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Query: UMLS:C0598766 (leukemogenesis)
 4,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study of Friend and Rauscher murine leukemia viruses has produced a variety of evidence regarding the nature of the target cell(s). These viruses produce in mice leukemias with a strong erythroid component. However, they are also pancytotic in their action, with demonstrable effects on differentiating myeloid and thromboid cells, the immuno-responsive cells, and the peripheral lymphoid cells as well. In addition, it has been noted that a variety of factors can influence disease expression, including the variety of mouse strain, the hematopoietic cell line being observed, and the tissue microenvironment in which leukemogenesis is taking place, as well as the viral substrain itself. The data available indicates that the target cells are definitely to be found among the most primitive of the hematopoietic progenitor cells of both the marrow and the spleen. However, from an analysis of this data it would appear that the virus target is not exclusively limited to a single type of hematopoietic precursor cell. Rather it is suggested that there is a closely related family of targets, consisting of the uncommitted pluripotent stem cell and the committed progenitor stem cells of the erythroid, myeloid, thromboid and immune cell lines. The evidence for each of these types of hematopoietic cells is reviewed.
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PMID:The role of committed and uncommitted hematopoietic stem cells as targets for Rauscher and Friend leukemia virus. 89 10

Treatment of mice with the immunomodulator pyran copolymer inhibited leukemogenesis produced by Friend leukemia virus (FLV) complex, as evidenced by inhibition of the spleen focus-forming virus and lymphatic leukemia virus, as well as by a significant decrease in splenomegaly. In this report we present data suggesting that the protective effect of pyran is mediated by macrophages. Protection was conferred on normal recipient mice when peritoneal exudate cells from pyran-treated mice were transferred to recipient mice infected 24 hr later with FLV. Animals receiving pyran-activated peritoneal cells had a significant reduction of splenomegaly and of titers of spleen focus-forming virus and lymphatic leukemia virus than did control animals. In contrast, when glycogen-elicited peritoneal exudate cells were transferred, the mice were not protected. Pyran-activated peritoneal cells, but not normal peritoneal cells, also inhibited FLV growth in vitro. Serum from pyran-treated, but not glycogen-treated, mice also transferred resistance to FLV-infected mice.
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PMID:Cellular and serum involvement in protection against Friend leukemia virus. 90 40

In their work authors have analyzed some epidemiologic and etiologic data that can be taken as the elements of risk in leukemogenesis. The investigations have been done retrospectively in 212 children suffering from acute leukemia and treated in Pediatric Clinic in Beograd. Certain factors of risk are particularly studied as: repeated viral infections, repeated use of antibiotics, diagnostic and therapeutic irradiation of children, familiar data on congenital anomalies and cancer and same harmful prezygotic and prenatal influences of possible significance. The authors also presented the results of their cytogenetic investigations obtained from 32 children. It is especially pointed out the significance of detailed data taken from patients suffering from these diseases.
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PMID:[Epidemiology and etiology of acute leukoses in children]. 92 29

Growth of tumors was inhibited or enhanced in mice by a synthetic (pyran) or a biologic (corynebacterium parvum) immunopotentiator. Marked inhibition of leukemogenesis induced by Friend leukemia virus was produced by prophylactic intraperitoneal treatment with pyran, while intravenous treatment with pyran (in the same dose and regimen) significantly enhanced growth of tumor virus. Paradoxical effects were also seen with the biologic immunopotentiator C. parvum in solid tumor systems. Treatment with C. parvum either potentiated disease or had no effect on the life span of most mice bearing the Lewis lung carcinoma. In contrast, the same treatment could produce a high percentage of tumor regressions in mice bearing the MCA 2182 sarcoma, although the effect was somewhat variable. These data, which show that a change in route of drug administration or in the type of tumor treated may reverse the effect of treatment, emphasize that the mechanism of action of immunopotentiators must be elucidated before consistent beneficial treatment of tumor viruses or tumors can be achieved.
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PMID:Paradoxical effects of immunopotentiators on tumors and tumor viruses. 93 3

The correlation of murine leukemia virus (MuLV) infection and leukemogenesis was examined by XC plaque assay in W/F rats neonatally infected with the rat-adapted Gross virus (RAGV). Thymic lymphomas developed in 100% of infected rats, with a mean latent period of 64 days. The virus infectivity was first detected in the thymus as early as 15 days after the virus infection; the titer steadily increased thereafter until the development of thymic lymphoma. No other tissues of virus-infected rats showed virus infectivity until the development of localized thymic lymphoma, though sera of a few rats showed low infectivity titers. In rats with generalized leukemia, however, high titers were detected in the sera and leukemic tissues. In untreated controls, all tissues tested invariably showed negative titers for MuLV infectivity at any age up to 7 months after birth. The results indicated that those tissue sites were common to both RAGV infectivity and the leukemogenic process, with the primary involvement of the thymus, and that the appearance of RAGV infectivity in various tissues represented the expression of the oncogenic genome of RAGV.
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PMID:Type C RNA viruses and leukemogenesis: association of Gross strain of murine leukemia virus infection and leukemogenesis in rats. 99 3

Cytologic and cytogenetic studies were performed on the bone marrow cells in atomic bomb-exposed patients who had prolonged periods of blood disorders with termination of acute leukemia (group I, 6 cases) and without the termination (group II, 6 cases), and survivors who were in apparent good health (group III, 85 cases). All but one patient in group I, who were examined at the preleukemic state, had abnormal clones. In 4 out of 6 of group I patients, morphologic abnormalities of bone marrow cells taken 3-10 years before leukemic development were found, such as giant neutrophils or basophils, binucleated granulocytes or megakaryocytes, and bridge formation of chromatid in metaphases. All patients in group II had stable types of chromosome aberrations. The types of cytologic abnormalities were similar to those in group I, but the frequencies were a little less than those in group I. In group III, 14 persons were found to have stable types of chromosome aberrations, of which 11 persons had apparent but transient clone formations. Cytologic and clinical abnormalities were not observed in the group. The persistent and high percentages of cytologic and cytogenetic abnormalities in patients with prolonged periods of blood disorders, regardless of history of radiation exposure, would suggest a preleukemic state, and also give some clue to the problems of leukemogenesis.
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PMID:Preleukemic states in atomic bomb survivors in Japan. 100 7

Mice were infected with the exogenous Moloney leukemia virus (M-MuLV) at two different stages of development. Either newborn mice (which can be considered as essentially fully differentiated animals) or preimplantation mouse embryos (at the 4-8 cell stage) were infected with M-MuLV. In both cases, animals that had developed an M-MuLV-induced leukemia were obtained. Two lines of evidence indicate that infection of preimplantation embryos, in contrast to infection of newborns, can lead to integration of the virus into the germ line. 1. Viremic males of the first backcross generation (N-1 generation) transmitted the virus to 50% of their offspring (N-2 generation) when mated with uninfected females. Likewise, a 50% transmission was observed from viremic N-2 and N-3 males to the next generations. 2. Molecular hybridization experiments revealed that viremic N-1 and N-2 animals carried one copy of M-MuLV per diploid mouse genome equivalent in all "non-target" organs tested. Together, both experiments indicate that the exogenous M-MuLV can be converted to an endogenous virus after infection of preimplantation embryos. The available evidence suggests that M-MuLV integrated into the germ line at one out of two possible integration sites. Thus, viremic backcross animals are heterozygous for a single Mendelian locus carrying the M-MuLV gene. During leukemogenesis an amplification of the M-MuLV from one copy to a maximum of four copies per diploid mouse genome equivalent takes place in the tumor tissues.
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PMID:Germ line integration and Mendelian transmission of the exogenous Moloney leukemia virus. 106 7

A case of epithelial thymoma occurring synchronously with Philadelphia chromosome-positive chronic myelogenous leukemia and urinary bladder carcinoma in a 76-year-old man is described. Thymomas have been associated with numberous hematologic, collagen-vascular and autoimmune disease states, as well as with an increased incidence of nonthymic malignancy. Human thymoma-associated leukemia is, however, extremely unusual, despite the well-documented role of the thymus in leukemogenesis in experimental animals. No previous literature reports of thymoma associated with chronic myelogeneous leukemia were found. A review of long-term followup data of surviving thymoma patients is necessary to determine if an increased propensity to develop leukemia is present in present in patients with thymoma.
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PMID:Thymoma and chronic myelogenous leukemia: a case report. 106 82

Friend leukemia virus (FV) suppressed the proliferative responses of spleen, lymph node, marrow, and thymus cell populations to various T- and B-cell mitogens. Cells taken from mice, e.g. BALB/c genetically susceptible to leukemogenesis in vivo were much more susceptible to suppression of mitogenesis in vitro than similar cells from genetically resistant mice, e.g., C57BL/6. Nylon wool-purified splenic T cells from BALB/c and C3H mice lost susceptibility to FV-induced suppression of mitogenesis but became suppressible by addition of 10% unfiltered spleen cell. Thus, FV mediates in vitro suppression of lymphocyte proliferation indirectly by "activating" a suppressor cell. The suppressor cell adhered to nylon wool but not to glass wool or rayon wool columns. Pretreatment of spleen cells with carbonyl iron and a magnet did not abrogate the suppressor cell function. Suppressor cells were not eliminated by treatment with rabbit antimouse immunoglobulin (7S) and complement (C). However, high concentrations of anti-Thy-1 plus C destroyed suppressor cells of the spleen; thymic suppressor cells were much more susceptible to anti-Thy-1 serum. Nude athymic mice were devoid of suppressor cells and their B-cell proliferation was relatively resistant to FV-induced suppression in vitro. The suppressor cells in the thymus (but not in the spleen) were eliminated by treatment of mice with cortisol. Thus, FV appears to mediate its suppressive effect on mitogen-responsive lymphocytes by affecting "T-suppressor cells." Spleen cells from C57BL/6 mice treated with 89Sr to destroy marrow-dependent (M) cells were much more suppressible by FV in virto than normal C57BL/6 spleen cells. However, nylon-filtered spleen cells of 89Sr-treated C57BL/6 mice were resistant to FV-induced suppression in vitro, indicating that the susceptibility of spleen cells from 89Sr-treated B6 mice is also mediated by suppressor cells. Normal B6 splenic T cells were rendered susceptible to FV-induced suppression of mitogenesis by addition of 10% spleen cells from 89Sr-treated B6 mice. Thus, M cells appear to regulate the numbers and/or functions of T-suppressor cells which in turn mediate the immunosuppressive effects of FV in vitro. Neither mitogen-responsive lymphocytes nor T-suppressor cells are genetically resistant or susceptible to FV. The genetic resistance to FV is apparently a function of M cells, both in vitro as well as in vivo.
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PMID:Mechanisms of genetic resistance to Friend virus leukemia. III. Susceptibility of mitogen-responsive lymphocytes mediated by T cells. 108 14

Differentiation of hemopoietic cells appears to depend upon specific interactions of certain cell-factors. The phenotypic abnormality in leukemia may involve an impairment in these interactions. In this report we present some of our views of leukemogenesis with respect to cell-factor interaction and the feasibility of experimental approaches to this problem. In culture, the interaction of myelogenous cells with factor(s) leading to differentiation can be measured either with a suspension mass culture method or by a solid (semi-soft) clonal method. The protein factors that support the growth of hemopoietic cells in suspension culture are termed growth stimulating factors (GSA) and in semi-solid culture, colony stimulating factors (CSA). Studies using conditioned medium prepared from phytohemagglutinin stimulated human lymphocytes (PHA-LyCM) and whole human embryo cells (WHE) revealed that GSA and CSA were not identical for growth of either normal human or leukemic leukocytes. In some cases maturation of leukemic leukocytes was observed. Fractionation of PHA-LyCM showed that there are three peaks for CSA. Each peak contains different fractions for supporting cellular proliferation, differentiation, and self-renewal of precursor cells in suspension culture. Apparently, each contains heterogenous species of protein factors some of which functionally overlap, while others do not.
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PMID:The phenotypic abnormality in leukemia: a defective cell-factor interaction? 108 22


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