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1. Reshetniak TM, Shirokova IE, Lisitskaia TL: [The role of hyperhomocysteinemia in systemic lupus erythematosus and antiphospholipid syndrome]. Ter Arkh; 2006;78(6):24-30
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  • [Title] [The role of hyperhomocysteinemia in systemic lupus erythematosus and antiphospholipid syndrome].
  • AIM: To assess the role of hyperhomocysteinemia (HHC) in development of vascular complications in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).
  • The patients had the disease for 14 +/- 11 years.
  • HHC (HC > 15 mcg/l) was diagnosed in 82 of 125 (66%) patients: in 59% patients of group 1, 67%--of group 2 and 76%--of group 3.
  • There was a relationship between HHC and digital necrosis (DN): 80% of DN patients had HHC while HHC was diagnosed in 57% patients free of DN (chi-square = 4.76, p = 0.03).
  • Elevated levels of HC in blood was registered in 43 of 55 (78%) APS patients with thromboses vs. 9 of 19 (47%) patients with APS free of thromboses (p = 0.03).
  • HHC occurred significantly more frequently in patients with arterial thromboses (in all 14 patients) than in patients with venous thromboses (in 16 of 23--69.6%, p = 0.03) and in the absence of thromboses (in 9 of 19, 47.4%, p = 0.04).
  • CONCLUSION: More than 50% patients with SLE and APS, irrespective of APS variants, had an elevated HC level in the blood.
  • [MeSH-major] Antiphospholipid Syndrome / epidemiology. Hyperhomocysteinemia / epidemiology. Hyperhomocysteinemia / physiopathology. Lupus Erythematosus, Systemic / epidemiology


2. Persaud SP, Donermeyer DL, Weber KS, Kranz DM, Allen PM: High-affinity T cell receptor differentiates cognate peptide-MHC and altered peptide ligands with distinct kinetics and thermodynamics. Mol Immunol; 2010 May;47(9):1793-801
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  • [Title] High-affinity T cell receptor differentiates cognate peptide-MHC and altered peptide ligands with distinct kinetics and thermodynamics.
  • Interactions between the T cell receptor and cognate peptide-MHC are crucial initiating events in the adaptive immune response.
  • In this work, we used M15, a high-affinity TCR engineered from the 3.L2 TCR system, to study the binding properties, thermodynamics, and specificity of two altered peptide ligands (APLs).
  • Our affinity measurements of the high-affinity TCR support the view that the wild type TCR binds these APLs in the millimolar affinity range, and hence very low affinities can still elicit biological functions.
  • As the identical TCR was analyzed with several structurally similar ligands, the distinct thermodynamic binding profiles provide a mechanistic perspective on how exquisite antigen specificity is achieved by the T cell receptor.

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  • [Copyright] (c) 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20334923.001).
  • [ISSN] 1872-9142
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI061173-05; United States / NIAID NIH HHS / AI / R37 AI024157-24; United States / NIAID NIH HHS / AI / AI024157-24; United States / NIAID NIH HHS / AI / P01 AI071195-040002; United States / NIAID NIH HHS / AI / R37 AI024157; United States / NIAID NIH HHS / AI / R01 AI061173-05; United States / NIAID NIH HHS / AI / P01 AI071195; United States / NIAID NIH HHS / AI / R01 AI061173; United States / NIAID NIH HHS / AI / AI071195-040002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class II; 0 / Ligands; 0 / Peptides; 0 / Receptors, Antigen, T-Cell
  • [Other-IDs] NLM/ NIHMS191933; NLM/ PMC2860700
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3. Shen H, Li R, Xiao H, Zhou Q, Cui Q, Chen J: Higher serum clozapine level is associated with increased antiphospholipid antibodies in schizophrenia patients. J Psychiatr Res; 2009 Mar;43(6):615-9
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  • [Title] Higher serum clozapine level is associated with increased antiphospholipid antibodies in schizophrenia patients.
  • OBJECTIVES: This study was to evaluate the relationship between clozapine and aPL in schizophrenia patients.
  • A fasting blood sample was taken for serum aPL and serum clozapine level.
  • Serum aPL were measured by ELISA technique and HPLC method was used for the determination of serum clozapine level.
  • RESULTS: The unmedicated schizophrenia patients showed higher IgG aCL level [mean+/-SD: 1.51+/-0.81 and 1.25+/-0.13 U, respectively (t=2.77, df=111, p<0.01)] and IgM aCL level [mean+/-SD: 1.53+/-0.54. and 1.33+/-0.15 U, respectively (t=-2.98, df=111, p<0.01)] compared with the healthy controls.
  • The comparison of the clozapine-treated schizophrenia patients and the healthy controls showed significant difference in IgG aCL level [mean+/-SD: 1.74+/-0.90 and 1.25+/-0.13 U, respectively (t=-4.77, df=124, p<0.01)] and IgM aCL level [mean+/-SD: 1.62+/-0.83 and 1.33+/-0.15 U, respectively (t=-4.35, df=124, p<0.01)].
  • In clozapine-treated schizophrenia patients, the results of Pearson correlation coefficients showed that there was a significant positive relationship between serum IgM aCL and serum clozapine level (r=0.461, p<0.01), and serum IgG aCL were significantly correlated with serum IgM aCL (r=0.279, p<0.05).
  • Stepwise multiple regression analysis was performed with various characteristics, such as duration of medication, daily dose and serum clozapine level as candidate factors for serum aCL (IgG and IgM isotypes) in clozapine-treated schizophrenia patients.
  • Only serum clozapine level was able to enter into the regression model of IgM aCL (Model R(2)=0.212, p<0.05).
  • CONCLUSIONS: A higher serum clozapine level is associated with an increased aPL in schizophrenia patients.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Antipsychotic Agents / blood. Clozapine / blood. Schizophrenia / blood

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  • (PMID = 18976782.001).
  • [ISSN] 0022-3956
  • [Journal-full-title] Journal of psychiatric research
  • [ISO-abbreviation] J Psychiatr Res
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antipsychotic Agents; 0 / Immunoglobulin G; 0 / Immunoglobulin M; J60AR2IKIC / Clozapine
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4. Matsuura E, Kobayashi K, Lopez LR: Atherosclerosis in autoimmune diseases. Curr Rheumatol Rep; 2009 Feb;11(1):61-9
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  • Circulating oxLDL/beta2GPI complexes and autoantibodies to these complexes have been demonstrated in patients with systemic lupus erythematosus and antiphospholipid syndrome.
  • The in vitro macrophage uptake of oxLDL/beta2GPI complexes increased significantly in the presence of antiphospholipid antibodies (anti-beta2GPI), suggesting that macrophage Fcgamma receptors are involved in the lipid intracellular influx that leads to foam cell formation.
  • These findings provide an immunologic explanation for the accelerated development of atherosclerosis seen in systemic lupus erythematosus and antiphospholipid syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Atherosclerosis / complications. Lupus Erythematosus, Systemic / complications

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  • (PMID = 19171113.001).
  • [ISSN] 1534-6307
  • [Journal-full-title] Current rheumatology reports
  • [ISO-abbreviation] Curr Rheumatol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigen-Antibody Complex; 0 / Autoantibodies; 0 / Lipoproteins, LDL; 0 / beta 2-Glycoprotein I; 0 / oxidized low density lipoprotein
  • [Number-of-references] 64
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5. Asou N: [Treatment of acute promyelocytic leukemia]. Nihon Rinsho; 2007 Jan 28;65 Suppl 1:483-7
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  • [Title] [Treatment of acute promyelocytic leukemia].
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 17474452.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  • [Number-of-references] 15
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6. Motta S, Monti M: Photodynamic therapy-a promising treatment option for autoimmune skin ulcers: a case report. Photochem Photobiol Sci; 2007 Nov;6(11):1150-1
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  • We describe a 38-year-old woman with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) who developed two symmetric paramalleolar ulcers with similar diameters, depths and borders, that were successfully treated with photodynamic therapy with 5-aminolevulinic acid (ALA-PDT).
  • [MeSH-minor] Adult. Aminolevulinic Acid / therapeutic use. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / drug therapy. Antiphospholipid Syndrome / pathology. Female. Humans. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / drug therapy. Lupus Erythematosus, Systemic / pathology. Photosensitizing Agents / therapeutic use

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  • (PMID = 17973045.001).
  • [ISSN] 1474-905X
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
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7. Ostertag MV, Liu X, Henderson V, Pierangeli SS: A peptide that mimics the Vth region of beta-2-glycoprotein I reverses antiphospholipid-mediated thrombosis in mice. Lupus; 2006;15(6):358-65
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  • [Title] A peptide that mimics the Vth region of beta-2-glycoprotein I reverses antiphospholipid-mediated thrombosis in mice.
  • Antiphospholipid (aPL) antibodies bind to beta2glycoprotein I (beta2GPI) and cause endothelial cell (EC) activation and thrombosis in mice. beta2GPI binds to EC through its Vth domain and induces their activation.
  • TIFI is a 20 amino acid synthetic peptide that shares similarity with the Vth domain of beta2GPI.
  • Our objectives were to examine the ability of TIFI to affect aPL-mediated thrombosis in mice and the interactions of TIFI, beta2GPI with phospholipid surfaces and target cells.
  • CD1 mice were injected with IgG from a patient with antiphospholipid syndrome (IgG-APS) or with control IgG-NHS and with either TIFI or with control peptide (VITT).
  • Inhibition and competition studies were done using aPL antibodies, cardiolipin (CL) liposomes in the presence of varying amounts of TIFI and beta2GPI.
  • TIFI reverted the beta2GPI-dependent binding of aPL antibodies to CL liposomes in a dose-dependent fashion.
  • This effect was abrogated by addition of beta2GPI, suggesting that TIFI displaces the binding of beta2GPI to phospholipids.
  • The data indicate that TIFI abrogates thrombogenic properties of aPL in mice by competing with beta2GPI and preventing its binding to target cells.
  • [MeSH-major] Antiphospholipid Syndrome / immunology. Fibrinolytic Agents / therapeutic use. Peptides / therapeutic use. Thrombosis / prevention & control. beta 2-Glycoprotein I / chemistry
  • [MeSH-minor] Amino Acid Sequence. Animals. Antibodies, Antiphospholipid / blood. Antibodies, Antiphospholipid / immunology. Antibodies, Antiphospholipid / toxicity. Binding, Competitive. Cardiolipins / immunology. Cells, Cultured. Endothelium, Vascular / drug effects. Endothelium, Vascular / physiopathology. Enzyme-Linked Immunosorbent Assay. Humans. Immunoglobulin G / toxicity. Liposomes. Macrophages / drug effects. Macrophages / immunology. Male. Mice. Molecular Mimicry. Molecular Sequence Data. Neutralization Tests. Protein Binding / drug effects. Protein Structure, Tertiary

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  • (PMID = 16830882.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / G12-RR03034; United States / NIGMS NIH HHS / GM / S02GM08248
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Cardiolipins; 0 / Fibrinolytic Agents; 0 / Immunoglobulin G; 0 / Liposomes; 0 / Peptides; 0 / TIFI peptide; 0 / beta 2-Glycoprotein I
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8. Bizzaro N, Tonutti E, Villalta D, Tampoia M, Tozzoli R: Prevalence and clinical correlation of anti-phospholipid-binding protein antibodies in anticardiolipin-negative patients with systemic lupus erythematosus and women with unexplained recurrent miscarriages. Arch Pathol Lab Med; 2005 Jan;129(1):61-8
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  • [Title] Prevalence and clinical correlation of anti-phospholipid-binding protein antibodies in anticardiolipin-negative patients with systemic lupus erythematosus and women with unexplained recurrent miscarriages.
  • CONTEXT: Anti-phospholipid antibodies (aPL) are a heterogeneous group of autoantibodies, the presence of which is associated with thrombotic events and miscarriage.
  • OBJECTIVE: To establish whether antibodies directed against phospholipid-binding plasma proteins such as beta(2)-glycoprotein I (beta(2)GPI), prothrombin (PT), and annexin V (Anx V) constitute a risk factor for thromboembolism in patients with systemic lupus erythematosus (SLE) and for miscarriage in women with recurrent pregnancy loss (RPL), independently of the presence of the classic anticardiolipin (aCL) antibodies, and whether their determination together with that of aCL would help to increase the diagnostic sensitivity of aPL tests.
  • DESIGN: The prevalence of various antibodies directed toward phospholipids (CL and other anionic phospholipids [APL]) and phospholipid-binding proteins (beta(2)GPI, PT, and Anx V) was determined by immunoenzymatic methods in 311 serum samples.
  • PATIENTS: Twenty-five patients with aCL-positive primary anti-phospholipid syndrome (pAPS); 89 patients with SLE, 23 of whom had thrombotic complications (SLE/APS) and 66 of whom had no thrombosis; and 77 women with unexplained recurrent pregnancy loss comprised our study group.
  • RESULTS: Immunoglobulin (Ig) G and/or IgM aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies were detected in 25 (100%), 20 (80%), 15 (60%), and 6 (24%), respectively, of the 25 aCL-positive pAPS patients; IgG and/or IgM aCL, aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies were detected in 33 (37%), 42 (47%), 31 (35%), 40 (45%), and 12 (13%) of the 89 SLE patients, respectively.
  • Of the 56 SLE patients who proved to be aCL negative, anti-beta(2)GPI was present in 3 patients (5%), anti-PT in 13 (23%) patients, and anti-Anx V in 5 (9%) patients.
  • In the subset of 23 SLE/APS patients, IgG anti-PT prevalence was higher than that of the other autoantibodies (87% vs 70% aCL, 66% aAPL, 57% anti-beta(2)GPI, and 4% anti-Anx V), and in 26% of cases, IgG anti-PT was the only antibody present.
  • Anti-PT had a slightly lower specificity than aCL (46% vs 49%); however, the occurrence of both antibodies brought the specificity to 92.4%.
  • The highest risk for thrombosis in SLE patients was associated with the presence of IgG anti-PT antibody (odds ratio [OR] 15.3, P < .001, vs 6.5 aCL, 3.5 aAPL, 3.4 anti-beta(2)GPI, 0.2 anti-Anx V).
  • Fifty-one of the 77 women with recurrent pregnancy loss were negative for all antibodies investigated; the prevalence of IgG and/or IgM aCL, aAPL, anti-beta(2)GPI, anti-PT, and IgG anti-Anx V antibodies was 6% (5), 12% (9), 6% (5), 16% (12), and 17% (13), respectively.
  • Of the 67 aCL-negative women, none had anti-beta(2)GPI antibodies, 7 (11%) were anti-PT positive, and 13 (19%) were anti-Anx V positive.
  • In the subgroup of 26 recurrent pregnancy loss patients who had at least one antibody, anti-Anx V was present in 50% of cases (in 42% as the sole antibody) and was the only antibody significantly associated with miscarriage (P = .02).
  • CONCLUSIONS: The results of this study indicate that it is useful to measure anti-PT antibodies in addition to the more widely used aCL and anti-beta(2)GPI antibodies in the prognostic evaluation of SLE patients for the risk of thrombosis, and the results also confirm that anti-Anx V antibodies may play an important role in recurrent pregnancy loss.
  • [MeSH-major] Abortion, Spontaneous / blood. Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / blood. Lupus Erythematosus, Systemic / blood
  • [MeSH-minor] Adult. Annexin A5 / blood. Annexin A5 / immunology. Autoantibodies / blood. Cardiolipins / immunology. Enzyme-Linked Immunosorbent Assay / methods. Female. Glycoproteins / blood. Glycoproteins / immunology. Humans. Male. Middle Aged. Phospholipids / immunology. Pregnancy. Prevalence. Prothrombin / immunology. Thromboembolism / etiology. beta 2-Glycoprotein I

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  • (PMID = 15628909.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Cardiolipins; 0 / Glycoproteins; 0 / Phospholipids; 0 / beta 2-Glycoprotein I; 9001-26-7 / Prothrombin
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9. Pourrat O, Jollit C, Gombert JM, Boinot C, Pierre F: Clinical relevance of the recent update of the classification criteria for definite antiphospholipid syndrome: an obstetric medicine clinic series of 107 patients. J Thromb Haemost; 2006 Oct;4(10):2276-7
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  • [Title] Clinical relevance of the recent update of the classification criteria for definite antiphospholipid syndrome: an obstetric medicine clinic series of 107 patients.
  • [MeSH-major] Antiphospholipid Syndrome / classification. Antiphospholipid Syndrome / diagnosis
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. Female. Humans. Lupus Coagulation Inhibitor / blood. Partial Thromboplastin Time. Phospholipids / chemistry. Pregnancy. Pregnancy Complications / classification. Pregnancy Complications / diagnosis. Pregnancy Complications / immunology. Prognosis. Retrospective Studies

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  • [CommentOn] J Thromb Haemost. 2006 Feb;4(2):295-306 [16420554.001]
  • (PMID = 16869832.001).
  • [ISSN] 1538-7933
  • [Journal-full-title] Journal of thrombosis and haemostasis : JTH
  • [ISO-abbreviation] J. Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Lupus Coagulation Inhibitor; 0 / Phospholipids
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10. Tsukamoto H, Irie A, Chen YZ, Takeshita K, Kim JR, Nishimura Y: TCR ligand avidity determines the mode of B-Raf/Raf-1/ERK activation leading to the activation of human CD4+ T cell clone. Eur J Immunol; 2006 Jul;36(7):1926-37
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  • [Title] TCR ligand avidity determines the mode of B-Raf/Raf-1/ERK activation leading to the activation of human CD4+ T cell clone.
  • The interactions between peptide/MHC complexes and their cognate TCR are essential for various T cell responses.
  • However, the relationship between the avidity of TCR ligand and the subsequent intracellular signaling through the TCR is still unclear.
  • To investigate the effects of TCR ligand avidity on TCR-mediated signaling, we established L cells expressing HLA-DR4 molecules covalently linked with agonistic peptide (high-affinity ligand) or altered peptide ligand (APL; low-affinity ligand) at various densities as APC for a cognate human CD4(+) T cell clone.
  • Using this system, we demonstrated that the T cell clone stimulated with APL/HLA-DR4 complexes presented at an excessive density provoked the up-regulation of CD69, IL-2 production and proliferation, but no detectable phosphorylation of ZAP-70/LAT/SLP-76.
  • The strength and duration of B-Raf/ERK activations closely correlated with the density of the TCR ligand.
  • A knockdown approach confirmed that B-Raf activation was indispensable for the APL-induced T cell responses.
  • These observations suggest that the differences in TCR-peptide/MHC interactions reflect the strength and duration of B-Raf/Raf-1/ERK activation in the human CD4(+) T cells.
  • [MeSH-minor] Amino Acid Sequence. Animals. Aotidae. Cell Transformation, Viral. Cells, Cultured. Clone Cells. Enzyme Activation / immunology. HLA-DR4 Antigen / physiology. Herpesvirus 2, Saimiriine. Humans. Jurkat Cells. L Cells (Cell Line). Ligands. Mice. Mice, Inbred C57BL. Molecular Sequence Data. NIH 3T3 Cells. PC12 Cells. Rats


11. El Bougrini J, Pampin M, Chelbi-Alix MK: Arsenic enhances the apoptosis induced by interferon gamma: key role of IRF-1. Cell Mol Biol (Noisy-le-grand); 2006;52(1):9-15
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  • We have shown earlier that IFNgamma and As2O3 act synergistically in acute promyelocytic leukemia cells to upregulate IRF-1 expression and to induce apoptosis.
  • Here, we show that in the human fibrosarcoma cell line 2fTGH, As2O3 prolongs IFNgamma-induced STAT1 phosphorylation resulting in persistent binding of STAT1 to GAS motif leading to an increase in IRF-1 expression which correlated with both higher anti-proliferative effect and increased apoptosis.

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  • (PMID = 16914093.001).
  • [ISSN] 1165-158X
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / GAS1 protein, human; 0 / GPI-Linked Proteins; 0 / Growth Inhibitors; 0 / Interferon Regulatory Factor-1; 0 / Membrane Proteins; 0 / STAT1 Transcription Factor; 82115-62-6 / Interferon-gamma; N712M78A8G / Arsenic
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12. Vassilakopoulos TP, Pangalis GA, Siakantaris MP, Levidou G, Yiakoumis X, Floudas C, Gribabis D, Bouros S, Metaxas I, Dimitriadou EM, Pantazi L, Tsoukala C, Korkolopoulou P, Andreopoulos A, Vaiopoulos G: Kikuchi's lymphadenopathy: a relatively rare but important cause of lymphadenopathy in Greece, potentially associated with the antiphospholipid syndrome. Rheumatol Int; 2010 May;30(7):925-32
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  • [Title] Kikuchi's lymphadenopathy: a relatively rare but important cause of lymphadenopathy in Greece, potentially associated with the antiphospholipid syndrome.
  • Kikuchi-Fujimoto disease is a form of reactive lymphadenopathy, which was firstly described in Japan, but is uncommon in the Western world.
  • We retrospectively reviewed the medical records of nine cases of adult or adolescent Kikuchi's disease diagnosed in a single Haematology Unit in Athens, Greece between 1990 and 2006.
  • The median leukocyte count was 4.7 x 10(9)/l (2.2-4.9) with a normal differential in 7/9 patients.
  • One patient had clinical and laboratory evidence of primary antiphospholipid syndrome (APLS).
  • In conclusion, Kikuchi's disease represents a rare but important diagnostic possibility for patients presenting with lymphadenopathy in Greece and other western countries.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / physiopathology. Histiocytic Necrotizing Lymphadenitis / diagnosis. Histiocytic Necrotizing Lymphadenitis / physiopathology
  • [MeSH-minor] Adolescent. Adult. Antibodies, Antiphospholipid / analysis. Antibodies, Antiphospholipid / blood. Autoimmune Diseases / diagnosis. Autoimmune Diseases / epidemiology. Autoimmune Diseases / physiopathology. Comorbidity. Diagnosis, Differential. Diagnostic Errors / prevention & control. Female. Greece. Humans. Leukocyte Count. Lymph Nodes / pathology. Male. Prevalence. Spleen / pathology. Spleen / physiopathology. Splenomegaly / diagnosis. Splenomegaly / epidemiology. Splenomegaly / physiopathology. Young Adult

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  • (PMID = 19693507.001).
  • [ISSN] 1437-160X
  • [Journal-full-title] Rheumatology international
  • [ISO-abbreviation] Rheumatol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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13. Kwaan HC, Huyck T: Thromboembolic and bleeding complications in acute leukemia. Expert Rev Hematol; 2010 Dec;3(6):719-30
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  • [Title] Thromboembolic and bleeding complications in acute leukemia.
  • The risk of both thromboembolic and bleeding complications is high in acute leukemia.
  • This double hazard has a significant negative impact on the morbidity and mortality of patients with this disease.
  • The clinical manifestations of both complications show special features specific to the form of acute leukemia.
  • Recognition of these characteristics is important in the diagnosis and management of acute leukemia.
  • In this article, several additional issues are addressed, including the features of bleeding and thrombosis in acute promyelocytic leukemia, the current understanding of the leukostasis syndrome and the iatrogenic complications including catheter-associated thrombosis, and the adverse effects of therapeutic agents used in acute leukemia.
  • [MeSH-major] Hemorrhage / etiology. Leukemia / complications. Thromboembolism / etiology
  • [MeSH-minor] Acute Disease. Blood Vessels / pathology. Drug-Related Side Effects and Adverse Reactions. Humans. Thrombophilia. Thrombosis / complications. Thrombosis / epidemiology

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  • (PMID = 21091148.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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14. Bassani MA, de Oliveira AB, Oliveira Neto AF: Noninvasive ventilation in a pregnant patient with respiratory failure from all-trans-retinoic-acid (ATRA) syndrome. Respir Care; 2009 Jul;54(7):969-72
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  • We saw a 34-year-old pregnant woman with acute promyelocytic leukemia, who developed acute respiratory failure from all-trans-retinoic acid (ATRA) syndrome.
  • She was discharged from the intensive care unit after 12 days.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Pregnancy Complications, Neoplastic / drug therapy. Respiration, Artificial. Respiratory Insufficiency / chemically induced. Tretinoin / adverse effects


15. Tincani A, Casu C, Cartella S, Ziglioli T, Cattaneo R: [Antiphospholipid antibody: laboratory, pathogenesis and clinical manifestations]. Reumatismo; 2010 Jan-Mar;62(1):65-75
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  • [Title] [Antiphospholipid antibody: laboratory, pathogenesis and clinical manifestations].
  • Antiphospholipid antibodies (aPL) represent a heterogeneous group of antibodies that recognize various antigenic targets including beta2 glycoprotein I (beta2GPI), prothrombin (PT), activated protein C, tissue plasminogen activator, plasmin and annexin A2.
  • The most commonly used tests to detect aPL are: lupus anticoagulant (LAC), a functional coagulation assay, anticardiolipin antibody (aCL) and anti-beta2GPI antibody (anti-beta2GPI), which are enzyme-linked immunoassay (ELISA).
  • Clinically aPL are associated with thrombosis and/or with pregnancy morbidity.
  • Apparently aPL alone are unable to induce thrombotic manifestations, but they increase the risk of vascular events that can occur in the presence of another thrombophilic condition; on the other hand obstetrical manifestations were shown to be associated not only to thrombosis but mainly to a direct antibody effect on the trophoblast.
  • [MeSH-major] Antibodies, Anticardiolipin. Antibodies, Antiphospholipid. Antiphospholipid Syndrome. Lupus Coagulation Inhibitor. Pregnancy Complications. Thrombosis / immunology

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  • (PMID = 20390120.001).
  • [ISSN] 0048-7449
  • [Journal-full-title] Reumatismo
  • [ISO-abbreviation] Reumatismo
  • [Language] ita
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 69
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16. Asai E, Okouchi M, Momiyama M, Kajikawa A, Ueda K: Free flap failure in an anticardiolipin antibody-positive patient with neoplasm--a case report. Microsurgery; 2010;30(3):238-41
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  • Laboratory findings, 7 days postoperatively, showed high levels of immunoglobulin G anticardiolipin antibody.
  • This case does not match the criteria for antiphospholipid syndrome, but some English-language reports have shown rising antiphospholipid antibody levels, particularly anticardiolipin antibodies, in patients with neoplasm.
  • In those cases, levels have normalized after successful therapy.
  • Antiphospholipid antibody levels should be examined before surgery to identify risks of hypercoagulability.

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  • (PMID = 20049910.001).
  • [ISSN] 1098-2752
  • [Journal-full-title] Microsurgery
  • [ISO-abbreviation] Microsurgery
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin
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17. Le Hello C, Blacher J, Conard J, Piette JC, Constans J: [Thrombophilias and peripheral arterial occlusive disease]. J Mal Vasc; 2008 Sep;33(3):126-36
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  • [Title] [Thrombophilias and peripheral arterial occlusive disease].
  • Peripheral arterial occlusive disease is a frequent disease due to the classical vascular risk factors such as smoking, diabetes mellitus, dyslipidemia, and hypertension.
  • Despite these risk factors, many thrombophilias (physiological inhibitors defects, Factor V Leiden and 20210A prothrombin gene variant, antiphospholipid antibodies, mild hyperhomocysteinemia 15-30micromol/l) can be evoked in some clinical forms of peripheral arterial occlusive disease.
  • Screening for these thrombophilias is justified in patients with venous thromboembolic disease, or signs of antiphospholipid syndrome and possibly in different situations such as premature atheroma of lower limbs, chronic ischaemia, evolutive disease despite adapted treatment and revascularisation failures without evident technical explanation.
  • Except for the antiphospholipid syndrome, there is currently no consensus for systematic screening of thrombophilia and treatment in patients with peripheral arterial occlusive disease.

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  • (PMID = 18554834.001).
  • [ISSN] 0398-0499
  • [Journal-full-title] Journal des maladies vasculaires
  • [ISO-abbreviation] J Mal Vasc
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antithrombins; 0 / factor V Leiden; 9001-24-5 / Factor V; 9001-26-7 / Prothrombin
  • [Number-of-references] 62
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18. Rush EA, Schlesinger KW, Watkins SC, Redner RL: The NPM-RAR fusion protein associated with the t(5;17) variant of APL does not interact with PML. Leuk Res; 2006 Aug;30(8):979-86
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  • [Title] The NPM-RAR fusion protein associated with the t(5;17) variant of APL does not interact with PML.
  • The PML protein localizes to regions of the nucleus known as nuclear bodies or PODs.
  • However, in t(15;17) Acute Promyelocytic Leukemia (APL) blasts, PML is found in a micro-punctate pattern.
  • In order to test the hypothesis that delocalization of PML from PODs is necessary for APL, we investigated the interaction of the t(5;17) APL fusion protein NPM-RAR with PML.
  • NPM-RAR localizes diffusely throughout the nucleoplasm.
  • NPM-RAR does not alter the localization of PML in transfected HeLa cells, and does not associate with PML in vitro.
  • These studies suggest that NPM-RAR does not interact with PML.
  • [MeSH-major] Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 5 / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. COS Cells. Cercopithecus aethiops. HeLa Cells. Humans. Polymerase Chain Reaction / methods. Promyelocytic Leukemia Protein. Protein Binding. Sensitivity and Specificity

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  • [CommentIn] Acta Haematol. 2016;136(1):1-15 [27089249.001]
  • (PMID = 16504291.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R29 CA67346
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NPM-RARalpha protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Promyelocytic Leukemia Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
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19. Etsuda H, Miyamoto A, Nakajima Y, Hakamata N, Yamauchi Y, Akita T, Fukuda M: [Acute myocardial infarction with variable clinical manifestations: probable catastrophic primary antiphospholipid antibody syndrome: a case report]. J Cardiol; 2005 Oct;46(4):155-60
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  • [Title] [Acute myocardial infarction with variable clinical manifestations: probable catastrophic primary antiphospholipid antibody syndrome: a case report].
  • A 62-year-old diabetic man was admitted to our hospital because of acute myocardial infarction.
  • Emergent coronary angiography showed multiple thromboembolic occlusions in the distal circumflex and anterior descending arteries.
  • These clinical manifestations and laboratory findings suggested catastrophic antiphospholipid antibody syndrome.
  • Acute myocardial infarction is rare as the initial manifestation of catastrophic antiphospholipid antibody syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Myocardial Infarction / etiology
  • [MeSH-minor] Anticoagulants / therapeutic use. Coronary Angiography. Diabetic Retinopathy / complications. Diagnosis, Differential. Humans. Kidney Diseases / complications. Male. Middle Aged. Prognosis


20. Onetti L, Villafañe S, Menso E, Drenkard C, Gamron S, Barberis G, Onetti CM: [Hyperhomocysteine like thrombocytic risk factor in patient with systemic lupus erythematous with antiphospholipid syndrome]. Rev Fac Cien Med Univ Nac Cordoba; 2005;62(1):21-5
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  • [Title] [Hyperhomocysteine like thrombocytic risk factor in patient with systemic lupus erythematous with antiphospholipid syndrome].
  • [Transliterated title] Hiperhomocisteinemia como factor de riesgo trombótico en pacientes con lupus eritematoso sistémico y síndrome antifosfolípido.
  • OBJECTIVES: to detect the prevalence of hyperhcy in SLE patients with and without antiphospholipid syndrom; to compare the Hcy levels between those patients and healthy controls and to determine the correlation between hyperhcy and antiphospholipid antibodies.
  • PATIENTS AND METHODS: we studied 44 SLE patients: 17 had antiphospholipid syndrom and 27 didn't have it, and we compared them to 24 healthy controls.
  • STATISTICAL ANALYSIS: cualytative variables: chi square or Fischer's; cuantitative variables: Student's T test or Mann-Whitney's test.
  • Hyperhcy was present in 27 SLE patients (61,4%), 12 of them had antiphospholipid syndrom.
  • 15(75%) of them had hiperhcy.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Hyperhomocysteinemia / complications. Lupus Erythematosus, Systemic / physiopathology. Thrombosis / etiology
  • [MeSH-minor] Adult. Aged. Antibodies, Antiphospholipid / blood. Argentina. Female. Homocysteine / blood. Humans. Male. Middle Aged. Risk Factors. Venous Thrombosis / blood

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  • (PMID = 16281418.001).
  • [ISSN] 0014-6722
  • [Journal-full-title] Revista de la Facultad de Ciencias Médicas (Córdoba, Argentina)
  • [ISO-abbreviation] Rev Fac Cien Med Univ Nac Cordoba
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0LVT1QZ0BA / Homocysteine
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21. Filip B, Milczarek M, Wietrzyk J, Chodyński M, Kutner A: Antitumor properties of (5E,7E) analogs of vitamin D3. J Steroid Biochem Mol Biol; 2010 Jul;121(1-2):399-402
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  • The analogs were examined for their antiproliferative activity in vitro against human breast cancer cells (MCF-7) and promyelocytic leukemia (HL-60) cells.
  • The studies of calcemic activity in vivo showed that analogs PRI-2208 and PRI-2209 did not influence the serum calcium level in doses, in which 1alpha,25(OH)2D3 or (24R)-1,24(OH)2D3 significantly increased this level.

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20227499.001).
  • [ISSN] 1879-1220
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 1C6V77QF41 / Cholecalciferol; SY7Q814VUP / Calcium
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22. Zhang X, Lian Z, Padden C, Gerstein MB, Rozowsky J, Snyder M, Gingeras TR, Kapranov P, Weissman SM, Newburger PE: A myelopoiesis-associated regulatory intergenic noncoding RNA transcript within the human HOXA cluster. Blood; 2009 Mar 12;113(11):2526-34
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  • We have identified an intergenic transcriptional activity that is located between the human HOXA1 and HOXA2 genes, shows myeloid-specific expression, and is up-regulated during granulocytic differentiation.
  • The novel gene, termed HOTAIRM1 (HOX antisense intergenic RNA myeloid 1), is transcribed antisense to the HOXA genes and originates from the same CpG island that embeds the start site of HOXA1.
  • HOTAIRM1 is the most prominent intergenic transcript expressed and up-regulated during induced granulocytic differentiation of NB4 promyelocytic leukemia and normal human hematopoietic cells; its expression is specific to the myeloid lineage.
  • Its induction during retinoic acid (RA)-driven granulocytic differentiation is through RA receptor and may depend on the expression of myeloid cell development factors targeted by RA signaling.
  • Knockdown of HOTAIRM1 quantitatively blunted RA-induced expression of HOXA1 and HOXA4 during the myeloid differentiation of NB4 cells, and selectively attenuated induction of transcripts for the myeloid differentiation genes CD11b and CD18, but did not noticeably impact the more distal HOXA genes.

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  • (PMID = 19144990.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / U01 HG003147; United States / NIDDK NIH HHS / DK / R01 DK054369; United States / NIDDK NIH HHS / DK / DK54369; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CO / N01-CO-12400; United States / NHGRI NIH HHS / HG / U01-HG003147
  • [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 / DNA, Intergenic; 0 / HOXA2 protein, human; 0 / Homeodomain Proteins; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / Regulatory Sequences, Ribonucleic Acid; 0 / Transcription Factors; 0 / homeobox A1 protein; 0 / long non-coding RNA HOTAIRM1, human; 157907-48-7 / HoxA protein; EC 2.7.7.- / RNA Polymerase II
  • [Other-IDs] NLM/ PMC2656274
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23. Jiang WQ, Zhong ZH, Henson JD, Reddel RR: Identification of candidate alternative lengthening of telomeres genes by methionine restriction and RNA interference. Oncogene; 2007 Jul 12;26(32):4635-47
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  • We reported previously that sequestration of MRE11/RAD50/NBS1 complexes represses ALT-mediated telomere length maintenance, and suppresses formation of ALT-associated promyelocytic leukemia (PML) bodies (APBs).
  • APBs are PML bodies containing telomeric DNA and telomere-binding proteins, and are observed only in a small fraction of cells within asynchronously dividing ALT-positive cell populations.
  • We combined methionine restriction with RNA interference to test whether the following proteins are required for APB formation: PML body-associated proteins, PML and Sp100; telomere-associated proteins, TRF1, TRF2, TIN2 and RAP1; and DNA repair proteins, MRE11, RAD50, NBS1 and 53BP1.

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  • (PMID = 17297460.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRE11A protein, human; 0 / NBN protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / Rad50 protein, human; 0 / TINF2 protein, human; 0 / TP53BP1 protein, human; 0 / Telomere-Binding Proteins; 0 / Telomeric Repeat Binding Protein 1; 0 / Telomeric Repeat Binding Protein 2; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 135844-47-2 / Sp100 protein, human; 143220-95-5 / PML protein, human; AE28F7PNPL / Methionine; EC 6.5.1.- / DNA Repair Enzymes
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24. Wu L, Xiao B, Jia X, Zhang Y, Lü S, Chen J, Long M: Impact of carrier stiffness and microtopology on two-dimensional kinetics of P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) interactions. J Biol Chem; 2007 Mar 30;282(13):9846-54
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  • [Title] Impact of carrier stiffness and microtopology on two-dimensional kinetics of P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1) interactions.
  • Interactions of P-selectin with P-selectin glycoprotein ligand-1 (PSGL-1) were used to demonstrate such effects by presenting the molecules on three carrier systems: human red blood cells (RBCs), human promyelocytic leukemia HL-60 cells, and polystyrene beads.
  • These results demonstrate that the carrier stiffness and microtopology of a receptor influences its rate of encountering and binding a surface ligand but does not subsequently affect the stability of binding.

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  • (PMID = 17267403.001).
  • [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 / Membrane Glycoproteins; 0 / P-Selectin; 0 / P-selectin ligand protein
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25. Kondo M, Nakabayashi Y, Sugiyama A, Tominaga T, Shinohara K: A case of acute promyelocytic leukemia showing transient thrombocytosis caused by increased interleukin-6 and thrombopoietin after treatment with all-trans retinoic acid and chemotherapy. Gan To Kagaku Ryoho; 2009 May;36(5):827-30
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  • [Title] A case of acute promyelocytic leukemia showing transient thrombocytosis caused by increased interleukin-6 and thrombopoietin after treatment with all-trans retinoic acid and chemotherapy.
  • A patient with acute promyelocytic leukemia(APL)treated with all-trans retinoic acid(ATRA)and chemotherapy for remission induction developed marked thrombocytosis after bone marrow recovery.
  • During thrombocytosis, plasma levels of interleukin-6(IL-6)were elevated while those of thrombopoietin(TPO)were not elevated.
  • However, the plasma level of TPO was markedly elevated at the nadir after post remission chemotherapy.
  • These findings suggest that in APL patients, thrombocytosis after treatment with ATRA and or chemotherapy may be caused by increased plasma levels of both of IL-6 and TPO.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Interleukin-6 / blood. Leukemia, Promyelocytic, Acute / drug therapy. Thrombocytosis / drug therapy. Thrombopoietin / blood. Tretinoin / therapeutic use


26. Marai I, Tincani A, Balestrieri G, Shoenfeld Y: Anticardiolipin and anti-beta-2-glycoprotein I antibodies. Autoimmunity; 2005 Feb;38(1):33-8
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  • [Title] Anticardiolipin and anti-beta-2-glycoprotein I antibodies.
  • The anticardiolipin (aCL) antibody test was first established in 1983, using cardiolipin (negatively charged phospholipid) as an antigen in a solid-phase immunoassAy.
  • The wide use of this test was determinant in the definition of the "aCL or antiphospholipid syndrome" (APS).Later, it was demonstrated that aCL antibodies do not recognize anionic phospholipids but are directed against plasma proteins bound to anionic phospholipids, mainly beta-2-glycoprotein I, which is now considered as the autoantigen in APS.
  • Anti-beta-2-glycoprotein I (anti-beta2GPI) is not yet accepted as a serological criterion for APS, but most investigators would consider a patient with anti-beta2GPI antibodies and clinical features of APS to have the syndrome. aCL and anti-beta2GPI are a heterogeneous group of antibodies with different clinical significances and can be present in different autoimmune diseases as well as in infectious diseases.
  • [MeSH-major] Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Glycoproteins / immunology
  • [MeSH-minor] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / immunology. Autoimmune Diseases / immunology. Female. History, 20th Century. Humans. Pregnancy. beta 2-Glycoprotein I

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  • (PMID = 15804703.001).
  • [ISSN] 0891-6934
  • [Journal-full-title] Autoimmunity
  • [ISO-abbreviation] Autoimmunity
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Glycoproteins; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 60
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27. Mohsen H, Faouzi A, Khaldoun BH, Fatma A, Hanéne H, Zohra D, Habib G, Fethi B, Faouzi M, Mohamed BF: [Abnormalities of haemostasis in myocardial infarction with normal coronary artery]. Tunis Med; 2005 Nov;83(11):675-80
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  • [Transliterated title] Anomalies de l'hemostase dans l'infarctus du myocarde sur coronaires angiographiquement saines: a propos de 39 cas.
  • Myocardial infarction with normal coronary artery is ussually inaugural, with electric and clinical characteristics similar to those with atheroma.
  • They were 33 males and 6 females aged between 22 and 75 years (44 + 13 years), in whom the deficiency in protein C and S. antithrombin, activated protein C resistance and antiphospholipid antibodies were assessed.
  • RESULTS: Concurrent abnormalities of haemostasis were found in 10 patients: Antiphospholipid antibodies, found in 5 patients constitute the most frequent abnormality.
  • [MeSH-major] Blood Coagulation Disorders / diagnosis. Coronary Angiography. Myocardial Infarction / blood
  • [MeSH-minor] Activated Protein C Resistance / diagnosis. Adult. Aged. Antibodies, Antiphospholipid / blood. Antithrombins / analysis. Antithrombins / deficiency. Coronary Vessels / pathology. Female. Humans. Immunoglobulin G / blood. Male. Middle Aged. Protein C / analysis. Protein C Deficiency / diagnosis. Protein S / analysis. Protein S Deficiency / diagnosis. Retrospective Studies

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  • (PMID = 16422365.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Tunisia
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antithrombins; 0 / Immunoglobulin G; 0 / Protein C; 0 / Protein S
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28. Iero M, Squarcina P, Romero P, Guillaume P, Scarselli E, Cerino R, Carrabba M, Toutirais O, Parmiani G, Rivoltini L: Low TCR avidity and lack of tumor cell recognition in CD8(+) T cells primed with the CEA-analogue CAP1-6D peptide. Cancer Immunol Immunother; 2007 Dec;56(12):1979-91
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  • [Title] Low TCR avidity and lack of tumor cell recognition in CD8(+) T cells primed with the CEA-analogue CAP1-6D peptide.
  • The use of "altered peptide ligands" (APL), epitopes designed for exerting increased immunogenicity as compared with native determinants, represents nowadays one of the most utilized strategies for overcoming immune tolerance to self-antigens and boosting anti-tumor T cell-mediated immune responses.
  • However, the actual ability of APL-primed T cells to cross-recognize natural epitopes expressed by tumor cells remains a crucial concern.
  • In the present study, we show that CAP1-6D, a superagonist analogue of a carcinoembriyonic antigen (CEA)-derived HLA-A*0201-restricted epitope widely used in clinical setting, reproducibly promotes the generation of low-affinity CD8(+) T cells lacking the ability to recognized CEA-expressing colorectal carcinoma (CRC) cells.
  • Short-term T cell cultures, obtained by priming peripheral blood mononuclear cells from HLA-A*0201(+) healthy donors or CRC patients with CAP1-6D, were indeed found to heterogeneously cross-react with saturating concentrations of the native peptide CAP1, but to fail constantly lysing or recognizing through IFN- gamma release CEA(+)CRC cells.
  • Characterization of anti-CAP1-6D T cell avidity, gained through peptide titration, CD8-dependency assay, and staining with mutated tetramers (D227K/T228A), revealed that anti-CAP1-6D T cells exerted a differential interaction with the two CEA epitopes, i.e., displaying high affinity/CD8-independency toward the APL and low affinity/CD8-dependency toward the native CAP1 peptide.
  • Our data demonstrate that the efficient detection of self-antigen expressed by tumors could be a feature of high avidity CD8-independent T cells, and underline the need for extensive analysis of tumor cross-recognition prior to any clinical usage of APL as anti-cancer vaccines.
  • [MeSH-minor] Antibody Affinity. Antigens, Neoplasm / chemistry. Cancer Vaccines. Colorectal Neoplasms / metabolism. Epitopes / chemistry. HLA-A Antigens / chemistry. HLA-A2 Antigen. Immunotherapy / methods. Leukocytes, Mononuclear / metabolism. Ligands. Peptides / chemistry. Risk. T-Lymphocytes / metabolism

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  • (PMID = 17564703.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CAP1-6D; 0 / Cancer Vaccines; 0 / Epitopes; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / Ligands; 0 / Oligopeptides; 0 / Peptides; 0 / Receptors, Antigen, T-Cell
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29. Zhou GB, Zhang J, Wang ZY, Chen SJ, Chen Z: Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy. Philos Trans R Soc Lond B Biol Sci; 2007 Jun 29;362(1482):959-71
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  • [Title] Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy.
  • To turn a disease from highly fatal to highly curable is extremely difficult, especially when the disease is a type of cancer.
  • However, we can gain some insight into how this can be done by looking back over the 50-year history of taming acute promyelocytic leukaemia (APL).
  • APL is the M3 type of acute myeloid leukaemia characterized by an accumulation of abnormal promyelocytes in bone marrow, a severe bleeding tendency and the presence of the chromosomal translocation t(15;17) or variants.
  • APL was considered the most fatal type of acute leukaemia five decades ago and the treatment of APL was a nightmare for physicians.
  • Great efforts have been made by scientists worldwide to conquer this disease.
  • A rational and intriguing hypothesis, to induce differentiation of APL cells rather than killing them, was raised in the 1970s.
  • Laudably, the use of all-trans retinoic acid (ATRA) in treating APL resulted in terminal differentiation of APL cells and a 90-95% CR rate of patients, turning differentiation therapy in cancer treatment from hypothesis to practice.
  • When arsenic trioxide (ATO) was used to treat relapsed APL not only the patients but also the ancient drug were revived.
  • ATO exerts dose-dependent dual effects on APL cells: at low concentration, ATO induces partial differentiation, while at relatively high concentration, it triggers apoptosis.
  • Of note, both ATRA and ATO trigger catabolism of the PML-RARalpha fusion protein which is the key player in APL leukaemogenesis generated from t(15;17), targeting the RARalpha (retinoic acid receptor alpha) or promyelocytic leukaemia (PML) moieties, respectively.
  • Hence, in treating APL both ATRA and ATO represent paradigms for molecularly targeted therapy.
  • At molecular level, ATRA and ATO synergistically modulate multiple downstream pathways/cascades.
  • Strikingly, a clearance of PML-RARalpha transcript in an earlier and more thorough manner, and a higher quality remission and survival in newly diagnosed APL are achieved when ATRA is combined with ATO, as compared to either monotherapy, making APL a curable disease.
  • Thus, the story of APL can serve as a model for the development of curative approaches for disease; it suggests that molecularly synergistic targeted therapies are powerful tools in cancer, and dissection of disease pathogenesis or anatomy of the cancer genome is critical in developing molecular target-based therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

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  • (PMID = 17317642.001).
  • [ISSN] 0962-8436
  • [Journal-full-title] Philosophical transactions of the Royal Society of London. Series B, Biological sciences
  • [ISO-abbreviation] Philos. Trans. R. Soc. Lond., B, Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 90
  • [Other-IDs] NLM/ PMC2435563
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30. Tebo AE, Jaskowski TD, Hill HR, Branch DW: Clinical relevance of multiple antibody specificity testing in anti-phospholipid syndrome and recurrent pregnancy loss. Clin Exp Immunol; 2008 Dec;154(3):332-8
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  • [Title] Clinical relevance of multiple antibody specificity testing in anti-phospholipid syndrome and recurrent pregnancy loss.
  • We wanted to evaluate whether testing for anti-phosholipid antibodies other than anti-cardiolipin (aCL) and anti-beta-2 glycoprotein I (abeta2GPI) immunoglobulin (Ig)G and IgM identifies patients with recurrent pregnancy loss (RPL) who may be positive for anti-phospholipid syndrome (APS).
  • In a cross-sectional study comprising 62 patients with APS, 66 women with RPL, 50 healthy blood donors and 24 women with a history of successful pregnancies, we tested IgM and IgG antibodies to phosphatidic acid, phosphatidyl choline, phosphatidyl ethanolamine, phosphatidyl glycerol, phosphatidyl inositol and phosphatidyl serine with and without beta-2 glycoprotein I (beta2GPI) from a single manufacturer as well as aCL and abeta2GPI antibodies.
  • Diagnostic accuracies of individual and combined anti-phospholipid (aPL) assays were assessed by computing sensitivities, specificities, positive predictive values and negative predictive values together with their 95% confidence intervals.
  • The overall combined sensitivity of the non-recommended aPL assays was not significantly higher than that of the aCL and aB2GPI tests.
  • Multiple aPL specificities in RPL group is not significantly different from controls and therefore of no clinical significance.
  • [MeSH-major] Abortion, Habitual / immunology. Antiphospholipid Syndrome / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Antiphospholipid / blood. Antibody Specificity. Autoantibodies / blood. Biomarkers / blood. Cross-Sectional Studies. Female. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. Male. Middle Aged. Pregnancy. Sensitivity and Specificity. Young Adult. beta 2-Glycoprotein I / blood

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  • (PMID = 18826497.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Biomarkers; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / beta 2-Glycoprotein I
  • [Other-IDs] NLM/ PMC2633231
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31. Zhou J, Zhang Y, Li J, Li X, Hou J, Zhao Y, Liu X, Han X, Hu L, Wang S, Zhao Y, Zhang Y, Fan S, Lv C, Li L, Zhu L: Single-agent arsenic trioxide in the treatment of children with newly diagnosed acute promyelocytic leukemia. Blood; 2010 Mar 4;115(9):1697-702
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  • [Title] Single-agent arsenic trioxide in the treatment of children with newly diagnosed acute promyelocytic leukemia.
  • The aim of this study was to determine the efficacy and safety of treatment of pediatric acute promyelocytic leukemia (APL) with single-agent arsenic trioxide (ATO).
  • A total of 19 children (< or = 15 years of age) with newly diagnosed APL were treated with single-agent ATO for remission induction and postremission therapy.
  • With a median follow-up of 53 months (range, 23-76 months), the calculated 5-year overall survival and event-free survival were 83.9% and 72.7%, respectively, which are comparable with results achieved by the use of ATRA plus chemotherapy, which is the standard therapy for APL.
  • ATO resistance was observed in only 1 patient with a complex karyotype.
  • The results indicate the high efficacy and safety of single-agent ATO regimens in the treatment of children with de novo APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Karyotyping. Male. Neutropenia / chemically induced. Remission Induction. Time Factors

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  • (PMID = 20029047.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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32. Stern C, Chamley L: Antiphospholipid antibodies and coagulation defects in women with implantation failure after IVF and recurrent miscarriage. Reprod Biomed Online; 2006 Jul;13(1):29-37
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  • [Title] Antiphospholipid antibodies and coagulation defects in women with implantation failure after IVF and recurrent miscarriage.
  • Testing for antiphospholipid antibodies or thrombophilia is commonly carried out, and interpretation of results in the light of the current evidence is extremely difficult.
  • This paper reviews the purported pathogenetic mechanisms and clinical associations between both antiphospholipid antibodies and inherited thrombophilias, and reproductive failure.
  • The current management strategies are also critically evaluated and recommendations are made for optimal, evidence-based clinical practice.
  • [MeSH-major] Abortion, Habitual / blood. Abortion, Habitual / immunology. Antibodies, Antiphospholipid / blood. Embryo Implantation / immunology. Thrombophilia / blood

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  • (PMID = 16820106.001).
  • [ISSN] 1472-6483
  • [Journal-full-title] Reproductive biomedicine online
  • [ISO-abbreviation] Reprod. Biomed. Online
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Anticoagulants; 0 / Immunoglobulins, Intravenous
  • [Number-of-references] 96
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33. Fischer MJ, Rauch J, Levine JS: The antiphospholipid syndrome. Semin Nephrol; 2007 Jan;27(1):35-46
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  • [Title] The antiphospholipid syndrome.
  • The antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the clinical association of antiphospholipid autoantibodies (aPL) with a syndrome of hypercoagulability that can affect any blood vessel, irrespective of type or size.
  • We also discuss the impact that APS may have on pre-existing renal disease as well as current recommendations for treatment of APS.

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  • (PMID = 17336687.001).
  • [ISSN] 0270-9295
  • [Journal-full-title] Seminars in nephrology
  • [ISO-abbreviation] Semin. Nephrol.
  • [Language] ENG
  • [Grant] None / None / / 67101; Canada / Canadian Institutes of Health Research / / 67101
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 32
  • [Other-IDs] NLM/ CAMS2313; NLM/ PMC3440307
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34. Laskin CA, Spitzer KA, Clark CA, Crowther MR, Ginsberg JS, Hawker GA, Kingdom JC, Barrett J, Gent M: Low molecular weight heparin and aspirin for recurrent pregnancy loss: results from the randomized, controlled HepASA Trial. J Rheumatol; 2009 Feb;36(2):279-87
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  • OBJECTIVE: To compare live birth rates in women with recurrent pregnancy loss (RPL) and either autoantibodies or a coagulation abnormality, treated with low molecular weight heparin plus aspirin (LMWH/ASA) or ASA alone, and to place our results in context with other randomized clinical trials (RCT) with similar cohorts.
  • METHODS: The HepASA Trial was an RCT including patients with a history of RPL and at least 1 of the following: antiphospholipid antibody (aPL), an inherited thrombophilia, or antinuclear antibody.
  • Treatment groups were stratified by aPL status and history of early versus late pregnancy losses.
  • RESULTS: Over 4 years, 859 women with RPL were screened: 88 (10.2%) fulfilled inclusion criteria, became pregnant and were randomized to receive either LMWH/ASA or ASA alone. aPL were present in 42 (47.7%) patients in each group.
  • Neither number of prior losses nor aPL status was correlated with pregnancy outcome.
  • Mean change in BMD did not differ by treatment group at either the lumbar spine (p = 0.57) or femoral neck (p = 0.15).
  • RCT since 2000 for aPL positive women with RPL and similar inclusion criteria report a mean live birth rate of 75% with either LMWH or ASA.
  • Regardless of treatment regimen, number of prior losses, or aPL positivity, almost 80% of women in our RPL cohort had a successful pregnancy outcome.
  • [MeSH-minor] Adult. Antibodies, Antinuclear / immunology. Anticoagulants / administration & dosage. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / drug therapy. Antiphospholipid Syndrome / physiopathology. Bone Density / drug effects. Cohort Studies. Female. Humans. Platelet Aggregation Inhibitors / administration & dosage. Pregnancy. Thrombophilia / complications. Thrombophilia / drug therapy. Thrombophilia / physiopathology. Treatment Outcome


35. Si J, Mueller L, Schuler A, Simon J, Collins SJ: The retinoic acid receptor/CaMKII interaction: pharmacologic inhibition of CaMKII enhances the differentiation of myeloid leukemia cells. Blood Cells Mol Dis; 2007 Nov-Dec;39(3):307-15
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  • [Title] The retinoic acid receptor/CaMKII interaction: pharmacologic inhibition of CaMKII enhances the differentiation of myeloid leukemia cells.
  • Certain myeloid leukemia cells, particularly the acute promyelocytic leukemia (APL) subset, undergo terminal granulocytic differentiation in response to retinoic acid (RA).
  • RA mediates its biologic effects through specific retinoic acid receptors (RARs) which serve as ligand-activated nuclear transcription factors.
  • We have observed significant cross-talk between these Ca(++) and RA signaling pathways that regulates the differentiation of myeloid leukemia cells.
  • We observe that CaMKIIgamma is the CaMK that is predominantly expressed in myeloid cells.
  • This enzyme localizes to the promoter of RAR target genes, physically interacts with and phosphorylates RARalpha and inhibits RAR transcriptional activity.
  • KN-62, a pharmacological inhibitor of the CaMKs, enhances both retinoic acid receptor transcriptional activity as well as the terminal in vitro differentiation of certain myeloid leukemia cell lines including HL-60.
  • Nevertheless, our observations suggest that CaMKIIgamma may provide a new therapeutic target for the treatment of the RA-responsive human myeloid leukemias.

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  • [RetractionIn] Blood Cells Mol Dis. 2009 May-Jun;42(3):300 [19388154.001]
  • (PMID = 17644368.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA118971-02; United States / NHLBI NIH HHS / HL / HL54881; United States / NCI NIH HHS / CA / R01 CA118971; United States / NCI NIH HHS / CA / R01 CA118971-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 127191-97-3 / KN 62; 5688UTC01R / Tretinoin; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2
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36. Pagnoux C, Korach JM, Guillevin L: Indications for plasma exchange in systemic lupus erythematosus in 2005. Lupus; 2005;14(11):871-7
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  • [Title] Indications for plasma exchange in systemic lupus erythematosus in 2005.
  • Plasma exchange can remove putative pathogenic autoantibodies and circulating immune complexes from the blood of patients with systemic lupus erythematosus (SLE).
  • We review herein the principal historical steps of the use of plasma exchange to treat SLE, based upon the main trials and case reports that have highlighted its most pertinent indications.
  • Acute life-threatening manifestations and severe therapy-resistant manifestations, like refractory SLE renal disease, diffuse alveolar hemorrhage, neuropsychiatric SLE, thrombotic thrombocytopenic purpura, catastrophic antiphospholipid syndrome, hyperviscosity syndrome and cryoglobulinemia, are the indications for which plasma exchange might have a beneficial therapeutic role.
  • Although few SLE patients undergo plasma exchange each year nowadays (10-20 per year in France), adverse events are very rare and recent advances in plasma exchange technologies, like immunoadsorption, might, in the future, counterbalance their cost and broaden their place in the therapeutic armamentarium for SLE.
  • [MeSH-major] Lupus Erythematosus, Systemic / therapy. Plasma Exchange / methods. Plasma Exchange / trends

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  • (PMID = 16335578.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 100
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37. Markowski TR, Martin DB, Kao GF, Lutz L, Deng A, Gaspari AA: Leukemia cutis: a presenting sign in acute promyelocytic leukemia. Arch Dermatol; 2007 Sep;143(9):1220-1
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  • [Title] Leukemia cutis: a presenting sign in acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Leg Dermatoses / diagnosis. Middle Aged

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  • (PMID = 17875899.001).
  • [ISSN] 0003-987X
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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38. Lu J, Chew EH, Holmgren A: Targeting thioredoxin reductase is a basis for cancer therapy by arsenic trioxide. Proc Natl Acad Sci U S A; 2007 Jul 24;104(30):12288-93
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  • Arsenic trioxide (ATO) is an effective cancer therapeutic drug for acute promyelocytic leukemia and has potential anticancer activity against a wide range of solid tumors.

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  • (PMID = 17640917.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Enzyme Inhibitors; 0 / Oxides; EC 1.8.1.9 / Thioredoxin-Disulfide Reductase; GAN16C9B8O / Glutathione; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC1940330
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39. Walter MJ, Park JS, Ries RE, Lau SK, McLellan M, Jaeger S, Wilson RK, Mardis ER, Ley TJ: Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha. Proc Natl Acad Sci U S A; 2005 Aug 30;102(35):12513-8
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  • [Title] Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.
  • Recently, haploinsufficiency for PU.1 has been shown to cause a shift in myelomonocytic progenitor fate toward the myeloid lineage.
  • We have previously shown that transgenic mice expressing PML-RARalpha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a large (>20 Mb) interstitial deletion of chromosome 2 that includes PU.1.
  • To directly assess the relevance of levels of expression of PU.1 for leukemia progression, we bred hCG-PR mice with PU.1+/- mice and assessed their phenotype.
  • Young, nonleukemic hCG-PR x PU.1+/- mice developed splenomegaly because of the abnormal expansion of myeloid cells in their spleens. hCG-PR x PU.1+/- mice developed a typical APL syndrome after a long latent period, but the penetrance of disease was 84%, compared with 7% in hCG-PR x PU.1+/+ mice (P < 0.0001).
  • The residual PU.1 allele in hCG-PR x PU.1+/- APL cells was expressed, and complete exonic resequencing revealed no detectable mutations in nine of nine samples.
  • However, PR expression in U937 myelomonocytic cells and primary murine myeloid bone marrow cells caused a reduction in PU.1 mRNA levels.
  • Therefore, the loss of one copy of PU.1 through a deletional mechanism, plus down-regulation of the residual allele caused by PR expression, may synergize to expand the pool of myeloid progenitors that are susceptible to transformation, increasing the penetrance of APL.

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  • (PMID = 16113082.001).
  • [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 / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / R01 CA083962; United States / NCI NIH HHS / CA / CA101937; United States / NCI NIH HHS / CA / CA83962
  • [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 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Trans-Activators; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ PMC1188022
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40. Campos B, Chames M, Lantry JM, Bill JP, Eis A, Brockman D, Neil J, Tischner E, Barton J, Wong C, Schwemberger S, Cornelius J, Myatt L, Baeza I, Hnat M: Determination of non-bilayer phospholipid arrangements and their antibodies in placentae and sera of patients with hypertensive disorders of pregnancy. Placenta; 2006 Feb-Mar;27(2-3):215-24
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  • [Title] Determination of non-bilayer phospholipid arrangements and their antibodies in placentae and sera of patients with hypertensive disorders of pregnancy.
  • Antiphospholipid antibodies (APA) in circulation are also associated with vascular diseases.
  • In fact, the pathology of placentae from PE and Antiphospholipid syndrome patients is similar; atherosis, thrombosis and infarction, and endothelium activation represent the pathological mechanisms.
  • We identified a new antibody which recognizes non-bilayer phospholipid arrangements (NPA) in membrane models and in cell membranes in vivo, and which triggered an autoimmune-like disease in mice.
  • Results showed increased levels of NPA in the syncytiotrophoblast, extravillous cytotrophoblast, syncytial knots and the amnion epithelial cell membranes of the placenta, as well as increases in NPA and NPA antibodies in sera from HDP patients, when compared with controls.
  • [MeSH-major] Antibodies, Antiphospholipid / analysis. Membrane Lipids / analysis. Phospholipids / analysis. Placenta / chemistry. Pre-Eclampsia / etiology

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  • (PMID = 16338467.001).
  • [ISSN] 0143-4004
  • [Journal-full-title] Placenta
  • [ISO-abbreviation] Placenta
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / HD40363
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Membrane Lipids; 0 / Phospholipids
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41. Hasan SK, Mays AN, Ottone T, Ledda A, La Nasa G, Cattaneo C, Borlenghi E, Melillo L, Montefusco E, Cervera J, Stephen C, Satchi G, Lennard A, Libura M, Byl JA, Osheroff N, Amadori S, Felix CA, Voso MT, Sperr WR, Esteve J, Sanz MA, Grimwade D, Lo-Coco F: Molecular analysis of t(15;17) genomic breakpoints in secondary acute promyelocytic leukemia arising after treatment of multiple sclerosis. Blood; 2008 Oct 15;112(8):3383-90
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  • [Title] Molecular analysis of t(15;17) genomic breakpoints in secondary acute promyelocytic leukemia arising after treatment of multiple sclerosis.
  • Therapy-related acute promyelocytic leukemia (t-APL) with t(15;17) translocation is a well-recognized complication of cancer treatment with agents targeting topoisomerase II.
  • Analysis of 12 cases of mitoxantrone-related t-APL in MS patients revealed an altered distribution of chromosome 15 breakpoints versus de novo APL, biased toward disruption within PML intron 6 (11 of 12, 92% vs 622 of 1022, 61%: P = .035).
  • Despite this intron spanning approximately 1 kb, breakpoints in 5 mitoxantrone-treated patients fell within an 8-bp region (1482-9) corresponding to the "hotspot" previously reported in t-APL, complicating mitoxantrone-containing breast cancer therapy.
  • Another shared breakpoint was identified within the approximately 17-kb RARA intron 2 involving 2 t-APL cases arising after mitoxantrone treatment for MS and breast cancer, respectively.
  • Analysis of PML and RARA genomic breakpoints in functional assays in 4 cases, including the shared RARA intron 2 breakpoint at 14 446-49, confirmed each to be preferential sites of topoisomerase IIalpha-mediated DNA cleavage in the presence of mitoxantrone.
  • This study further supports the presence of preferential sites of DNA damage induced by mitoxantrone in PML and RARA genes that may underlie the propensity to develop this subtype of leukemia after exposure to this agent.

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  • (PMID = 18650449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077683; United States / NIGMS NIH HHS / GM / R01 GM033944; United States / NIGMS NIH HHS / GM / GM33944; United States / NCI NIH HHS / CA / R01CA077683
  • [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 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 9007-49-2 / DNA; BZ114NVM5P / Mitoxantrone; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC2954750
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42. Zhang L, Chen YM, Zou Y, Chen XJ, Yang WY, Wang SC, Wang JX, Zhu XF: [Retrospective analysis of 76 children with acute promyelocytic leukemia]. Zhonghua Er Ke Za Zhi; 2009 Sep;47(9):710-3
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  • [Title] [Retrospective analysis of 76 children with acute promyelocytic leukemia].
  • OBJECTIVE: There are very limited data on childhood acute promyelocytic leukemia (APL), especially childhood APL treated with arsenic trioxide (As(2)O(3)).
  • METHOD: Between January 1999 and December 2007, 76 children (< 18 years) with newly diagnosed APL were included.
  • The 5-year cumulative incidence of relapse was 13.8%, whereas event-free (EFS), disease-free (DFS) and overall survival rates were 79.5%, 86.3% and 90.5%, respectively.
  • CONCLUSION: As(2)O(3) is an effective and well tolerable therapy for children with APL and it may be used in those who not only cannot bear side effects of ATRA but also the newly diagnosed and relapsed APL.
  • [MeSH-major] Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 20021798.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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43. Ravandi F, Estey E, Jones D, Faderl S, O'Brien S, Fiorentino J, Pierce S, Blamble D, Estrov Z, Wierda W, Ferrajoli A, Verstovsek S, Garcia-Manero G, Cortes J, Kantarjian H: Effective treatment of acute promyelocytic leukemia with all-trans-retinoic acid, arsenic trioxide, and gemtuzumab ozogamicin. J Clin Oncol; 2009 Feb 1;27(4):504-10
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  • [Title] Effective treatment of acute promyelocytic leukemia with all-trans-retinoic acid, arsenic trioxide, and gemtuzumab ozogamicin.
  • PURPOSE: We examined the outcome of patients with newly diagnosed acute promyelocytic leukemia (APL) treated with all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) with or without gemtuzumab ozogamicin (GO) but without traditional cytotoxic chemotherapy.
  • PATIENTS AND METHODS: From February 2002 to March 2008, 82 patients with APL were treated with a combination of ATRA plus ATO.
  • From July 2007, the second cohort of 17 patients received ATRA and ATO concomitantly on day 1.
  • Monitoring for PML-RARA fusion gene was conducted after induction and throughout consolidation and follow-up.
  • Seven patients died at a median of 4 days (range, 1 to 24 days) after inclusion in the study from disease-related complications.
  • CONCLUSION: The combination of ATRA and ATO (with or without GO) as initial therapy for APL was effective and safe and can substitute chemotherapy-containing regimens.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 19075265.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / gemtuzumab; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC4881307
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44. Ma J: Advances in management of acute promyelocytic leukemia with arsenic trioxide. Chin J Integr Med; 2007 Jun;13(2):92-4
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  • [Title] Advances in management of acute promyelocytic leukemia with arsenic trioxide.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 17609904.001).
  • [ISSN] 1672-0415
  • [Journal-full-title] Chinese journal of integrative medicine
  • [ISO-abbreviation] Chin J Integr Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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45. Pan M, Chu M, Sun Y, Song X, Zhu J: [Preparation and characterization of quantum dots-peptides bioconjugations and their specificity related to recognizing tumor cells]. Sheng Wu Yi Xue Gong Cheng Xue Za Zhi; 2007 Jun;24(3):577-81
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  • Water-soluble CdTe quantum dots synthesized in aqueous solution have been conjugated with peptide LyP-1 using N-Succinimidyl 3-[2-pyridyldithio]-propionate (SPDP) as a cross-linking reagent.
  • Capillary electrophoresis (CE), UV-Vis absorption and photoluminescent (PL) spectra suggested that the peptide had been successfully linked to the QDs.
  • The QDs-peptides conjugates could specifically recognize the lung adenoma cancer cells (SPCA-1), but did not recognize promyelocytic leukemia cells (HL-60).

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  • (PMID = 17713265.001).
  • [ISSN] 1001-5515
  • [Journal-full-title] Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi
  • [ISO-abbreviation] Sheng Wu Yi Xue Gong Cheng Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / LyP-1 protein, mouse; 0 / Oligopeptides; 0 / Peptides; 0 / Peptides, Cyclic; 99896-85-2 / arginyl-glycyl-aspartic acid
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46. Crowder C, Dahle Ø, Davis RE, Gabrielsen OS, Rudikoff S: PML mediates IFN-alpha-induced apoptosis in myeloma by regulating TRAIL induction. Blood; 2005 Feb 1;105(3):1280-7
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  • [Title] PML mediates IFN-alpha-induced apoptosis in myeloma by regulating TRAIL induction.
  • Interferon (IFN) induces expression of proapoptotic genes and has been used in the clinical treatment of multiple myeloma.
  • The promyelocytic leukemia (PML) gene is an IFN-induced target that encodes a tumor suppressor protein.
  • PML protein is typically localized within discrete speckled nuclear structures termed PML nuclear bodies (NBs).
  • Herein, we show that growth inhibition effects of IFN-alpha in myeloma cells correlate with PML NBs and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induction, whereas known IFN targets including signal transducer and activator of transcription-1 (STAT1), STAT3, p38, and Daxx cannot account for these differential responses.
  • RNAi silencing of PML blocks IFN-alpha-induced apoptosis in myeloma cells and correspondingly down-regulates TRAIL expression.
  • These results demonstrate that PML and TRAIL play important roles in IFN-induced apoptosis and identify TRAIL as a novel downstream transcriptional target of PML.
  • Identification of PML and PML NBs as effectors of IFN responses provides insights into mechanisms by which tumor cells exhibit resistance to this class of agents and may prove useful in assessing treatment regimens.
  • [MeSH-major] Apoptosis / drug effects. Interferon-alpha / pharmacology. Membrane Glycoproteins / physiology. Neoplasm Proteins / physiology. Nuclear Proteins / physiology. Transcription Factors / physiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Apoptosis Regulatory Proteins. Cell Division / drug effects. Cell Line, Tumor. Humans. Leukemia, Promyelocytic, Acute. Multiple Myeloma. RNA, Small Interfering / genetics. TNF-Related Apoptosis-Inducing Ligand. Transfection. Tumor Suppressor Proteins

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  • (PMID = 15459016.001).
  • [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 / Apoptosis Regulatory Proteins; 0 / Interferon-alpha; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
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47. Liu BH, Wu TS, Yu FY, Su CC: Induction of oxidative stress response by the mycotoxin patulin in mammalian cells. Toxicol Sci; 2007 Feb;95(2):340-7
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  • When cell-permeating fluorescent dyes were used as indicators of the generation of reactive oxygen species (ROS), we found that PAT treatment directly increased intracellular oxidative stress in human embryonic kidney (HEK293) and human promyelocytic leukemia (HL-60) cells.
  • Lipid peroxidation levels were also significantly increased in HL-60 cells and mouse kidney homogenates treated with PAT.
  • Pretreatment of HEK293 cells with Tiron, a free radical scavenger, reduced the phosphorylation levels of extracellular signal-regulated kinase (ERK) 1/2 elicited by PAT.
  • The ERK1/2 signaling pathway inhibitor, U0126, also significantly decreased the levels of ROS associated with PAT treatment.

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  • (PMID = 17090621.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Free Radical Scavengers; 0 / Reactive Oxygen Species; 95X2BV4W8R / Patulin; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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48. Araujo FD, Stracker TH, Carson CT, Lee DV, Weitzman MD: Adenovirus type 5 E4orf3 protein targets the Mre11 complex to cytoplasmic aggresomes. J Virol; 2005 Sep;79(17):11382-91
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  • [Title] Adenovirus type 5 E4orf3 protein targets the Mre11 complex to cytoplasmic aggresomes.
  • Rearrangement of Mre11 and Rad50 by Ad5 E4orf3 is not dependent on interactions with Nbs1 or promyelocytic leukemia protein nuclear bodies.

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  • (PMID = 16103189.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA097093; United States / NIAID NIH HHS / AI / AI43341; United States / NCI NIH HHS / CA / CA97093
  • [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 / Adenovirus E4 Proteins; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / MRE11A protein, human; 0 / Multiprotein Complexes; 0 / NBN protein, human; 0 / Nuclear Proteins; 0 / Rad50 protein, human; 0 / Tubulin; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ PMC1193610
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49. van Os GM, Urbanus RT, Agar C, Meijers JC, de Groot PG: Antiphospholipid syndrome. Current insights into laboratory diagnosis and pathophysiology. Hamostaseologie; 2010 Aug;30(3):139-43
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  • [Title] Antiphospholipid syndrome. Current insights into laboratory diagnosis and pathophysiology.
  • The antiphospholipid syndrome (APS) is a non-inflammatory autoimmune disease characterized by the presence of antiphospholipid antibodies (aPL) in the plasma of patients with vascular thrombosis, recurrent complications of pregnancy, or both (1, 2).
  • The presence of aPL in plasma of patients can be detected with either a prolongation of phospholipid dependent coagulation tests (lupus anticoagulant, LAC), or with solid phase immune assays against the protein beta2-glycoprotein I (beta2-GPI) or the phospholipid cardiolipin (anti-beta2-GPI antibody ELISA and anti-cardiolipin antibody ELISA, respectively) (3).
  • To solve this dispute, an international consensus meeting was organized in Sapporo in 1999 to formulate classification criteria for patients with the antiphospholipid syndrome (4).
  • This is very unfortunate because the specificity of the different aPL assays to detect the clinical manifestations that characterize APS are disputable.
  • One of the aims of defining the criteria was to initiate studies to determine the value of the different anti-phospholipid antibody assays to serve as biomarker for the risk of thrombosis and pregnancy morbidity.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / physiopathology
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. Antibodies, Antiphospholipid / physiology. Clinical Laboratory Techniques. Female. Humans. Pregnancy. Pregnancy Complications / blood

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  • (PMID = 20680233.001).
  • [ISSN] 0720-9355
  • [Journal-full-title] Hämostaseologie
  • [ISO-abbreviation] Hamostaseologie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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50. Tennent-Brown BS, Wilkins PA, Lindborg S, Russell G, Boston RC: Assessment of a point-of-care lactate monitor in emergency admissions of adult horses to a referral hospital. J Vet Intern Med; 2007 Sep-Oct;21(5):1090-8
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  • BACKGROUND: Blood lactate concentration [LAC] is considered a useful indicator of disease severity in horses.
  • HYPOTHESIS: It was hypothesized that results from a POC lactate monitor would be in agreement with a laboratory-based measurement of [LAC].
  • [LAC] was measured with whole blood (AWB) and plasma (APL) by means of a POC monitor (Accutrend) and compared with results from whole blood measured by a laboratory blood gas analyzer (NOVA).
  • Agreement (p +/- SE) was closest between APL and NOVA (0.97 +/- 0.01); an average observed difference of 0.15 +/- 0.89 (mean +/- SD) and 95% limits of agreement (LOA) -1.89, 1.59 also were found.
  • CONCLUSIONS AND CLINICAL IMPORTANCE: Results indicate close agreement between NOVA and the POC monitor when [LAC] was measured with plasma.

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  • (PMID = 17939569.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 33X04XA5AT / Lactic Acid
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51. Ortona E, Capozzi A, Colasanti T, Conti F, Alessandri C, Longo A, Garofalo T, Margutti P, Misasi R, Khamashta MA, Hughes GR, Valesini G, Sorice M: Vimentin/cardiolipin complex as a new antigenic target of the antiphospholipid syndrome. Blood; 2010 Oct 21;116(16):2960-7
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  • [Title] Vimentin/cardiolipin complex as a new antigenic target of the antiphospholipid syndrome.
  • Antiphospholipid syndrome (APS) is an autoimmune disease characterized by arterial and venous thrombosis, recurrent abortions, and antiphospholipid antibodies (aPL).
  • However, it is possible to find patients with clinical signs of APS who persistently test negative for aPL (seronegative APS, or SN-APS).
  • We tested sera from patients with SN-APS with a proteomic approach by analyzing endothelial cell-surface membrane proteins.
  • Our results prompt to identify vimentin as a "new" cofactor for aPL, which may represent a useful tool mainly in SN-APS patients.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Autoantibodies / immunology. Cardiolipins / immunology. Vimentin / immunology

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  • [CommentIn] Blood. 2010 Oct 21;116(16):2867-9 [20966174.001]
  • (PMID = 20634382.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Cardiolipins; 0 / NF-kappa B; 0 / Vimentin; EC 2.7.11.1 / IRAK1 protein, human; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases
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52. Graw-Panzer KD, Verma S, Rao S, Miller ST, Lee H: Venous thrombosis and pulmonary embolism in a child with pneumonia due to Mycoplasma pneumoniae. J Natl Med Assoc; 2009 Sep;101(9):956-8
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  • [Title] Venous thrombosis and pulmonary embolism in a child with pneumonia due to Mycoplasma pneumoniae.
  • A 13-year-old boy with Mycoplasma pneumoniae pulmonary infection developed deep vein thrombosis and pulmonary embolism.
  • He was found to have protein S deficiency and transient antiphospholipid antibodies.
  • Though uncommon, it is important to consider venous thromboembolic disease in children whose clinical course is atypically severe.
  • [MeSH-major] Lupus Erythematosus, Systemic / complications. Pneumonia, Mycoplasma / complications. Pulmonary Embolism / etiology. Venous Thrombosis / etiology
  • [MeSH-minor] Adolescent. Anticoagulants / therapeutic use. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / immunology. Heparin / therapeutic use. Humans. Male. Protein S Deficiency / complications. Protein S Deficiency / immunology. Warfarin / therapeutic use


53. Miesbach W, Chapman J, Scharrer I: Focal seizures after treatment with fluvastatin in a patient with a history of catastrophic antiphospholipid syndrome. J Neurol Sci; 2005 Nov 15;238(1-2):93-5
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  • [Title] Focal seizures after treatment with fluvastatin in a patient with a history of catastrophic antiphospholipid syndrome.
  • The symptoms appeared one day after start of the treatment with fluvastatin (40 mg) administered in order to diminish the endothelial activation induced by antiphospholipid antibodies (aPL).
  • The patient suffered from severe manifestations of the antiphospholipid syndrome (APS) including Catastrophic Antiphospholipid Syndrome (CAPS, Asherson's syndrome).
  • [MeSH-major] Antiphospholipid Syndrome / complications. Epilepsies, Partial / chemically induced. Fatty Acids, Monounsaturated / adverse effects. Hydroxymethylglutaryl-CoA Reductase Inhibitors / adverse effects. Indoles / adverse effects. Seizures / chemically induced


54. Cheunsuchon B, Rungkaew P, Chawanasuntorapoj R, Pattaragarn A, Parichatikanond P: Prevalence and clinicopathologic findings of antiphospholipid syndrome nephropathy in Thai systemic lupus erythematosus patients who underwent renal biopsies. Nephrology (Carlton); 2007 Oct;12(5):474-80
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  • [Title] Prevalence and clinicopathologic findings of antiphospholipid syndrome nephropathy in Thai systemic lupus erythematosus patients who underwent renal biopsies.
  • AIM: To determine the prevalence of antiphospholipid syndrome nephropathy (APSN) in Thai systemic lupus erythematosus (SLE) patients who underwent renal biopsy and to compare the relationship of renal histopathology and other significant clinical parameters between SLE patients with and without APSN.
  • METHODS: A retrospective analysis was undertaken in systemic lupus erythematosus patients (n = 150, 44 <15 years old, 106 0e;15 years old) who underwent renal biopsy.
  • The specimens were evaluated for histological features of APSN and other significant clinical parameters.
  • The result of antiphospholipid antibodies, clinical course, and renal function from chart review were analysed.
  • RESULTS: The prevalence of APSN in systemic lupus erythematosus patients who underwent renal biopsies was 34% (16% in <15-year-old group, 41.5% in > or =15-year-old group).
  • APSN was associated with more severe hypertension (P = 0.002 for systolic and P = 0.004 for diastolic blood pressure), acute renal failure (P = 0.003), persistent heavy proteinuria (P < 0.001 for 4+ proteinuria), severe lupus nephritis (class III and IV, P = 0.014, high activity and chronicity indices, P < 0.001) and a tendency to progress to end-stage renal disease.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / epidemiology. Kidney / pathology. Kidney Diseases / etiology. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / physiopathology
  • [MeSH-minor] Adolescent. Adult. Biopsy. Child. Child, Preschool. Chronic Disease. Disease Progression. Female. Humans. Infant. Kidney Failure, Chronic / etiology. Male. Middle Aged. Prevalence. Retrospective Studies. Severity of Illness Index. Thailand


55. de Meis E, Monteiro RQ, Levy RA: Lung adenocarcinoma and antiphospholipid antibodies. Autoimmun Rev; 2009 May;8(6):529-32
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  • [Title] Lung adenocarcinoma and antiphospholipid antibodies.
  • Thrombosis is a frequent finding in cancer patients, being referred to as a poor prognostic factor.
  • A number of studies have demonstrated the presence of antiphospholipid antibodies (aPL) in cancer patients, suggesting a potential role in tumor-associated thrombosis.
  • A prospective analysis has been performed in a group of lung adenocarcinoma patients in respect to the presence of aPL and thrombotic manifestations.
  • On the other hand, patients that displayed IgM anti-beta2-glycoprotein I (abeta2GPI) (22/80) showed an unexpected decrease in thrombosis risk (2/22, with IgM abeta2GPI vs 18/58, without IgM abeta2GPI RR=0.29; p=0.04).
  • Considerations on the mechanisms that link cancer, thrombosis and aPL are discussed in this article.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / immunology. Antibodies, Antiphospholipid / blood. Lung Neoplasms / diagnosis. Lung Neoplasms / immunology

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  • (PMID = 19185619.001).
  • [ISSN] 1873-0183
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I
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56. Takenokuchi M, Nakamachi Y, Yoneda K, Joo K, Kawano S, Tatsumi E, Saigo K, Kumagai S: Quantitative detection of PML-RARalpha fusion transcript by real-time PCR with a single primer pair. J Clin Lab Anal; 2009;23(4):223-30
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  • [Title] Quantitative detection of PML-RARalpha fusion transcript by real-time PCR with a single primer pair.
  • Quantitative detection of minimal residual disease has prognostic value for some leukemias.
  • Acute promyelocytic leukemia (APL) is characterized by the specific PML-RARalpha fusion gene from t(15;17).
  • Added to three PML-RARalpha isoforms, alternative spliced forms of PML exons give rise to multiple isoforms even within a single patient.
  • To date, multiple primer pairs for the detection of the various PML-RARalpha transcripts have been designed, potentially generating some nonspecific amplification products.
  • Here, we established a real-time quantitative PCR (RQ-PCR) strategy with a single primer pair using LightCycler (sp-RQ-PCR), which could simultaneously detect three isoforms with equal specificity and sensitivity as well as alternative spliced forms.
  • Results obtained with sp-RQ-PCR for 39 samples from 15 APL patients and 31 non-APL samples were compared with those with TaqMan assay with three primer pairs.
  • In two of the APL samples, PML-RARalpha was detected in the TM, but not in the sp-RQ-PCR or nested PCR.
  • Furthermore, the sp-RQ-PCR showed no positive results for the 31 non-APL samples, whereas the TM identified 13% (4/31) as positive.
  • Electrophoresis detected some artifacts in the TM, which do not correspond to PML-RARalpha.
  • We conclude that our sp-RQ-PCR is specific enough to identify various forms of PML-RARalpha and yields no false-positive results.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. Receptors, Retinoic Acid / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19623654.001).
  • [ISSN] 1098-2825
  • [Journal-full-title] Journal of clinical laboratory analysis
  • [ISO-abbreviation] J. Clin. Lab. Anal.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / RNA, Neoplasm; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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57. Sayarlioglu M, Topcu N, Harman M, Guntekin U, Erkoc R: A case of antiphospholipid syndrome presenting with pulmonary truncus and main pulmonary artery thrombosis. Rheumatol Int; 2005 Jan;25(1):65-8
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  • [Title] A case of antiphospholipid syndrome presenting with pulmonary truncus and main pulmonary artery thrombosis.
  • In patients with antiphospholipid syndrome (APS), thromboembolism and pulmonary hypertension are the most common pulmonary manifestations.
  • Thrombotic obstruction at the level of the main and/or proximal pulmonary arteries is rare.
  • We report a 40-year-old woman without any history of previous arterial and/or venous thrombosis who presented with severe dyspnea and was found to have pulmonary hypertension and positivity for anticardiolipin antibodies.
  • Computed tomography revealed pulmonary truncus thrombosis extending to both right and left pulmonary arteries.
  • This is the first reported case with thrombosis of pulmonary truncus and main pulmonary arteries concurrent with APS.
  • [MeSH-major] Antiphospholipid Syndrome / pathology. Pulmonary Artery / pathology. Pulmonary Embolism / pathology
  • [MeSH-minor] Adult. Antibodies, Anticardiolipin / blood. Diagnosis, Differential. Echocardiography. Fatal Outcome. Female. Humans. Hypertension, Pulmonary / etiology. Hypertension, Pulmonary / pathology. Radiography, Thoracic. Tomography, X-Ray Computed

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  • [Cites] Ann Thorac Surg. 1998 Dec;66(6):1919-24 [9930469.001]
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  • (PMID = 15378261.001).
  • [ISSN] 0172-8172
  • [Journal-full-title] Rheumatology international
  • [ISO-abbreviation] Rheumatol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin
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58. Andreoli L, Malacarne F, Ceribelli A, Kutschera I, Tincani A: Anti-cardiolipin and anti-beta2-glycoprotein I antibodies: performance of new commercial ELISA kits. Ann N Y Acad Sci; 2007 Aug;1109:531-7
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  • [Title] Anti-cardiolipin and anti-beta2-glycoprotein I antibodies: performance of new commercial ELISA kits.
  • Antiphospholipid antibodies (aPL) are known to be pathogenic in experimental models and are predictive of thrombosis and miscarriages in patients, so it is important to correctly evaluate their presence for identifying patients at risk.
  • Despite many years of work, the standardization of aPL ELISA remains an open problem, so evaluation of newly introduced commercial preparations is mandatory.
  • A total of 80 sera were collected (10 primary antiphospholipid syndromes (APSs), 10 APSs associated with systemic lupus erythematosus, 20 infectious diseases, 20 rheumatoid arthritis and 20 normal blood donors) and tested for IgG/IgM anti-cardiolipin and anti-beta2GPI antibodies on commercial ELISA kits (ETI) by DiaSorin and on home-made ELISA.

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  • (PMID = 17785342.001).
  • [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 / Antibodies; 0 / Cardiolipins; 0 / beta 2-Glycoprotein I
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59. Stein E, McMahon B, Kwaan H, Altman JK, Frankfurt O, Tallman MS: The coagulopathy of acute promyelocytic leukaemia revisited. Best Pract Res Clin Haematol; 2009 Mar;22(1):153-63
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  • [Title] The coagulopathy of acute promyelocytic leukaemia revisited.
  • Since the initial description of the disease, the life-threatening coagulopathy associated with acute promyelocytic leukaemia (APL) has been the defining clinical characteristic.
  • Historically, this uncommon subtype of acute myeloid leukaemia has been associated with a high mortality rate during induction therapy, most frequently attributable to haemorrhage.
  • Since the introduction of all-trans retinoic acid (ATRA) into the therapy of all patients with APL, disease-free survival and overall survival have improved dramatically, such that the disease is now highly curable.
  • As a result, while the predominant clinical manifestation of the coagulopathy is haemorrhage, thromboembolic events may occur both at presentation and during therapy.
  • A major recent finding is the high expression of annexin II in the leukaemic cells from patients with APL.
  • Annexin II is a protein with high affinity for plasminogen and tissue-type plasminogen activator (tPA), and also acts as a cofactor for plasminogen activation by tPA.
  • Annexin II is expressed in high amounts in cerebral microvascular endothelial cells, perhaps accounting for the relatively high incidence of intracranial haemorrhage in APL compared with other sites.
  • Recent studies have found that microparticles containing tissue factor, tPA, plasminogen activator inhibitor-1 and annexin II have been found in the plasma of APL patients, suggesting a role in pathogenesis of the coagulopathy.
  • The most important factor may be the early introduction of ATRA at the first suspicion of a diagnosis of APL, before it is confirmed genetically.
  • [MeSH-major] Blood Coagulation Disorders / complications. Hemorrhage / complications. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 19285282.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009207
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Annexin A2; 5688UTC01R / Tretinoin; 9001-91-6 / Plasminogen; EC 3.4.21.68 / Tissue Plasminogen Activator
  • [Number-of-references] 64
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60. Avetisov SE, Smirnova TV, Kozlovskaia NL, Kazarian EE, Budzinskaia MV: [Multifocal electroretinography in ophtalmological symptoms in patients with antiphospholipid syndrome]. Vestn Oftalmol; 2009 Jan-Feb;125(1):46-9
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  • [Title] [Multifocal electroretinography in ophtalmological symptoms in patients with antiphospholipid syndrome].
  • The paper describes the first experience in using multifocal electroretinography (mfERG) in patients with antiphospholipid syndrome (APS).
  • In the latter, thrombogenesis is mosaic in most cases so the techniques providing a spatial imaging of the pathological process is of interest in the examination of patients with this disease.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Electroretinography / methods. Retina / physiopathology. Retinal Diseases / physiopathology
  • [MeSH-minor] Adolescent. Adult. Diagnosis, Differential. Humans. Middle Aged. Visual Field Tests. Visual Fields / physiology. Young Adult

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  • (PMID = 19284102.001).
  • [ISSN] 0042-465X
  • [Journal-full-title] Vestnik oftalmologii
  • [ISO-abbreviation] Vestn Oftalmol
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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61. Singh A, Blank M, Shoenfeld Y, Illges H: Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-beta2-glycoprotein-I autoantibodies. Rheumatol Int; 2008 May;28(7):661-5
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  • [Title] Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-beta2-glycoprotein-I autoantibodies.
  • The sCD21 is able to bind all known ligands such as CD23, sCD23, Epstein-Barr virus and C3d in immune complexes.
  • Here, we show the serum levels of sCD21 in sera the of antiphospholipid syndrome (APS) patients.
  • Antiphospholipid syndrome is an autoimmune disorder in which autoantibodies cause heart attack, stroke and miscarriage.
  • Antiphospholipid syndrome may appear as primary or in association with systemic lupus erythromatosus (SLE) and other autoimmune diseases.
  • Here, we ask whether APS patients have different sCD21 titers compared to healthy persons and whether sCD21 levels correlate with the presence of anti-beta2-GPI autoantibodies.
  • We show that autoimmune APS patients have significantly reduced amounts of sCD21 in their sera, irrespective of the presence of anti-beta2-GPI autoantibodies.
  • In our APS patients cohort additional SLE, vasculities, DVT (deep vein thrombosis), fetal loss or thrombosis did not correlate to the reduced level of sCD21.
  • [MeSH-major] Antiphospholipid Syndrome / blood. Autoantibodies / blood. Receptors, Complement 3d / blood. beta 2-Glycoprotein I / immunology

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  • [Cites] J Immunol. 1985 Oct;135(4):2687-94 [2411809.001]
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  • (PMID = 18172655.001).
  • [ISSN] 0172-8172
  • [Journal-full-title] Rheumatology international
  • [ISO-abbreviation] Rheumatol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Receptors, Complement 3d; 0 / beta 2-Glycoprotein I
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62. Kondo H, Nakayama M, Ishikawa H: [Mitral valve replacement for mitral valve stenosis and insufficiency in a patient with antiphospholipid syndrome and systemic lupus erythematosus; report of a case]. Kyobu Geka; 2010 Dec;63(13):1173-5
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  • [Title] [Mitral valve replacement for mitral valve stenosis and insufficiency in a patient with antiphospholipid syndrome and systemic lupus erythematosus; report of a case].
  • She was previously diagnosed as antiphospholipid syndrome (APS) because of previous pregnancy morbidity and cerebral infarction.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Heart Valve Prosthesis Implantation. Lupus Erythematosus, Systemic / complications. Mitral Valve Insufficiency / surgery. Mitral Valve Stenosis / surgery


63. Bougie JK, Lim T, Farah CA, Manjunath V, Nagakura I, Ferraro GB, Sossin WS: The atypical protein kinase C in Aplysia can form a protein kinase M by cleavage. J Neurochem; 2009 May;109(4):1129-43
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  • We have cloned the atypical PKC from Aplysia, PKC Apl III.
  • Instead, over-expression of PKC Apl III in Aplysia sensory neurons leads to production of a PKM fragment of PKC Apl III.
  • Moreover, nervous system enriched spliced forms of PKC Apl III show enhanced cleavage.
  • PKC Apl III could also be activated through phosphorylation downstream of phosphoinositide 3-kinase.


64. Bokarev IN, Arshinov AV, Mel'nikov AL: [Antiphospholipid syndrome: modern problems]. Klin Med (Mosk); 2007;85(11):4-8
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  • [Title] [Antiphospholipid syndrome: modern problems].
  • The article describes the historical aspects of the formation of the notion antiphospholipid syndrome (AFS) as well as the development of the conception of its clinical symptoms and laboratory tests confirming the diagnosis.
  • Special attention is paid to the modern interpretation of the notion of AFS, which excludes a number of clinical symptoms and laboratory tests and defines more clearly the use of the rest of clinical and laboratory signs.
  • Theoretical concepts of the pathogenetic mechanisms of the development of this disease and its association with congenital thrombofilias are adduced.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology

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  • (PMID = 18219947.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Number-of-references] 29
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65. Choi SH, Worswick S, Byun HM, Shear T, Soussa JC, Wolff EM, Douer D, Garcia-Manero G, Liang G, Yang AS: Changes in DNA methylation of tandem DNA repeats are different from interspersed repeats in cancer. Int J Cancer; 2009 Aug 1;125(3):723-9
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  • Hypomethylation of DNA repetitive elements is a common finding in cancer, but very little is known about the DNA methylation changes of different types of DNA repetitive elements, such as interspersed repeats (LINE1 and Alu Yb8) and tandem repeats (Sat-alpha, NBL-2 and D4Z4).
  • In all we studied 10 different tissues from four individuals undergoing autopsy, 34 paired normal and tumor tissues from patients with bladder cancer, 58 patients with chronic myelogenous leukemia and 23 patients with acute promyelocytic leukemia.
  • In bladder cancer we found clear hypomethylation of LINE1, Alu Yb8, Sat-alpha and NBL-2.
  • Conversely, we found an increase in the DNA methylation levels of D4Z4 from normal to cancer.
  • In contrast leukemia showed no significant changes in the DNA methylation of LINE1 and Alu Yb8, but DNA methylation increases in NBL-2 and D4Z4 tandem repeats.
  • Our findings show that the changes in DNA methylation levels of individual DNA repetitive elements are unique for each repetitive element, which may reflect distinct epigenetic factors and may have important implications in the use of DNA methylation of repetitive elements as global DNA methylation biomarkers.

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  • (PMID = 19437537.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA086871; United States / NIEHS NIH HHS / ES / P30 ES007048; United States / NIEHS NIH HHS / ES / 5P30ES07048; United States / NCI NIH HHS / CA / P01 CA86871
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS587075; NLM/ PMC4086885
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66. Dutta P, Sazawal S, Kumar R, Saxena R: Does acute promyelocytic leukemia in Indian patients have biology different from the West? Indian J Pathol Microbiol; 2008 Jul-Sep;51(3):437-9
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  • [Title] Does acute promyelocytic leukemia in Indian patients have biology different from the West?
  • Acute promyelocytic leukemia (APML) is a well-characterized malignancy with typical clinico-hematological and molecular features.
  • This study was conducted to determine the clinico-hematological profile of APML in India.
  • Thirty-five patients with APML presenting to Hematology Department, AIIMS, New Delhi, between July 2003 and June 2005 were evaluated for presenting clinical features, hemogram, peripheral smear, bone marrow morphology and cytochemistry.
  • Reverse transcriptase PCR (RT-PCR) for PML-RARalpha was done in all cases.
  • Male-to-female ratio was 0.9:1 (males--17 and females--18) with median age 25 years (range 11-57 years).
  • RT-PCR showed PML-RARalpha in 33/35 cases with the bcr3 isoform being present in 24/33 positive cases (72.7%).
  • The two cases negative for PML-RARalpha showed typical morphology and responded to ATRA.
  • APML in India has certain unusual features, which may reflect a different biology.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 18723985.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Azo Compounds; 0 / Naphthalenes; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.- / Esterases
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67. Riviello C, Ammannati F, Lamassa M, Mariotti F, Mennonna P, Parretti E, Tondi F, Mello G: Atypical onset of antiphospholipid syndrome in pregnancy: a case report. Thromb Res; 2005;115(5):405-8
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  • [Title] Atypical onset of antiphospholipid syndrome in pregnancy: a case report.
  • BACKGROUND: We present a case of an atypical onset of antiphospholipid syndrome (APS).
  • After 1 month, laboratory tests revealed high level of antiphospholipid antibodies.
  • After 6 weeks, antiphospholipid antibodies, tested again, result positive.
  • CONCLUSION: Antiphospholipid antibodies often cause pregnancy complications, but, to our knowledge, this is the first report of an association of antiphospholipid antibodies, with cerebral cavernoma thrombosis and early onset HELLP syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Pregnancy Complications, Hematologic
  • [MeSH-minor] Abortion, Spontaneous. Adult. Antibodies, Antiphospholipid / blood. Cerebral Hemorrhage / complications. Cerebral Hemorrhage / diagnosis. Cerebral Hemorrhage / surgery. Female. HELLP Syndrome / complications. HELLP Syndrome / diagnosis. Humans. Pregnancy. Prognosis. Risk Factors. Thrombosis / complications. Thrombosis / diagnosis

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  • (PMID = 15733974.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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68. Riccioni R, Pasquini L, Mariani G, Saulle E, Rossini A, Diverio D, Pelosi E, Vitale A, Chierichini A, Cedrone M, Foà R, Lo Coco F, Peschle C, Testa U: TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL. Haematologica; 2005 May;90(5):612-24
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  • [Title] TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL.
  • BACKGROUND AND OBJECTIVES: The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is regarded as a potential anticancer agent.
  • The present study was designed to evaluate the sensitivity to TRAIL-induced apoptosis in acute myeloblastic leukemias (AML).
  • DESIGN AND METHODS: TRAIL/TRAIL receptor (TRAIL-R) expression and sensitivity to TRAIL-mediated apoptosis were explored in 79 AML patients, including 17 patients with acute promyelocytic leukemia (APL).
  • RESULTS: In non-APL AML we observed frequent expression of TRAIL decoy receptors (TRAIL-R3 and TRAIL-R4), while TRAIL-R1 and TRAIL-R2 expression was restricted to AML exhibiting monocytic features.
  • Total leukemic blasts, as well as AML colony-forming units (AML-CFU), were invariably resistant to TRAIL-mediated apoptosis.
  • APL express membrane-bound TRAIL on their surface and exhibit a pattern of TRAIL-R expression similar to that observed in the other types of AML.
  • Before, during and after retinoic acid treatment APL cells are TRAIL-resistant.
  • The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression.
  • INTERPRETATION AND CONCLUSIONS: The analysis of experimental APL models (i.e., U937 cells engineered to express PML/RAR-Eo and NB4 cells) provided evidence that PML/RAR-Eo expression was associated with downmodulation of TRAIL-R1 and with resistance to TRAIL-mediated apoptosis.
  • We suggest that AML blasts, including APL blasts, are resistant to TRAIL-mediated apoptosis, a phenomenon seemingly related to the expression of TRAIL decoy receptors on these cells.
  • Finally, APL blasts express membrane-bound TRAIL that could confer an immunologic privilege to these cells.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / physiology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Agents / pharmacology. Caspase 3 / analysis. Caspase 8 / analysis. Cell Differentiation / drug effects. Cell Membrane / metabolism. Cytarabine / pharmacology. Etoposide / pharmacology. Female. GPI-Linked Proteins. Granulocytes / drug effects. HL-60 Cells / pathology. Humans. Hydroxyurea / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Monocytes / drug effects. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. U937 Cells / drug effects

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  • (PMID = 15921376.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; X6Q56QN5QC / Hydroxyurea
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69. Savickiene J, Treigyte G, Gineitis A, Navakauskiene R: A critical role of redox state in determining HL-60 cell granulocytic differentiation and apoptosis via involvement of PKC and NF-kappaB. In Vitro Cell Dev Biol Anim; 2010 Jun;46(6):547-59
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  • Here, a causal relationship among redox state, granulocytic differentiation induced by all-trans retinoic acid (RA) or dibutyryl cAMP (dbcAMP) and apoptosis have been studied in the human acute promyelocytic leukaemia HL-60 cells.
  • The modulation of intracellular reactive oxygen species levels by D: , L: -buthionine-(S, R) sulfoximide (BSO), and N: -acetyl-L: -cysteine (NAC) caused inducer- and time-dependent or stage-specific effects on HL-60 cell growth inhibition, differentiation and subsequent apoptosis.

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  • (PMID = 20224971.001).
  • [ISSN] 1543-706X
  • [Journal-full-title] In vitro cellular & developmental biology. Animal
  • [ISO-abbreviation] In Vitro Cell. Dev. Biol. Anim.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / NF-kappa B; EC 2.7.11.13 / Protein Kinase C; WYQ7N0BPYC / Acetylcysteine
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70. Karasawa M, Yamane A, Mitsui T, Irisawa H, Sakura T, Matsushima T, Tsukamoto N, Nojima Y, Miyawaki S: Long-term persistence of host cells detected by X-chromosome gene-based assay in patients undergoing gender-mismatched hematopoietic stem cell transplantation. Am J Hematol; 2005 Oct;80(2):101-5
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  • After restriction digestion of samples, we detected a small number of female-derived cells within a large population of male-derived cells, with a sensitivity from 0.1% to 0.05%.
  • Chimerism was examined in four patients with myeloid malignancies: two patients with acute myeloid leukemia (AML) from myelodysplastic syndrome (MDS), and one patient each with AML M3 and AML M4.
  • All patients underwent myeloablative conditioning regimens and exhibited good clinical results during a median follow-up period of 6.6 years (range, 3.4-7.5 years).
  • [MeSH-minor] Adult. Chromosomes, Human, X. Female. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Myeloid / therapy. Longitudinal Studies. Middle Aged. Receptors, Androgen / genetics. Sensitivity and Specificity. Sex Factors

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16184584.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Receptors, Androgen
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71. Crowther M, Crowther MA: Intensity of warfarin coagulation in the antiphospholipid syndrome. Curr Rheumatol Rep; 2010 Feb;12(1):64-9
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  • [Title] Intensity of warfarin coagulation in the antiphospholipid syndrome.
  • Antiphospholipid syndrome is a condition with an increased propensity for both arterial and venous thrombosis.
  • [MeSH-major] Anticoagulants / therapeutic use. Antiphospholipid Syndrome / drug therapy. Thromboembolism / prevention & control. Warfarin / therapeutic use

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  • (PMID = 20425536.001).
  • [ISSN] 1534-6307
  • [Journal-full-title] Current rheumatology reports
  • [ISO-abbreviation] Curr Rheumatol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 5Q7ZVV76EI / Warfarin
  • [Number-of-references] 27
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72. Mimura Y, Takahashi K, Kawata K, Akazawa T, Inoue N: Two-step colocalization of MORC3 with PML nuclear bodies. J Cell Sci; 2010 Jun 15;123(Pt 12):2014-24
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  • [Title] Two-step colocalization of MORC3 with PML nuclear bodies.
  • Many functional subdomains, including promyelocytic leukemia nuclear bodies (PML NBs), are formed in the mammalian nucleus.
  • Various proteins are constitutively or transiently accumulated in PML NBs in a PML-dependent manner.
  • MORC3 (microrchidia family CW-type zinc-finger 3), also known as NXP2, which consists of GHL-ATPase, a CW-type zinc-finger and coiled-coil domains, is localized in PML NBs, where it recruits and activates p53 to induce cellular senescence.
  • Interestingly, we found that MORC3 can form PML-independent nuclear domains (NDs) in mouse hematopoietic cells and even in Pml-deficient cells.
  • Here, we show that MORC3 colocalizes with PML by a two-step molecular mechanism: the PML-independent formation of MORC3 NDs by the ATPase cycle, and the association of MORC3 with PML via the SUMO1-SUMO-interacting motif (SIM).
  • Furthermore, the SUMOylation of MORC3 at five sites was involved in the association of MORC3 with PML, and SUMO1-unmodified MORC3 formed NDs independently of PML.
  • [MeSH-major] Adenosine Triphosphatases / metabolism. DNA-Binding Proteins / metabolism. Intranuclear Inclusion Bodies / metabolism. Nuclear Proteins / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Animals. HeLa Cells. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Mice. Protein Structure, Tertiary. Protein Transport. SUMO-1 Protein / genetics. SUMO-1 Protein / metabolism

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  • (PMID = 20501696.001).
  • [ISSN] 1477-9137
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / MORC3 protein, human; EC 3.6.1.- / MORC3 protein, mouse
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73. Chu Q, Amano O, Kanda Y, Kunii S, Wang Q, Sakagami H: Tumor-specific cytotoxicity and type of cell death induced by gefitinib in oral squamous cell carcinoma cell lines. Anticancer Res; 2009 Dec;29(12):5023-31
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  • [Title] Tumor-specific cytotoxicity and type of cell death induced by gefitinib in oral squamous cell carcinoma cell lines.
  • Gefitinib alone and combined with docetaxel induced internucleosomal DNA fragmentation and caspase-3 activation in human promyelocytic leukemia HL-60 cells, but not in HSC-2 or T98G cells.


74. Kwaan HC: Double hazard of thrombophilia and bleeding in leukemia. Hematology Am Soc Hematol Educ Program; 2007;:151-7
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  • [Title] Double hazard of thrombophilia and bleeding in leukemia.
  • Thrombotic complications in acute leukemia are often overlooked because bleeding complications generally dominate the clinical picture.
  • While there are many thrombogenic factors shared by both solid tumors and leukemia, many additional prothrombotic features are present in leukemia.
  • In addition, comorbid conditions including hereditary thrombophilia, infection, endothelial cell activation by cytokines, antiphospholipid syndrome and acquired activated protein C resistance are major contributory factors.

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  • (PMID = 18024623.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 44
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75. Basova LV, Kurnikov IV, Wang L, Ritov VB, Belikova NA, Vlasova II, Pacheco AA, Winnica DE, Peterson J, Bayir H, Waldeck DH, Kagan VE: Cardiolipin switch in mitochondria: shutting off the reduction of cytochrome c and turning on the peroxidase activity. Biochemistry; 2007 Mar 20;46(11):3423-34
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  • Upon interaction with anionic phospholipids, particularly mitochondria-specific cardiolipin (CL), cytochrome c (cyt c) loses its tertiary structure and its peroxidase activity dramatically increases.
  • CL-induced peroxidase activity of cyt c has been found to be important for selective CL oxidation in cells undergoing programmed death.
  • During apoptosis, the peroxidase activity and the fraction of CL-bound cyt c markedly increase, suggesting that CL may act as a switch to regulate cyt c's mitochondrial functions.
  • Using cyclic voltammetry and equilibrium redox titrations, we show that the redox potential of cyt c shifts negatively by 350-400 mV upon binding to CL-containing membranes.
  • Further, CL/cyt c complexes are not effective in scavenging superoxide anions and are not effectively reduced by ascorbate.
  • Thus, both redox properties and functions of cyt c change upon interaction with CL in the mitochondrial membrane, diminishing cyt c's electron donor/acceptor role and stimulating its peroxidase activity.

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  • (PMID = 17319652.001).
  • [ISSN] 0006-2960
  • [Journal-full-title] Biochemistry
  • [ISO-abbreviation] Biochemistry
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070755; United States / NIOSH CDC HHS / OH / R01 OH008282; United States / NIAID NIH HHS / AI / U19 AI068021; United States / NIAID NIH HHS / AI / U19 AI 068021; None / None / / R01 HL070755-08; United States / NHLBI NIH HHS / HL / R01 HL061411; United States / NHLBI NIH HHS / HL / HL 61411; United States / NHLBI NIH HHS / HL / HL 70755; United States / NIOSH CDC HHS / OH / OH 008282; United States / NHLBI NIH HHS / HL / R01 HL070755-08
  • [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] United States
  • [Chemical-registry-number] 0 / 1,1',2,2'-tetraoleoylcardiolipin; 0 / Cardiolipins; 0 / Liposomes; 9007-43-6 / Cytochromes c; EC 1.11.1.- / Peroxidases; EC 1.9.3.1 / Electron Transport Complex IV; PQ6CK8PD0R / Ascorbic Acid
  • [Other-IDs] NLM/ NIHMS62066; NLM/ PMC3356783
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76. Varjo SJ, Hautala JT, Wiedmer SK, Riekkola ML: Small diamines as modifiers for phosphatidylcholine/phosphatidylserine coatings in capillary electrochromatography. J Chromatogr A; 2005 Jul 15;1081(1):92-8
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  • The phospholipid coatings consisted of 1 mM of 8:2 mol% phosphatidylcholine (PC)/phosphatidylserine (PS) and 5 mM of modifier in buffer solutions (acetate, phosphate, or Tris) at pH 4.0-7.4.
  • The results showed that under optimal conditions, the small linear diamines increased the packing density of anionic phospholipids, leading to improved separations.
  • While buffers with amino groups take part in the phospholipid bilayer formation, buffers like phosphate may even have negative effect on coating formation.
  • The factors affecting phospholipid coatings with diamines as modifiers are clarified.

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  • (PMID = 16013604.001).
  • [ISSN] 0021-9673
  • [Journal-full-title] Journal of chromatography. A
  • [ISO-abbreviation] J Chromatogr A
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Buffers; 0 / Coated Materials, Biocompatible; 0 / Diamines; 0 / Ethylenediamines; 0 / Liposomes; 0 / Phosphatidylcholines; 0 / Phosphatidylserines; 0 / Steroids; 023C2WHX2V / Tromethamine; 60V9STC53F / ethylenediamine; 64431-96-5 / 1,3-bis(tris(hydroxymethyl)methylamino)propane; CB3ISL56KG / trimethylenediamine; RWW266YE9I / HEPES
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77. Zhong Q, Gvozdenovic-Jeremic J, Webster P, Zhou J, Greenberg ML: Loss of function of KRE5 suppresses temperature sensitivity of mutants lacking mitochondrial anionic lipids. Mol Biol Cell; 2005 Feb;16(2):665-75
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  • [Title] Loss of function of KRE5 suppresses temperature sensitivity of mutants lacking mitochondrial anionic lipids.
  • Disruption of PGS1, which encodes the enzyme that catalyzes the committed step of cardiolipin (CL) synthesis, results in loss of the mitochondrial anionic phospholipids phosphatidylglycerol (PG) and CL.
  • To understand the essential functions of mitochondrial anionic lipids at elevated temperatures, we isolated suppressors of pgs1Delta that grew at 37 degrees C.
  • Stabilization of the cell wall with osmotic support alleviated the cell wall defects of pgs1Delta and suppressed the temperature sensitivity of all CL-deficient mutants.
  • These findings demonstrated that mitochondrial anionic lipids are required for cellular functions that are essential in cell wall biogenesis, the maintenance of cell integrity, and survival at elevated temperature.

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  • (PMID = 15563612.001).
  • [ISSN] 1059-1524
  • [Journal-full-title] Molecular biology of the cell
  • [ISO-abbreviation] Mol. Biol. Cell
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL062263; United States / NHLBI NIH HHS / HL / HL-62263
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Anions; 0 / Antigens, Bacterial; 0 / Cardiolipins; 0 / Codon, Nonsense; 0 / Enzyme Inhibitors; 0 / Fluorescent Dyes; 0 / Glycoproteins; 0 / Indoles; 0 / KRE5 protein, S cerevisiae; 0 / Phosphatidylglycerols; 0 / Polysaccharides, Bacterial; 0 / Saccharomyces cerevisiae Proteins; 0 / beta-Glucans; 0 / capsular polysaccharide K1; 1398-61-4 / Chitin; 47165-04-8 / DAPI; 9051-97-2 / beta-1,3-glucan; 9Z22C3QQCJ / nikkomycin
  • [Other-IDs] NLM/ PMC545902
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78. Rantalainen KI, Christensen PA, Hafrén A, Otzen DE, Kalkkinen N, Mäkinen K: Interaction of a potyviral VPg with anionic phospholipid vesicles. Virology; 2009 Dec 5;395(1):114-20
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  • [Title] Interaction of a potyviral VPg with anionic phospholipid vesicles.
  • Typically, this type of protein gains a more stable structure upon interactions or posttranslational modifications.
  • It is possible that this stabilization favored the formation of alpha-helical structures.
  • Limited tryptic digestion showed that the interaction with anionic vesicles protected certain, otherwise accessible, trypsin cleavage sites.
  • [MeSH-major] Phospholipids / metabolism. Potyviridae / metabolism. Ribonucleoproteins / metabolism. Viral Nonstructural Proteins / metabolism

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  • (PMID = 19800647.001).
  • [ISSN] 1096-0341
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phospholipids; 0 / Ribonucleoproteins; 0 / Viral Nonstructural Proteins
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79. Mora JR, Knoll JH, Rogan PK, Getts RC, Wilson GS: Dendrimer FISH detection of single-copy intervals in acute promyelocytic leukemia. Mol Cell Probes; 2006 Apr;20(2):114-20
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  • [Title] Dendrimer FISH detection of single-copy intervals in acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (AML-M3) is characterized by a translocation between chromosomes 15 and 17 [t(15;17)].
  • The detection of t(15;17) at the single cell level, is commonly done by fluorescence in situ hybridization (FISH) using recombinant locus specific genomic probes greater than 14 kilobases kb in length.
  • To allow a more thorough study of t(15;17), we designed small (0.9-3.6 kb), target-specific, single-copy probes from the human genome sequence.
  • (1) dendrimers modified with anti-biotin antibodies for detection of biotinylated bound probes, and (2) dendrimers modified with 45-base long oligonucleotides designed from the single-copy probes, for direct detection of the target region.
  • Furthermore, the scFISH probes were successfully detected on metaphase cells with anti-biotin dendrimer conjugates and on interphase cells with 45-base modified dendrimers.
  • [MeSH-major] Genome, Human. Leukemia, Promyelocytic, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. DNA Probes / chemistry. Dendrimers / chemistry. Humans. In Situ Hybridization, Fluorescence. Interphase. Metaphase

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  • (PMID = 16460913.001).
  • [ISSN] 0890-8508
  • [Journal-full-title] Molecular and cellular probes
  • [ISO-abbreviation] Mol. Cell. Probes
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM08359
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Probes; 0 / Dendrimers
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80. Shishido-Hara Y, Higuchi K, Ohara S, Duyckaerts C, Hauw JJ, Uchihara T: Promyelocytic leukemia nuclear bodies provide a scaffold for human polyomavirus JC replication and are disrupted after development of viral inclusions in progressive multifocal leukoencephalopathy. J Neuropathol Exp Neurol; 2008 Apr;67(4):299-308
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  • [Title] Promyelocytic leukemia nuclear bodies provide a scaffold for human polyomavirus JC replication and are disrupted after development of viral inclusions in progressive multifocal leukoencephalopathy.
  • Progressive multifocal leukoencephalopathy is a fatal demyelinating disorder due to human polyomavirus JC infection in which there are viral inclusions in enlarged nuclei of infected oligodendrocytes.
  • We report that the pathogenesis of this disease is associated with distinct subnuclear structures known as promyelocytic leukemia nuclear bodies (PML-NBs).
  • Postmortem brain tissues from 5 patients with the disease were examined.
  • Affected cells with enlarged nuclei contained distinct dot-like subnuclear PML-NBs that were immunopositive for PML protein and nuclear body protein Sp100.
  • Major and minor viral capsid proteins and proliferating cell nuclear antigen, an essential component for DNA replication, colocalized with PML-NBs.
  • By in situ hybridization, viral genomic DNA showed dot-like nuclear accumulation, and by electron microscopy, virus-like structures clustered in subnuclear domains, indicating that PML-NBs are the site of viral DNA replication and capsid assembly.
  • When viral progeny production was advanced, PML-NBs were disrupted.
  • 1) PML-NBs allow for efficient viral propagation by providing scaffolds, 2) disruption of PML-NBs is independent of the ubiquitin-proteasome pathway, and 3) this disruption probably heralds oligodendrocyte degeneration and the resulting demyelination.

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  • (PMID = 18379438.001).
  • [ISSN] 0022-3069
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Ubiquitin; 143220-95-5 / PML protein, human
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81. Lin J, Han LX, Qian J, Wang YL, Qian Z, Yang XF, Sheng XJ: [Quantification of PML/RAR alpha fusion gene transcripts in patients with acute promyelocytic leukemia by using real-time quantitative PCR]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Jun;25(3):319-21
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  • [Title] [Quantification of PML/RAR alpha fusion gene transcripts in patients with acute promyelocytic leukemia by using real-time quantitative PCR].
  • OBJECTIVE: To establish and evaluate a real time quantitative PCR (RQ-PCR) method for detection and quantification the PML/RAR alpha fusion gene transcripts in patients with acute promyelocytic leukemia (APL).
  • METHODS: Three pairs of primers and TaqMan probe were designed for detecting the most frequent PML/RAR alpha transcripts (L-form, S-form and V-form) and normal ABL was used as an internal control.
  • A real time PCR condition was established to detect PML/RAR alpha and ABL positive templates with a series of dilutions.
  • To evaluate this assay, bone marrow samples from 6 APL patients were detected.
  • The median absolute and normalized amount of PML/RAR alpha fusion gene transcripts were 4.27 x 10(3)-3.36 x 10(5) copies/50 ng (median 4.33 x 10(4)copies/50 ng) and 29.38%-600.53% (median 48.12%) respectively.
  • One case showed significant decrease of PML/RAR alpha fusion gene transcripts after induction therapy compared to that at the time of diagnosis, while the fusion transcripts significantly increased after relapsed.
  • CONCLUSION: RQ-PCR is a sensitive, reliable quantitative assay and can be used in the diagnosis of APL and measurement of MRD.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 18543226.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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82. Kantarjian H, O'Brien S, Cortes J, Wierda W, Faderl S, Garcia-Manero G, Issa JP, Estey E, Keating M, Freireich EJ: Therapeutic advances in leukemia and myelodysplastic syndrome over the past 40 years. Cancer; 2008 Oct 1;113(7 Suppl):1933-52
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  • [Title] Therapeutic advances in leukemia and myelodysplastic syndrome over the past 40 years.
  • Major therapeutic progress has been accomplished in leukemia and myelodysplastic syndrome (MDS) over the past 40 years, which may not be fully appreciated by the larger medical community.
  • The objective of this review was to briefly highlight the treatment breakthroughs in leukemia and MDS.
  • Therapeutic progress happened through better understanding of disease pathophysiologies and rational development of targeted agents, like imatinib mesylate in chronic myeloid leukemia (CML), and through astute, empirical discoveries in the clinic, like all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia (APL) and chlorodeoxyadenosine in hairy cell leukemia (HCL).
  • Today, the 5- to 10-year survival rates in patients with APL and HCL exceed 80%.
  • In patients with adult acute lymphocytic leukemia, modern intensive regimens have improved the 5-year survival rates from 20% up to 40%.
  • In patients with chronic lymphocytic leukemia, chemoimmunotherapy recently produced high rates of quality responses and improved long-term outcome.
  • In younger patients with acute myeloid leukemia (AML), the 5-year survival rates range from 40% to 50%, although elderly AML remains a therapeutic challenge.
  • Much therapeutic progress has been witnessed in leukemia and MDS, and much more is expected to occur soon.
  • [MeSH-major] Leukemia / therapy. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Myelodysplastic Syndromes / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Humans. Leukemia, Hairy Cell / mortality. Leukemia, Hairy Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy


83. Au WY, Kumana CR, Lam CW, Cheng VC, Shek TW, Chan EY, Liu R, Kwong YL: Solid tumors subsequent to arsenic trioxide treatment for acute promyelocytic leukemia. Leuk Res; 2007 Jan;31(1):105-8
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  • [Title] Solid tumors subsequent to arsenic trioxide treatment for acute promyelocytic leukemia.
  • Arsenic trioxide (As(2)O(3)) is highly efficacious for acute promyelocytic leukemia (APL).
  • Three APL patients (de novo, 2; therapy-related, 1) in a cohort of 59 cases given oral-As(2)O(3) for induction and maintenance treatment developed secondary cancers (nasopharyngeal carcinoma, 2; colonic adenocarcinoma, 1) at 16, 36 and 55 months post-As(2)O(3) therapy.
  • [MeSH-major] Adenocarcinoma / chemically induced. Arsenicals / adverse effects. Arsenicals / therapeutic use. Colonic Neoplasms / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Nasopharyngeal Neoplasms / chemically induced. Neoplasms / chemically induced. Oxides / adverse effects. Oxides / therapeutic use

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  • (PMID = 16725199.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Growth Inhibitors; 0 / Oxides; S7V92P67HO / arsenic trioxide
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84. Terashi H, Hashimoto S, Uchiyama S: [Beta2-glycoprotein I polymorphism]. Brain Nerve; 2008 Nov;60(11):1333-8
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  • In our study, stroke patients with antiphospholipid antibodies (APL) were significantly younger and were more likely to be women than stroke patients without APL.
  • Valvular heart disease, neurological complications, and hematological disorders were more frequent in the APL-positive group.
  • The mean value of thrombin-antithrombin III complex was significantly lower in the APL-positive group. beta2-Glyoprotein I (beta2-GPI) is the antigen primarily responsible for APL.
  • At the DNA level, 4 different types of allelic polymorphisms have been detected in beta2-GPI.
  • [MeSH-minor] Adult. Alleles. Antibodies, Antiphospholipid / genetics. Antiphospholipid Syndrome / genetics. Female. Genotype. Humans. Leucine / genetics. Male. Middle Aged. Platelet Factor 4. Risk Factors. Valine / genetics. beta-Thromboglobulin

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  • (PMID = 19069167.001).
  • [ISSN] 1881-6096
  • [Journal-full-title] Brain and nerve = Shinkei kenkyū no shinpo
  • [ISO-abbreviation] Brain Nerve
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / beta 2-Glycoprotein I; 0 / beta-Thromboglobulin; 37270-94-3 / Platelet Factor 4; GMW67QNF9C / Leucine; HG18B9YRS7 / Valine
  • [Number-of-references] 22
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85. Vogrinc Z, Trbojević-Cepe M, Coen D, Vitale K, Stavljenić-Rukavina A: Apolipoprotein H (apoH)-dependent autoantibodies and apoH protein polymorphism in selected patients showing lupus anticoagulant activity. Clin Chem Lab Med; 2005;43(1):17-21
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  • Apolipoprotein H (apoH) is considered to be a necessary cofactor for the binding of certain antiphospholipid antibodies to anionic phospholipids.
  • Some apoH-dependent antiphospholipid antibodies also exert lupus anticoagulant (LA) activity, which seems to depend on antiphospholipid antibody epitope specificity.
  • We selected patients with confirmed LA activity and none or low titers of anticardiolipin antibodies that had been sent to the laboratory for routine antiphospholipid antibody determination.
  • Many of them had some clinical manifestation of antiphospholipid syndrome.
  • Antibodies to apoH were determined with a commercially available anticardiolipin/apoH ELISA kit.
  • Our results showed that 47/74 (63.5%) of our selected LA-positive patients also had elevated apoH-dependent antiphospholipid antibody titers.

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  • (PMID = 15653437.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Glycoproteins; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / Protein Isoforms; 0 / beta 2-Glycoprotein I
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86. Membre A, Wahl D, Latger-Cannard V, Max JP, Lacolley P, Lecompte T, Regnault V: The effect of platelet activation on the hypercoagulability induced by murine monoclonal antiphospholipid antibodies. Haematologica; 2008 Apr;93(4):566-73
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  • [Title] The effect of platelet activation on the hypercoagulability induced by murine monoclonal antiphospholipid antibodies.
  • BACKGROUND: To identify the mechanisms of the hypercoagulability associated with antiphospholipid antibodies, we investigated antibody-mediated platelet activation and interference of antibodies with phospholipid-dependent reactions.
  • Platelet activation was assessed by phospholipid-related platelet procoagulant activity.
  • RESULTS: Both monoclonal antibodies mimicked the effect of IgG in 11 out of a series of 40 patients with antiphospholipid antibodies in thrombography.
  • In the presence of their target, 7F6G and 28F4 at 200 microg/mL exhibited comparatively low and high binding to platelets and elicited low and high levels of procoagulant phospholipids on platelet surface, respectively.
  • In platelet-poor plasma, these antibodies induced a 1.6 and >12-fold increase in IC(50)-APC, respectively, thus providing evidence for a procoagulant effect independent of platelet activation.
  • In platelet-rich plasma, this anticoagulant effect was significantly less (23% decrease in ETP(0)), demonstrating that a high increase in procoagulant surfaces by platelet activation significantly antagonizes the anticoagulant effect of antiphospholipid antibodies.
  • In both types of plasma, the inhibition of thrombin generation (reduced ETP(0)) was less than the inhibition of activated protein C activity (increased IC(50)-APC).
  • CONCLUSIONS: Our findings show that platelet activation reinforces the hypercoagulability induced by competition between antiphospholipid antibodies/target complexes and pro- and anticoagulant complexes for phospholipid surfaces.
  • [MeSH-major] Antibodies, Antiphospholipid / pharmacology. Blood Coagulation / drug effects. Immunoglobulin G / pharmacology. Platelet Activation / drug effects. Thrombophilia / immunology
  • [MeSH-minor] Animals. Antibody Specificity. Blood Platelets / immunology. Humans. Lupus Coagulation Inhibitor / physiology. Mice. Phospholipids / physiology. Platelet-Rich Plasma. Protein C / physiology. Prothrombin / immunology. Thrombin / biosynthesis. Thrombin Time. beta 2-Glycoprotein I / immunology

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  • (PMID = 18322249.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Immunoglobulin G; 0 / Lupus Coagulation Inhibitor; 0 / Phospholipids; 0 / Protein C; 0 / beta 2-Glycoprotein I; 9001-26-7 / Prothrombin; EC 3.4.21.5 / Thrombin
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87. Han DH, Kim JH: Difference in growth suppression and apoptosis induction of EGCG and EGC on human promyelocytic leukemia HL-60 cells. Arch Pharm Res; 2009 Apr;32(4):543-7
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  • [Title] Difference in growth suppression and apoptosis induction of EGCG and EGC on human promyelocytic leukemia HL-60 cells.
  • Growth suppression and apoptosis inducing effect of (-)-epigallocatechin 3-gallate (EGCG) and (-)-epigallocatechin (EGC) were studied against human promyeolcytic leukemia, HL-60 cells.
  • The expression level of Bcl-2 was decreased and caspase-3 was activated by EGCG or EGC treatment.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Catechin / analogs & derivatives. Cell Proliferation / drug effects. Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 19407972.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Proto-Oncogene Proteins c-bcl-2; 1617-55-6 / gallocatechol; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3
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88. Podrazilová L, Peterová V, Olejárová M, Seidl Z, Dostál C: [Antiphospholipid syndrome--the description of two cases]. Vnitr Lek; 2006 Jan;52(1):89-94
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  • [Title] [Antiphospholipid syndrome--the description of two cases].
  • Antiphospholipid syndrome (APS) often occurs in young people, it is defined by the presence of venous or arterial thromboses, repeated miscarriages, thrombocytopenias and increased levels of antiphospholipid antibodies.
  • Clinical symptoms are different, there is often experienced the phlebothrombosis of lower limbs, miscarriages or neurological symptoms characterized by transient ischemic attacks (TIA).
  • If APS is associated with other system disease, most often with systemic lupus erythematosus (SLE), it is called secondary APS.
  • At another elder patient there was stated the diagnosis of non-differentiated disease of bonding agent with secondary APS with cardial, pneumonic and neurological clinical symptoms.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis
  • [MeSH-minor] Adult. Aged. Antibodies, Antiphospholipid / analysis. Female. Humans. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / diagnosis. Lupus Erythematosus, Systemic / immunology

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  • [CommentIn] Vnitr Lek. 2006 Jan;52(1):17-20 [16526193.001]
  • (PMID = 16526206.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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89. Guvendag Guven ES, Okur H, Beksac MS: Placental fas/fas ligand expression in early pregnancy losses. Am J Reprod Immunol; 2008 Jul;60(1):1-7
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  • [Title] Placental fas/fas ligand expression in early pregnancy losses.
  • PROBLEM: The aim of this study was to compare the expression levels of Fas and Fas ligand (FasL) in first-trimester placentas obtained from spontaneous abortions in patients with antiphospholipid antibody syndrome (APS) or factor V (FV) Leiden mutation, compared with values in placentas from induced abortions in patients negative for these conditions.
  • [MeSH-major] Abortion, Spontaneous / metabolism. Antigens, CD95 / biosynthesis. Fas Ligand Protein / biosynthesis. Placenta / metabolism
  • [MeSH-minor] Antiphospholipid Syndrome / complications. Factor V / metabolism. Female. Flow Cytometry. Fluorescent Antibody Technique. Humans. Immune Tolerance / physiology. Pregnancy. Pregnancy Trimester, First

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  • (PMID = 18422813.001).
  • [ISSN] 1046-7408
  • [Journal-full-title] American journal of reproductive immunology (New York, N.Y. : 1989)
  • [ISO-abbreviation] Am. J. Reprod. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / factor V Leiden; 9001-24-5 / Factor V
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90. Bozic B, Cucnik S, Kveder T, Rozman B: Avidity of anti-beta-2-glycoprotein I antibodies. Autoimmun Rev; 2005 Jun;4(5):303-8
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  • [Title] Avidity of anti-beta-2-glycoprotein I antibodies.
  • Since affinity refers to monovalent binding of antibodies to a monovalent epitope, the majority of data on the binding of anti-beta2-glycoprotein I antibodies (anti-beta2-GPI) characterized their avidity rather than affinity.
  • Anti-beta2-GPI were generally believed to be of low avidity, but heterogeneous avidity of patients' IgG anti-beta2-GPI has been demonstrated.
  • High avidity anti-beta2-GPI monoclonals were reported to possess higher pathogenicity than low avidity anti-beta2-GPI.
  • Polyclonal high avidity anti-beta2-GPI were found to be more common in patients with antiphospholipid syndrome (APS) and associated with thrombosis.
  • Some conformational changes of beta2-GPI are required for the binding of polyclonal anti-beta2-GPI to the antigen: neither high density of the antigen nor high avidity of the anti-beta2-GPI alone is sufficient for the recognition.
  • Avidity of anti-beta2-GPI should be considered in any attempt of inter-laboratory standardisation and/or evaluation of anti-beta2-GPI enzyme-linked immunosorbent assay (ELISA).

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  • (PMID = 15990078.001).
  • [ISSN] 1568-9972
  • [Journal-full-title] Autoimmunity reviews
  • [ISO-abbreviation] Autoimmun Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Glycoproteins; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 40
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91. Yamasaki Y, Narain S, Yoshida H, Hernandez L, Barker T, Hahn PC, Sobel ES, Segal MS, Richards HB, Chan EK, Reeves WH, Satoh M: Autoantibodies to RNA helicase A: a new serologic marker of early lupus. Arthritis Rheum; 2007 Feb;56(2):596-604
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  • OBJECTIVE: To investigate the clinical and immunologic significance of autoantibodies to RNA helicase A (RHA) in patients with systemic rheumatic diseases.
  • RESULTS: Anti-RHA was observed in 17 (6.2%) of 276 patients with systemic lupus erythematosus (SLE), 2 patients with antiphospholipid antibodies, and 3 other patients, but anti-RHA was not observed in any patient with polymyositis/dermatomyositis, systemic sclerosis, rheumatoid arthritis, or Sjögren's syndrome.
  • Anti-RHA was present in only 2.9% of African American patients, compared with 6.0% of white patients and 12-25% of patients of other races; this was in striking contrast to the frequency of anti-Sm in African American patients (27.2%).
  • Among patients with SLE, anti-RHA was common in young patients (26% of those whose initial visit was at an age younger than 20 years versus 3-4% of those who were initially seen at ages 20-49 years) and at an early stage of disease (23% of those whose first clinic visit was within 1 year of disease onset versus 2-8% of those whose first visit was at least 1 year after disease onset).
  • In 9 of 11 patients, levels of anti-RHA decreased to <10% of the initial value within 9-37 months, while levels of coexisting anti-Ro or anti-Su remained the same.
  • New specificities developed in 2 patients (anti-nuclear RNP and anti-Sm, and anti-ribosomal P, respectively).
  • These data suggest that the level of anti-RHA diminishes over time, and that anti-RHA is regulated via a mechanism different from that for other lupus-related autoantibodies.
  • CONCLUSION: Anti-RHA is a new serologic marker for SLE.
  • It is produced mainly in young non-African Americans at an early stage of their disease.
  • Anti-RHA has a unique tendency to diminish over time.
  • The production of anti-RHA may depend on a process restricted to early SLE, or it may be highly sensitive to treatment.
  • [MeSH-major] Autoantibodies / blood. DEAD-box RNA Helicases / immunology. Lupus Erythematosus, Systemic / diagnosis. Lupus Erythematosus, Systemic / immunology. Neoplasm Proteins / immunology

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  • (PMID = 17265494.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI-39645; United States / NIAID NIH HHS / AI / AI-47859; United States / NIAMS NIH HHS / AR / AR-050661; United States / NIAMS NIH HHS / AR / AR-40391; United States / NCRR NIH HHS / RR / M01-RR-00082
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Autoantigens; 0 / Neoplasm Proteins; 0 / Ribonucleoproteins, Small Nuclear; 0 / snRNP Core Proteins; EC 3.6.1.- / DHX9 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
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92. Surga N, Makdassi R, Choukroun G, Vandwalle J, Petit J, Saint F: [Adrenal hemorrhage acutised by adrenocorticotropin hormone]. Prog Urol; 2010 Jun;20(6):425-9
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  • We associated a clinical, endocrine and radiologic staging to treat those patients.
  • Two patients suffered of the condition of the antiphospholipid syndrome.
  • The clinical attitude has thus to be defined clearly.
  • The patient must be under close clinical evaluation.
  • Antiphospholipid syndrome must also be excluded.

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  • [Copyright] Copyright 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20538206.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hormones; 16960-16-0 / Cosyntropin; 53468-06-7 / adrenocorticotropin zinc
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93. Binet F, Girard D: Novel human neutrophil agonistic properties of arsenic trioxide: involvement of p38 mitogen-activated protein kinase and/or c-jun NH2-terminal MAPK but not extracellular signal-regulated kinases-1/2. J Leukoc Biol; 2008 Dec;84(6):1613-22
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  • Arsenic trioxide (ATO) is known for treating acute promyelocytic leukemia and for inducing apoptosis and mitogen-activated protein kinases (MAPKs) in promyelocytes and cancer cells.

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  • (PMID = 18728151.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Reactive Oxygen Species; BBX060AN9V / Hydrogen Peroxide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; 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 / p38 Mitogen-Activated Protein Kinases; EC 3.4.24.- / Gelatinases; S7V92P67HO / arsenic trioxide; SY7Q814VUP / Calcium
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94. Gigante A, Gasperini ML, Cianci R, Barbano B, Giannakakis K, Di Donato D, Fuiano G, Amoroso A: Antiphospholipid antibodies and renal involvement. Am J Nephrol; 2009;30(5):405-12
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  • [Title] Antiphospholipid antibodies and renal involvement.
  • Antiphospholipid antibodies are a heterogeneous group of autoantibodies associated with the hypercoagulable state affecting all vascular districts with thrombosis named antiphospholipid syndrome (APS).
  • APS is an autoimmune disease with multifactorial etiology that includes cellular, molecular, genetic and pathogenic mechanisms.
  • The APS clinical features are a combination of arterial and/or venous thrombosis, hematological events, recurrent fetal losses, neurological disorders and intra-abdominal manifestations.
  • Clinical features include hypertension, renal artery stenosis, thrombotic microangiopathy and other histological manifestations of the nephropathy (APSN), venous renal thrombosis, APSN in the course of systemic lupus erythematosus and renal failure.
  • APSN is an independent risk factor that should be included in the classification criteria for definite APS with characteristic clinical and histological features.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / immunology. Kidney / immunology. Kidney Diseases / immunology