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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used a producer NIH 3T3 cell line that secretes, together with the helper Moloney murine leukemia virus (Mo-MuLV), a transducing recombinant virus containing the neomycin-resistance gene linked to the Mo-MuLV long terminal repeat (LTR). By infecting three embryonal carcinoma cell lines, PCC4.aza1R, F9tk-, and Nulli-SCC1, with this recombinant virus, we have isolated many transductant clones that stably express the integrated neomycin-resistance gene. These clonal transductant lines consist of undifferentiated embryonal carcinoma cells as judged by morphology, tumorigenicity in 129/Sv mice, and cell-surface antigenic markers. Analysis of the integrated recombinant viral genes by Southern blot hybridization revealed that some of the lines have single copies, whereas others have multiple copies, probably in multiple sites. Although these transductant lines contained many copies of helper Mo-MuLV integrated in the cellular genome, expression of these helper viruses was not detected either by reverse transcriptase activity or by X-C plaque assay. Two F9tk--derived, G418-resistant transductant lines were superinfected with a second recombinant transducing virus that contains the herpes simplex virus thymidine kinase gene flanked by the Mo-MuLV LTR. The frequency of transduction to yield clones able to grow in hypoxanthine/aminopterin/thymidine medium was similar to that of the parental F9tk- cells. These results suggest that the expression of the neomycin-resistance gene, linked to MoMuLV LTR in the transductant embryonal carcinoma cell clones, is due to a cisacting mechanism(s).
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PMID:Isolation of embryonal carcinoma cell lines that express integrated recombinant genes flanked by the Moloney murine leukemia virus long terminal repeat. 385 93

We present a general strategy for the efficient insertion of recombinant retroviral vector DNA into the mouse germ line via infection of preimplantation mouse embryos. Transgenic mice were generated that harbor a replication-competent recombinant retrovirus (delta Mo + Py M-MuLV) that lacks the Moloney murine leukemia virus (M-MuLV)-type enhancer sequence in the long terminal repeat (LTR). Instead, the LTR contains an enhancer element that permits polyoma virus F101 to grow in undifferentiated F9 embryonal carcinoma cells. Expression studies in different tissues of animals transgenic for delta Mo + Py M-MuLV indicate possibilities to target and modulate expression of retroviral recombinants in mice via their LTR enhancer sequences. In addition, 16 transgenic mice were generated that harbor proviral DNA of a defective recombinant retrovirus carrying a mutant dihydrofolate reductase gene.
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PMID:Efficient insertion of genes into the mouse germ line via retroviral vectors. 386 22

An assay to determine the mechanism of regulation of embryonal carcinoma cells by the blastocyst, which is based on a comparison of tumors produced when the cancer cells are cloned alone or after incorporation into blastocysts, was refined by labeling embryonal carcinoma cells with fluorescent microspheres and by following their fate after injection into the blastocysts. Through the use of the new techniques, it was observed that cells of one line of nullipotent embryonal carcinoma were controlled at the 50% level, those from another were not controlled, and those from a multipotent but undifferentiated line were controlled in almost absolute fashion. Single Sarcoma 180 of L1210 leukemia cells were not controlled when injected into the blastocele, but C1300 neuroblastoma cells were partially controlled. None of these tumors have a normal cellular counterpart in the blastocyst, as does embryonal carcinoma, but neurulation follows blastulation by only a few days, so that the neuroblastoma cells may be regulated at that time. Parietal yolk sac carcinoma cells, which have a counterpart in the late blastocyst, were not controlled. On the basis of these data, it is postulated that, if one embryonic field can regulate its closely related cancer, then there may be an embryonic field capable of regulating each carcinoma.
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PMID:Specificity of the control of tumor formation by the blastocyst. 627 73

An ultrastructural survey of 11 human tumors passaged in N:NIH(S) (nu/nu) mice showed two instances of type C virus production. In one instance type C virus particles were observed in the endothelial murine stromal cell component of an embryonal carcinoma but not in the human tumor cells. In another instance type C virus particles were seen replicating in the chondroblastic human cells of a xenografted osteosarcoma. The type C virus produced in the human cells failed to transform NIH/3T3 cells, the C-127 rat cell line, or mink cells. Nucleic acid hybridization studies in which a human endogenous retroviral probe and a xenotropic murine leukemia virus envelope probe were used suggested that the retrovirus present in the human osteosarcoma cells is related to murine leukemia viruses. Intracisternal A-particles (IAP) were also detected in the human osteosarcoma cells. Their presence in the human cells was demonstrated by simultaneous visualization of IAP and human HLA determinants at the cell surface. The literature on type C virus infection of human cells and tumors grafted in nude mice is reviewed.
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PMID:Murine type C retroviruses and intracisternal A-particles in human tumors serially passaged in nude mice. 631 Feb 1

Moloney murine leukaemia virus (M-MuLV) infection of embryonal carcinoma (EC) cells results in the integration of proviral DNA into the host cell genome, but not in virus production. One suggested explanation for the lack of viral gene expression in EC cells has been methylation of the integrated viral DNA. However, subsequent reports indicated that integration of the M-MuLV DNA occurs soon after infection, but that viral DNA methylation occurs considerably later. Nevertheless, viral gene expression is not observed even at early times. One possible explanation is that certain M-MuLV regulatory sequences do not function in EC cells. We now present evidence which supports this hypothesis.
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PMID:Non-function of a Moloney murine leukaemia virus regulatory sequence in F9 embryonal carcinoma cells. 632 96

Early mouse embryos exposed to Moloney leukaemia virus (M-MuL V) produce substrains of mice, designated Mov-1 to Mov-14, that transmit the virus genetically from one generation to the next. In some substrains the inserted viral genome becomes activated at specific stages of embryogenesis and the available evidence suggests that these viral genomes are developmentally regulated. The effect of cellular differentiation on virus expression was investigated by introducing M-MuL V into preimplantation or postimplantation mouse embryos, or into embryonal carcinoma cells (EC cells) in tissue culture. Whereas preimplantation embryos or EC cells did not permit virus expression, efficient replication occurred in postimplantation embryos or in differentiated cells. The viral genomes introduced into early embryos were highly methylated and non-infectious when analysed in the adult. In contrast, viral genomes introduced into postimplantation embryos remained unmethylated and were infectious in a transfection assay. Similarly, de novo methylation occurred in undifferentiated EC cells but not in differentiated derivatives. These results demonstrate an efficient de novo methylation activity which appears to be involved in the repression of genes introduced into pluripotent embryonic cells and is not observed in cells of the postimplantation embryo or in differentiated cells growing in culture. Integration of M-MuL V into the germ line can lead to recessive lethal mutations. This has been shown for the Mov-13 substrain, as animals homozygous at the Mov-13 locus die between Days 13 and 14 of embryogenesis. This suggests that viral integration occurred in a chromosomal region that is active during, and crucial for, embryonic development.
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PMID:Retroviruses and mouse embryos: a model system in which to study gene expression in development and differentiation. 655 10

The purpose of this study was to determine whether the neurula stage mouse embryo can regulate tumor formation of C-1300-3 neuroblastoma cells. Five neuroblastoma cells were injected into the second somite of neurula stage embryos, and their ability to form tumors was tested, 24 hr later, by transplanting the portion of the embryo containing the cancer cells into the testes of adult mice. Only one-third the number of tumors was obtained in comparison with controls in which (i) five neuroblastoma cells were injected into blocks of liver tissue that were then transplanted into the testes of adult animals or (ii) five C-1300-3 neuroblastoma cells were injected directly into the testes. When five C-1300-3 cells were injected into somites, which had been dissected from embryos, and the injected somites were placed in animals, significantly fewer tumors were obtained in relationship with controls. Although it is not known whether the neuroblastoma cells are induced to differentiate or are killed by the embryonic tissue, the effect appeared to be specific because the tumor-forming ability of L1210 leukemia, B-16 melanoma, embryonal carcinoma 247, and a parietal yolk sac carcinoma was unaffected by somites.
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PMID:The neurula stage mouse embryo in control of neuroblastoma. 659 4

A review was made on 1,437 cases of testicular malignancies reported in the Annual of the Pathological Autopsy Cases in Japan between 1967 and 1976. They were 417 cases of germinal testicular cancer and 1,027 cases of secondary tumors, the ratio between the two being 1:2.46. The primary disease of 966 cases of secondary tumors was known: It was leukemia in 541 cases (56%), cancer in 188 cases (19.4%) and lymphosarcoma in 184 cases (19.0%), in decreasing order of frequency. The histological classification of the 410 germinal cell carcinoma given clear description was type I, II, III, IV and V according to Dixon and Moore's classification in 34.4%, 38.5%, 3.7%, 10.2% and 13.2%, respectively. There were 369 cases consisting of only one histological type, which was seminoma, embryonal carcinoma, teratoma, teratocarcinoma and choriocarcinoma in 38.2%, 39.0%, 3.8% 10.0% and 9.0% of these cases, respectively. The pattern of metastasis was analyzed for these 369 cases. There was no significant difference in the pattern of lymph node metastasis between the 5 groups, but there was a slight difference between seminoma and embryonal carcinoma. There was a significant difference in the pattern of distant metastasis between the 5 groups and between choriocarcinoma and seminoma, choriocarcinoma and embryonal carcinoma, and, choriocarcinoma and teratocarcinoma. It is questionable whether the findings at autopsy directly relate to prognosis, but considering from the pattern of metastasis at autopsy, the adult germinal cell testicular tumors can be divided into the three groups: seminoma, choriocarcinoma and embryonal carcinoma + teratocarcinoma + teratoma.
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PMID:[A review of the cases of testicular tumors reported in the Annual of Pathological Autopsy Cases in Japan]. 668 45

We have investigated the block to expression of Moloney murine leukemia virus in murine embryonal carcinoma (EC) cells. Infected EC cells were found to contain up to 100 integrated proviral genomes. However, expression of virus as measured by XC plaque and virus-specific RNA synthesis did not occur at significant levels, in contrast to productively infected differentiated cells. Analysis of the DNA in the infected EC cells revealed that the proviral genomes were highly methylated, as shown by their resistance to cleavage by Sma I. Integrated proviral genomes in infected differentiated cells were readily cut by Sma I and thus were not methylated at these sites. Transfection of DNA from infected EC cells to cells permissive for virus expression failed to induce virus expression. The proviral genomes, however, were potentially infectious because they induced XC plaques when the recipient cells for transfection were treated with 5-azacytidine. This drug is believed to interfere with DNA methylation. We conclude that expression of proviral genomes introduced into EC cells is suppressed and that this inactivation can be correlated with the de novo methylation of the viral DNA. De novo methylation activity thus may be a characteristic of early embryonic cells.
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PMID:De novo methylation, expression, and infectivity of retroviral genomes introduced into embryonal carcinoma cells. 695 93

Hemorrhage from brain tumor was confirmed clinically, surgically, or on autopsy in 94 of 1861 cases (5.1%) treated during the past 18 years: 49 of 311 pituitary adenomas (15.8%) and 45 of 1550 other brain tumors (2.9%). The higher incidence of hemorrhage from pituitary adenoma was statistically significant (p less than 0.001). In brain tumors other than pituitary adenoma, the incidence of hemorrhage was significantly higher in the patients under 14 years old (17 of the 322 cases, 5.3%) than in the patients over 15 years old (28 of the 1228 cases; 2.3%) (p less than 0.001). Nineteen patients showed no evidence of clinical symptoms related to bleeding. Twenty-six patients had a definite history of an acute episode that suggested sudden bleeding. In 11 of these, the apoplectic syndrome was the initial presenting symptoms. The incidence of hemorrhage was not statistically correlated with sex. The hemorrhage was intratumoral in 30 cases, intracerebral in 7, subarachnoid in 7, and subdural in 1. The tumors were supratentorial in 36 cases, pineal in 1, and infratentorial in 8. Primary and metastatic choriocarcinoma and primary embryonal carcinoma seemed to cause hemorrhage most frequently. The following precipitating factors were found in 7 of the 17 patients aged under 14: ventricular drainage in 2, ventriculoperitoneal shunt in 2, carotid angiography in 1, head injury in 1, and leukemia in 1. Seven of the 17 patients under 14 years old died of massive bleeding from the tumor. Unless there is evidence of vascular disease such as cerebral aneurysm, vascular malformation, or hypertensive cerebrovascular disease, intracranial hemorrhage should be suspected of being due to a brain tumor.
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PMID:Spontaneous intracranial hemorrhage caused by brain tumor: its incidence and clinical significance. 709 93


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