Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was made of the properties of human lymphoid cell line RPMI-6410 derived from peripheral blood of a patient with acute myeloblastic leukaemia. The lymphoblastoid cell line was found to be resistant to 5-brom-deoxyuridine and to have a low thymidine kinase activity. The modal chromosome number for RPMI-6410 is 46-47 XY. The karyotype includes marker chromosomes: two large submetacentrics --M1 and M2, and two small acrocentrics--M3 and M4. Ways of marker chromosome formation are discussed. The properties of RPMI-6410 line make it possible to use it for somatic cell hybridization, in particular, for obtaining hybridoma synthesizing human monoclonal antibodies.
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PMID:[Biochemically labelled human lymphoblastoid cell line. I. Its karyotypic, growth and physiological characteristics]. 385 83

Soluble immune response suppressor (SIRS), a protein of Mr 14,000, is a lymphokine produced by interferon- or concanavalin A-activated suppressor T cells and is oxidized to its activated form, SIRSox, by H2O2 produced by macrophages. SIRSox inhibits antibody secretion by B lymphocytes and cell division by normal or transformed cell lines. Effects of purified growth factors on suppression of antibody secretion were examined to determine whether any would oppose the inhibitory effects of SIRS or SIRSox. Interleukin 1 (IL-1), interleukin 2 (IL-2), and epidermal growth factor (EGF) each inhibited SIRS-mediated suppression of antibody secretion by cultured mouse spleen cells. Inhibition of SIRS activity was most effective when growth factors were added late in the culture period. IL-1, IL-2, and EGF also blocked suppression by SIRSox. However, EGF and IL-1 blocked suppression by SIRSox only when added 3-6 hr before addition of SIRSox, whereas IL-2 blocked suppression by SIRSox when added before or up to 3 hr after addition of SIRSox. Further evaluation showed that IL-2, but not EGF or IL-1, reversed inhibition of antibody secretion by SIRSox in a time- and concentration-dependent manner. With 50 units of IL-2 per 0.5-ml culture, reversal was complete within 1 hr. The ability of growth factors to interfere with inhibition of cell division by SIRSox was examined with the human B-cell leukemia RPMI-1788. This cell line binds EGF but is not known to have cell surface receptors for IL-1 or IL-2. EGF (0.3-1 ng/ml), when added to RPMI-1788 cultures 4-6 hr before SIRSox, interfered with the ability of SIRSox to inhibit cell division. Taken together, these data indicate that growth factors interfere with both the immunosuppressive and growth inhibitory properties of SIRSox in both heterogeneous and homogeneous cell populations.
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PMID:Inhibition of soluble immune response suppressor activity by growth factors. 387 57

A simple and convenient method for efficiently establishing 8-azaguanine-resistant mutant leukemia and myeloma cell lines (for example, the T cell lines Jurkat and CCRF-CEM, human myeloid/macrophage-like cell lines HL60 and U937, Burkitt lymphoma line Raji and the human myeloma line RPMI 8226), is described. The method relies on culturing the cell lines in RPMI 1640 medium containing 8-azaguanine and supplemented with 15% heat-inactivated fetal calf serum and large amounts of amino acids and vitamins, and removes the necessity for pretreatment with mutagenic reagents such as ethyl methylsulfonate or X-irradiation. The possibility of obtaining mutant cell lines using the method described here is about 15 times greater than using media without high levels of amino acids and vitamins. Hybridomas produced between mitogen-activated human peripheral blood lymphocytes and an 8-azaguanine-resistant Jurkat mutant cell line (established by this method) were shown to produce soluble T cell-derived macrophage activating factor (MAF)-like material.
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PMID:A simple method for efficiently establishing 8-azaguanine-resistant mutant human leukemia and myeloma cell lines. 390 63

We examined the effect of rate of temperature rise on the thermosensitivity of a murine lymphoblastic leukemia. L1210 cells suspended in RPMI 1630 medium:5% fetal bovine serum at pH 7.4 were heated from 37 degrees C-42 degrees C, or 44 degrees C over variable times (immediately, 30, 60, 120, 180 min) in a circulating water bath controlled by an electronic temperature programmer. Survival of the cells using a soft agar clonogenic assay was plotted against the time at final temperature so that a Do (min of heat required to reduce survival by 63% on the exponential portion of the survival curve) could be calculated as an estimate of thermosensitivity. Cells heated from 37 degrees C-42 degrees C over a time period of 30 min (10 degrees C/h) were less thermosensitive (Do 62.7 +/- 12.5 min) as compared to those exposed immediately to 42 degrees C (Do 38.5 +/- 2.2 min). Cells heated over a period of 180 min (1.6 degrees C/h) showed almost no death even after 4 h at 42 degrees C. Thermosensitivity of cells heated to several other high temperatures was also a function of rate of heating. This relative thermal resistance induced by slow heating was not a result of a change in membrane cholesterol content or fatty acid composition. Similarly, there was no difference between cells heated at slow and fast rates in cell cycle distribution or in cellular protein concentration. The major heat shock protein of Mr 70,000, which was induced by immediate heating, was not synthesized at the same high rate 1-12 h after heat treatment by the cells made thermotolerant with slow heating. We conclude that the thermosensitivity of this neoplastic cell can be altered considerably by the rate of heating. This alteration is not due to a change in membrane lipids. Furthermore, the heat shock protein at Mr 70,000 which was synthesized after immediate heating could not be demonstrated in the gradually heated L1210 leukemia cells.
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PMID:Influence of rate of heating on thermosensitivity of L1210 leukemia: membrane lipids and Mr 70,000 heat shock protein. 394 70

The specificity of guinea pig erythrocyte (GPE) rosettes for feline peripheral blood lymphocytes was studied. Of the GPE rosette-positive cells from peripheral blood, 54% were monocytes, 29% were granulocytes, and only 17% were lymphocytes. Results were similar for rosettes incubated at 4 C and those incubated at 37 C. Mononuclear cells separated with polyvinylpyrrolidone-coated silica formed fewer monocyte rosettes (49%) and more granulocyte rosettes (34%) than did cells separated with sodium diatrizoate-Ficoll (60% monocyte rosettes and 18% granulocyte rosettes), whereas the percentage of lymphocyte rosettes was similar for both media. Mononuclear cells suspended in Eagle's minimum essential medium had a higher percentage of monocyte rosettes (75%) and a lower percentage of granulocyte rosettes (12%) than did cells suspended in RPMI 1640 medium (59% monocyte rosettes and 27% granulocyte rosettes). The percentage of lymphocyte rosettes was similar in the 2 media. Two sequential 45-minute plastic adherent cell depletions decreased monocyte rosettes to 51% and increased lymphocyte rosettes to 23% compared with 63% monocyte rosettes and 12% lymphocyte rosettes before adherent cell depletion. The granulocyte rosettes were unchanged by plastic adherent cell depletion. The percentage of rosette-positive cells (9%) was not significantly affected by incubation at 4 C or 37 C, cell separation with polyvinylpyrrolidone-coated silica or lymphocyte separation medium, or suspension in Eagle's minimum essential medium or RPMI 1640 medium. Plastic adherent cell depletion decreased the percentage of rosette-positive cells. Feline thymocytes were 38% to 80% GPE rosette-positive and a feline leukemia virus-infected lymphoblastic cell line (F422) was 88% GPE rosette-positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Guinea pig erythrocyte rosette formation as a nonspecific cell surface receptor assay in the cat. 395 30

The growth inhibitory activity of human recombinant leucocyte A interferon (Ro22-8181: alpha-interferon) against 23 human cultured cell lines derived from leukemias and lymphomas was measured quantitatively by regrowth assay. Daudi cells were the most sensitive to it. Two T-cell lines (RPMI-8402, HUT78), three B-cell lines (Raji, Ly16, A3/Kawakami), one non-T, non-B acute lymphoblastic leukemia (ALL) cell line (KOPN-1) and three myelomonocytoid cell lines (U937, THP-1, ML-1) were moderately or slightly sensitive. Although the levels of sensitivity of these cell lines were different, cells could be killed by the recombinant alpha-interferon. Morphological changes in the sensitive cells treated with it were decreases in mitosis, pyknosis and fragmentation of the cells. Thirteen other cultured cell lines were not sensitive. The results indicated that the growth inhibitory activity of recombinant alpha-interferon is not always cell lineage-specific. There were only three cell lines whose sensitivity, expressed by the concentration required for 90% growth inhibition, was less than the several hundred units per milliliter that has usually been obtained as blood levels in clinical trials. These three included one of 10 T-cell lines and two of seven B-cell lines; none of six non-T, non-B ALL and myelomonocytoid cell lines were that sensitive. Among virus-associated cell lines, only Epstein-Barr virus-associated B-cell lines were sensitive to the interferon; adult T-cell leukemia virus-associated T-cell lines were not sensitive. It was demonstrated that recombinant alpha-interferon has a time-dependent, but not a concentration-dependent cytocidal action, indicating that optimal therapeutic schedules of recombinant alpha-interferon for cancer may be daily long-term treatment, not single or short-term large-dose therapy.
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PMID:Time-dependent cytotoxic action of human recombinant alpha-interferon (Ro22-8181) in vitro and the sensitivity of various cultured leukemia and lymphoma cell lines to it. 398 16

Ten human leukemia-lymphoma cell lines were tested for the growth-inhibitory effects of harringtonine (HT). HT was most active against HL-60 acute promyelocytic leukemia cells and least active against DND-41 acute lymphoblastic leukemia cells, with a 70-fold differential activity. Sensitivity of the cell lines is, in decreasing order: HL-60 greater than RPMI-8402 greater than DND-39A congruent to ML-2 congruent to MOLT-3 congruent to KG-1 greater than Daudi congruent to NALL-1 greater than BALM-2 greater than DND-41. The cell lines with rapid cell growth tended to be more sensitive to HT. To further elucidate the selectivity of the differential sensitivity, uptake and release of HT were compared in HL-60 and DND-41 cells. Uptake of [3H]HT into HL-60 and DND-41 cells showed no difference; however, the binding of [3H]HT to cellular components was greater than 16-fold higher in HL-60 cells than DND-41 cells. There were also minor, but significant differences in the inhibition of [3H]leucine incorporation into proteins of these two cell lines in the presence of 1 microgram/ml HT. To test whether the biological effects of HT are related to the concentration of, or exposure time to, HT, KG-1 cells were exposed to HT for different periods of time and the growth-inhibitory effects were compared. Increasing exposure time from 1 h to 3 h resulted in a 100-fold decrease in concentration X exposure time (c X t) at ID50; from 3 h to 6 h, in a 20-fold decrease at ID70; and from 6 h to 24 h, in a 16-fold decrease at ID90. HT was not inactivated by cells up to 24 h. These results indicate that (a) the sensitivity of different cell lines to HT may be related to the degree of HT binding; and (b) the effects of HT are more dependent on exposure time than concentration. Continuous infusion is thus rational for clinical trials of this drug, and the degree of HT binding to leukemic cells may be predictive of clinical response.
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PMID:Biologic and pharmacologic effects of harringtonine on human leukemia-lymphoma cells. 399 83

Estrogen receptors (ER) and androgen receptors (AR) were determined in a series of 23 leukemia or lymphoma cell lines including 8 T-cell lines, 12 B-cell lines, and 3 non lymphoid cell lines. The phenotypic characterization of these cells by currently available immunological markers provides an estimate of their stage of differentiation. The result indicate that none of the investigated cell lines bear simultaneously ER and AR. Four were found to bear ER: U266, RPMI 8226, HL60, IARC/310/LT2, and four to express AR: RAJI, IARC/301/LTI, U937, REH6. The presence of cytosolic receptors was always associated with that of nuclear receptors. The expression of either ER or AR is restricted to discrete maturation stages of different haemopoietic cell lineages. Thus AR were found among the most immature lines of the T, B or monocytic lineage but they could be detected neither in the promyelocytic line HL60, nor in the pluripotential K562. The present results are in keeping with the demonstration of AR in some leukaemic blasts or in non Hodgkin's lymphomas. In contrast with AR, ER are present in two myeloma cell lines, in the promyelocytic cell line, HL60 and in a T-cell line bearing the phenotype of mature suppressor/cytotoxic T cells.
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PMID:Distribution of androgen and estrogen receptors among lymphoid and haemopoietic cell lines. 407 52

A monoclonal antibody designated 'antibody 390' (Ab 390) with anti-human Thy-1 reactivity was prepared by the hybridoma technique from the splenocytes of BALB/c mice immunized with human fetal brain. This antibody was shown to have anti-human Thy-1 reactivity because (1) it precipitated a molecule with a molecular weight of about 24,000 daltons, (2) it had a pattern of reactivity similar to that of previously described anti-human Thy-1 antibodies and (3) purified human Thy-1 antigen specifically inhibited binding of Ab 390 to a known antigen-positive cell line. It was the intent of this study to investigate the distribution of Thy-1 on normal and malignant haematopoietic cells in humans and non-human primates. We show here that Ab 390 did not react with human peripheral blood leucocytes, bone marrow cells or splenocytes by immunofluorescence but did react with subcapsular and cortical fetal thymocytes by peroxidase-antiperoxidase immunohistology. A section of fetal spleen demonstrated staining of connective tissue and blood vessels and rare reactive lymphocytes. Adult spleen contained Thy-1-positive cells surrounding the white pulp and in the marginal zone, but single-cell suspensions of splenocytes did not react with Ab 390. Ab 390 was tested against a variety of fresh human leukaemia cells and human cell lines and was shown to react with only the acute lymphoblastic leukaemia T cell lines RPMI 8402 and HPB-MLT. Non-human primate studies revealed reactivity with a number of T cell lines from New World primates (cotton-topped and red-bellied marmosets) and peripheral blood granulocytes (owl monkey). Our studies support previous findings that suggest that human Thy-1 may be a marker for early T lymphocytes in man, and its distribution on non-human primate T cell lines suggests the same for certain species of non-human primates. Not consistent with the distribution on human cells was the demonstration of Ab 390 reactivity with owl monkey granulocytes.
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PMID:A monoclonal antibody recognizing human Thy-1: distribution on human and non-human primate haematopoietic cells. 615 74

A human leukemia-associated antigen (LAA) has been identified by immunofluorescence and electrophoretic analyses. LAA was detected on the surfaces of cells from patients with acute lymphocytic leukemia (ALL) as well as on the surfaces of leukemia cells from the established cell lines NALM-1, NALM-16, MOLT-4, CCRF-CEM, and RPMI 8402. The antigen was not detected on BALM-1 or Raji cells (established B-cell lines), bone marrow cells from ALL patients in remission, or on blood lymphocytes from normal donors. This antigen was most frequently associated with common ALL (cALL); however, cells from 2 of 12 patients with T-cell ALL and 1 patient with B-cell ALL also expressed this antigen. Under reduced conditions, the antigen had an approximate molecular mass of 100,000 daltons as determined by sodium dodecyl sulfate--polyacrylamide gel electrophoresis and autoradiographic analysis and appeared to be the same cALL antigen that has recently been described by others. The probability that LAA is a normal differentiation antigen was discussed.
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PMID:Identification of a leukemia-associated antigen of human acute lymphocytic leukemia. 615 21


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