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)

To evaluate the role of human endogenous retroviruses in vivo, we examined their expressions in various organs from autopsy cases by Northern blot and RT-PCR. ERV3 (HERV-R) mRNA was expressed in many organs, and the level of expression in individuals and organs considerably differed. However, expression in the adrenal gland showed consistently high levels in every individual. lambda 4-1 (HERV-E) mRNA was expressed less compared with that of ERV3, and could not be detected in the adrenal gland by Northern blot, although the expression of lambda 4-1 generally correlated with that of ERV-3 in placentas. We also examined the effect of cytokines on the transcriptional regulation of ERV3 in vitro. Although the level of ERV3 expression in cultured synovial cells did not change after IL-1 beta treatment, the level in cultured proximal tubular epithelial cells was upregulated. The evidence suggests that distinct regulatory pathways may exist for the expression of human endogenous retroviruses in different cell types.
Leukemia 1997 Apr
PMID:Human endogenous retroviruses: expression in various organs in vivo and its regulation in vitro. 920 24

Plasma concentrations of interleukines 1, 3, 6, 8 and platelet derived growth factor (PDGF) were estimated in 45 patients with leukaemias. Among patients were 12 with acute myeloblastic leukaemia-AML (type M1 according to FAB classification), 9 with chronic granulocytic leukaemia-CGL, 10 with blastic crisis of CGL (CGL-BC) and 14 with chronic lymphocytic leukaemia-CLL (in 1 and 2 stage according to Rai classification). Additionally the concentration of IL-3 was measured in 10 patients with exacerbation of CLL. Control group consisted of 12 health volunteers. The concentrations of interleukines and PDGF were determined by means of radioimmunoassay or immunoradiometric assay. In the patients with AML, CGL-BC and CLL significant increase of concentrations of IL-1B, IL-6 were found. The patients suffers from CGL and CGL-BC had increase concentrations of IL-3, but patients with CLL-interleukin 8. The concentrations of PDGF were significantly decreased in the patients with AML, CGL-BC, and CGL. The differences of concentrations of studied interleukines can confirm their great significance in proliferation of leukaemic cells. The decrease of concentrations of PDGF in myelocytic leukaemias may reflect thrombopoietic disturbances in these illnesses.
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PMID:[Examination of interleukin levels and growth factor from blood platelets in leukemia]. 928 10

Induction of hepatocyte growth factor/scatter factor (HGF/SF) may be one of the critical steps in organ regeneration, wound healing, and embryogenesis. We previously reported the production of HGF/SF from various human leukemia cell lines and a high level of the growth factor in blood and bone marrow plasma from patients with various types of leukemia. We determined here the effects of hematopoietic cytokines on HGF/SF production in human leukemia cell lines, KG-1, a myeloid cell line, and RPMI-8226, a B cell line. Interferon (IFN)-gamma remarkably stimulated HGF/SF production in both cell lines at concentrations of more than 0.1 or 1 IU/ml. IFN-alpha and IFN-beta were as effective as IFN-gamma in RPMI-8226 cells, but less than IFN-gamma in KG-1 cells. HGF/SF gene expression in KG-1 cells was also up-regulated by IFN-gamma. Granulocyte colony-stimulating factor (G-CSF), granulocyte/macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-5 and IL-6 had no effect on HGF/SF production in the 2 leukemia cell lines. We also determined the effects of HGF/SF inducers known for human fibroblasts on the growth factor production in leukemia cells. Out of phorbol 12-myristate 13-acetate (PMA), cholera toxin, IL-1 beta, and tumor necrosis factor (TNF)-alpha, the former three were as effective as IFN-gamma in KG-1 cells, but only TNF-alpha stimulated HGF/SF production in RPMI-8226 cells, whose effect was less than those of IFN-alpha, IFN-beta, and IFN-gamma. The effect of IFN-gamma in KG-1 cells was synergistic with that of PMA. In contrast with the effect in leukemia cells, HGF/SF induction by IFN-gamma in human skin fibroblasts was much less than that by PMA or cholera toxin. These results indicated that IFN-gamma is a potent inducer of HGF/SF in human leukemia cells. This finding suggests the presence of a homeostatic control mechanism in liver regeneration and repair: hepatic injury, DNA synthesis inhibition, or apoptosis caused by IFN-gamma is subsequently overcome by cytokine-induced HGF/SF, a potent promoter of liver DNA synthesis.
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PMID:Induction of hepatocyte growth factor/scatter factor by interferon-gamma in human leukemia cells. 939 61

The cytokines belong to the group of main factors regulating of leukaemia cell proliferation. Most of information comprised in the literature concern the behaviour of single cytokines in the cell culture in vitro. In the organism of leukaemia patient many different cytokines, adhesion molecules, growth factors and other substances probably act in the same time. Therefore the aim of study was the determination of plasma concentrations of interleukin 1B, 3, 4, 6, 8, G-CSF and P-selection in 26 patients with acute myeloblastic leukaemia-aml, among them 14 patient in the course of exacerbation-aml-e and 12 being in the remission-aml-r, classified as type M1 and M2 according to the FAB classification. Control group consisted of 15 healthy volunteers. The cytokine measurements were performed by means of immunoradiometric, immunoenzymatic and radioimmunologic kits. In the patients with aml-e significant increase of plasma concentrations of IL-1B, IL-3, IL-6, G-CSF, P-selectin and essential decrease of IL-4 was found. Significant decrease of IL-4 and P-selecting concentrations in the patients with aml-r and lack of changes in IL-8 concentrations in the both groups of patients was demonstrated. The observed differences of concentrations may additionally confirm the role of studied cytokines and P-selectin in the regulation of leukaemia cell proliferation.
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PMID:[Cytokines in acute myeloid leukemia]. 982 57

Treatment of human leukemia THP-1 cells with bufalin, a specific inhibitor of Na(+)-K(+)-ATPase, sequentially induces c-fos and inflammatory cytokines interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) gene expressions before the appearance of mature phenotypes of monocytic cells. In this study we examined the signal transduction leading to bufalin-induced gene expressions. Bufalin selectively activated extracellular signal-regulated kinase (ERK), compared with other mitogen-activated protein (MAP) kinase family members. Pretreatment of THP-1 cells with PD-98059, an inhibitor of the ERK-kinase cascade, abolished bufalin-induced c-fos and IL-1 beta gene expressions, indicating that the ERK-kinase cascade mediates the induction of inflammatory cytokines by bufalin. Inhibition of the Na(+)/Ca(2+) exchanger by KB-R7943 and of protein kinase C (PKC) by Ro-31-8220 suppressed ERK activation and gene expressions of c-fos and IL-1 beta. These findings suggest that Na(+)-K(+)-ATPase inhibition by bufalin induces calcium influx and thereby activates PKC and ERK. In cells treated with an inhibitor of p38 MAP kinases, SB-203580, bufalin-mediated ERK activation became persistent and the induction of IL-1 beta and TNF-alpha expressions was significantly augmented. These results suggest that cross talk in bufalin-mediated ERK activation is negatively regulated by endogenous p38 MAP kinase activations.
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PMID:ERK signaling mediates the induction of inflammatory cytokines by bufalin in human monocytic cells. 1071 38

A 73-year-old man with acute adult T-cell leukemia (ATL) in remission was re-admitted to our hospital due to drowsiness, headache, and bilateral knee joint pain on May 17, 1998. On admission, examinations revealed decreased serum sodium concentration (112 mEq/l), low plasma osmotic pressure (259 mOsm/l), and elevated antidiuretic hormone(5.6 pg/ml). Cerebrospinal fluid examination showed an increased number of abnormal flower-like lymphocyte (951/microliter). Brain computed tomography and magnetic resonance imaging found no abnormality in the hypothalamus or pituitary gland. These findings yielded a diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Though ATL patients typically exhibit a variety of clinical symptoms, SIADH is rarely one of the complications. Further investigation showed that IL-1 beta and IL-6 concentrations were increased in spinal fluid but not in serum. Recently, it has been reported that exogeneous IL-6 is an inducer of ADH secretion, and that primary ATL cells and HTLV-I infected cell lines can produce IL-6. In this case, we speculated that IL-6 produced by ATL cells that infiltrated a cerebral lesion may have played an important role in the development of SIADH.
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PMID:[Syndrome of inappropriate antidiuretic hormone secretion associated with meningeal infiltration of tumor cells and elevated interleukin-1 beta and interleukin-6 in cerebrospinal fluid of a patient with adult T-cell leukemia]. 1072 44

Some cytokines play an important role in aetiology and pathogenesis of leukaemia. Majority of data available in the literature relates to a single cytokine in the cell culture in vitro. In patients with chronic myelogenous leukaemia several different cytokines are probably active. Therefore, this study aimed to determine the concentrations of interleukin-1 beta, G-CSF, L-selectin in leukaemia cell culture supernatant, broken granulocytes and plasma in the course of disease exacerbation and remission. Cytokines have been assayed with available immunoenzymatic kits of ELISA type. IL-1 beta, G-CSF and L-selectin levels have been increased in cell supernatant but IL-1 beta level has been decreased in non-stimulated broken granulocytes. G-CSF levels have been low both in stimulated and non-stimulated granulocytes. In comparison to control the lowered levels of G-CSF and L-selectin have been observed in blood plasma of patients with CML. Different levels of assayed cytokines and adhesion molecule may suggest their contribution to leukaemia cells proliferation regulation.
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PMID:[Diagnostic value of some cytokines levels in chronic myelogenous leukemia]. 1087 Apr 15

Six-membered peptide fragment TGENHR (HLDF-6) was identified in the HL-60 cell culture of human promyelocyte leukemia treated with retinoic acid when studying the differentiation factor HLDF of this cell line. HLDF-6 retains the ability of the full-size factor to induce the differentiation and arrest the proliferation of the starting HL-60 cells. It was shown that the synthetic peptide HLDF-6 has no specific receptors on the surface of the HL-60 cells but can affect the binding of interleukin IL-1 beta, a cytokine involved in proliferation, to the cell surface. It was found on a model of transplantable NSO myeloma that HLDF-6 has an antitumor activity.
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PMID:[Biologically active fragment of the differentiation factor from HL-60 cell line. Identification and properties]. 1100 40

Haptoglobin (Hp) is one of the acute-phase proteins and is mainly synthesized in the liver. During our study on the differentiation of leukemia cells, we have found that Hp is synthesized in human monocytic cells by all-trans retinoic acid (ATRA). The synthesis of Hp by ATRA is induced in a dose- and time-dependent manner. Hp cDNA cloned from ATRA-treated THP-1 cells corresponds to the Hp alpha 2(FS)-beta form. Whereas ATRA acted as a strong inducer in THP-1 cells, IL-1 beta, TNF-alpha, IL-6, and LPS had little effect on Hp gene expression in these cells. These findings suggest that THP-1 cells express the Hp gene through a signal pathway different from hepatocytes, and that ATRA is a potent Hp-inducer in these cells.
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PMID:Induction of haptoglobin by all-trans retinoic acid in THP-1 human monocytic cell line. 1139 64

We have shown previously that tumor necrosis factor-alpha (TNF-alpha) inhibits the growth and induces the differentiation of a murine myelomonocytic leukemia (WEHI-3B JCS cells) into macrophage-like cells. In this study, using reverse transcription polymerase chain reaction, we found that both endogenous interleukin-1 alpha and beta (IL-1 alpha, IL-1 beta) mRNA were up-regulated upon TNF-alpha induction. Exogenous IL-1 alpha and IL-1 beta also inhibited the growth as well as induced the differentiation of JCS cells, with IL-1 beta exerting a greater growth-inhibitory effect. Neutralizing anti-IL-1 alpha, anti-IL-1 beta and anti-TNF-alpha antibodies were further used to elucidate the role of IL-1 alpha, IL-1 beta and TNF-alpha in JCS cell differentiation. The results show that the IL-1 alpha-induced monocytic differentiation of JCS cells was effectively blocked by anti-IL-1 beta as well as anti-IL-1 beta antibodies and to a lesser extent by anti-TNF-alpha antibody. In contrast, the differentiation-inducing effect of IL-1 beta on JCS cells was only blocked by anti-IL-1 beta antibody but not by anti-IL-1 alpha or anti-TNF-alpha antibody. Finally, the TNF-alpha-induced monocytic differentiation of JCS cells was significantly blocked by anti-TNF-alpha and to a lesser extent by anti-IL-1 alpha and anti-IL-1 beta antibodies. Collectively, our results suggest that IL-1 beta alone may directly trigger JCS cell differentiation whereas the differentiation-inducing effect of IL-1 alpha may be via the endogenous production of IL-1 beta and/or TNF-alpha. In addition, IL-1 alpha and IL-1 beta may be involved, at least in part, in TNF-alpha-induced monocytic differentiation of the JCS leukemia cells.
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PMID:Involvement of interleukin-1 in the differentiation-inducing activity of tumor necrosis factor-alpha on a murine myeloid leukemia (WEHI-3B JCS). 2153 51


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