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Primary effusion lymphoma (PEL) was initially designated as a body-cavity-based lymphoma and recognized as a distinct clinical entity without a contiguous tumor mass.

PEL was first reported in patients with acquired immunodeficiency syndrome (AIDS) and the distinctive feature of PEL originally reported as a B-cell neoplasm characterized by infection of the tumor cells by human herpes virus 8 (HHV-8).

However, there have recently been several reports of PEL in patients without human immunodeficiency virus (HIV) or HHV-8 infection.

[MeSH-major] Antigens, CD4 / biosynthesis. DNA-Binding Proteins / genetics. Gene Rearrangement. Herpesvirus 8, Human / genetics. Lymphoma, Primary Effusion / genetics. Lymphopenia / therapy. T-Lymphocytes / metabolism

[MeSH-minor] Aged. Antineoplastic Agents / pharmacology. Dyspnea / diagnosis. HIV Infections / diagnosis. Humans. Immunophenotyping. Male. Pericardial Effusion

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(PMID = 18166773.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD4; 0 / Antineoplastic Agents; 0 / BCL6 protein, human; 0 / DNA-Binding Proteins

   

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The new compounds showed a wide range of potencies and efficacies on doxorubicin-resistant erythroleukemia K562 cells in the pirarubicin uptake assay.

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(PMID = 19140665.001).

[ISSN] 1520-4804

[Journal-full-title] Journal of medicinal chemistry

[ISO-abbreviation] J. Med. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclohexanols; 0 / Cyclohexylamines; 0 / P-Glycoprotein; 80168379AG / Doxorubicin; D58G680W0G / pirarubicin

   

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[Title] [Risk of neoplastic diseases in conditions of exposure to power magnetic fields--epidemiologic investigations].

Cancer risks of power magnetic fields are small and doubtful, but there exist confirmed epidemiologic investigations that in children living in homes where PMF intensity exceeds 0.3-0.4 microT (0.24-0.32 A/m) an increased risk of certain types of leukemias can be observed.

About one percent of children live under conditions of PMF exposure.

The authors also discuss the binding regulations on the protection of the general population and workers against power magnetic fields and they conclude that existing permissible exposure levels are incompatible with exposure conditions, the present state of knowledge and health threats.

[MeSH-major] Electromagnetic Fields / adverse effects. Electromagnetic Phenomena. Environmental Exposure / statistics & numerical data. Neoplasms / epidemiology. Neoplasms / etiology

[MeSH-minor] Adult. Brain Neoplasms / epidemiology. Brain Neoplasms / etiology. Causality. Child. Humans. Leukemia, Radiation-Induced / epidemiology. Leukemia, Radiation-Induced / etiology. Lymphoma / epidemiology. Lymphoma / etiology. Poland / epidemiology. Risk Assessment / statistics & numerical data. Risk Factors. Soft Tissue Neoplasms / epidemiology. Soft Tissue Neoplasms / etiology

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(PMID = 19746891.001).

[ISSN] 0465-5893

[Journal-full-title] Medycyna pracy

[ISO-abbreviation] Med Pr

[Language] pol

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Poland

[Number-of-references] 35

   

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[Title] Downregulation of the Spi-1/PU.1 oncogene induces the expression of TRIM10/HERF1, a key factor required for terminal erythroid cell differentiation and survival.

Sustained expression of the Spi-1/PU.1 and Fli-1 oncoproteins blocks globin gene activation in mouse erythroleukemia cells; however, only Spi-1/PU.1 expression inhibits the inclusion of exon 16 in the mature 4.1R mRNA.

This report demonstrates that Spi-1/PU.1 downregulation induces the activation of TRIM10/hematopoietic RING finger 1 (HERF1), a member of the tripartite motif (TRIM)/RBCC protein family needed for globin gene transcription.

Additionally, we demonstrate that TRIM10/HERF1 is required for the regulated splicing of exon 16 during late erythroid differentiation.

Altogether, these data indicate that primary Spi-1/PU.1 downregulation acts on late erythroid differentiation through at least two pathways, one of which requires TRIM10/HERF1 upregulation and parallels the Spi-1/PU.1-induced Fli-1 shutoff regulatory cascade.

[MeSH-major] Cell Differentiation / genetics. Erythroid Cells / metabolism. Hematopoiesis / physiology. Histocompatibility Antigens / metabolism. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism

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(PMID = 18560381.001).

[ISSN] 1748-7838

[Journal-full-title] Cell research

[ISO-abbreviation] Cell Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Blood Proteins; 0 / Carrier Proteins; 0 / Epb4.1 protein, mouse; 0 / Fli1 protein, mouse; 0 / Hemoglobins; 0 / Histocompatibility Antigens; 0 / Microfilament Proteins; 0 / Proto-Oncogene Protein c-fli-1; 0 / Proto-Oncogene Proteins; 0 / TRIM10 protein, human; 0 / TRIM10 protein, mouse; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; YOW8V9698H / Dimethyl Sulfoxide

   

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Kaposi's sarcoma-associated herpesvirus (KSHV) is the infectious viral agent associated with Kaposi's sarcoma and may also contribute to B-cell disorders, which include primary effusion lymphoma (PEL) and multicentric Castleman's disease.

In this report, we demonstrate that KSHV suppresses the interleukin-4 (IL-4)-stimulated immune response of B-lymphocyte activation and cell proliferation.

Importantly, knockdown of endogenous STAT6 dramatically increases the sensitivity of PEL cells to low-serum stress or chemical-mediated cellular apoptosis and reactivation of KSHV from latent replication.

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(PMID = 20719954.001).

[ISSN] 1098-5514

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA091792; United States / NIDCR NIH HHS / DE / DE014136; United States / NIDCR NIH HHS / DE / R01 DE014136; United States / NCI NIH HHS / CA / R00 CA126182-04; United States / NCI NIH HHS / CA / CA091792; United States / NCI NIH HHS / CA / K99 CA126182; United States / NIAID NIH HHS / AI / AI067037; United States / NCI NIH HHS / CA / R00 CA126182; United States / NIAID NIH HHS / AI / R01 AI067037; United States / NIDCR NIH HHS / DE / R01 DE017338; United States / NCI NIH HHS / CA / CA126182; United States / NIDCR NIH HHS / DE / DE17338; United States / NCI NIH HHS / CA / CA126182-04; United States / NCI NIH HHS / CA / CA072510

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 207137-56-2 / Interleukin-4

[Other-IDs] NLM/ PMC2953196

   

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[Title] KSHV G protein-coupled receptor inhibits lytic gene transcription in primary-effusion lymphoma cells via p21-mediated inhibition of Cdk2.

Infection with Kaposi sarcoma-associated herpesvirus (KSHV) is now known to be an etiologic force behind KS and primary-effusion lymphoma (PEL).

Over time, KSHV has pirated many human genes whose products regulate angiogenesis, inflammation, and the cell cycle.

Although it is considered a viral oncogene and causes KS-like lesions in mice, vGPCR expression results in cell-cycle arrest of KSHV-infected PEL cells.

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(PMID = 16150942.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA068 939; United States / NIAID NIH HHS / AI / K08-AI53 971

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / G protein-coupled receptor, Human herpesvirus 8; 0 / Immediate-Early Proteins; 0 / Receptors, Chemokine; 0 / Rta protein, Human herpesvirus 8; 0 / Trans-Activators; 0 / Viral Proteins; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2

[Other-IDs] NLM/ PMC1895347

   

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[Title] Induction of erythroid differentiation in human erythroleukemia cells by depletion of malic enzyme 2.

Higher expression of this enzyme correlates with the degree of cell de-differentiation.

We found that ME2 is expressed in K562 erythroleukemia cells, in which a number of agents have been found to induce differentiation either along the erythroid or the myeloid lineage.

These findings were accompanied by differentiation of K562 cells along the erythroid lineage, as confirmed by staining for glycophorin A and hemoglobin production.

Increased ROS levels, likely reflecting increased mitochondrial production, and a decreased NADPH/NADP+ ratio were noted but use of a free radical scavenger to decrease inhibition of ROS levels did not reverse the differentiation or apoptotic phenotype, suggesting that ROS production is not causally involved in the resultant phenotype.

As might be expected, depletion of ME2 induced an increase in the NAD+/NADH ratio and ATP levels fell significantly.

We also examined several intracellular signaling pathways and expression of transcription factors and intermediate filament proteins whose expression is known to be modulated during erythroid differentiation in K562 cells.

Metabolomic analysis, conducted to gain insight into intermediary metabolic pathways that ME2 knockdown might affect, showed that ME2 depletion resulted in high orotate levels, suggesting potential impairment of pyrimidine metabolism.

Collectively our data point to ME2 as a potentially novel metabolic target for leukemia therapy.

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(PMID = 20824065.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / K01 CA104700; United States / NIDDK NIH HHS / DK / T32 DK007199; United States / NCI NIH HHS / CA / K01-CA 104700

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] EC 1.1.1.37 / Malate Dehydrogenase; EC 1.1.1.37 / malic enzyme 2; human

[Other-IDs] NLM/ PMC2932743

   

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Biofilm formation results from the production of a matrix mainly comprised of exopolysaccharides. P. aeruginosa possesses several gene clusters which contribute to the formation of the matrix, including the pel genes.

Among the pel genes, pelC encodes an outer membrane protein, which may serve as a transporter of polysaccharide to the bacterial cell surface.

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[Copyright] 2009 Elsevier Masson SAS. All rights reserved.

(PMID = 19853003.001).

[ISSN] 1638-6183

[Journal-full-title] Biochimie

[ISO-abbreviation] Biochimie

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] France

[Chemical-registry-number] 0 / Bacterial Outer Membrane Proteins

   

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[Title] Phenylobacterium zucineum sp. nov., a facultative intracellular bacterium isolated from a human erythroleukemia cell line K562.

A bacterial strain HLK1(T) was isolated from the human erythroleukemia cell line K562.

The type strain is HLK1(T) (=CGMCC 1.3786(T), DSM=18354).

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(PMID = 16908113.001).

[ISSN] 0723-2020

[Journal-full-title] Systematic and applied microbiology

[ISO-abbreviation] Syst. Appl. Microbiol.

[Language] eng

[Databank-accession-numbers] GENBANK/ AY628697/ DQ311665/ DQ311666

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / DNA, Bacterial; 0 / DNA, Ribosomal; 0 / RNA, Ribosomal, 16S; EC 5.99.1.3 / DNA Gyrase

   

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[Title] Stem cells of GATA1-related leukemia undergo pernicious changes after 5-fluorouracil treatment.

In Gata1.05 gene knockdown mice, Gata1 expression deteriorates to 5% of wild-type allelic expression, a level insufficient for supporting normal erythropoiesis and one that leads to accumulation of erythroid progenitors that are readily transformed into erythroblastic leukemia.

To delineate characteristics of leukemic stem cells (LSCs), we analyzed LSCs of Gata1.05 leukemia, which have a potential to reestablish leukemia in mice.

MATERIALS AND METHODS: Leukemic cells isolated from the first recipient mice of Gata1.05 leukemia cells were divided into two fractions using Hoechst dye.

Fractionated cells were transplanted into second recipient, or analyzed gene expression profiles and cell-cycle status.

However, expression of hematopoietic stem cell (HSC)-related genes was upregulated in the LSP cells.

CONCLUSION: Based on this observation, distinct self-renewal regulatory mechanisms in LSCs may be considered as one of the causes of worsening of the features of leukemia after injury and relapse.

[MeSH-major] Fluorouracil / pharmacology. GATA1 Transcription Factor / metabolism. Leukemia / drug therapy. Stem Cells / drug effects

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(PMID = 19302918.001).

[ISSN] 1873-2399

[Journal-full-title] Experimental hematology

[ISO-abbreviation] Exp. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; U3P01618RT / Fluorouracil

   

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After the initial dramatic effects, observed in a Lewis lung carcinoma animal model, using a combination of thymosin alpha 1 (Talpha1) and interferon (IFN) after cyclophosphamide, a number of other preclinical models in mice (Friend erythroleukemia and B16 melanoma) and in rats (DHD/K12 colorectal cancer liver metastasis) have confirmed the efficacy of the combination therapy with Talpha1 and either IFN or IL-2 plus chemotherapy.

[MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. CD4-Positive T-Lymphocytes / drug effects. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / immunology. Disease Models, Animal. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Mice. Rats

The Lens. Cited by Patents in .

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(PMID = 17600290.001).

[ISSN] 0077-8923

[Journal-full-title] Annals of the New York Academy of Sciences

[ISO-abbreviation] Ann. N. Y. Acad. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / thymalfasin; 61512-21-8 / Thymosin

   

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[Title] Histone H4-lysine 20 monomethylation is increased in promoter and coding regions of active genes and correlates with hyperacetylation.

In the case of H3-Lys(4), H3-Lys(9), H3-Lys(27), and H4-Lys(20), the degree of methylation was variable from the mono- to the di- or trimethylated state, each of which was presumed to be involved in the organization of chromatin and the activation or repression of genes.

Here we investigated the interplay between histone H4-Lys(20) mono- and trim-ethylation and H4 acetylation at induced (beta-major/beta-minor glo-bin), repressed (c-myc), and silent (embryonic beta-globin) genes during in vitro differentiation of mouse erythroleukemia cells.

By using chromatin immunoprecipitation, we found that the beta-major and beta-minor promoter and the beta-globin coding regions as well as the promoter and the transcribed exon 2 regions of the highly expressed c-myc gene were hyperacetylated and monomethylated at H4-Lys(20).

Although activation of the beta-globin gene resulted in an increase in hyperacetylated, monomethylated H4, down-regulation of the c-myc gene did not cause a decrease in hyperacetylated, monomethylated H4-Lys(20), thus showing a stable pattern of histone modifications.

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(PMID = 16166085.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Butyrates; 0 / Chromatin; 0 / Cross-Linking Reagents; 0 / Heterochromatin; 0 / Histones; 0 / Isobutyrates; 0 / Proto-Oncogene Proteins c-myc; 1HG84L3525 / Formaldehyde; 8LL210O1U0 / isobutyric acid; 9004-22-2 / Globins; K3Z4F929H6 / Lysine

   

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[Title] Development of permissible exposure limits: the California experience.

The California OSHA Airborne Contaminant Advisory Committee reviewed several hundred substances and recommended occupational exposure limits with the intent of worker and employer protection.

[MeSH-major] Advisory Committees / organization & administration. Hazardous Substances / standards. Occupational Exposure / standards. Occupational Health / legislation & jurisprudence

[MeSH-minor] Animals. California. Communication. Humans. Maximum Allowable Concentration. National Institute for Occupational Safety and Health (U.S.) / standards. No-Observed-Adverse-Effect Level. Program Development. United States

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(PMID = 16967831.001).

[ISSN] 1077-3525

[Journal-full-title] International journal of occupational and environmental health

[ISO-abbreviation] Int J Occup Environ Health

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Hazardous Substances

   

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[Title] Expression of alpha-hemoglobin stabilizing protein and cellular prion protein in a subclone of murine erythroleukemia cell line MEL.

Alpha-Hemoglobin stabilizing protein (AHSP) functions as the erythroid-specific molecular chaperon for alpha-globin.

AHSP gene expression has been reported to be downregulated in hematopoietic tissues of animals suffering from prion diseases though the mechanism remains to be clarified.

Herein, we demonstrate that MELhipod8 cells, a subclone of murine erythroleukemia (MEL) cells, have prion protein (PrPc) on the cell surface and have highly inducible expression of the AHSP and alpha- and beta-globin genes, resembling the expression pattern of the PrP and AHSP genes in bipotential erythroid- and megakaryocyte-lineage cells followed by erythroid differentiation in normal erythropoiesis.

Moreover, MELhipod8 cells exhibit greater effective erythroid differentiation with a population of hemoglobinized normoblast-like cells than that observed for the parental MEL cells.

These findings suggest that MELhipod8 cells could provide a mechanism for downregulation of the AHSP gene in prion diseases.

[MeSH-minor] Animals. Cell Line, Tumor. Gene Expression Regulation. Leukemia, Erythroblastic, Acute. Mice. Time Factors

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(PMID = 18828445.001).

[ISSN] 0047-1917

[Journal-full-title] The Japanese journal of veterinary research

[ISO-abbreviation] Jpn. J. Vet. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Ahsp protein, mouse; 0 / Blood Proteins; 0 / Molecular Chaperones; 0 / PrPC Proteins

   

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No quercetin and ACN were found in plasma, while coumaric acid, 4-hydroxybenzoic acid (4HBA, 56 and 54% of pelargonidin-3-glucoside (Pel-glc) ingested with FS and SS, respectively) and protocatechuic acid (59 and 34% of cyanidin-3-glucoside ingested with FS and SS, respectively) over 8 h from strawberry consumption were retrieved in the plasma.

Pelargonidin glucuronide, pelargonidin glucoside and pelargonidin aglycone peaked in urine within 2 h of strawberry consumption, and the 24 h amount excreted was always approximately 0.9% of the Pel-glc dose ingested.

Furthermore, in the present study, the metabolism of Pel-glc was elucidated, and, for the first time, 4HBA was suggested to be a major human metabolite of Pel-glc.

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(PMID = 20487578.001).

[ISSN] 1475-2662

[Journal-full-title] The British journal of nutrition

[ISO-abbreviation] Br. J. Nutr.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Anthocyanins; 0 / Antioxidants; 0 / Phenols; 36-88-4 / Carotenoids; 45XWE1Z69V / alpha-carotene

   

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The model used is a murine erythroleukemia cell line (MEL cells).

These continuously cycling, immature red blood cells, arrested at an early stage in erythropoiesis, can be induced to progress further through the process by 72 h exposure to 1.8% DMSO.

The relative levels of three sequences: β globin, amino levulinate synthase, and carbonic anhydrase-1 are estimated by real-time PCR, using 18S rRNA as the reference sequence.

The changes in gene expression are robust and reproducible, enabling students to experience a "cutting edge" research technique in an undergraduate lab setting.

While the undergraduate student experience in practical classes with such sensitive techniques is often mixed, the changes in gene expression in this model are sufficiently great that students can gain the satisfaction of consistent results.

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[Copyright] Copyright © 2010 International Union of Biochemistry and Molecular Biology, Inc.

(PMID = 21567850.001).

[ISSN] 1539-3429

[Journal-full-title] Biochemistry and molecular biology education : a bimonthly publication of the International Union of Biochemistry and Molecular Biology

[ISO-abbreviation] Biochem Mol Biol Educ

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Acute erythroid leukemia (AML-M6) - Is it rare?

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(PMID = 27265109.001).

[ISSN] 1300-7777

[Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology

[ISO-abbreviation] Turk J Haematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Turkey

   

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OBJECTIVE: Megaloblastosis (i.e., megaloblastic transformation of erythroid precursor cells in the bone marrow) is the cytomorphological hallmark of megaloblastic anemia resulting from vitamin B12 and folate deficiency.

RESULTS: Derangement of DNA synthesis occurred due to an impaired de novo pathway of thymidylate synthesis in both vitamin-B12- and folate-deficient human megaloblastic bone marrows as well as in the bone marrows of rhesus monkeys and rats with experimentally induced folate deficiency.

On the other hand, megaloblastic changes in the bone marrow of human patients with myelodysplastic syndrome and erythroleukemia were not associated with this DNA synthetic abnormality.

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[Copyright] Copyright 2005 S. Karger AG, Basel

(PMID = 16103708.001).

[ISSN] 1011-7571

[Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre

[ISO-abbreviation] Med Princ Pract

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Genetic Markers; 0 / Histones; 9007-49-2 / DNA

   

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[Title] Multi-stage Friend murine erythroleukemia: molecular insights into oncogenic cooperation.

The Friend virus SFFV (Spleen Focus Forming Virus) provokes an acute erythroblastosis in susceptible strains of mice that progresses to overt erythroleukemia by a multi-step process.

For virologists, the Friend virus-induced disease has provided deep insights into the host mechanisms influencing susceptibility to retroviral infection and viremia.

For cell biologists and oncologists, this leukemia has been a powerful experimental model to identify critical oncogenes involved in a multi-stage process, to understand the contribution of host genes to cancer development, and to investigate the mechanisms leading to cell growth autonomy.

This model also provided an example of oncogenic reversion since Friend tumor cells can reinitiate their erythroid differentiation program when exposed in vitro to some chemical inducers.

The Friend model of leukemia progression recapitulates the two phases of human acute myeloid leukemia (AML).

Coupling of insights from studies on the Friend erythroleukemia with knowledge on AML might allow a better understanding of the molecular mechanisms involved in the evolution of leukemia in mice and men.

[MeSH-major] Cell Transformation, Neoplastic. Leukemia, Erythroblastic, Acute / virology. Oncogenes. Spleen Focus-Forming Viruses / pathogenicity

[MeSH-minor] Animals. Animals, Newborn. Cell Differentiation. Cell Proliferation. Humans. Leukemia, Myeloid, Acute / pathology. Male. Mice

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(PMID = 18983647.001).

[ISSN] 1742-4690

[Journal-full-title] Retrovirology

[ISO-abbreviation] Retrovirology

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Number-of-references] 132

[Other-IDs] NLM/ PMC2585586

   

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The iron(III) salen-type complexes [Fe(salen)(L)](n) (1-6) involving heterocyclic N-donor ligands HL {HL = 1H-imidazole (Himz), 1H-tetrazol-5-amine (Hatz), 5-methyl-1H-tetrazole (Hmtz), 1H-benzimidazole (Hbimz), 1H-1,2,4-triazole (Htriz) and 1H-benzotriazole (Hbtriz)} have been prepared and characterised by elemental analysis, FT IR, CI mass and (57)Fe Mössbauer spectroscopies, and variable temperature magnetic measurements.

The compounds have been tested for their SOD-like activity, DNA cleavage activity, and in vitro cytotoxicity against two human cancer cell lines: chronic myelogenous erythroleukemia (K562) and breast adenocarcinoma (MCF7).

[MeSH-minor] Adenocarcinoma / metabolism. Breast Neoplasms / metabolism. Cell Line, Tumor. Crystallography, X-Ray. DNA Cleavage. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Ligands. Spectroscopy, Mossbauer. Superoxide Dismutase / pharmacology

MedlinePlus Health Information. consumer health - Iron.

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(PMID = 19885536.001).

[ISSN] 1477-9234

[Journal-full-title] Dalton transactions (Cambridge, England : 2003)

[ISO-abbreviation] Dalton Trans

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ferric Compounds; 0 / Ligands; E1UOL152H7 / Iron; EC 1.15.1.1 / Superoxide Dismutase

   

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[Title] Transient activation of Ras-dependent signalling at the early stages of Herbimycin A induced erythroid differentiation of human K562 cells.

AIM: To study the dynamics of Ras-dependent signalling in the course of Herbimycin A induced erythroid differentiation of human erythroleukemia K562 cells.

Transient rise of Ras-GTP level at 3rd h of incubation in the presence of Herbimycin A correlated with the increase in tyrosine phosphorylation of proteins with apparent molecular weight of 210, 160, 140, 116 and 42 kDa, as well as with the activation of Erk2 and increase of binding of a set of pY-containing proteins with recombinant GST-fusion form of Ras activator, adaptor protein Grb2.

CONCLUSION: The obtained results suggest that time-dependent changes in Grb2-mediated network of protein-protein interaction events might define implication of Ras-dependent signalling in Herbimycin A-induced erythroid differentiation of K562 cells.

[MeSH-major] Enzyme Inhibitors / pharmacology. Erythroid Cells / cytology. Proto-Oncogene Proteins p21(ras) / metabolism. Quinones / pharmacology. Signal Transduction / physiology

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(PMID = 15812354.001).

[ISSN] 1812-9269

[Journal-full-title] Experimental oncology

[ISO-abbreviation] Exp. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Ukraine

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Benzoquinones; 0 / Enzyme Inhibitors; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / Lactams, Macrocyclic; 0 / Quinones; 146-91-8 / Guanosine Diphosphate; 1W306TDA6S / Rifabutin; 42HK56048U / Tyrosine; 70563-58-5 / herbimycin; 86-01-1 / Guanosine Triphosphate; EC 2.5.1.18 / Glutathione Transferase; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)

   

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Glycophorin A (GPA, CD235a) is a major membrane glycoprotein and marker of cells of the erythroid lineage.

The new panel complements the already known anti-glycophorin antibodies and offers several potential applications for, e.g., differential diagnosis of erythroleukemias, lineage analyses of erythroid cells, isolation of senescent erythrocytes, or a highly sensitive neuraminidase assay.

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[Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.

(PMID = 20727998.001).

[ISSN] 1878-1705

[Journal-full-title] International immunopharmacology

[ISO-abbreviation] Int. Immunopharmacol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Epitopes; 0 / Glycophorin; 0 / Sialoglycoproteins; EC 3.2.1.18 / Neuraminidase

   

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Spray foam applicators and assistants may be exposed to airborne MDI concentrations above the OSHA permissible exposure limit.

At these concentrations, OSHA recommends appropriate respiratory protection during spray foam application to prevent airborne MDI exposures above established limits and to protect against exposure to dichlorofluoroethane (HCFC-141b).

After 45 min, airborne concentrations were below the limit of quantitation (LOQ) of 0.036-microg per sample.

[MeSH-major] Air Pollutants, Occupational / analysis. Chlorofluorocarbons / analysis. Isocyanates / analysis. Occupational Exposure / analysis. Polyurethanes

[MeSH-minor] Canada. Chlorofluorocarbons, Ethane. Facility Design and Construction. Housing. Humans. Particle Size. Threshold Limit Values. United States

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(PMID = 17249149.001).

[ISSN] 1545-9624

[Journal-full-title] Journal of occupational and environmental hygiene

[ISO-abbreviation] J Occup Environ Hyg

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Air Pollutants, Occupational; 0 / Chlorofluorocarbons; 0 / Chlorofluorocarbons, Ethane; 0 / Isocyanates; 0 / Polyurethanes; 101-68-8 / 4,4'-diphenylmethane diisocyanate; 1717-00-6 / 1,1-dichloro-1-fluoroethane; 9009-54-5 / polyurethane foam

   

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INTRODUCTION: Acute myeloblastic leukemia (AML) is the most common form of acute leukemia in adults.

One major problem in this disease is the emergence of leukemic blast cells that are resistant to anticancer drugs.

One cause of MDR is the expression of the MDR1 gene and its product, P-glycoprotein (Pgp).

MATERIALS AND METHODS: The Pgp expressing cell line was established from a parental K562 (Erythroleukemia) cell line with increasing concentrations of doxorubicin, and named KDI/20.

The effect of PS-ODN was assessed at the cellular level by flow cytometry (for Pgp detection), and Rhodamine 123 assay (for functional assessment of Pgp) at the molecular level by RT-PCR (for MDR1/mRNA detection) and MTT assay in order to assess the sensitivity of cell to doxorubicin.

Therefore, our data showed that antisense can reverse the MDR phenotype at the transcription level and the PEI vector is more efficient than cationic lipid.

[MeSH-major] Drug Resistance, Multiple / drug effects. Leukemia / drug therapy. Oligonucleotides, Antisense / pharmacology. P-Glycoprotein / drug effects. RNA, Messenger / drug effects

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(PMID = 17852455.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Oligonucleotides; 0 / Oligonucleotides, Antisense; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / RNA, Messenger; 0 / Thionucleotides; 80168379AG / Doxorubicin

   

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A total of 22 BRET assays have been established for nine RTKs derived from four subfamilies [erythroblastic leukemia viral (v-erb-b) oncogene homolog (ErbB), platelet-derived growth factor (PDGF), neurotrophic tyrosine kinase receptor (TRK), vascular endothelial growth factor (VEGF)] monitoring the interactions with five effectors (Grb2, p85, Stat5a, Shc46, PLCgamma1).

RTK BRET assays are highly sensitive for quantifying ligand-independent (constitutive), agonist-induced, or antagonist-inhibited RTK activity levels.

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(PMID = 17715395.001).

[ISSN] 1521-0111

[Journal-full-title] Molecular pharmacology

[ISO-abbreviation] Mol. Pharmacol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Luminescent Proteins; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases

   

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[Title] Networking of differentially expressed genes in human cancer cells resistant to methotrexate.

These are especially useful to rationalize how external perturbations propagate through the expression of genes.

To address this issue in the case of drug resistance, we constructed biological association networks of genes differentially expressed in cell lines resistant to methotrexate (MTX).

METHODS: Seven cell lines representative of different types of cancer, including colon cancer (HT29 and Caco2), breast cancer (MCF-7 and MDA-MB-468), pancreatic cancer (MIA PaCa-2), erythroblastic leukemia (K562) and osteosarcoma (Saos-2), were used.

Genes deregulated in common between the different cancer cell lines served to generate biological association networks using the Pathway Architect software.

RESULTS: Dikkopf homolog-1 (DKK1) is a highly interconnected node in the network generated with genes in common between the two colon cancer cell lines, and functional validations of this target using small interfering RNAs (siRNAs) showed a chemosensitization toward MTX.

Members of the UDP-glucuronosyltransferase 1A (UGT1A) family formed a network of genes differentially expressed in the two breast cancer cell lines. siRNA treatment against UGT1A also showed an increase in MTX sensitivity.

Eukaryotic translation elongation factor 1 alpha 1 (EEF1A1) was overexpressed among the pancreatic cancer, leukemia and osteosarcoma cell lines, and siRNA treatment against EEF1A1 produced a chemosensitization toward MTX.

CONCLUSIONS: Biological association networks identified DKK1, UGT1As and EEF1A1 as important gene nodes in MTX-resistance.

Treatments using siRNA technology against these three genes showed chemosensitization toward MTX.

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(PMID = 19732436.001).

[ISSN] 1756-994X

[Journal-full-title] Genome medicine

[ISO-abbreviation] Genome Med

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2768990

   

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[Title] Organ-specific, developmental, hormonal and stress regulation of expression of putative pectate lyase genes in Arabidopsis.

Pectate lyases catalyse the eliminative cleavage of de-esterified homogalacturonan in pectin, a major component of the primary cell walls in higher plants.

In the completed genome of Arabidopsis, there are 26 genes (AtPLLs) that encode pectate lyase-like proteins.

Interestingly, all PLL genes are expressed in flowers.

Analysis of expression of all PLL genes in seedlings treated with hormones, abiotic stresses and elicitors of defense responses revealed significant changes in the expression of some PLLs without affecting the other PLLs.

The stability of transcripts of PLLs varied considerably among different genes.

[MeSH-major] Arabidopsis / genetics. Arabidopsis Proteins / genetics. Gene Expression Regulation, Plant. Polysaccharide-Lyases / genetics

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(PMID = 17447910.001).

[ISSN] 0028-646X

[Journal-full-title] The New phytologist

[ISO-abbreviation] New Phytol.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Arabidopsis Proteins; 0 / Deoxyadenosines; 0 / RNA, Messenger; 73-03-0 / cordycepin; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

   

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[Title] Elevation of clonal serum free light chains in patients with HIV-negative primary effusion lymphoma (PEL) and PEL-like lymphoma.

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(PMID = 19681885.001).

[ISSN] 1365-2141

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Immunoglobulin Light Chains

   

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Combining with the characterizations of the solid products by solid-state NMR, it is verified that different aggregates of organic amines with imidazolium cations, which is similar to self-assembled supramolecular analogues, could act as the structure-directing agents for selective tuning of the framework topologies such as AEL, AFI and LTA in the final solid products.

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(PMID = 20449358.001).

[ISSN] 1463-9084

[Journal-full-title] Physical chemistry chemical physics : PCCP

[ISO-abbreviation] Phys Chem Chem Phys

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Aluminum Compounds; 0 / Ionic Liquids; 0 / Phosphates; F92V3S521O / aluminum phosphate

   

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Of the 811 identified membrane proteins, six displayed significantly higher expression levels in the undifferentiated state compared with differentiating cells.

This group includes the established marker CD133/Prominin-1 as well as novel candidates for hESC surface markers: Glypican-4, Neuroligin-4, ErbB2, receptor-type tyrosine-protein phosphatase zeta (PTPRZ), and Glycoprotein M6B.

Our study also revealed 17 potential markers of hESC differentiation as their corresponding protein expression levels displayed a dramatic increase in differentiated embryonic stem cell populations.

[MeSH-minor] Animals. Biomarkers / metabolism. Cell Proliferation. Cells, Cultured. Culture Media, Conditioned. Gene Expression Regulation, Developmental. Humans. Mice. Phosphoproteins / analysis. Pluripotent Stem Cells / cytology. Proteomics. RNA, Messenger / genetics. RNA, Messenger / metabolism

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(PMID = 19151416.001).

[ISSN] 1535-9484

[Journal-full-title] Molecular & cellular proteomics : MCP

[ISO-abbreviation] Mol. Cell Proteomics

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Amino Acids; 0 / Biomarkers; 0 / Culture Media, Conditioned; 0 / Membrane Proteins; 0 / Phosphoproteins; 0 / Proteome; 0 / RNA, Messenger

[Other-IDs] NLM/ PMC2689770

   

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However, constitutive NF-kappaB activation can promote continuous lymphocyte proliferation and survival and has recently been recognized as a critical pathogenetic factor in lymphoma.

Various molecular events lead to deregulation of NF-kappaB signaling in Hodgkin disease and a variety of T- and B-cell non-Hodgkin lymphomas either up-stream or downstream of the central IkappaB kinase.

This review provides an overview of the NF-kappaB pathway and discusses the mechanisms of NF-kappaB deregulation in distinct lymphoma entities with defined aberrant pathways: Hodgkin lymphoma (HL), diffuse large B-cell lymphoma (DLBCL), mucosa-associated lymphoid tissue (MALT) lymphoma, primary effusion lymphoma (PEL), and adult T-cell lymphoma/leukemia (ATL).

[MeSH-minor] Hodgkin Disease / physiopathology. Humans. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Lymphocytes / physiology. Lymphoma, B-Cell / physiopathology. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / physiopathology. Lymphoma, Large B-Cell, Diffuse / physiopathology. Models, Biological. Oncogene Proteins, Viral / physiology. Prognosis. Signal Transduction / physiology. Translocation, Genetic

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(PMID = 17119127.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / NF-kappa B; 0 / Oncogene Proteins, Viral

[Number-of-references] 96

   

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[Title] Nitric oxide levels during erythroid differentiation in K562 cell line.

This study was designed to investigate the possible role of NO during erythroid differentiation in K562 erythroleukemia cells.

The chronic myelogenous leukemia (K562) cell line can be triggered in culture to differentiate along the erythrocytic pathway, in response to a variety of stimulatory agents.

We investigated NOx (nitrate+nitrite) levels in uninduced (control) and hemin-induced K562 cell lysates during erythroid differentiation.

Our results showed that NO levels decreased significantly on fourth and sixth day both in hemin-induced and control cells; the decrease was, however, more in hemin-induced group than in control group.

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(PMID = 17133771.001).

[ISSN] 0301-1208

[Journal-full-title] Indian journal of biochemistry & biophysics

[ISO-abbreviation] Indian J. Biochem. Biophys.

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Chemical-registry-number] 0 / Hemoglobins; 0 / Nitrates; 0 / Nitrites; 31C4KY9ESH / Nitric Oxide; 743LRP9S7N / Hemin

   

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Primary effusion lymphoma (PEL) is an aggressive neoplasm caused by human herpes virus-8 infection, and is generally resistant to chemotherapy.

Hybrid liposomes, composed of dimyristoylphosphatidylcholine (DMPC) and polyoxyethylene (21) dodecyl ether (C12(EO)21) (HL-21), were rapidly accumulated in the membrane of PEL cells.

HL-21 also increased membrane fluidity of PEL cells, and induced caspase-3 activation along with cell death.

These results suggest that HL-21 should be an effective and attractive regent for PEL treatment.

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[Copyright] 2010 Elsevier Inc. All rights reserved.

(PMID = 20138834.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Liposomes; 0AWH8BFG9A / polidocanol; 30IQX730WE / Polyethylene Glycols; U86ZGC74V5 / Dimyristoylphosphatidylcholine

   

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BACKGROUND: Primary effusion lymphoma (PEL) represents a peculiar lymphoma infected with human herpesvirus 8 (HHV-8) and occurs predominantly in human immunodeficiency virus (HIV)-infected patients.

The aim of the present study was to evaluate the immunologic and virological parameters, including HHV-8 viremia, of 5 HIV-infected patients with PEL whose disease was diagnosed and treated at our institute.

Biological parameters, such as latent and lytic HHV-8 antigen levels, plasma HHV-8 load, Epstein-Barr virus plasma DNA load, HIV-1 load, and CD4 cell count, were assessed before treatment, during therapy, and at follow-up.

RESULTS: Four patients were treated with chemotherapy and highly active antiretroviral therapy (HAART), and 1 was treated with HAART alone; 3 of 5 patients reached complete remission.

HHV-8 levels decreased after therapy in 4 patients.

CONCLUSIONS: Our analysis demonstrates that HHV-8 can be detected in the plasma at the onset of PEL; its prognostic role needs to be explored.

CD4 cell count seems to be the most important indicator of progression of PEL.

[MeSH-minor] Adult. Anti-HIV Agents. CD4 Lymphocyte Count. Disease Progression. Female. Gene Expression Regulation, Viral. Herpesvirus 8, Human. Humans. Male. Viral Load. Viral Proteins / metabolism. Viremia

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(PMID = 15824995.001).

[ISSN] 1537-6591

[Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America

[ISO-abbreviation] Clin. Infect. Dis.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Viral Proteins

   

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[Title] Retroviral insertional activation of the Fli-3 locus in erythroleukemias encoding a cluster of microRNAs that convert Epo-induced differentiation to proliferation.

Friend erythroleukemia has been used as an excellent system for the identification and characterization of oncogenes and tumor suppressor genes involved in neoplastic transformation.

Using this model, we have isolated a novel integration site designated Fli-3, from a Friend murine leukemia virus (F-MuLV)-induced erythroleukemia.

The Fli-3 transcription unit is a murine homologue of the human gene C13orf25 that includes a region encoding the mir-17-92 miRNA cluster.

C13orf25 is the target gene of 13q31 chromosomal amplification in human B-cell lymphomas and other malignancies.

The erythroleukemias that have acquired either insertional activation or amplification of Fli-3 express higher levels of the primary or mature miRNAs derived from mir-17-92.

The ectopic expression of Fli-3 in an erythroblastic cell line switches erythropoietin (Epo)-induced differentiation to Epo-induced proliferation through activation of the Ras and PI3K pathways.

These findings highlight the potential of the Fli-3 encoding mir-17-92 in the development of erythroleukemia and its important role in hematopoiesis.

[MeSH-major] Cell Differentiation / drug effects. Erythropoietin / pharmacology. Friend murine leukemia virus / genetics. Leukemia, Erythroblastic, Acute / metabolism. Leukemia, Erythroblastic, Acute / pathology. MicroRNAs / genetics. Viral Proteins / metabolism

[MeSH-minor] Animals. Base Sequence. Cell Line. Cell Proliferation / drug effects. Gene Expression Regulation, Neoplastic. Gene Expression Regulation, Viral. Humans. Mice. Multigene Family. Mutagenesis, Insertional / genetics. Transcription, Genetic / genetics

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(PMID = 17586726.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MicroRNAs; 0 / Viral Proteins; 11096-26-7 / Erythropoietin

   

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Late-stage erythroid cells synthesize large quantities of haemoglobin, a process requiring the co-ordinated regulation of globin and haem synthesis as well as iron uptake.

In the present study, we investigated the role of the ERK (extracellular-signal-regulated kinase) and p38 MAPK (mitogen-activated protein kinase) signalling pathways in MEL (mouse erythroleukaemia) cell differentiation.

We found that treatment of HMBA (hexamethylene bisacetamide)-induced MEL cells with the ERK pathway inhibitor UO126 results in an increase in intracellular haem and haemoglobin levels.

The transcript levels of the genes coding for β(major)-globin, the haem biosynthesis enzyme 5-aminolevulinate synthase 2 and the mitochondrial iron transporter mitoferrin 1 are up-regulated.

Reporter assays showed that globin promoter and HS2 enhancer-mediated transcription was under the control of MAPKs, as inhibition of the ERK and p38 MAPK pathways led to increased and decreased gene activity respectively.

Our present results suggest that the ERK1/2 and p38α/β MAPKs play antagonistic roles in HMBA-induced globin gene expression and erythroid differentiation.

These results provide a novel link between MAPK signalling and the regulation of haem biosynthesis and iron uptake in erythroid cells.

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(PMID = 20738258.001).

[ISSN] 1470-8728

[Journal-full-title] The Biochemical journal

[ISO-abbreviation] Biochem. J.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / P01 HL032262; United States / NIDDK NIH HHS / DK / R01 DK070838; Canada / Canadian Institutes of Health Research / / MOP-79361

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole; 0 / Acetamides; 0 / Antineoplastic Agents; 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Hemoglobins; 0 / Imidazoles; 0 / Nitriles; 0 / Pyridines; 0 / U 0126; 42VZT0U6YR / Heme; 9004-22-2 / Globins; E1UOL152H7 / Iron; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; LA133J59VU / hexamethylene bisacetamide

   

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While vIL-6 is generally considered to be a lytic gene, several reports have noted its low-level expression in latently infected primary effusion lymphoma (PEL) cultures, in the absence of other lytic gene expression.

Knockdown of vIL-6 expression in PEL cells led to markedly reduced cell growth in normal culture, independently of extracellular cytokines.

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(PMID = 18987143.001).

[ISSN] 1098-5514

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA076445; United States / NCI NIH HHS / CA / R01-CA76445

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / IL6R protein, human; 0 / Interleukin-6; 0 / Receptors, Interleukin-6; 0 / Viral Proteins; 0 / interleukin-6, RRV-HHV-8; 133483-10-0 / Cytokine Receptor gp130

[Other-IDs] NLM/ PMC2612405

   

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[Title] First case of bacteremia due to chromosome-encoded CfxA3-beta-lactamase-producing Capnocytophaga sputigena in a pediatric patient with acute erythroblastic leukemia.

Bacteremia due to Capnocytophaga sputigena occurred in a 4-year and 9-month-old Japanese girl patient with acute erythroblastic leukemia in Shinshu University Hospital, Japan.

The causative Capnocytophaga sputigena isolate was found to be a beta-lactamase-producer demonstrating to possess cfxA3 gene.

The gene responsible for the production of CfxA3-beta-lactamase was proved to be chromosome-encoded, by means of southern hybridization analysis.

[MeSH-major] Bacteremia / microbiology. Capnocytophaga / isolation & purification. Chromosomes, Bacterial. Leukemia, Erythroblastic, Acute / complications. beta-Lactamases / biosynthesis

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(PMID = 18499560.001).

[ISSN] 0949-2321

[Journal-full-title] European journal of medical research

[ISO-abbreviation] Eur. J. Med. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Anti-Bacterial Agents; EC 3.5.2.6 / beta-Lactamases

   

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[Title] The M type K15 protein of Kaposi's sarcoma-associated herpesvirus regulates microRNA expression via its SH2-binding motif to induce cell migration and invasion.

The KSHV open reading frame K15 is a KSHV-specific gene encoding a transmembrane protein.

The two K15 alleles resemble the latent membrane protein 2A (LMP2A) gene of Epstein-Barr virus (EBV) in their genomic locations and protein topology.

K15 therefore appears to be a hybrid of a distant evolutionary relative of EBV LMP1 and LMP2A.

In this study, we show that K15M is latently expressed in KSHV-positive PEL cells and knockdown of K15M in PEL cells reduces cell motility.

[MeSH-minor] Cell Line, Tumor. Cell Migration Assays. Gene Knockdown Techniques. Humans. Intracellular Membranes / chemistry. Lysosomes / chemistry. NF-kappa B / biosynthesis

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(PMID = 18971265.001).

[ISSN] 1098-5514

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / K15 protein, Human herpesvirus 8; 0 / MIRN21 microRNA, human; 0 / MIRN31 microRNA, human; 0 / MicroRNAs; 0 / NF-kappa B; 0 / Viral Proteins

[Other-IDs] NLM/ PMC2612383

   

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A single nucleotide polymorphism (SNP) in the sickle beta-globin gene (beta(S)) leads to sickle cell anemia.

RNA interference (RNAi) uses small interfering (si)RNAs for sequence-specific gene silencing.

A beta(S) siRNA with position 10 of the guide strand designed to align with the targeted beta(S) SNP specifically silences beta(S) gene expression without affecting the expression of the gamma-globin or normal beta-globin (beta(A)) genes.

Specific beta(S) silencing was demonstrated by using a luciferase reporter and full-length beta(S) cDNA transfected into HeLa cells and mouse erythroleukemia cells, where it was expressed in the context of the endogenous beta-globin gene promoter and the locus control region enhancers.

When this strategy was used to target beta(E), silencing was not limited to the mutant gene but also targeted the normal beta(A) gene. siRNAs, mismatched with their target at position 10, guided mRNA cleavage in all cases except when two bulky purines were aligned.

The specific silencing of the beta(S)-globin gene, as compared with beta(E), as well as studies of silencing SNP mutants in other diseases, indicates that siRNAs developed to target a disease-causing SNP will be specific if the mutant residue is a pyrimidine and the normal residue is a purine.

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(PMID = 16585504.001).

[ISSN] 0027-8424

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / 5 T32 HL007556-19; United States / NHLBI NIH HHS / HL / P01 HL 055435-11; United States / NIAID NIH HHS / AI / U19 AI056900; United States / NIAID NIH HHS / AI / AI056900; United States / NHLBI NIH HHS / HL / P01 HL055435; United States / NHLBI NIH HHS / HL / T32 HL007556

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 9004-22-2 / Globins; EC 1.13.12.5 / Luciferases, Renilla

[Other-IDs] NLM/ PMC1458679

   

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[Title] Effect of occupational stress and anxiety on natural killer lymphocyte activity of men and women employed in a university.

The aim of this study is the immune response of the staff of a university and a museum (referent group).

Blood samples were collected for determining NK cytotoxic activity vs human erythroleukaemia cells and the lymphocyte subsets CD45+, CD45+-CD3+, CD45+-CD3+-CD4+, CD45+-CD3+-CD8+, CD45+-CD3-CD8+, CD3+-CD16+-56+ and CD3+-CD19+.

Group F of men showed higher levels of occupational stress and both STAI I and II than groups E and G.

The scores of STAI I and II were negatively correlated with the cytotoxic activity expressed per ml of blood and/or total lymphocytes. and/or NK CD45+-CD16+-CD56+ cells.

[MeSH-minor] Adult. Female. Humans. Lymphocyte Subsets. Male. Middle Aged. Universities

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(PMID = 17291412.001).

[ISSN] 0394-6320

[Journal-full-title] International journal of immunopathology and pharmacology

[ISO-abbreviation] Int J Immunopathol Pharmacol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

   

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The mucins, MUC5AC and MUC5B, contribute to the viscoelastic properties of mucus, and are found at elevated levels in the airways of individuals with chronic respiratory diseases.

The T helper type 2 cell cytokine, IL-13, is known to regulate MUC5AC expression in goblet cells of the airways, although much less is known about the regulation of MUC5B expression.

NRG1beta1-induced expression of MU5AC and MUC5B was shown to involve v-erb-b2 erythroblastic leukemia viral oncogene homolog (ErbB) and ErbB3 receptors, but not ErbB4 receptors.

[MeSH-major] Gene Expression Regulation. Goblet Cells / metabolism. Mucin 5AC / biosynthesis. Mucin-5B / biosynthesis. Neuregulin-1 / metabolism

[MeSH-minor] Animals. Cell Line. Cells, Cultured. Chronic Disease. Humans. Interleukin-13 / metabolism. Mice. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphorylation / drug effects. Protein Kinase Inhibitors / pharmacology. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-2 / metabolism. Receptor, ErbB-3 / metabolism. Receptor, ErbB-4. Respiration Disorders / metabolism. Th2 Cells / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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(PMID = 19556605.001).

[ISSN] 1535-4989

[Journal-full-title] American journal of respiratory cell and molecular biology

[ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-13; 0 / MUC5AC protein, human; 0 / MUC5B protein, human; 0 / Mucin 5AC; 0 / Mucin-5B; 0 / NRG1 protein, human; 0 / Neuregulin-1; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Erbb4 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases

   

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3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (EC1.1.1.88) inhibitors (statins) reduce cholesterol synthesis and prevent cardiovascular disease; they can also inhibit prenylation of Ras and Rho proteins, and have anti-neoplastic effects.

We found that the HMG-CoA reductase inhibitor lovastatin markedly induced the expression of RhoA, B, and C in human erythroleukemia (HEL) cells.

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(PMID = 17920041.001).

[ISSN] 0006-2952

[Journal-full-title] Biochemical pharmacology

[ISO-abbreviation] Biochem. Pharmacol.

[Language] ENG

[Grant] United States / NIAMS NIH HHS / AR / R01 AR051300-07; United States / NIAMS NIH HHS / AR / AR051300-07; United States / NIAMS NIH HHS / AR / AR051300-09; United States / NIAMS NIH HHS / AR / R01-AR051300; United States / NIAMS NIH HHS / AR / AR051300-08; United States / NHLBI NIH HHS / HL / 5T32-HL07261; United States / NIAMS NIH HHS / AR / R01 AR051300-09; United States / NHLBI NIH HHS / HL / T32 HL007261; United States / NIAMS NIH HHS / AR / R01 AR051300; United States / NIAMS NIH HHS / AR / R01 AR051300-08

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / ARHGDIA protein, human; 0 / Guanine Nucleotide Dissociation Inhibitors; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / RHOC protein, human; 0 / rho Guanine Nucleotide Dissociation Inhibitor alpha; 0 / rho-Specific Guanine Nucleotide Dissociation Inhibitors; 124671-05-2 / RHOA protein, human; 86-01-1 / Guanosine Triphosphate; 9LHU78OQFD / Lovastatin; EC 3.6.5.2 / rho GTP-Binding Proteins; EC 3.6.5.2 / rhoA GTP-Binding Protein; EC 3.6.5.2 / rhoB GTP-Binding Protein

[Other-IDs] NLM/ NIHMS37750; NLM/ PMC2228324