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Query: UMLS:C0023418 (
leukemia
)
93,477
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Minute virus of mice (MVM), a non-defective parvovirus, has been shown to infect cultures of non-pluripotent differentiated teratocarcinoma-derived cells, but pluripotent (and "nullipotent")
embryonal carcinoma
cells derived from the same teratocarcinoma resist MVN infection. Somatic cell hybrids between an
embryonal carcinoma
line and Friend erythroblastic
leukemia
cells are also resistant to MVM, even though Friend cells are susceptible. Among three blastocyst-derived lines tested, only one, a parietal yolk sac cell line, resists MVM infection. These results suggest that teratocarcinoma cultures may provide useful systems in which to study the cellular factors which mediate susceptibility to this teratogenic and oncolytic virus.
...
PMID:Embryonal carcinoma cells (and their somatic cell hybrids) are resistant to infection by the murine parvovirus MVM, which does infect other teratocarcinoma-derived cell lines. 55 90
The expression of murine
leukemia
provirus in
embryonal carcinoma
(EC) cells is blocked by a mechanism still incompletely understood. The blockage is not overcome by deleting a large portion of the enhancer region (in U3) in recombinant retroviruses (M-MuLVneo delta Enh). This confirms the presence of negative elements outside the viral 82-bp repeats. However, a few sites in the genomes of EC cells permit M-MuLVneo delta Enh proviral expression. One such site, identified in PCC4, PCC3, and LT, was studied. The complete analysis of the mechanism of activation by Northern (RNA) blotting, cloning, and sequencing of partial cDNA copies of the viral transcript and of the site of integration establishes that viral transcripts are initiated from an upstream host-cell promoter and are spliced from a host donor to a cryptic viral acceptor at position 542 in the Moloney murine
leukemia
virus (M-MuLV) genome. In consequence, the mature transcripts are host cell-virus fusion transcripts from which M-MuLV sequences, including the cis-active negative elements of the 5' long terminal repeat-containing region, are absent. The provirus integrates apparently randomly into any of the three most proximal introns of the transcriptional unit. The host cell promoter contains a TATA box and 14 potential SpI binding sites included in a 1.0-kb GC-rich island. These elements promote gene expression of recombinant vectors in EC and differentiated cells. The mechanism described points to a mechanism by which retroviruses can be transcribed from upstream nonviral elements and can acquire host genes by 5' annexation of exons.
...
PMID:Capture of a cellular transcriptional unit by a retrovirus: mode of provirus activation in embryonal carcinoma cells. 132 Dec 82
Human
embryonal carcinoma
is thought to be a counterpart of mouse
embryonal carcinoma
, which has provided useful information for studying early molecular events in murine embryogenesis. A major practical problem in the use of human
embryonal carcinoma
for molecular pathological studies is the lack of an efficient expression system for foreign genes. The SR alpha promoter is a fusion promoter containing the SV 40 early promoter and the R segment and part of the U5 sequence of the long terminal repeat derived from human T-cell
leukemia
virus type I. We analyzed the expression pattern of the SR alpha promoter in human and mouse
embryonal carcinoma
lines and transgenic mouse tissues. Efficient and stable expression was detected in all cell lines tested, and tissues from all mice of four independent transgenic lines carrying the SR alpha-CAT vector showed a detectable level of CAT expression. These data suggest that the SR alpha promoter is useful for studies of both human
embryonal carcinoma
and transgenic mouse tissue. Using this expression system, we are now able to label human embryonal carcinomas with various genes, for example beta galactosidase, and follow their fate at the single-cell level in nude mice, where xenotransplanted human
embryonal carcinoma
expresses differentiation capability.
...
PMID:Expression pattern of SR alpha promoter in human embryonal carcinoma and transgenic tissues in mice. 133 14
Primordial germ cells (PGCs) are first identifiable as a population of about eight alkaline phosphatase-positive cells in the 7.0 days postcoitum mouse embryo. During the next 6 days of development they proliferate to give rise to the 25,000 cells that will establish the meiotic population. Steel factor is required for PGC survival both in vivo and in vitro and together with
leukaemia
inhibitory factor stimulates PGC proliferation in vitro. In feeder-dependent culture, PGCs will proliferate for up to 7 days, but their numbers eventually decline and their proliferative capacity is only a fraction of that seen in vivo. Here we report a further factor that stimulates PGC proliferation in vitro, basic fibroblast growth factor (bFGF). Furthermore, bFGF, in the presence of steel factor and
leukaemia
inhibitory factor, stimulates long-term proliferation of PGCs, leading to the derivation of large colonies of cells. These embryonic germ cells resemble embryonic stem cells, pluripotent cells derived from preimplantation embryos, or feeder-dependent
embryonal carcinoma
cells, pluripotent stem cells of PGC-derived tumours (teratomas and teratocarcinomas). To our knowledge, these results provide the first system for long-term culture of PGCs.
...
PMID:Long-term proliferation of mouse primordial germ cells in culture. 140 66
The pleiotropic biological actions of
leukaemia
inhibitory factor (LIF) on haemopoietic cells (macrophages and megakaryocytes), hepatocytes, osteoblasts, pre-adipocytes, embryonic stem cells, myoblasts and neuronal cells must be mediated through the interactions of LIF with specific cellular receptors. The demonstration by equilibrium binding analysis and autoradiography of LIF receptors on all of the above cells and cell lines suggests that each of these pleiotropic effects of LIF is mediated by direct interactions with the responding cells rather than by the indirect release of secondary cytokines. Despite the differing biological effects of LIF on these cells, equilibrium binding, kinetic analyses and receptor internalization studies have all suggested that these cells display essentially identical high affinity LIF receptors. Nevertheless, there is evidence on some cell types (granulocyte-macrophage colony-stimulating factor [GM-CSF] transgenic peritoneal cells and F9
embryonal carcinoma
cells) for a second class of low affinity LIF receptors (Kd = 1.5 nM versus Kd = 30 pM for high affinity receptors) which, LIF receptors (Kd = 1.5 nM versus Kd = 30 pM for high affinity receptors) which differ from the high affinity receptors only in kinetic dissociation rate. Moreover, the evidence suggests that low and high affinity receptors are structurally related and interconvertible, because detergent solubilization of LIF receptors from any cell type results in the quantitative conversion of high affinity receptors into low affinity receptors. As is the case for other related cytokine receptors, these data suggest that high affinity LIF receptors may be composed of two protein subunits--one responsible for LIF-specific low affinity binding and the other responsible for affinity conversion and cell signalling by the receptor. Such a model provides a possible explanation for the pleiotropy of LIF's biological actions.
...
PMID:Distribution and binding properties of receptors for leukaemia inhibitory factor. 142 15
Murine
embryonal carcinoma
(EC) cells do not normally express Moloney murine
leukemia
virus genes. Earlier, rare EC cell lines were isolated that expressed proviral neomycin resistance (neo) gene. This expression was dependent on cellular enhancer or promoter sequences that flank the proviral integration site. Four such integration sites, designated as Mint (for Moloney murine
leukemia
virus integration and expression sites in EC cells), have been mapped on mouse chromosomes. Minta, Mintb, Mintc and Mintd are unlinked and mapped on different chromosomes (Chr), Chr 10, Chr 1, Chr 5 and the X Chr, respectively. None of these loci appear to be linked to any known Mo-MuLV proviral integration sites previously mapped. These enhancer and promoter loci may represent a new set of genes active in undifferentiated embryonic cells.
...
PMID:Mapping of recombinant retrovirus integration sites that cause expression of the viral genome in murine embryonal carcinoma cells. 154 15
The embryonal long terminal repeat-binding protein, ELP, is present in undifferentiated mouse
embryonal carcinoma
cells. It binds to and suppresses transcription of the Moloney
leukemia
virus long terminal repeat in undifferentiated murine
embryonal carcinoma
cells. We report here that ELP is a mouse homolog of Drosophila FTZ-F1, which positively regulates transcription of the fushi tarazu gene in blastoderm-stage embryos of the fly. As members of the steroid receptor superfamily, ELP and FTZ-F1 have both DNA binding and putative ligand binding domains which are well conserved between the two. ELP and FTZ-F1 function in cells in the extremely early stage of development. A high degree of conservation between the two transcription factors during the evolution of these species indicates the importance of their functions in early-stage embryogenesis. In addition, the sequence elements they recognize do not contain repeat units, in contrast to other steroid receptors, which usually bind to either palindromic or direct repeat sequences.
...
PMID:Embryonal long terminal repeat-binding protein is a murine homolog of FTZ-F1, a member of the steroid receptor superfamily. 154 9
ELP, the embryonal LTR binding protein, is a member of the nuclear receptor superfamily and a mouse homologue of Drosophila FTZ-F1. ELP is expressed specifically in undifferentiated mouse
embryonal carcinoma
cells and participates in suppression of the Moloney murine
leukemia
virus genome. The zinc finger domain of the protein was fused with glutathione S-transferase and was successfully used for isolating genomic targets. Sixteen genomic fragments were isolated and twelve of them strongly interacted with ELP. Six of the ELP binding fragments were analyzed further. All of these contained the multiple binding sites for ELP, which matched well with the consensus binding sequence for FTZ-F1, YCAAGGYCR. Among these, three fragments functioned as negative regulatory elements in response to ELP, when placed upstream to the promoter region of the Moloney
leukemia
virus. These results indicate that ELP may function as a negative transcription factor for a variety of cellular sequences, in addition to suppressing expression of Moloney
leukemia
virus in early embryonal cells. It was also shown that the procedure employed here works well for isolation of genomic targets of transcription factors.
...
PMID:Isolation of high affinity cellular targets of the embryonal LTR binding protein, an undifferentiated embryonal carcinoma cell-specific repressor of Moloney leukemia virus. 157 38
A case of embryonal carcinoma of the testis after acute myelomonocytic
leukemia
is reported. The interval between the initial diagnosis of
leukemia
and the appearance of
embryonal carcinoma
was almost three years. Although the patient had received neither irradiation nor alkylating agents, the case is regarded as one of secondary malignancy. Possible contributing factors are discussed.
...
PMID:Embryonal carcinoma of the testis after acute myelomonocytic leukemia: a case report. 164 34
We reported previously that composite DNA constructed from a mammalian plasmid (L factor) and foreign gene can be reestablished as a plasmid in mouse
embryonal carcinoma
(F9) cells after transfection and the plasmid-bearing F9 cells undergo normal in vitro differentiation in response to retinoic acid, an inducer for F9 cell differentiation. We constructed F9 cells bearing plasmidal L factor DNA in which a reporter (chloramphenicol acetyltransferase; CAT) gene was placed under the control of a differentiation-responsive viral (Moloney murine
leukemia
virus or simian virus 40) enhancer-promoter. When such plasmid-bearing cells were treated with retinoic acid, the CAT gene was inducibly expressed. These results indicate that mammalian gene expression can be studied with the plasmidal expression vector which is structurally dissociated from complex chromosomes.
...
PMID:Induction of CAT gene expression on a plasmid vector (L factor) by retinoic acid in mouse embryonal carcinoma (F9) cells. 166 27
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