Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598766 (leukemogenesis)
4,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The oncornavirus related proteins associated with the surface of normal and malignant thymocytes were studied. Three virion-associated proteins (gp69/71, p45, p30) were associated with lymphoma cells from about 70% of the tumors studied. Two virion-associated proteins (gp69/71 and p45 were associated with normal thymocytes form some but not all strains of mice. In gp69/71- mice, conversion to the gp69/71+ phenotype accompanied leukemogenesis. An interesting difference in the apparent molecular size of virus related antigens of the 70,000 dalton size class was detected in lymphoma cells present in involved spleens as compared to involved thymuses. Mice infected as neonates with Scripps leukemia virus make antibody to gp69/71 and some make antibodies to molecules associated with the surface of their own tumors. The significance of the restricted presence of antigens coded for by the viral genome to the surface of some differentiated cells is discussed in reference to (a) the relationship between virion, leukemia associated, and differentiation dependent markers, and (b) the possible consequence to the host of having similar antigenic determinants on three independent structures with replicative potential (virus, normal thymocytes, and tumor cells).
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PMID:The oncornavirus glycoprotein gp69/71: a constituent of the surface of normal and malignant thymocytes. 4 9

Leukemic cells from all human chronic granulocytic leukemia (CGL) and some acute myelomonocytic leukemia (AMML) donors are lysed by rabbit antisera to a purified glycoprotein of Friend murine leukemia virus (FLV gp71) in a microcytotoxicity assay. These antisera are not cytotoxic to cells from patients with acute myelocytic leukemia (AML), acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), or to peripheral blood lymphocytes from normal donors. A goat antiserum to gradient purified FLV in addition to reacting with cells from CGL and AMML donors also reacted with cells from AML patients and some ALL donors. However, this antiserum failed to react with cells from CLL patients. Peripheral blood and bone marrow leukocytes prepared from leukemic patients in clinical remission failed to react with antisera to FLV and FLV gp71. Absorption experiments demonstrated that the antigen on CGL cells which is reacting with the antiserum to FLV gp71 is also present on normal human platelets and neutrophils. Similar absorption studies showed that the antigen on AML cells detected by the FLV antiserum is not present on normal leukocytes and platelets and appears to be related to the major internal p30 antigens of mammalian RNA tumor viruses. Another antigenic relationship between oncornaviruses and membrane antigens of human leukemia cells was shown by the ability of FLV antigens to absorb the cytotoxic reactivity of nonhuman primate antisera detecting human leukemia-associated antigens. FLV and FLV gp71 antigens were able to absorb all cytotoxic activity of monkey and chimpanzee antisera to human myeloid leukemia antigens when these antisera were tested with CGL cells. These two approaches to an analysis of cross-reactivity indicate that the antigenic determinant(s) detected by the cytotoxic reactions of the FLV gp71 antiserum with human CGL cells is different from the determinant on FLV gp71 which is responsible for the inhibition of the reactivity of simian antisera with CGL cells. Since the goat and rabbit antisera to FLV and FLV gp71 are able to distinguish AML from CGL cells by direct cytotoxicity testing and absorption, they may be valuable reagents for the serological diagnosis of myeloid leukemia. In addition, since peripheral blood cells from AML and CGL patients in clinical remission were seronegative, the antisera may be valuable as management aids. The data in this report indicates that whatever the mechanism of leukemogenesis is in man, cells from CGL and AML patients possess certain membrane antigens which cross-react with FLV structural components such as p30 and gp71.
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PMID:Relationships between membrane antigens of human leukemic cells and oncogenic RNA virus structural components. 5 69

Problems relating to immunoselection of neoplastic, in particular leukemic, cell lines are reviewed. Since there is ample evidence that specific immune reactions of the host against malignant neoplastic cells do occur, it becomes important to consider the effectiveness and the relevance of immunity in suppression or elimination of neoplastic growth. Emphasis is placed on experimental results obtained in syngeneic tumor-host combinations, because they more closely resemble the situation of spontaneous tumorigenesis or leukemogenesis than xenogeneic or allogeneic model systems. Studies of types of neoplasia observed in cases of human immunodeficiency syndromes offer an important insight into problems involved in immunoselection of leukemic cell lines: the marked predominance of leukemias and lymphoreticular neoplasias in immunodeficient patients invites speculation on both the mechanisms of leukemogenesis and the relative importance of the immune system in eliminating malignant neoplastic cells.
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PMID:Problems relating to immunoselection of leukemias. 6 43

The potential of embryonic thymus organ cultures for studies on relations of endogenous MuLV, lymphoid cells and thymic microenvironment to lymphoma development were evaluated. Four main findings are reported. First, thymuses of 14-day-old CBA and AKR embryos could be maintained in organ cultures for at least 9 weeks with sustained production of lymphocytes. Lymphopoiesis in CBA and AKR thymuses were not grossly different. Secondly, an indirect immunofluorescence (IF) technique demonstrated spontaneous appearance of MuLV-antigen-containing cells in AKR, but not in CBA thymuses. Such spontaneous MuLV expression first occurred after 16 days of organ culture, thereafter infrequently and at random in individual thymus cultures. Thirdly, incubation of AKR and CBA thymuses in lymphoma extract containing AKR-type MuLV at initiation of organ cultures induced MuLV-antigen-containing cells. These were first detected after 7-14 days in culture, somewhat earlier and initially more frequently in AKR than in CBA thymuses. In the former, induction was accompanied by a clear reduction in the number of lymphocytes per thymus. Fourthly, iododeoxyuridine (IdUrd) treatment of AKR thymuses on cultute day 0, 3 or 7 decreased the number of lymphocytes per thymus and induced appearance of MuLV-antigen containing cells, assayed 8-20 days later. The IdUrd effect was most marked on day 0, and decreased sucessively on days 3 and 7. IdUrd had a much slighter effect on CBA thymuses, causing a lower reduction in cell numbers and inducing few MuLV-antigen cells. These main results clearly demonstrate the potential usefulness of the organ culture system for studied on leukemogenesis. It may be directly applied to answer several questions raised by detailed findings in our study.
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PMID:Spontaneous and induced appearance of murine leukemia virus antigen containing cells in organ cultures of embryonic mouse thymus. 7 Apr 15

Various inbred strains of mice respond immunologically to genetically transmitted ecotropic C-type viruses. Part of this response is T cell blastogenesis with type specificity for the viral envelope glycoprotein gp71. Of those nonviremic, nonleukemic strains, and F1 crosses examined, in which virus expression occurs early in life, gp71-specific blastogenic T cells were detected within the first 2 months of age and temporally preceded the development of a humoral immune response. However, in the viremic, highly leukemic strain of AKR mice, gp71-specific T cell blastogenesis in vitro was readily detectable throughout the preleukemic phase, the first 5 months of age. In appropriate F1 crosses and backcrosses, the persistent in vitro blastogenic response segregated with viremia and leukemia. These data suggest that in vivo T cell stimulation by endogenous viral gp71, caused by viremia, may contribute to virus-induced leukemogenesis in mice.
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PMID:Mechanisms of C-type viral leukemogenesis. I. Correlation of in vitro lymphocyte blastogenesis to viremia and leukemia. 9 Jul 8

1. Work over the past years and especially results of the past few years indicate that type-C viral or viral related genetic information exists in humans. 2. We do not know how this information entered humans or whether it causes disease, but it is of interest that the probes from the viruses used to detect this information are from the very same viruses which we find can affect growth and differentiation of some human hematopoietic cells. 3. The status of actual virus isolates from humans, though encouraging because of similarities of isolates from five different laboratories, remain very perplexing and so far have not been especially informative to human leukemogenesis. 4. In the near future we hope to clone in bacteria the viral related sequences detected in human DNA in order to more precisely determine their chemical and biological properties. The HL-60 system may also afford an opportunity to purify receptors for CSF. When CSF and other, perhaps more important, regulatory factors are purified, we would like to determine if they bind differently to leukemic and normal cells.
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PMID:Cellular and virological studies directed to the pathogenesis of the human myelogenous leukemias. 9 83

Trisomy of chromosome 15 is a highly regular feature of murine T-cell leukemogenesis. We have studied the chromosomal constitution of 7,12-dimethylbenza(a)anthracene (DMBA)-induced T-cell leukemias in C57BL X CBAT6T6 F1 mice. The CBAT6T6-derived chromosome T(14:15)6 was regularly duplicated whereas the C57BL-derived normal chromosome 15 was only present in one copy. It was concluded that the gene(s) that tend to duplicate in parallel with the neoplastic transformation of the prothymocyte to an overt leukemic cell have a greater chance of duplicating and/or may have a stronger promoting effect on leukemogenesis if stronger promoting effect on leukemogenesis if located on the CBA-derived, structurally rearranged T(14:15)6 than the corresponding genes located on the C57BL-derived normal chromosome 15.
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PMID:Non-random duplication of chromosome 15 in murine T-cell leukemias induced in mice heterozygous for translocation T(14:15)6. 10 28

It is well admitted that blast cells of the thymic subcapsular zone play an important role in murine leukemogenesis. Previous ultrastructural investigations have revealed the morphological heterogeneity of this population which is formed by lymphoblasts, X cells and ring shaped nucleolus cells. These aspects could correspond to different positions in the cell cycle of an unique cell type. After administration of vinblastine, a drug blocking mitosis in metaphasis, the percentage of lymphoblasts decreases whereas the percentage of X cells increases. There is no modification of the number of ring-shaped nucleolus cells. This suggests that at least a part of lymphoblasts gives rise to x cells.
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PMID:[Effect of vinblastine on the blast population of the thymus subcapsular zone in the mouse]. 16 Nov 92

Cyclic adenosine 3':5'-monophosphate (cyclic AMP) levels were slightly increased in preleukemic AKR mouse thymus cells, compared with nonleukemic thymus cells, but were markedly reduced in leukemic cells. Adenylate cyclase activity rose during the preleukemic and leukemic phases of leukemogenesis. Although the drop of epinephrine-induced stimulation of thymus adenylate cyclase in the preleukemic phase was probably age related, there was an additional decrease of adenylate cyclase activation by epinephrine in leukemic cells. Cyclic AMP phosphodiesterase activity was slightly higher in preleukemic cells and more than fourfold AKR thymus. These observations suggest that cyclic AMP phosphodiesterase is largely responsible for the low levels of cyclic AMP in leukemic cells. Significant changes in cyclic AMP metabolism are already detectable before neoplastic cells may be found in the thymus.
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PMID:Changes in lymphoid cyclic adenosine 3':5'-monophosphate metabolism during murine leukemogenesis. 16 59

Friend leukemia virus suppresses the proliferative responses of normal thymus-dependent (T) and bursa equivalent-dependent (B) lymphocytes from spleen, thymus, lymph node, and bone marrow to mitogens. The suppressive effect of Friend virus complex (FV) requires fully infectious virions. Friend erythroleukemic cells, washed to removed extracellular virus, fail to suppress concanavalin A (Con-A)-induced mitogenesis of normal spleen cells. This indicates that FV does not mediate its immunosuppressive effect via transformed erythropoietic cells. The in vitro suppressive effect of FV on lymphocyte mitogenesis is under host genetic control. Spleen, bone marrow, and thymus cells from strains of mice susceptible to FV-induced leukemogenesis in vivo were quite susceptible to the suppressive effects of FV in vitro. On the other hand, similar cells from strains of mice such as C57BL/6 resistant to Friend erythroleukemia, were quite resistant to in virto immunosuppression by FV. Mitogenesis of splenic T cells from resistant B6 mice, previously treated with 89Sr, became susceptible to suppression by FV. This indicated that the in vitro resistance of lymphocytes to FV-induced suppression is not an intrinsic property of T cells, but is controlled by marrow-dependent (M) cells which are selectively eliminated by treatment with 89Sr. M-cell function does not develop in mice less than 3-wk old. The Con A response by thymus cells from 2-wk-old B6 mice was susceptible to suppression by FV, further supporting the concept that M cells may regulate the genetic resistance to FV.
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PMID:Mechanisms of genetic resistance to Friend virus leukemia in mice. II. Resistance of mitogen-responsive lymphocytes mediated by marrow-dependent cells. 17 9


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