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Query: UMLS:C0596978 (Leukemia)
 15,069 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection by exogenous avian leukosis viruses (ALVs) causes economic loss from neoplastic mortality and from impaired performance of subclinically infected chickens. This paper reviews progress in research related to natural infection and its control. Subgroup A ALVs causing lymphoid leukosis are the most common viruses in the field, but variant viruses can arise and cause losses. In Israel in recent years, epidemic outbreaks of haemangiosarcomas caused by a virus of unusual cytopathogenicity have occurred. In the UK, an ALV belonging to a new subgroup for chickens has been recently isolated; this virus is able to cause myeloid leukosis and nephromas. ALV infection of commercial stock is controlled by virus eradication schemes that prevent vertical transmission of ALV from one generation to the next. In this regard, endogenous leukosis viruses and ev loci, notably ev21 linked to the K slow-feathering gene, have been shown to have a detrimental influence on responses to infection by exogenous ALVs, and on the success of eradication schemes. Tolerogenic properties of the ev loci are involved. Attention has also been directed to whether ev loci have any direct influence on performance traits. Although eradication provides the main means of controlling ALV, the development of transgenic techniques in chickens has renewed interest in genetic resistance, and some progress has also been made in developing recombinant vaccines.
Leukemia 1992
PMID:Developments in avian leukosis research. 131 66

v-erb-B is the principal transforming gene of avian erythroblastosis virus, a replication defective retrovirus that transforms erythroid and fibroblast cells in vitro and causes erythroleukemia and fibrosarcoma in vivo. We have used a recombinant murine retrovirus, based on the truncated genome of Moloney murine leukemia virus and containing a chimeric gag-v-erb-B gene, to determine the murine hematopoietic cells transformed by v-erb-B. Infection of day 16.5 murine embryonal cells in liquid culture with this virus resulted in the outgrowth of foci of loosely to non-adherent hematopoietic cells which grew in close association with an adherent monolayer. After several weeks in culture a clonal population of transformed pre-B-lymphocytes emerged from this transformation initiated, though still growth factor dependent, population. These transformed cells were growth factor independent, and were tumorigenic in syngeneic mice. The results indicate that although v-erb-B can initiate transformation of murine hematopoietic cells, additional events are required for establishment of the fully transformed growth factor independent, tumorigenic phenotype. This v-erb-B induced progression from growth factor dependence to independence provides an in vitro model system for analysing events involved in the initiation and maintenance of leukemia.
Leukemia 1992 Jan
PMID:Transformation of murine pre-B-lymphocytes by v-erb-B: progression to growth factor independence and tumorigenicity. 173 10

The receptor for human macrophage colony stimulating factor (CSF-1R) was introduced into hematopoietic cell lines of myeloid and T-lymphoid origin, both of which normally do not express the CSF-1R. Infection of an interleukin-3 (IL-3)-dependent mouse myeloid cell line (FDC-P1) with a high titer retroviral vector expressing the human c-fms c-DNA, enabled CSF-1-dependent proliferation in short-term liquid culture assays as well as in clonal culture systems. CSF-1-dependent cell lines could be established after sorting for CSF-1R positive cells. In contrast to FDC-P1 cells, expression of the CSF-1R in CTLL cells, an IL-2-dependent mouse cytotoxic T-cell line, and in T-cell growth factor III/P40-dependent helper T-cells, ST2/K9.4a2, did not lead to CSF-1-dependent proliferation. These observations lead to the conclusion that ectopically expressed CSF-1R may function on certain myeloid cells where it is normally not expressed, suggesting the presence of signal transduction pathways which can be utilized by that foreign receptor. In contrast, it appears that T-lymphoid cells lack such a signalling mechanism, indicating that quite different modes of transducing mitogenic signals from the cell membrane to the nucleus must have developed during myeloid and T-lymphoid differentiation.
Leukemia 1991 Jan
PMID:Expression of human CSF-1 receptor induces CSF-1-dependent proliferation in murine myeloid but not in T-lymphoid cells. 182 80

The hematopoietic disregulation in adult mice induced by the malignant histiocytosis sarcoma virus (MHSV) and the Harvey murine sarcoma virus (Ha-MuSV), which both possess c-Ha-ras-related oncogenic sequences, was investigated. Spleen focus formation induced by MHSV and Ha-MuSV was not restricted by the Fv-2 resistance locus in congenic DDD and C57BL/6 mice, unlike leukemogenesis induced by Friend virus, Rauscher virus, and the myeloproliferative sarcoma virus (MPSV). C57BL/6 mice were much more resistant to MHSV and Ha-MuSV-induced spleen focus formation than DDD mice regardless of their Fv-2 state. Infection of DDD mice with MHSV caused a systemic histiocytic neoplasia, best described as murine malignant histiocytosis. Transformed histiocytic cells proliferated excessively in the bone marrow, spleen, and lymph nodes and, in the final stages of the disease, in all major parenchymal organs. The Ha-MuSV caused a strikingly different benign histiocytic tumor in DDD mice and, unlike MHSV, did not induce a rapid, progressive splenomegaly in C57BL/6 mice. Infection of DDD mice with MHSV induced a rapid and synchronized depletion of early and late erythroid precursor cell pools. In MHSV-infected C57BL/6 mice comparable changes were observed with dissimilar kinetics. Macrophage colony-forming cells of MHSV-infected mice were increased in number and proliferated independently of stimulating growth factors. The disease induced by MHSV in mice can thus serve as a model for malignant histiocytosis in humans.
Leukemia 1987 Jan
PMID:Murine retrovirus-induced malignant histiocytosis, an experimental model for the disease in humans. 282 12

The occurrence of potential leukemia cells (PLC) among bone marrow, spleen, and thymus of AKR mice during the preleukemic period was tested by an in vivo transplantation bioassay. The presence of PLC in 30- and 75-day-old AKR mice was demonstrated mostly among bone marrow cells, less in spleen, and was lacking in thymus. Occurrence of PLC in young AKR mice was shown to be thymus independent. However, progression of PLC from young donors (14-80 days old) into overt leukemia following transplantation into F1 recipients was shown to be dependent on specific host conditions including an intact thymus and an Fv-1nn allele. In contrast, PLC from 7-9-month-old AKR mice or frank leukemic cells when transplanted grew in any intact or thymectomized histocompatible host, thereby indicating their autonomous growth state. Infection of 2-week-old AKR mice with the dual-tropic virus DTV-70 induced characteristic changes in the thymus and accelerated leukemia development. DTV-70 inoculation into 14-day-old AKR mice did not change the spontaneous PLC distribution pattern in the tested host organs within 30 days postinfection, nor did it change PLC-specific host requirements for further progression into leukemic cells; however, it enhanced PLC transition to autonomous leukemic cells. The preferential cell tropism of DTV-70 for target cells (prothymocytes) among bone marrow and young spleen cells rather than for thymocytes was also demonstrated in an in vitro-in vivo test. The dual tropic virus may act as a promoter on preexisting PLC (present mostly among bone marrow cells) by enhancing their ability to progress into autonomous leukemic cells.
Leukemia 1987 May
PMID:Enhanced AKR leukemogenesis by the dual tropic viruses. I. The time and site of origin of potential leukemic cells. 282 20

The data are presented on the activation of endogenous retrovirus in vaccinia virus--malignant transformed cells of rat tissue culture. Infection of the cells by Mazurenko mouse leukemia virus induced rat sarcoma virus. The latter was formed as a result of recombination of sarcoma virus-specific sequences received from the rat cells malignantly transformed by vaccinia virus and virus-helper (Mazurenko mouse leukemia virus).
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PMID:[Isolation of sarcoma virus from noninbred rats]. 284 34

Alterations in the circulating CD5+ B-lymphocyte population, in vitro GP51 expression, and in vivo tax/rex expression that may precede lymphomagenesis were characterized prospectively in ten experimentally BLV-infected sheep. Infection with pathogenetic BLV resulted in a significant expansion of the circulating CD5+ B-lymphocyte population in six infected sheep. Of the remaining four infected sheep that did not have persistently elevated CD5+ B-lymphocyte counts, three developed lymphoid neoplasia within 14 months post-inoculation. Neoplastic cells from two of these three sheep were CD5- B-lymphocytes, while cells from the third were CD5+ B-lymphocytes. In vitro GP51 expression was a consistent feature of circulating lymphocytes from all three sheep developing tumors, but high level tax/rex gene transcription was not detected in circulating lymphocytes prior to lymphomagenesis. Neither in vitro GP51 expression nor high level tax/rex gene transcription was associated with expansion of the CD5+ B-lymphocyte population in sheep with significantly elevated CD5+ B-lymphocyte counts. These observations indicate that BLV infection in sheep results in expansion of the circulating CD5+ B-lymphocyte population, and that this expansion is not required for the subsequent development of BLV-associated lymphoid neoplasia.
Leukemia 1994 Nov
PMID:Association of GP51 expression and persistent CD5+ B-lymphocyte expansion with lymphomagenesis in bovine leukemia virus infected sheep. 752 91

Leukemia cell infiltration and the induction of lethal hematopoietic disease in immune-deficient SCID mice transplanted with human T cell acute lymphoblastic T leukemia (T-ALL) cells occurred only when the cells possessed mutant p53 genes and lacked a wild-type allele or when T-ALL cells lacking p53 protein were infected with specific mutant p53 genes. A series of six mutant p53 genes were cloned from relapse T-ALL-derived cell lines and were constructed into defective retroviral expression vectors. Viruses encoding mutant p53 proteins were used to infect relapse T-ALL cells in a study designed to compare their pathogenic potency. The mutant p53 genes possessed a distinct hierarchy in vivo and in vitro: mutants inducing the greatest increase in proliferation of different T-ALL lines in vitro and colony formation in methylcellulose cultures also induced tissue invasiveness of infected T-ALL cells in vivo. Mutant p53 gene transfer to a cell line lacking p53 protein showed that the more potent p53 mutants possessed a distinctive dominant oncogenic activity in vitro and in vivo. The dominant oncogenic activity of these mutant p53 proteins was not dependent on the presence of and on complex formation with wild-type p53 protein. These "hot" p53 mutations thus represent bona fide gain-of-function mutations. Infection of p53-negative T-ALL cells with viruses encoding gain-of-function mutant p53 genes resulted in the acquisition of metastatic potential and tissue invasiveness. Taken together, our results suggest that specific mutant p53 genes play a role in the generation of lymphohematopoietic metastatic potential and tissue invasiveness as assayed in SCID mice, whereas the expression of wild-type p53 is capable of keeping this metastatic potential in check.
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PMID:Gain-of-function mutations of the p53 gene induce lymphohematopoietic metastatic potential and tissue invasiveness. 808 50

The thymus is the primary site of T cell ontogeny and selection during fetal and neonatal development. Previous studies have established that the thymus is also a site of HIV-1 infection, as early as the first trimester of pregnancy. Alteration of the thymocyte maturation process by HIV-1 could impact on the peripheral T cell population and interfere with immune responses. A neonatal thymic organ culture system was established to study HIV-1 infection within the thymus. We have shown that this primary tissue isolate can support a productive HIV-1 infection. Infection occurred without detectable thymocyte cytopathology. The ability to infect the developing thymocyte within an intact micro environment will enable us to further establish the kinetics of acute HIV-1 thymic infection and its consequences on lymphocyte maturation.
Leukemia 1994 Apr
PMID:Neonatal HIV-1 thymic infection. 815 85

The ras gene products play a fundamental role in signal transduction in haemopoiesis. In this study, we have examined the effects of ras upon haemopoietic cell proliferation and differentiation, using two human cell lines which represent different stages of haemopoietic cell maturation. When a mutant H12-ras gene (codon 12: gly-->asp) was expressed in the monoblastic cell line, U937, marked inhibition of growth was seen together with morphological, functional and immunophenotypic evidence of monocytic maturation. Infection of U937 cells with a c-myc retrovirus produced similar changes strongly suggesting that Myc plays an important role in this action of Ras. By contrast, expression of H12-ras promoted factor-independent growth of the multipotent cell line, TF-1. Furthermore, mutant ras dramatically enhanced the growth of TF-1 cells in the presence of added GM-CSF or erythropoietin, but did not influence the state of differentiation of these cells. These data clearly indicate that in haemopoietic cells, Ras may promote either proliferation or differentiation depending upon cell type and/or state of maturation.
Leukemia 1996 Jan
PMID:Mutant ras promotes haemopoietic cell proliferation or differentiation in a cell-specific manner. 855 43


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