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It was determined that substitution at the C6-position of the benzo[b]thiophene core with a three-atom spacer yielded optimal HDAC1 inhibition and anti-proliferative activity in murine erythroleukemia (SC-9) cells.

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(PMID = 17576064.001).

[ISSN] 0960-894X

[Journal-full-title] Bioorganic & medicinal chemistry letters

[ISO-abbreviation] Bioorg. Med. Chem. Lett.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Thiophenes

   

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The measured gas concentrations were generally below the permissible exposure limits (PELs) established by the Occupational Safety and Health Administration (OSHA) throughout the year except for the NH3 concentrations in cold weather (December, January, and February).

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(PMID = 20437782.001).

[ISSN] 1096-2247

[Journal-full-title] Journal of the Air & Waste Management Association (1995)

[ISO-abbreviation] J Air Waste Manag Assoc

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 142M471B3J / Carbon Dioxide; 7664-41-7 / Ammonia; YY9FVM7NSN / Hydrogen Sulfide

   

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[Title] Gab1 transduces PI3K-mediated erythropoietin signals to the Erk pathway and regulates erythropoietin-dependent proliferation and survival of erythroid cells.

Knockdown of Gab1 by the introduction of the Gab1 siRNA expression vector into F-36P human erythroleukemia (F-36P-Gab1-siRNA) cells resulted in a reduction of cell proliferation and survival in response to EPO.

LY294002 inhibited EPO-induced tyrosine phosphorylation of Gab1 and its association with Grb2 in human primary EPO-sensitive erythroid cells.

Taken together, these results suggest that Gab1 couples PI3K-mediated EPO signals with the Ras/Erk pathway and that Gab1 plays an important role in EPOR-mediated signal transduction involved in the proliferation and survival of erythroid cells.

[MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Erythroid Cells / cytology. Erythropoietin / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Phosphatidylinositol 3-Kinases / metabolism

[MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Proliferation. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. GRB2 Adaptor Protein / metabolism. Gene Knockdown Techniques. Humans. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / metabolism. Leukemia, Erythroblastic, Acute / metabolism. Morpholines / pharmacology. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism. Receptors, Erythropoietin / metabolism. SOS1 Protein / metabolism

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(PMID = 19665053.001).

[ISSN] 1873-3913

[Journal-full-title] Cellular signalling

[ISO-abbreviation] Cell. Signal.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / GAB1 protein, human; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / Morpholines; 0 / Receptors, Erythropoietin; 0 / SOS1 Protein; 11096-26-7 / Erythropoietin; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11

   

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The development of a low-cost, simple colorimetric sensor array capable of the detection and identification of toxic gases is reported.

Striking visual identification of 3 toxic gases has been shown at the IDLH (immediately dangerous to life and health) concentration, at the PEL (permissible exposure level), and at a level well below the PEL.

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(PMID = 19918616.001).

[ISSN] 1364-5528

[Journal-full-title] The Analyst

[ISO-abbreviation] Analyst

[Language] ENG

[Grant] United States / NIEHS NIH HHS / ES / ES016011-03; United States / NIEHS NIH HHS / ES / U01 ES016011; United States / NIEHS NIH HHS / ES / U01 ES016011-03; United States / NIEHS NIH HHS / ES / U01ES016011

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

[Publication-country] England

[Chemical-registry-number] 0 / Air Pollutants; 0 / Coloring Agents; 0 / Gases; 0 / Membranes, Artificial; 0UZA3422Q4 / Sulfur Dioxide; 4R7X1O2820 / Chlorine; 7664-41-7 / Ammonia

[Other-IDs] NLM/ NIHMS229255; NLM/ PMC2947824

   

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Here we have used Friend murine leukemia virus (F-MuLV)-induced erythroleukemia to investigate factors of the splenic microenvironment that may make it fertile for the expansion and survival of malignant erythroblasts.

Cytokine protein arrays revealed that F-MuLV-infected splenocytes secreted elevated levels of interleukin-6 (IL-6), vascular endothelial growth factor-A (VEGF-A), macrophage chemoattractant protein-5 (MCP-5), soluble tumor necrosis factor receptor-1 (sTNFR1), IL-12p70, tumor necrosis factor-alpha (TNF-alpha), and IL-2 over normal splenocytes.

Furthermore, in vivo administration of a neutralizing antibody to VEGF-A extended survival times of erythroleukemic mice in comparison with controls.

These findings suggest that VEGF-A and MCP-5 are potentially pivotal paracrine mediators occurring within the diseased splenic microenvironment capable of promoting disease acceleration and expansion of erythroleukemic blasts.

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(PMID = 15701719.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA-41233

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

[Publication-country] United States

[Chemical-registry-number] 0 / Angiogenic Proteins; 0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Inflammation Mediators; 0 / Monocyte Chemoattractant Proteins; 0 / Vascular Endothelial Growth Factor A

[Other-IDs] NLM/ PMC1895028

   

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[Title] [Apoptosis induced by NNAMB, a novel polyamine conjugate, in human erythroleukemia K562 cells and its mechanism].

OBJECTIVE: To investigate the apoptosis-inducing effects of NNAMB, a novel polyamine conjugate, in erythroleukemia K562 cells and its molecular mechanism.

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(PMID = 19062712.001).

[ISSN] 0253-3766

[Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]

[ISO-abbreviation] Zhonghua Zhong Liu Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / Anthracenes; 0 / NNAMB compound; 0 / Polyamines; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; U87FK77H25 / Spermidine

   

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[Title] Sequences of polycythemia-type Friend spleen focus-forming virus in clone-745-derived mouse erythroleukemia cells.

Friend leukemia virus complex consists of a replication-competent virus plus one of two replication-incompetent viruses, spleen focus-forming virus anemia virus or spleen focus-forming virus polycythemia virus.

The replication-incompetent viruses induce rapid malignant transformation of erythroid precursor cells.

However, lines containing the anemia-type virus require erythropoietin and another agent such as dimethyl sulfoxide for optimal erythrodifferentiation, whereas those containing the polycythemia-type virus do not require or respond to erythropoietin.

Sequence analysis demonstrates that they contain the polycythemia-type virus and not the anemia-type virus.

[MeSH-minor] Animals. Cell Differentiation. Cell Line, Transformed. Leukemia, Experimental / virology. Mice. Molecular Sequence Data. RNA, Viral / genetics. Retroviridae Infections / virology. Sequence Analysis, RNA. Tumor Virus Infections / virology

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(PMID = 19347245.001).

[ISSN] 1432-8798

[Journal-full-title] Archives of virology

[ISO-abbreviation] Arch. Virol.

[Language] eng

[Databank-accession-numbers] GENBANK/ FJ556972/ FJ556973

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

[Publication-country] Austria

[Chemical-registry-number] 0 / RNA, Viral

   

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OBJECTIVE: The LIM-finger protein LMO2 forms a transcription factor complex with other hematopoietic regulator proteins, such as TAL1 (SCL), LDB1, GATA1, 2, and 3, in the promoters of several erythroid genes.

In vivo hematopoiesis in transgenic mice with wild-type and LIM-modified Lmo2 was studied morphologically and by measuring the progenitor cells in fetal liver.

Their effects on the erythroid differentiation of the dimethylsulfoxide (DMSO)-induced murine erythroleukemia (MEL) cells were evaluated.

Overexpression of wild-type LMO2 is known to have dominant negative inhibitory effects on erythropoietic development.

DMSO-induced erythroid differentiation of the MEL cells was inhibited by the overexpressed LMO2 with mutant LIM2 but not by the LMO2 with modified LIM1.

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(PMID = 15911088.001).

[ISSN] 0301-472X

[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 / Adaptor Proteins, Signal Transducing; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins

   

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These ultrasmall SWNTs are fabricated in the elliptical nanochannels of an AlPO-11 (AEL) single crystal.

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(PMID = 18764364.001).

[ISSN] 0031-9007

[Journal-full-title] Physical review letters

[ISO-abbreviation] Phys. Rev. Lett.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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The accumulation of Hsp70 and Hdj 1 in human erythroleukemia K562 cells was stimulated by heat stress (43 degrees C, 60 min).

The level of Hsp70 chaperone activity in cell extracts was estimated using original technique.

The results of the study indicate that Hsp70 chaperone activity is regulated by the level of its cochaperones, especially Hdj 1.

This finding confirms the possibility of using peptide approach for regulation of Hsp70 function at the cellular and organismal levels.

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(PMID = 16706166.001).

[ISSN] 0041-3771

[Journal-full-title] Tsitologiia

[ISO-abbreviation] Tsitologiia

[Language] rus

[Publication-type] Comparative Study; English Abstract; Journal Article

[Publication-country] Russia (Federation)

[Chemical-registry-number] 0 / BCL2-associated athanogene 1 protein; 0 / Culture Media; 0 / DNA-Binding Proteins; 0 / DNAJB1 protein, human; 0 / HSP40 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Transcription Factors; 8L70Q75FXE / Adenosine Triphosphate

   

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[Title] Exogenous wild-type p53 gene improved survival of nude mice injected with murine erythroleukemia cell line through amelioration of hemorheological changes.

OBJECTIVES: Previous investigations have shown that human wild-type p53 gene (WTp53) inhibits the growth of leukemia and tumor cells in vitro.

In the present study, the authors used nude mice and examined the therapeutic role of p53 gene for erythroleukemia in vivo in the absence of MHC effects.

METHODS: The nude mice were injected with murine erythroleukemia cells (MEL), MEL cells transfected with wild-type p53 gene (MEL-W), and MEL cells transfected with mutated p53 gene (MEL-M).

RESULTS: The results showed that WTp53 restrained the growth of erythroleukemia cells in vivo and reduced the erythroleukemia tumorigenesis in the microcirculation by improving the hemorheological and biophysical properties of MEL cells, which helped to prolong the life span of nude mice suffering from erythroleukemia.

CONCLUSION: These results contribute to our knowledge on the use of wild-type p53 gene for the treatment of erythroleukemia disease.

[MeSH-major] Leukemia, Erythroblastic, Acute / pathology. Leukemia, Erythroblastic, Acute / physiopathology. Tumor Suppressor Protein p53 / genetics

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(PMID = 17365670.001).

[ISSN] 1073-9688

[Journal-full-title] Microcirculation (New York, N.Y. : 1994)

[ISO-abbreviation] Microcirculation

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53

   

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We investigated whether human erythroleukemia (HEL) cells were able to bind, metabolise and transport the main endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG).

Indeed, 2-AG itself drove HEL cells towards megakaryocytic differentiation, as it enhanced expression of beta3 integrin subunit, a megakaryocyte/platelet surface antigen, and glycoprotein VI, a late marker of megakaryocytes; in parallel, it reduced the amount of messenger RNA encoding for glycophorin A, a marker of erythroid phenotype.

In addition, classical inducers of megakaryocyte differentiation reduced 2-AG synthesis (although they did not affect the binding efficiency of CB(2) receptors), suggesting that levels of this endocannabinoid may be critical for committing HEL cells towards the megakaryocytic lineage.

[MeSH-major] Arachidonic Acids / pharmacology. Cannabinoid Receptor Modulators / biosynthesis. Cannabinoid Receptor Modulators / pharmacology. Cell Differentiation / drug effects. Endocannabinoids. Gene Expression Regulation / drug effects. Glycerides / pharmacology. Megakaryocytes / metabolism

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(PMID = 18820887.001).

[ISSN] 0946-2716

[Journal-full-title] Journal of molecular medicine (Berlin, Germany)

[ISO-abbreviation] J. Mol. Med.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Arachidonic Acids; 0 / Cannabinoid Receptor Modulators; 0 / Endocannabinoids; 0 / Glycerides; 0 / Polyunsaturated Alkamides; 8D239QDW64 / glyceryl 2-arachidonate; UR5G69TJKH / anandamide

   

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Primary effusion lymphoma (PEL) is a rare B-cell lymphoma caused by Kaposi's sarcoma-associated herpesvirus (KSHV).

PEL is poorly responsive to standard cytotoxic chemotherapy and portends a poor survival.

It is known that KSHV encodes two lytic genes, ORF36 (phosphotransferase) and KSHV ORF21 (thymidine kinase), which can phosphorylate ganciclovir and azidothymidine, respectively.

Here, we have explored whether these genes can be used as therapeutic targets for PEL.

PEL arises in pleural spaces and other effusions that provide a hypoxic environment.

Based on Northern blot analysis, exposure of PEL cells to hypoxia up-regulated the expression of both ORF36 and ORF21.

Using a newly developed nonradioactive reverse-phase high-performance liquid chromatography/mass spectrometry method to separate and quantify the phosphorylated forms of ganciclovir and azidothymidine, we found that PEL cells exposed to hypoxia produced increased amounts of the toxic triphosphates of these drugs.

Moreover, we found that hypoxia increased the cell toxicity of ganciclovir and azidothymidine in PEL cells but had no significant effect on the herpesvirus-negative cell line CA46.

These findings may have clinical applicability in the development of effective therapies for PEL or other KSHV-related malignancies.

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(PMID = 17638913.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / Intramural NIH HHS / /

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antiviral Agents; 4B9XT59T7S / Zidovudine; P9G3CKZ4P5 / Ganciclovir

   

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The mean concentration of silica before 1986 was an extremely high level of 8.6 mg/m(3), and then remarkably dropped after 1986, with the level of 2.4 mg/m(3) from 1986 to 1989, 2.7 mg/m(3) from 1990 to 2002 and 2.7 mg/m(3) from 2003 to 2008.

Silica concentrations among jobs were significantly different, with highest level in melting (4.4 mg/m(3)), followed by cast shakeout and finishing (3.4 mg/m(3)), pouring (3.4 mg/m(3)), sand preparation (2.4 mg/m(3)), moulding (2.1 mg/m(3)) and core-making (1.7 mg/m(3)).

Mean concentration of asbestos dust in melting was a relative high level of 2.0 mg/m(3).

Benzene and its homologues existed in cast shakeout and finishing, and the level of benzene, toluene, xylene was 0.2 mg/m(3), 0.1 mg/m(3) and 1.3 mg/m(3), respectively.

Mean concentration of benzo(a) pyrene was a low level of 1.80 x 10(-4) microg/m(3).

Intensity of heat stress was high in melting, pouring and cast shakeout and finishing, with the level of 30 degrees C, 29 degrees C and 26 degrees C, respectively.

Noise was high in cast shakeout and finishing and core-making, with the level of 93.1 dB(A) and 89.5 dB(A), respectively.

CONCLUSION: Occupational hazards in environment of the foundry are diversified and their concentrations exceed permissible exposure limits stipulated by the national occupational hygienic standards.

[MeSH-major] Dust / analysis. Hazardous Substances / analysis. Occupational Exposure

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(PMID = 20465956.001).

[ISSN] 1001-9391

[Journal-full-title] Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases

[ISO-abbreviation] Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Dust; 0 / Hazardous Substances

   

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This analysis highlighted both known differences in serum and citrated plasma such as fibrinogens, and reproducible differences in peptide abundances from proteins such as soluble activin receptor-like kinase 7b and glycoprotein m6b.

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(PMID = 16052625.001).

[ISSN] 1615-9853

[Journal-full-title] Proteomics

[ISO-abbreviation] Proteomics

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / P41 RR018522; United States / NCI NIH HHS / CA / CA78722; United States / NCRR NIH HHS / RR / RR18522

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Blood Proteins; 0 / Ions; 0 / Peptides; 0 / Proteins; 0 / Proteome; 9001-32-5 / Fibrinogen; EC 3.4.21.4 / Trypsin

[Other-IDs] NLM/ NIHMS15646; NLM/ PMC2041806

   

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[Title] Schizophrenia is not associated with the ERBB3 gene in a Han Chinese population sample: Results from case-control and family-based studies.

ERBB3 (v-erb-b2 erythroblastic leukemia viral oncogene homolog 3), encoding a receptor of neuregulin-1 (NRG1), has been considered a functional candidate gene for schizophrenia susceptibility.

In order to investigate a relationship between ERBB3 gene and schizophrenia in the Chinese population, case-control and family-based studies were carried out in 470 cases matched by controls, and in 532 family trios.

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(PMID = 21637446.001).

[ISSN] 1678-4685

[Journal-full-title] Genetics and molecular biology

[ISO-abbreviation] Genet. Mol. Biol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Brazil

[Other-IDs] NLM/ PMC3036886

[Keywords] NOTNLM ; ERBB3 gene / schizophrenia

   

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Primary effusion lymphoma (PEL) is a rare type of lymphoma related to herpesvirus-8 (HHV-8), and considered an AIDS-defining condition.

The authors describe a case of PEL with cardiac involvement occurring in an HIV-positive patient treated with HAART and chemotherapy, who achieved complete remission and long survival.

[MeSH-major] Antiretroviral Therapy, Highly Active. HIV Infections / complications. HIV Infections / drug therapy. HIV Long-Term Survivors. Heart Neoplasms / secondary. Lymphoma, Primary Effusion / complications. Lymphoma, Primary Effusion / diagnosis

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(PMID = 18845471.001).

[ISSN] 1386-6532

[Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology

[ISO-abbreviation] J. Clin. Virol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Netherlands

   

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[Title] Comparison of childhood myelodysplastic syndrome, AML FAB M6 or M7, CCG 2891: report from the Children's Oncology Group.

BACKGROUND: Myelodysplastic syndromes (MDS), acute erythroleukemia (FAB M6), and acute megakaryocytic leukemia (FAB M7) have overlapping features.

PROCEDURE: Children without Down syndrome or acute promyelocytic leukemia who were newly diagnosed with primary myelodysplastic syndrome or acute myeloid leukemia (AML) M6 or M7 were compared to children with de novo AML M0-M5.

RESULTS: The presentation and outcomes of the 132 children diagnosed with MDS (60 children), AML FAB M6 (19 children), or AML FAB M7 (53 children) were similar.

Children with AML FAB M7 were diagnosed at a significantly younger age (P = 0.001).

Children with MDS, M6, or M7 had significantly lower white blood cell (WBC) counts (P = 0.001), lower peripheral blast counts (P < 0.001), and an increased frequency of -7/7q- (P = 0.003) at presentation.

All three groups had significantly inferior overall survival (OS) (P < 0.001) and event free survival (P < 0.001) compared with the 748 children diagnosed with AML FAB M0-M5 when assessed from entry on study.

However, when assessed from successful completion of induction therapy, the 5-year OS (P = 0.090)(49.1 vs. 56.9%) and disease-free survival (DFS) (P = 0.113)(38.0 vs. 46.3%) therapy were not significantly different from other children with AML.

CONCLUSIONS: Childhood AML FAB M6 and AML M7 resemble MDS in presentation, poor induction success rates, and outcomes.

[MeSH-major] Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis

[MeSH-minor] Acute Disease. Child. Child, Preschool. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Male. Prognosis. Remission Induction. Survival Rate. Treatment Outcome

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(PMID = 16856158.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

   

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METHODS AND RESULTS: Effects of selected cytokines and growth factors on megakaryocyte expression of FcgammaRIIa were assessed with phorbol 12-myristate 13-acetate (PMA)-differentiated human erythroleukemia (HEL) cells and with thrombopoietin-differentiated CD34 stem cells and compared with those obtained with myelocytic cell lines and a monocytic cell lines.

This effect of IFNgamma may contribute to greater platelet expression of FcgammaRIIa in patients with atherosclerotic vascular disease.

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(PMID = 19372459.001).

[ISSN] 1524-4636

[Journal-full-title] Arteriosclerosis, thrombosis, and vascular biology

[ISO-abbreviation] Arterioscler. Thromb. Vasc. Biol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Fc gamma receptor IIA; 0 / Receptors, IgG; 82115-62-6 / Interferon-gamma

   

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The WW domain containing E3 ubiquitin protein ligase 1 (WWP1) is a homologous to the E6-associated protein C terminus-type E3 ligase frequently overexpressed in human prostate and breast cancers due to gene amplification.

Here, we showed that WWP1 upregulates and maintains erythroblastic leukemia viral oncogene homolog 2 (ErbB2) and epithelial growth factor receptor (EGFR) in multiple cell lines.

[MeSH-major] Genes, erbB-2. Receptor, Epidermal Growth Factor / genetics. Receptor, ErbB-2 / genetics. Ubiquitin-Protein Ligases / metabolism

[MeSH-minor] Breast Neoplasms / genetics. Breast Neoplasms / pathology. Carrier Proteins / genetics. Carrier Proteins / physiology. Cell Division. Cell Line, Tumor. Cell Survival. Epidermal Growth Factor / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. Female. Gene Amplification. Gene Deletion. Gene Expression Regulation, Neoplastic. Humans. Male. Phosphorylation. Prostatic Neoplasms / genetics. Prostatic Neoplasms / pathology

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(PMID = 18724389.001).

[ISSN] 1476-5594

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Carrier Proteins; 0 / RNF11 protein, human; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / WWP1 protein, human

   

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The application of this method was tested on ubiquitin-protein conjugates in the brains of Niemann-Pick type C disease mouse and in heat-shocked K562 erythroleukemia cells.

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(PMID = 18358228.001).

[ISSN] 1096-0309

[Journal-full-title] Analytical biochemistry

[ISO-abbreviation] Anal. Biochem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Detergents; 0 / Membrane Proteins; 0 / Npc1 protein, mouse; 0 / Proteins; 0 / Ubiquitin; 0 / flotillins; 368GB5141J / Sodium Dodecyl Sulfate

   

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Importantly, during latency, only a small number of viral encoded genes are expressed.

This viral gene expression pattern contributes to the establishment of long-term infection as well as the ability of the virus to evade the immune system.

Previous studies have been shown that the replication and transcription activator (RTA) encoded by ORF50 activates it downstream genes and initiates viral lytic reactivation through functional interaction with RBP-Jkappa, the major downstream effector of the Notch signaling pathway.

This indicates that RTA can usurp the conserved Notch signaling pathway and mimic the activities of intracellular Notch1 to modulate gene expression.

In this report, we show that the activated intracellular domain of Notch1 (ICN) is aberrantly accumulated in KSHV latently infected pleural effusion lymphoma (PEL) cells.

[MeSH-minor] B-Lymphocytes. Cell Line. Gene Expression Regulation, Viral. Humans. Promoter Regions, Genetic. Protein Binding. Sarcoma, Kaposi / metabolism. Sarcoma, Kaposi / virology. Transcriptional Activation

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(PMID = 16701788.001).

[ISSN] 0042-6822

[Journal-full-title] Virology

[ISO-abbreviation] Virology

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA 072510; United States / NCI NIH HHS / CA / CA 091792; United States / NIDCR NIH HHS / DE / DE 01436

[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 / Receptor, Notch1

   

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Primary effusion lymphoma (PEL) is a Human Herpesvirus-8 (HHV-8)-associated tumor, which releases several cytokines such as IL-6, IL-10 and VEGF and its growth seems to be dependent on them in vitro or in vivo.

The iDC obtained in the presence of PEL supernatants showed reduction of FITC-dextran uptake, reduction of MLR allostimulatory activity and altered expression of surface molecules, suggesting that cytokines released by PEL adversely affect DC differentiation.

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(PMID = 18680763.001).

[ISSN] 0165-2478

[Journal-full-title] Immunology letters

[ISO-abbreviation] Immunol. Lett.

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Cytokines

   

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The characterization of exposure was conducted by means of an extensive survey of several persistent organic pollutants (PAHs, PCBs, DDTs, PBDEs, HCHs, HCB) measured in seven core sediments from the Sunderban wetlands, obtaining a dataset with more than 2200 analyses.

The three different approaches chosen for risk assessment of the Sunderban were the consensus SQGs obtained by TEC (threshold effect concentration), PEC (probable effect concentration) and EEC (extreme effect concentration), the threshold/probable effect level (TEL/PEL) approach and, finally, the ERL-ERM guidelines, including the m-ERM-Q (mean ERM quotient).

A different sensitivity for toxicity assessment due to quality guidelines was obtained, as the consensus SQGs based on TEC were less conservative and protective than the TEL and ERL approaches, while the use of m-ERM-Q seems to be the most powerful tool to predict the toxicity related to a contaminant mixture.

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(PMID = 18718633.001).

[ISSN] 1879-1298

[Journal-full-title] Chemosphere

[ISO-abbreviation] Chemosphere

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Soil Pollutants; 0 / Water Pollutants, Chemical

   

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NK cells are large granular lymphocytes that represent a critical component of the innate immunity.

Significant numbers of CD56dimCD16+ cytotoxic and CD56-CD16+ immature NK cells appeared in peripheral blood (PB), peritoneal cavity, spleen, bone marrow and liver of the mice.

The NOD/SCID mice engrafted with human NK cells exhibited antitumor activity against K562 erythroleukemia in vitro and in vivo.

[MeSH-minor] Animals. Cell Death / immunology. Cell Line, Tumor. Cells, Cultured. Fetal Blood / cytology. Fetal Blood / transplantation. GPI-Linked Proteins. Humans. Immunity, Innate. K562 Cells. Lymphocyte Activation / immunology. Mice. Mice, Inbred NOD. Mice, SCID. Transduction, Genetic

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(PMID = 16304638.001).

[ISSN] 0014-2980

[Journal-full-title] European journal of immunology

[ISO-abbreviation] Eur. J. Immunol.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, CD; 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / Receptors, IgG

   

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[Title] Kaposi's sarcoma-associated herpesvirus/human herpesvirus type 8-positive solid lymphomas: a tissue-based variant of primary effusion lymphoma.

Kaposi's sarcoma-associated herpesvirus (KSHV), also termed human herpesvirus type 8, is consistently identified in Kaposi's sarcoma, primary effusion lymphoma (PEL), and multicentric Castleman's disease.

All KSHV-positive solid lymphomas exhibited PEL-like cell morphology.

To investigate the relationship of these disorders to PEL and to other AIDS-associated diffuse large cell lymphomas, KSHV-positive solid lymphomas were tested for the expression of a set of genes that were previously shown by gene profiling analysis to define PEL tumor cells.

The results showed that expression of this set of genes in KSHV-positive lymphomas is similar to that of PEL but distinct from KSHV-negative AIDS-associated diffuse large cell lymphomas.

Because pathobiological features of KSHV-positive solid lymphomas closely mimic those of PEL, our results suggest that KSHV-positive solid lymphomas should be considered as a tissue-based variant of classical PEL, irrespective of HIV status.

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(PMID = 15681470.001).

[ISSN] 1525-1578

[Journal-full-title] The Journal of molecular diagnostics : JMD

[ISO-abbreviation] J Mol Diagn

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA037295; United States / NCI NIH HHS / CA / R37 CA037295; United States / NCI NIH HHS / CA / CA-37295

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

[Publication-country] United States

[Other-IDs] NLM/ PMC1876263

   

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[Title] A chemosensory system that regulates biofilm formation through modulation of cyclic diguanylate levels.

Mutations in a gene called wspF, part of a putative chemosensory signal-transduction operon, have been shown to result in cell aggregation and altered colony morphology.

The WspF phenotypes depend on the presence of WspR, which is a member of a family of signal transduction proteins known as response regulators.

WspR contains a GGDEF domain known to catalyze formation of a cytoplasmic signaling molecule cyclic diguanylate (c-diGMP).

We observed increased cellular levels of c-diGMP and increased biofilm formation in a wspF mutant.

Expression of a protein predicted to catalyze degradation of c-diGMP reversed the phenotypes of a wspF mutant and inhibited biofilm initiation by wild-type cells, indicating that the presence of c-diGMP is necessary for biofilm formation.

A transcriptome analysis showed that expression levels of at least 560 genes were affected by a wspF deletion.

The psl and pel operons, which are involved in exopolysaccharide production and biofilm formation, were expressed at high levels in a wspF mutant.

Together, the data suggest that the wsp signal transduction pathway regulates biofilm formation through modulation of cyclic diguanylate levels.

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(PMID = 16186483.001).

[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 / NIGMS NIH HHS / GM / R01 GM056665; United States / NIGMS NIH HHS / GM / GM056665

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

[Publication-country] United States

[Chemical-registry-number] 0 / Bacterial Proteins; 147336-22-9 / Green Fluorescent Proteins; 61093-23-0 / bis(3',5')-cyclic diguanylic acid; H2D2X058MU / Cyclic GMP

[Other-IDs] NLM/ PMC1234902

   

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[Title] Expression profiling of formalin-fixed paraffin-embedded primary breast tumors using cancer-specific and whole genome gene panels on the DASL® platform.

BACKGROUND: The cDNA-mediated Annealing, extension, Selection and Ligation (DASL) assay has become a suitable gene expression profiling system for degraded RNA from paraffin-embedded tissue.

We examined assay characteristics and the performance of the DASL 502-gene Cancer Panel v1 (1.5K) and 24,526-gene panel (24K) platforms at differentiating nine human epidermal growth factor receptor 2- positive (HER2+) and 11 HER2-negative (HER2-) paraffin-embedded breast tumors.

Unequal-variance t-statistics tested for differences in expression levels between HER2 + and HER2 - tumors.

Inter-panel correlations of expression values for the common 498 genes across the two panels ranged between 0.485-0.573.

In both panels, erythroblastic leukemia viral oncogene homolog 2 (ERBB2) was the most differentially expressed gene between the HER2 + and HER2 - tumors and seven additional genes had p-values < 0.05 and log2 -fold changes > |0.5| in expression between HER2 + and HER2 - tumors: topoisomerase II alpha (TOP2A), cyclin a2 (CCNA2), v-fos fbj murine osteosarcoma viral oncogene homolog (FOS), wingless-type mmtv integration site family, member 5a (WNT5A), growth factor receptor-bound protein 7 (GRB7), cell division cycle 2 (CDC2), and baculoviral iap repeat-containing protein 5 (BIRC5).

The top 52 discriminating probes from the 24K panel are enriched with genes belonging to the regulatory networks centered around v-myc avian myelocytomatosis viral oncogene homolog (MYC), tumor protein p53 (TP53), and estrogen receptor α (ESR1).

Network analysis with a two-step extension also showed that the eight discriminating genes common to the 1.5K and 24K panels are functionally linked together through MYC, TP53, and ESR1.

CONCLUSIONS: The relative RNA abundance obtained from two highly differing density gene panels are correlated with eight common genes differentiating HER2 + and HER2 - breast tumors.

Network analyses demonstrated biological consistency between the 1.5K and 24K gene panels.

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(PMID = 21172013.001).

[ISSN] 1755-8794

[Journal-full-title] BMC medical genomics

[ISO-abbreviation] BMC Med Genomics

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA129949; United States / NCI NIH HHS / CA / CA129949; United States / NCI NIH HHS / CA / CA150083

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

[Publication-country] England

[Chemical-registry-number] EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2

[Other-IDs] NLM/ PMC3022545

   

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[Title] PU.1 directly regulates cdk6 gene expression, linking the cell proliferation and differentiation programs in erythroid cells.

Most leukemia cells are blocked from undergoing terminal differentiation and also exhibit uncontrolled proliferation.

Dysregulated expression of transcription factor PU.1 is strongly associated with Friend virus-induced erythroleukemia.

PU.1 inhibits erythroid differentiation by binding to and inhibiting GATA-1.

PU.1 also may be involved in controlling proliferation of erythroid cells.

We reported previously that the G(1) phase-specific cyclin-dependent kinase 6 (CDK6) also blocks erythroid differentiation.

We now report that PU.1 directly stimulates transcription of the cdk6 gene in both normal erythroid progenitors and erythroleukemia cells, as well as in macrophages.

We propose that PU.1 coordinates proliferation and differentiation in immature erythroid cells by inhibiting the GATA-1-mediated gene expression program and also by regulating expression of genes that control progression through the G(1) phase of the cell cycle, the period during which the decision to differentiate is made.

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(PMID = 19955566.001).

[ISSN] 1083-351X

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

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01 HL078381; United States / NCI NIH HHS / CA / 2P30CA13330; United States / NHLBI NIH HHS / HL / HL078381; United States / NIGMS NIH HHS / GM / 5T32GM07288; United States / NIGMS NIH HHS / GM / T32 GM007288

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

[Publication-country] United States

[Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; EC 2.7.11.22 / Cdk6 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 6

[Other-IDs] NLM/ PMC2823399

   

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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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The rationale for this study is based on the observation that alteration of gene transcription represents a very promising approach to control the expression of selected genes and could be obtained using different molecules acting on the interactions between DNA and transcription factors (TFs).

Antiproliferative activity was assayed on different human cell lines, including erythroleukemia K562, B-lymphoid Raji, T-lymphoid Jurkat and erythroleukemia HEL cell lines.

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(PMID = 16789890.001).

[ISSN] 1573-4064

[Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))

[ISO-abbreviation] Med Chem

[Language] eng

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

[Publication-country] United Arab Emirates

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Transcription Factors; 9007-49-2 / DNA

   

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Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma (PEL), and multicentric Castleman's disease.

We screened multiple TLR agonists for their ability to initiate KSHV replication in latently infected PEL.

Agonists specific for TLR7/8 reactivated latent KSHV and induced viral lytic gene transcription and replication.

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(PMID = 19564611.001).

[ISSN] 1091-6490

[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 / NCI NIH HHS / CA / R01 CA109232; United States / NIDCR NIH HHS / DE / DE018281-03; United States / NIAID NIH HHS / AI / T32 AI007419; United States / NIDCR NIH HHS / DE / R01 DE018304-02; United States / NCI NIH HHS / CA / T32 CA009156; United States / NIDCR NIH HHS / DE / R01 DE018281-03; United States / NIDCR NIH HHS / DE / DE018304-01; United States / NIDCR NIH HHS / DE / R01 DE018304; United States / NIDCR NIH HHS / DE / R01 DE018304-01; United States / NIDCR NIH HHS / DE / R01 DE018304-03; United States / NIDCR NIH HHS / DE / DE018304-02; United States / NIDCR NIH HHS / DE / DE018304-03; United States / NIDCR NIH HHS / DE / R01 DE018281; United States / NIAID NIH HHS / AI / F32 AI078735; United States / NCI NIH HHS / CA / R01 CA096500

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8

[Other-IDs] NLM/ PMC2710638

   

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[Title] Decursin and PDBu: two PKC activators distinctively acting in the megakaryocytic differentiation of K562 human erythroleukemia cells.

Phorbol 12,13-dibutyrate (PDBu) induces the megakaryocytic differentiation of K562 human erythroleukemia cells through PKC activation.

All these results indicate that decursin and phorbol ester are PKC activators distinctively acting in megakaryocytic differentiation and PKC modulation in K562 leukemia cells.

[MeSH-major] Cell Differentiation. Leukemia, Erythroblastic, Acute / pathology. Megakaryocytes / pathology. Phorbol 12,13-Dibutyrate / pharmacology. Protein Kinase C / metabolism. Pyranocoumarins / pharmacology

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(PMID = 15992925.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzopyrans; 0 / Butyrates; 0 / Pyranocoumarins; 37558-16-0 / Phorbol 12,13-Dibutyrate; 5928-25-6 / decursin; EC 2.7.11.13 / Protein Kinase C

   

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Sampling, detection, identification, and quantitation of all compounds were readily achieved in times of less than 2 min, with detection limits ranging from 800 parts per trillion to 3 parts per million depending on the analyte.

For all but one analyte, detection limits were well below (3.5-130 times below) permissible exposure limits.

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(PMID = 18181580.001).

[ISSN] 0003-2700

[Journal-full-title] Analytical chemistry

[ISO-abbreviation] Anal. Chem.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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Primers of multiplex PCR were designed to amplify specific regions of the EBV EBNA1, CMV IE2, and KSHV LANA genes.

To assess diagnostic and pre-clinical applications with this method, we utilized KSHV-positive primary effusion lymphoma (PEL) cells, EBV-positive Burkitt's lymphoma cells, CMV-infected fibroblast cells, and clinically prepared peripheral blood leukocytes (PBLs) that had been infected with viruses.

[MeSH-minor] Blood Donors. Cell Line. Cytomegalovirus Infections / diagnosis. Cytomegalovirus Infections / epidemiology. Cytomegalovirus Infections / virology. DNA, Viral / analysis. Epstein-Barr Virus Infections / diagnosis. Epstein-Barr Virus Infections / epidemiology. Epstein-Barr Virus Infections / virology. Prevalence. Sarcoma, Kaposi / diagnosis. Sarcoma, Kaposi / epidemiology. Sarcoma, Kaposi / virology. Sensitivity and Specificity

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[Copyright] (c) 2006 Wiley-Liss, Inc.

(PMID = 17063511.001).

[ISSN] 0146-6615

[Journal-full-title] Journal of medical virology

[ISO-abbreviation] J. Med. Virol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Viral

   

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Sequencing of c-Myc coding sequences revealed that c-Myc in KSHV-positive primary effusion lymphoma (PEL) cell lines is wild type in the N-terminal region that regulates c-Myc protein stability.

Despite this, c-Myc in PEL cells is stabilized.

We now show that LANA increases the level of phosphorylated extracellular signal-regulated kinase 1 (ERK1) and increases ERK phosphorylation of c-Myc on Ser62.

LANA-mediated manipulation of c-Myc function is likely to contribute to KSHV-associated tumorigenesis through the induction of c-Myc regulated cellular genes, as well as by the stimulation of cell cycle progression.

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(PMID = 17634226.001).

[ISSN] 0022-538X

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P01 CA113239

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Viral; 0 / MYC protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Ubiquitin; 0 / latency-associated nuclear antigen; 2ZD004190S / Threonine; 452VLY9402 / Serine; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.26 / Glycogen Synthase Kinase 3

[Other-IDs] NLM/ PMC2045471

   

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[Title] Epigenetic alteration of the NF-κB-inducing kinase (NIK) gene is involved in enhanced NIK expression in basal-like breast cancer.

Basal-like breast cancers are triple-negative (estrogen receptor negative, progesterone receptor negative, erythroblastic leukemia viral oncogene homolog 2 (ERBB2) negative) tumors with an aggressive clinical behavior that lacks effective molecular targets for therapy.

Here, we report that enhanced NIK expression, which is exclusively observed in the basal-like subtype rather than the luminal-like subtype or non-tumorigenic mammary epithelial cells, is caused by epigenetic alteration of the NIK gene.

However, histone H3 acetylation levels were up-regulated in the basal-like subtype.

Thus, NIK and genes induced by the NIK-mediated constitutive NF-κB activation could be therapeutic targets of basal-like breast cancer.

[MeSH-major] Breast Neoplasms / genetics. Epigenesis, Genetic. Gene Expression Regulation, Neoplastic / genetics. Protein-Serine-Threonine Kinases / genetics

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[Copyright] © 2010 Japanese Cancer Association.

(PMID = 20735436.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histones; 0 / NF-kappa B; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 614OI1Z5WI / Valproic Acid; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.25 / NF-kappa B kinase; M801H13NRU / Azacitidine

   

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[Title] Glycolytic inhibition by mutation of pyruvate kinase gene increases oxidative stress and causes apoptosis of a pyruvate kinase deficient cell line.

OBJECTIVE: SLC3 is a Friend erythroleukemic cell line established from the Pk-1(slc) mouse, a mouse model of red blood cell type-pyruvate kinase (R-PK) deficiency.

DNA microarray analysis was performed to examine gene-expression profiles between the two transfectants and parental SLC3.

The forced expression of R-PK significantly decreased cells at the sub G0/G1 stage in an expression-level dependent manner.

Microarray analysis showed that proapoptotic genes, such as Bad, Bnip3, and Bnip3l, were downregulated in the transfectants.

In addition, peroxiredoxin 1 (Prdx1) and other antioxidant genes, such as Cat, Txnrd1, and Glrx1 were also downregulated.

CONCLUSION: These results indicated that glycolytic inhibition by R-PK gene mutation augmented oxidative stress in the Friend erythroleukemia cell, leading to activation of hypoxia-inducible factor-1 as well as downstream proapoptotic gene expression.

Thus, R-PK plays an important role as an antioxidant during erythroid differentiation.

[MeSH-minor] Animals. Apoptosis. Cell Line. Cell Line, Tumor. Erythrocytes / enzymology. Flow Cytometry. Genetic Predisposition to Disease. Leukemia, Erythroblastic, Acute. Mice. Oligonucleotide Array Sequence Analysis

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(PMID = 17662887.001).

[ISSN] 0301-472X

[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] EC 2.7.1.40 / Pyruvate Kinase

   

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[Title] Activation of Prn-p gene and stable transfection of Prn-p cDNA in leukemia MEL and neuroblastoma N2a cells increased production of PrP(C) but not prevented DNA fragmentation initiated by serum deprivation.

We observed that murine erythroleukemia (MEL) cells arrested in phase G(1) undergo transcriptional activation of Prn-p gene.

Here, we explored the potential role of activation of Prn-p gene and cytosolic accumulation of PrP(C) in growth arrest, differentiation, and apoptotic DNA fragmentation by stably transfecting MEL and N2a cells with Prn-p cDNA.

Our results indicate that (a) Induction of terminal differentiation of stably transfected MEL cells led to growth arrest, activation of Prn-p gene, concomitant expression of transfected Prn-p cDNA, suppression of bax gene, cytosolic accumulation of PrP(C), and DNA fragmentation.

(b) similarly, serum deprivation promoted growth arrest, apoptosis/necrosis associated with DNA fragmentation in parental N2a and N2a13 cells that produced relative high level of PrP(C) and not PrP(SC).

These data indicate that activation of Prn-p gene and expression of transfected Prn-p cDNA in cells of both hematopoietic and neuronal origin occurred concomitantly, and led to cytosolic accumulation of PrP(C) and DNA damage induced by serum deprivation.

[MeSH-major] Apoptosis. DNA Fragmentation. Leukemia, Erythroblastic, Acute / metabolism. Neuroblastoma / metabolism. PrPC Proteins / biosynthesis. Prions / biosynthesis. Transcriptional Activation

[MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Proliferation. Culture Media, Serum-Free / metabolism. Cytosol / metabolism. Dimethyl Sulfoxide / pharmacology. Flow Cytometry. Gene Expression Regulation, Neoplastic. Mice. RNA, Messenger / biosynthesis. Time Factors. Transfection. Up-Regulation. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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[Copyright] (c) 2007 Wiley-Liss, Inc.

(PMID = 17186498.001).

[ISSN] 0021-9541

[Journal-full-title] Journal of cellular physiology

[ISO-abbreviation] J. Cell. Physiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Bax protein, mouse; 0 / Culture Media, Serum-Free; 0 / PrPC Proteins; 0 / Prions; 0 / Prnp protein, mouse; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; YOW8V9698H / Dimethyl Sulfoxide

   

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Primary effusion lymphoma (PEL) is a rare lymphoma of B-cell origin, developed in serous cavities.

PEL tumor cells are latently infected with Kaposi sarcoma-associated herpesvirus (KSHV) and in most cases co-infected with Epstein-Barr virus (EBV).

In 15 primary PEL tumors including 10 EBV-positive cases, we analyzed the fused terminal repeat (TR) regions of KSHV episomes using pulsed-field gel electrophoresis and Southern blot.

On the same genomic DNA samples, the cellular clonality was assessed by Southern blot and PCR detection of monoclonal immunoglobulin heavy chain (IGH) VDJ gene rearrangements, associated in the EBV-infected cases, with Southern blot analysis of the fused termini of EBV episomes.

Monoclonal IGH gene rearrangements were detected in 13 tumors using Southern blot, in 11 cases using PCR, and in all cases considering both methods.

However, only 5 PEL tumors were found to be monoclonally infected with KSHV.

We hypothesized that the apparent discrepancy between viral and cellular clonalities in PEL might be due to several phenomena including complex mechanisms of genomic recircularization, insertion of duplicated sequences into the TR region and simultaneous infection of tumor cells with defective KSHV variants.

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[Copyright] Copyright 2005 Wiley-Liss, Inc.

[CommentIn] Int J Cancer. 2006 Oct 1;119(7):1746-8; author reply 1749-50 [16671085.001]

(PMID = 15700304.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Immunoglobulin Heavy Chains

   

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[Title] Quantitative determination of hexamethylene diisocyanate (HDI), 2,4-toluene diisocyanate (2,4-TDI) and 2,6-toluene diisocyanate (2,6-TDI) monomers at ppt levels in air by alkaline adduct coordination ionspray tandem mass spectrometry.

Once sensitized, some workers could react to isocyanate monomers at concentrations below 1% of the Permissible Exposure Limit of 5 ppb in air.

Currently available methods are not sufficiently sensitive to adequately evaluate isocyanates present at these levels in workplace air.

The analytical method's linearity was measured for a concentration range varying from the limit of detection of 0.04-0.13 ng mL(-1), depending on the monomer, up to approximately 32 ng mL(-1) for every isocyanate monomer, all with correlation coefficients (R(2)) greater than 0.999.

The analytical method's lower limit of quantification combined with an adapted sampling strategy allow the quantification of isocyanate monomers down to 0.04 ppt for an 8 h work shift when a lithium adduct is used, which is more than 300 times lower than the most sensitive method currently available.

This novel method can be used to confirm the very low level of isocyanate monomers for the safe reassignment of sensitized workers and it is also useful for charting the isocyanate dispersion tail in workplace environments.

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(PMID = 15690096.001).

[ISSN] 1464-0325

[Journal-full-title] Journal of environmental monitoring : JEM

[ISO-abbreviation] J Environ Monit

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Air Pollutants, Occupational; 0 / Cyanates; 0 / Isocyanates; 0I70A3I1UF / 1,6-hexamethylene diisocyanate; 17X7AFZ1GH / Toluene 2,4-Diisocyanate; 91-08-7 / 2,6-diisocyanatotoluene

   

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The suitability of atmospheric pressure chemical ionization mass spectrometry as sensing instrumentation for the real-time monitoring of low levels of toxic compounds is assessed, especially with respect to public safety applications.

Tandem MS methods were implemented in selected cases for improved selectivity, sensitivity, and limits of detection.

Limits of detection in the parts-per-billion and parts-per-trillion range were achieved for this set of analytes.

In all cases detection limits were well below the compounds' permissible exposure limits (PELs), even in the presence of added complex mixtures of alkanes.

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(PMID = 16568176.001).

[ISSN] 0003-2654

[Journal-full-title] The Analyst

[ISO-abbreviation] Analyst

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Air Pollutants; 0 / Chemical Warfare Agents

   

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To examine this, we analyzed whether HLA-G5 affects the proliferation of UT7/EPO and HEL erythroleukemia cells and characterized the mechanism by which HLA-G5 influences erythropoietin receptor (EPOR) signaling.

We show that HLA-G5 inhibits the proliferation of UT7/EPO cells, the EPOR signaling of which is similar to that of normal erythroid progenitors.

Involvement of JAK2 in erythroid cell proliferation has been highlighted by the role of JAK2 V617F mutation in polycythemia vera (PV), a myeloproliferative disorder characterized by erythroid lineage overproduction.

Clinical relevance is provided by analysis of PV patients who carry JAK2 V617F mutation, showing that HLA-G5 inhibits the formation of erythropoietin-independent erythroid colonies.

[MeSH-minor] Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Colony-Forming Units Assay. Erythroid Precursor Cells / drug effects. Erythropoietin / physiology. G1 Phase / drug effects. HLA-G Antigens. Humans. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Janus Kinase 2 / metabolism. Leukemia, Erythroblastic, Acute / pathology. Microspheres. Mutation, Missense. Phosphorylation / drug effects. Point Mutation. Protein Processing, Post-Translational / drug effects. Recombinant Fusion Proteins / pharmacology. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism

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(PMID = 18059484.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; 0 / Receptors, Erythropoietin; 0 / Recombinant Fusion Proteins; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / STAT5 Transcription Factor; 11096-26-7 / Erythropoietin; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2

   

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The cytotoxicity of DON and DONGLU were compared in cell culture using human erythroleukemia cell line K562.

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(PMID = 17507135.001).

[ISSN] 0278-6915

[Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

[ISO-abbreviation] Food Chem. Toxicol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Coloring Agents; 0 / Glucuronides; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Trichothecenes; 298-93-1 / thiazolyl blue; EC 3.2.1.31 / Glucuronidase; I2ZWO3LS3M / Trypan Blue; JT37HYP23V / deoxynivalenol

   

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Interestingly, gamma-secretase cleaves several proteins including Notch, E-cadherin, CD44 and ErbB-4 (erythroblastic leukemia viral oncogene homolog 4), which are important modulators of angiogenesis.

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(PMID = 15878319.001).

[ISSN] 0014-2999

[Journal-full-title] European journal of pharmacology

[ISO-abbreviation] Eur. J. Pharmacol.

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Carbamates; 0 / Dipeptides; 0 / L 685458; 0 / N-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester; 0 / N-benzyloxycarbonyl-valyl-leucyl-leucinal; 0 / Oligopeptides; 0 / Protease Inhibitors; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse

   

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[Title] Noise exposure and hearing conservation in U.S. coal mines--a surveillance report.

This study examines the patterns and trends in noise exposure documented in data collected by Mine Safety and Health Administration inspectors at U.S. coal mines from 1987 through 2004.

During this period, MSHA issued a new regulation on occupational noise exposure that changed the regulatory requirements and enforcement policies.

The exposure reduction was accompanied by an increase of shift length as represented by dosimeter sample duration.

For coal miners exposed above the permissible exposure level, use of hearing protection devices increased from 61% to 89% during this period.

Participation of miners exposed at or above the action level in hearing conservation programs rapidly reached 86% following the effective date of the noise rule.

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(PMID = 17162478.001).

[ISSN] 1545-9624

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

[ISO-abbreviation] J Occup Environ Hyg

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Filopodial protrusions induced by glycoprotein M6a exhibit high motility and aids synapse formation.

M6a is a neuronal membrane glycoprotein whose expression diminishes during chronic stress.

M6a overexpression in rat primary hippocampal neurons induces the formation of filopodial protrusions that could be spine precursors.

As the filopodium and spine motility has been associated with synaptogenesis, we analysed the motility of M6a-induced protrusions by time-lapse imaging.

Our data demonstrate that the motile protrusions formed by the neurons overexpressing M6a were more abundant and moved faster than those formed in control cells.

When different putative M6a phosphorylation sites were mutated, the neurons transfected with a mutant lacking intracellular phosphorylation sites bore filopodia, but these protrusions did not move as fast as those formed by cells overexpressing wild-type M6a.

This suggests a role for M6a phosphorylation state in filopodium motility.

Furthermore, we show that M6a-induced protrusions could be stabilized upon contact with presynaptic region.

The behavior of filopodia from M6a-overexpressing cells and control cells was alike.

Thus, M6a-induced protrusions may be spine precursors that move to reach presynaptic membrane.

We suggest that M6a is a key molecule for spine formation during development.

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(PMID = 20074218.001).

[ISSN] 1460-9568

[Journal-full-title] The European journal of neuroscience

[ISO-abbreviation] Eur. J. Neurosci.

[Language] eng

[Grant] United States / Howard Hughes Medical Institute / /

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

[Publication-country] France

[Chemical-registry-number] 0 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins

   

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[Title] Occupational exposure to trichloroethylene is associated with a decline in lymphocyte subsets and soluble CD27 and CD30 markers.

Occupational cohort and case-control studies suggest that trichloroethylene (TCE) exposure may be associated with non-Hodgkin lymphoma (NHL) but findings are not consistent.

Personal exposure measurements were taken over a three-week period before blood collection.

Ninety-six percent of workers were exposed to TCE below the current US Occupational Safety and Health Administration Permissible Exposure Limit (100 p.p.m.

The total lymphocyte count and each of the major lymphocyte subsets including CD4+ T cells, CD8+ T cells, natural killer (NK) cells and B cells were significantly decreased among the TCE-exposed workers compared with controls (P < 0.05), with evidence of a dose-dependent decline.

Further, there was a striking 61% decline in sCD27 plasma level and a 34% decline in sCD30 plasma level among TCE-exposed workers compared with controls.

This is the first report that TCE exposure under the current Occupational Safety and Health Administration workplace standard is associated with a decline in all major lymphocyte subsets and sCD27 and sCD30, which play an important role in regulating cellular activity in subsets of T, B and NK cells and are associated with lymphocyte activation.

[MeSH-major] Antigens, CD27 / blood. Antigens, CD30 / blood. Biomarkers / metabolism. Lymphocyte Subsets / drug effects. Occupational Exposure. Trichloroethylene / adverse effects

[MeSH-minor] Case-Control Studies. Humans. Lymphocyte Count. Molecular Epidemiology

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(PMID = 20530238.001).

[ISSN] 1460-2180

[Journal-full-title] Carcinogenesis

[ISO-abbreviation] Carcinogenesis

[Language] eng

[Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P30ES01896; United States / NIEHS NIH HHS / ES / P42ES04705

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

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD30; 0 / Biomarkers; 290YE8AR51 / Trichloroethylene

[Other-IDs] NLM/ PMC2930801

   

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[Title] Ezrin is a target for oncogenic Kit mutants in murine erythroleukemia.

The model of erythroleukemia caused by Spi-1/PU.1 transgenesis in mice is a multistage disease.

A preleukemic step is characterized by an acute proliferation of proerythroblasts due to the arrest of differentiation provoked by Spi-1/PU.1.

To gain insights into the mechanisms of the leukemic progression, we performed proteomic profiling analyses of proerythroblasts isolated at the 2 stages of the disease.

Our results indicate that the level of ezrin, a membrane cytoskeletal crosslinker, is increased in the leukemic cells.

Another recurrent oncogenic form of tyrosine kinases (Flt3) most frequently involved in human myeloid leukemia was also able to phosphorylate ezrin.

These findings point to a new role for ezrin as signaling player in the development of leukemia, being a downstream effector of oncogenic tyrosine kinases in leukemic blasts.

[MeSH-major] Cytoskeletal Proteins / metabolism. Leukemia, Erythroblastic, Acute / metabolism. Proto-Oncogene Proteins c-kit / metabolism

[MeSH-minor] Animals. Cell Line. Cell Proliferation. Erythroblasts / cytology. Erythroblasts / metabolism. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Mutation / genetics. Peptides / genetics. Peptides / metabolism. Phosphotyrosine / metabolism. Protein-Tyrosine Kinases / metabolism

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(PMID = 18182570.001).

[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 / Cytoskeletal Proteins; 0 / Peptides; 0 / ezrin; 129712-62-5 / lambda Spi-1; 21820-51-9 / Phosphotyrosine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

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[Title] Selection of non-P-glycoprotein mediated high-level etoposide resistant cell lines by adriamycin with P-gp inhibitors.

In murine erythroleukemia (MEL) A20 cells (grown in 20 ng/ml adriamycin), mutation(s) producing 10-fold adriamycin (doxorubicin) resistance emerged via an unknown mechanism.

Exposure of A20 cells to further stepwise increasing concentrations of ADR in combination with MDR modulators (PSC833 and verapamil) aimed to amplify the undetermined A20 mechanism while controlling P-glycoprotein (P-gp) overexpression.

Resistance to vincristine was unchanged, but resistance to etoposide (VP-16) was 3.7-fold higher in A40P than A20 (itself 97-fold higher than wild-type).

No mutations in the coding sequence of topoisomerase IIalpha could be located to account for the high etoposide resistance levels.

[MeSH-minor] ATP Binding Cassette Transporter, Sub-Family B / antagonists & inhibitors. ATP Binding Cassette Transporter, Sub-Family B / genetics. ATP Binding Cassette Transporter, Sub-Family B / metabolism. ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette Transporters / metabolism. Animals. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Antineoplastic Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Cyclosporins / pharmacology. DNA Topoisomerases, Type II / genetics. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Daunorubicin / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Multiple / genetics. Gene Expression Regulation, Neoplastic / drug effects. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Verapamil / pharmacology

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(PMID = 16465381.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / P-30 DK 34928

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

[Publication-country] Greece

[Chemical-registry-number] 0 / ATP Binding Cassette Transporter, Sub-Family B; 0 / ATP-Binding Cassette Transporters; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Cyclosporins; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / multidrug resistance protein 3; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; CJ0O37KU29 / Verapamil; EC 5.99.1.3 / DNA Topoisomerases, Type II; Q7ZP55KF3X / valspodar; ZS7284E0ZP / Daunorubicin

   

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Primary effusion lymphoma (PEL) is a recently recognized disease that occurs most often in immunosuppressed patients, either with human immunodeficiency virus (HIV) or in the posttransplantation setting, and it occasionally occurs in nonimmunosuppressed patients.

PEL rarely responds to systemic chemotherapy, and the prognosis is poor, with a median survival time of less than 6 months for most cohorts.

A standard treatment for PEL has not yet been identified.

We describe a patient with HIV-seronegative PEL who relapsed after combination chemotherapy and then underwent successful treatment with high-dose chemotherapy (HDC) and autologous stem cell transplantation (ASCT).

The treatment was well tolerated, and the patient has been in remission for 12 months after HDC and ASCT.

[MeSH-minor] Disease-Free Survival. HIV Seropositivity. Humans. Male. Middle Aged. Prognosis. Recurrence. Transplantation, Autologous

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(PMID = 16757433.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan