of Friend murine leukemia virus (F-MuLV) in normal and tumor-bearing C57BL/6J (B6) mice were examined. Two syngeneic fibrosarcoma-inducing cell lines were used: Cells from a 3-methylcholanthrene-induced fibrosarcoma syngeneic to B6 mice (MCA-FS) and cells from a Harvey murine sarcoma virus-transformed, nonproducer sarcoma syngeneic to B6 mice (H-NP) were described in the preceding study. Both cell lines lacked ecotropic viral expression. F-MuLV produced in vitro was rarely able to infect normal adult B6 tissue in vivo and lacked pathogenic potential. Adult animals receiving F-MuLV remained clinically normal during 20 months of follow-up and had no detectable viremia, although some had persistently infected thymuses and long bones. In animals receiving a single dose of F-MuLV given to superinfect either the MCA-FS or the H-NP induced tumors, virion antigens were found only in tumor tissue and not in the normal host organs studied. Infectious virus was abundant in tumors; occasionally, it was found in thymuses and long bones of animals bearing superinfected H-NP tumors but rarely in other organs. Localization of F-MuLV in MCA-FS tumors appeared to be more selective with rare contamination of host organs. The presence of a rescuable sarcoma genome in H-NP may explain the discrepancy between MCA-FS and H-NP tumors. The possibility of increasing the efficiency and selectivity of infection as well as the therapeutic application of this technique are discussed.
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PMID:In vivo antigenic modification of tumor cells. II. Distribution of virus in sarcoma-bearing mice. 694 82


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