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1. Ioachimescu OC, Stoller JK: Diffuse alveolar hemorrhage: diagnosing it and finding the cause. Cleve Clin J Med; 2008 Apr;75(4):258, 260, 264-5 passim
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  • [Title] Diffuse alveolar hemorrhage: diagnosing it and finding the cause.
  • Diffuse alveolar hemorrhage is an acute, life-threatening event, and repeated episodes can lead to organizing pneumonia, collagen deposition in small airways, and, ultimately, fibrosis.
  • Among the many conditions it can accompany are Wegener granulomatosis, microscopic polyangiitis, Goodpasture syndrome, connective tissue disorders, antiphospholipid antibody syndrome, infectious or toxic exposures, and neoplastic conditions.
  • [MeSH-minor] Acute Disease. Adrenal Cortex Hormones / therapeutic use. Bronchoscopy. Humans. Immunosuppressive Agents / therapeutic use. Prognosis. Risk Factors. Vasculitis

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  • (PMID = 18491433.001).
  • [ISSN] 0891-1150
  • [Journal-full-title] Cleveland Clinic journal of medicine
  • [ISO-abbreviation] Cleve Clin J Med
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Immunosuppressive Agents
  • [Number-of-references] 62
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2. Eshel R, Ben-Zaken O, Vainas O, Nadir Y, Minucci S, Polliack A, Naparstek E, Vlodavsky I, Katz BZ: Leukomogenic factors downregulate heparanase expression in acute myeloid leukemia cells. Biochem Biophys Res Commun; 2005 Oct 7;335(4):1115-22
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  • [Title] Leukomogenic factors downregulate heparanase expression in acute myeloid leukemia cells.
  • Heparanase is a heparan sulfate-degrading endoglycosidase expressed by mature monocytes and myeloid cells, but not by immature hematopoietic progenitors.
  • Heparanase gene expression is upregulated during differentiation of immature myeloid cells.
  • PML-RARalpha and PLZF-RARalpha fusion gene products associated with acute promyelocytic leukemia abrogate myeloid differentiation and heparanase expression.
  • AML-Eto, a translocation product associated with AML FAB M2, also downregulates heparanase gene expression.
  • We found that retinoic acid that dissociates PML-RARalpha from the DNA, and which is used to treat acute promyelocytic leukemia patients, restores heparanase expression to normal levels in an acute promyelocytic leukemia cell line.
  • The retinoic acid effects were also observed in primary acute promyelocytic leukemia cells and in a retinoic acid-treated acute promyelocytic leukemia patient.
  • Histone deacetylase inhibitor reverses the downregulation of heparanase expression induced by the AML-Eto fusion gene product in M2 type AML.
  • In summary, we have characterized a link between leukomogenic factors and the downregulation of heparanase in myeloid leukemic cells.
  • [MeSH-major] Glucuronidase / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukocytes / metabolism. Proto-Oncogene Proteins / metabolism. Transcription Factors / metabolism

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  • (PMID = 16112651.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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3. Tabe Y, Konopleva M, Kondo Y, Contractor R, Tsao T, Konoplev S, Shi Y, Ling X, Watt JC, Tsutsumi-Ishii Y, Ohsaka A, Nagaoka I, Issa JP, Kogan SC, Andreeff M: PPARgamma-active triterpenoid CDDO enhances ATRA-induced differentiation in APL. Cancer Biol Ther; 2007 Dec;6(12):1967-77
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  • [Title] PPARgamma-active triterpenoid CDDO enhances ATRA-induced differentiation in APL.
  • Acute promyelocytic leukemia (APL) is associated with oncogenic PML-RARalpha that acts as a dominant negative transcriptional repressor of retinoic acid (RA) receptor target genes by recruiting histone deacetylase (HDAC).
  • In addition to RAR targets, PML-RARalpha silence a wide range of nuclear receptor target genes including PPARgamma targets.
  • All-trans-retinoic acid (ATRA), a ligand for the RA receptor (RAR), restores normal retinoid signaling and induces terminal differentiation of APL cells; however, APL cells can develop resistance to ATRA.
  • Using ATRA sensitive NB4 and ATRA-resistant derivative MR2 cell lines, we demonstrate that PPARgamma ligand 2-cyano-3, 12-dioxooleana-1, 9-dien-28-oic acid (CDDO) enhances pro-apoptotic and differentiating effects of ATRA in ATRA-sensitive NB4 cells and partially reverses ATRA resistance in MR2 cells.
  • The CDDO/ATRA combination synergistically induces RARbeta2 expression both in ATRA-sensitive and -resistant APL cells.
  • In an in vivo mouse model of APL, CDDO derivative CDDO-methyl ester markedly enhanced ATRA-induced maturation and extended the survival of mice.
  • In summary, these results provide rationale for the combined targeting of RAR and PPARgamma nuclear receptors in the therapy of APL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Oleanolic Acid / analogs & derivatives. PPAR gamma / drug effects. Tretinoin / pharmacology

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  • (PMID = 18075297.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA49639; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / R01 CA89346
  • [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 / 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; 0 / Antineoplastic Agents; 0 / Histones; 0 / LG 100268; 0 / Nicotinic Acids; 0 / PPAR gamma; 0 / RNA, Small Interfering; 0 / Receptors, Retinoic Acid; 0 / Tetrahydronaphthalenes; 0 / retinoic acid receptor beta; 5688UTC01R / Tretinoin; 6SMK8R7TGJ / Oleanolic Acid; CEG1Q6OGU1 / methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate
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4. Obón Azuara B, Ortas Nadal MR, Gutiérrez Cía I, Bustamante Rodríguez R, Velilla Soriano C, Villanueva Anadón B: [Mortality due to heart involvement in the catastrophic antiphospholipid syndrome]. An Med Interna; 2008 May;25(5):229-30
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  • [Title] [Mortality due to heart involvement in the catastrophic antiphospholipid syndrome].
  • We reported a CAPS case, possibily afterward sting wasp triggering, with acute heart failure during evolution.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Heart Failure / etiology. Heart Failure / mortality
  • [MeSH-minor] Acute Disease. Fatal Outcome. Female. Humans. Middle Aged


5. Mahmoud IS, Sughayer MA, Mohammad HA, Awidi AS, EL-Khateeb MS, Ismail SI: The transforming mutation E17K/AKT1 is not a major event in B-cell-derived lymphoid leukaemias. Br J Cancer; 2008 Aug 5;99(3):488-90
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  • Considering the importance of the PI3K/AKT pathway in mediating survival and antiapoptotic signals in the B-cell types of chronic lymphocytic leukaemia (CLL) and acute lymphoblastic leukaemia (ALL), we sequenced the AKT1 exon 3 for the above mentioned mutation in 87 specimens, representing 45 CLLs, 38 ALLs and 4 prolymphocytic leukaemia (PLL) cases, which are all of B-cell origin.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Transformation, Neoplastic / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Promyelocytic, Acute / genetics. Point Mutation. Proto-Oncogene Proteins c-akt / genetics

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  • (PMID = 18665177.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2527790
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6. Cervera R, CAPS Registry Project Group: Catastrophic antiphospholipid syndrome (CAPS): update from the 'CAPS Registry'. Lupus; 2010 Apr;19(4):412-8
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  • [Title] Catastrophic antiphospholipid syndrome (CAPS): update from the 'CAPS Registry'.
  • Although less than 1% of patients with the antiphospholipid syndrome (APS) develop the catastrophic variant, its potentially lethal outcome emphasizes its importance in clinical medicine today.
  • In order to put together all of the published case reports as well as the new diagnosed cases from all over the world, an international registry of patients with catastrophic APS (CAPS Registry) was created in 2000 by the European Forum on Antiphospholipid Antibodies (see http://www.med.ub.es/MIMMUN/FORUM/CAPS.HTM).
  • Currently, it documents the entire clinical, laboratory and therapeutic data of more than 300 patients whose data has been fully registered.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Registries
  • [MeSH-minor] Adolescent. Adult. Antibodies, Antiphospholipid / immunology. Catastrophic Illness. Child. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 20353979.001).
  • [ISSN] 1477-0962
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
  • [Investigator] Cervera R; Bucciarelli S; Espinosa G; Erkan D; Shoenfeld Y; Asherson RA; Amigo MC; Barile-Fabris L; Boffa JJ; Boffa MC; Chávez I; Chapman J; Davidson C; Denes AE; Derksen RH; Coto JF; Disdier P; Egan RM; Ehrenfeld M; Enriquez R; Falcini F; Fang LS; García-Carrasco M; Grandone JT; Gurjal A; Hayem G; Hughes GR; Inam S; Kant KS; Khamashta MA; Kitchens CS; Kupferminc MJ; de Larrañaga G; Levy RA; Lockshin MD; Lui SF; Maddison PJ; Mekori YA; Miyamae T; Moore J; Moutsopoulos HM; Muñoz-Rodríguez FJ; Musial J; Nakajima A; Neuwelt MC; Parke A; Piette JC; Praprotnik S; Roca B; Rojas-Rodriguez J; Roldan R; Sawitzke AD; Schaar CG; Shoenfeld Y; Sipek-Dolnicar A; Spyropoulos AC; Sinico R; Stojanovich L; Tan D; Tektonidou M; Veloso MP; Wislowska M
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7. Kusakabe M, Suzukawa K, Nanmoku T, Obara N, Okoshi Y, Mukai HY, Hasegawa Y, Kojima H, Kawakami Y, Ninomiya H, Nagasawa T: Detection of the STAT5B-RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G-banding. Eur J Haematol; 2008 May;80(5):444-7
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  • [Title] Detection of the STAT5B-RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G-banding.
  • Acute promyelocytic leukemia (APL) is characterized by chromosomal rearrangements of 17q21, leading to fusion of the gene-encoding retinoic acid receptor alpha (RARA) with a number of alternative partner genes.
  • We report a rare case of APL with STAT5B-RARA fusion transcript and the normal chromosome 17 on G-banding.
  • Administration of all trans-retinoic acid improved disseminated intravascular coagulation without decrease of the leukemia cells in his peripheral blood and bone marrow.
  • The molecular mechanism of fusion between STAT5B and RARA by chromosomal rearrangement is discussed based on the data from genome database.
  • Clinical characteristics of APL with STAT5B-RARA are also discussed.
  • [MeSH-major] Chromosomes, Human, Pair 17 / genetics. Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. STAT5 Transcription Factor / analysis. STAT5 Transcription Factor / genetics. Transcription, Genetic / genetics

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  • [CommentIn] Eur J Haematol. 2009 Nov;83(5):499-501 [19624718.001]
  • (PMID = 18221386.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / STAT5 Transcription Factor; 0 / STAT5-RARalpha protein, human
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8. Scheinemann K, Weitzman S, Hitzler J, Doyle J, Abla O: Isolated central nervous system relapse in childhood acute promyelocytic leukemia. J Pediatr Hematol Oncol; 2008 Feb;30(2):160-2
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  • [Title] Isolated central nervous system relapse in childhood acute promyelocytic leukemia.
  • Central nervous system (CNS) involvement is rare in acute promyelocytic leukemia (APL).
  • We describe a 13-year-old boy with APL who developed an isolated CNS relapse after first-line treatment with all-trans retinoic acid and chemotherapy.
  • A second remission was achieved with a regimen consisting of intrathecal chemotherapy, intravenous high-dose cytarabine, and oral 6-mercaptopurine.
  • Prognostic factors of CNS relapse in children with APL are needed to define the indications for CNS prophylaxis in this group of patients.
  • [MeSH-major] Central Nervous System Neoplasms / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18376270.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
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9. Asou N: [Treatment of acute promyelocytic leukemia]. Nihon Rinsho; 2007 Jan 28;65 Suppl 1:483-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. Jain D, Singh T, Arora P: Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report. J Med Case Rep; 2007;1:147
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  • [Title] Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report.
  • BACKGROUND: Acute promyelocytic leukemia (APL) accounts for less than 10% of pediatric AML.
  • Cases of APL in Down syndrome (DS) have been described in the literature rarely and it is rarer still to find the microgranular variant (M3v) of APL in trisomy 21 patients.
  • CASE PRESENTATION: We present a case of a five-year-old female with Down syndrome diagnosed with acute promyelocytic leukemia (APL).
  • Based on this morphology and cytochemistry, a diagnosis of APL microgranular variant (M3v) was made.
  • CONCLUSION: This case report emphasizes the importance of a high index of suspicion in the diagnosis of acute promyelocytic leukemia microgranular variant in Down syndrome.

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  • (PMID = 18036234.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2211491
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11. Cervera R, Espinosa G: Antiphospholipid syndrome: long-time research on pathogenic mechanisms has finally lead to new therapeutic strategies. Expert Opin Ther Targets; 2010 Dec;14(12):1279-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiphospholipid syndrome: long-time research on pathogenic mechanisms has finally lead to new therapeutic strategies.
  • The antiphospholipid syndrome is characterized by the presence of arterial or venous thrombosis or recurrent miscarriages in a patient with positive laboratory tests for antiphospholipid antibodies (anticardiolipin antibodies and/or lupus anticoagulant and/or anti-beta2-glycoprotein I).
  • Despite the strong association between antiphospholipid antibodies and thrombosis and obstetric morbidity, their pathogenic role in the development of these clinical features has not been fully elucidated.
  • [MeSH-major] Antibodies, Monoclonal, Murine-Derived / pharmacology. Anticoagulants / therapeutic use. Antiphospholipid Syndrome / drug therapy. Immunologic Factors / pharmacology
  • [MeSH-minor] Abortion, Habitual / immunology. Abortion, Habitual / pathology. Antibodies, Anticardiolipin / physiology. Antibodies, Antiphospholipid / immunology. Female. Humans. Lupus Coagulation Inhibitor / immunology. Lupus Coagulation Inhibitor / physiology. Pregnancy. Pregnancy Complications / drug therapy. Pregnancy Complications / immunology. Rituximab. Thrombosis / immunology. Thrombosis / pathology. Venous Thrombosis / immunology. beta 2-Glycoprotein I / immunology. beta 2-Glycoprotein I / physiology

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  • (PMID = 21058919.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Anticoagulants; 0 / Immunologic Factors; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I; 4F4X42SYQ6 / Rituximab
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12. Lee KW, Kim HJ, Lee YS, Park HJ, Choi JW, Ha J, Lee KT: Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte. Carcinogenesis; 2007 Sep;28(9):1928-36
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  • [Title] Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte.
  • We investigated the in vitro effects of acteoside on the proliferation, cell cycle regulation and differentiation of HL-60 human promyelocytic leukemia cells.
  • DNA flow cytometric analysis indicated that acteoside blocked cell cycle progression at the G1 phase in HL-60 human promyelocytic leukemia cells.
  • Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent protein kinase (CDK)2, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E were reduced by acteoside, whereas the steady-state level of CDK4 was unaffected.
  • The protein and mRNA levels of CDK inhibitors (cyclin-dependent kinase inhibitors), such as p21(CIP1/WAF1) and p27(KIP1), were gradually increased after acteoside treatment in a time-dependent manner.
  • Our results further suggest that acteoside is a potent inducer of differentiation of HL-60 cells based on biochemical activities and the expression level of CD14 cell surface antigen.
  • In conclusion, the onset of acteoside-induced G1 arrest of HL-60 cells prior to the differentiation appears to be tightly linked to up-regulation of the p21(CIP1/WAF1) and p27(KIP1) levels and decreases in the CDK2, CDK4 and CDK6 activities.
  • These findings, for the first time, reveal the mechanism underlying the anti-proliferative effect of acteoside on human promyelocytic HL-60 cells.

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  • (PMID = 17634406.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Glucosides; 0 / Phenols; 0 / Stilbenes; 61276-17-3 / acteoside; 62229-50-9 / Epidermal Growth Factor; NI40JAQ945 / Tetradecanoylphorbol Acetate; Q369O8926L / resveratrol
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13. Shah AA, Higgins JP, Chakravarty EF: Thrombotic microangiopathic hemolytic anemia in a patient with SLE: diagnostic difficulties. Nat Clin Pract Rheumatol; 2007 Jun;3(6):357-62
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  • INVESTIGATIONS: At a general hospital, the investigations included brain MRI, echocardiography, laboratory tests including measurement of the amount of protein excreted daily, platelet count, levels of lactate dehydrogenase, creatinine and anticardiolipin antibodies, direct Coombs' test, peripheral blood smear, and measurement of blood pressure.
  • At a tertiary institution the investigations included physical examination, electroencephalography, brain MRI, magnetic resonance angiography, repetition of laboratory tests plus measurement of von Willebrand factor-cleaving protease activity, measurement of levels of antibodies to double-stranded DNA and platelets, and renal biopsy.
  • DIAGNOSIS: Thrombotic microangiopathic hemolytic anemia with a possible underlying diagnosis of malignant hypertension, antiphospholipid antibody syndrome, catastrophic antiphospholipid antibody syndrome, thrombotic thrombocytopenic purpura, or active SLE.
  • MANAGEMENT: At the general hospital, therapy included a single dose of intravenous cyclophosphamide 500 mg, eight daily plasma exchange treatments, three daily infusions of methylprednisolone 1 g followed by methylprednisolone 60 mg every 8 h, an infusion of rituximab 657 mg and ultrafiltration via hemodialysis.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Hypertension, Malignant / diagnosis. Lupus Erythematosus, Systemic / complications. Lupus Nephritis / diagnosis. Purpura, Thrombotic Thrombocytopenic / diagnosis. Purpura, Thrombotic Thrombocytopenic / therapy
  • [MeSH-minor] Adult. Anemia, Hemolytic / etiology. Diagnosis, Differential. Erythrocytes. Erythrocytes, Abnormal. Female. Humans. Plasma Exchange. Seizures / etiology. Thrombocytopenia / etiology. Vascular Diseases / complications. Vascular Diseases / etiology. Vascular Diseases / pathology

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  • (PMID = 17538567.001).
  • [ISSN] 1745-8382
  • [Journal-full-title] Nature clinical practice. Rheumatology
  • [ISO-abbreviation] Nat Clin Pract Rheumatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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14. Ashrafuzzaman M, Andersen OS, McElhaney RN: The antimicrobial peptide gramicidin S permeabilizes phospholipid bilayer membranes without forming discrete ion channels. Biochim Biophys Acta; 2008 Dec;1778(12):2814-22
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  • [Title] The antimicrobial peptide gramicidin S permeabilizes phospholipid bilayer membranes without forming discrete ion channels.
  • We examined the permeabilization of lipid bilayers by the beta-sheet, cyclic antimicrobial decapeptide gramicidin S (GS) in phospholipid bilayers formed either by mixtures of zwitterionic diphytanoylphosphatidylcholine and anionic diphytanoylphosphatidylglycerol or by single zwitterionic unsaturated phosphatidylcholines having various hydrocarbon chain lengths, with and without cholesterol.
  • In the zwitterionic bilayers formed by the phosphatidylcholines, without or with cholesterol, the peptide concentrations and membrane potentials required to initiate membrane permeabilization vary little as function of bilayer thickness and cholesterol content.
  • In the zwitterionic phosphatidylcholine bilayers, the effect of GS does not depend on the polarity of the transmembrane potential; however, in bilayers formed from mixtures of phosphatidylcholines and anionic phospholipids, the polarity of the transmembrane potential becomes important, with the GS-induced conductance events being much more frequent when the GS-containing solution is positive relative to the GS-free solution.
  • Overall, these results suggest that GS does not form discrete, well-defined, channel-like structures in phospholipid bilayers, but rather induces a wide variety of transient, differently sized defects which serve to compromise the bilayer barrier properties for small electrolytes.

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  • (PMID = 18809374.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM021342-26; United States / NIGMS NIH HHS / GM / R01 GM021342; United States / NIGMS NIH HHS / GM / GM 21342; United States / NIGMS NIH HHS / GM / R01 GM021342-26
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Ion Channels; 0 / Lipid Bilayers; 0 / Phospholipids; 1405-97-6 / Gramicidin
  • [Other-IDs] NLM/ NIHMS82601; NLM/ PMC2614689
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15. Russell AI, Cunninghame Graham DS, Chadha S, Roberton C, Fernandez-Hart T, Griffiths B, D'Cruz D, Nitsch D, Whittaker JC, Vyse TJ: No association between E- and L-selectin genes and SLE: soluble L-selectin levels do correlate with genotype and a subset in SLE. Genes Immun; 2005 Aug;6(5):422-9
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  • [Title] No association between E- and L-selectin genes and SLE: soluble L-selectin levels do correlate with genotype and a subset in SLE.
  • Altered function of selectin glycoprotein adhesion molecules may modulate severity and organ-specific manifestations of autoimmune and inflammatory disease via changes in leukocyte trafficking.
  • We identified increased levels of soluble L-selectin (sL-selectin), but not soluble E-selectin (sE-selectin) in 278 European-Caucasian lupus patients compared to 230 healthy siblings (P=0.002).
  • sL-selectin levels were markedly elevated in patients with IgG antiphospholipid autoantibodies (P=0.002), suggesting that perhaps sL-selectin defines a subgroup of lupus with vasculopathy. sL-selectin level was also influenced by two L-selectin polymorphisms: 665C>T, F206L in the epidermal growth factor-like domain (P=0.015) and rs12938 in the 3'-untranslated region (P=0.06).
  • Having shown increased sL-selectin levels in lupus patients, we used genetics to investigate whether this was a secondary phenomena or the result of an underlying genetic mechanism.
  • [MeSH-major] E-Selectin / genetics. Genetic Predisposition to Disease. L-Selectin / genetics. Lupus Erythematosus, Systemic / genetics. Polymorphism, Single Nucleotide. Quantitative Trait Loci / genetics
  • [MeSH-minor] Adult. Antibodies, Antiphospholipid / blood. Chromosomes, Human, Pair 1 / genetics. Female. Humans. Male. Middle Aged. Risk Factors

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  • (PMID = 15902275.001).
  • [ISSN] 1466-4879
  • [Journal-full-title] Genes and immunity
  • [ISO-abbreviation] Genes Immun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / E-Selectin; 126880-86-2 / L-Selectin
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16. 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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17. Sato J, Kawakami T, Nakabayashi K, Fukuoka K, Hirano K, Terado Y, Yokoyama K, Ohtsuka T, Ohkura Y, Fujioka Y, Kurata A: Multiple aortic aneurysms complicated by a rupture in the systemic lupus erythematosus: a case report. Pathol Res Pract; 2008;204(11):845-50
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  • At 59 years of age, she was found to be affected by antiphospholipid antibody syndrome (APS).
  • Although SLE with APS is common, a complication of the disease by CMN, multiple AAs, or ruptured AA has been described in several cases to date.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Age of Onset. Antiphospholipid Syndrome / complications. Fatal Outcome. Female. Humans. Middle Aged

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  • (PMID = 18653288.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones
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18. Cavazzana A, Ruffatti A, Tonello M, Bortolati M, De Moerloose P, Reber G: An analysis of experimental conditions influencing the anti-beta2-glycoprotein I ELISA assay results. Ann N Y Acad Sci; 2007 Aug;1109:484-92
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  • [Title] An analysis of experimental conditions influencing the anti-beta2-glycoprotein I ELISA assay results.
  • Five components of the anti-beta(2)-glycoprotein I (abeta(2)GPI) enzyme-linked immunosorbent assay (ELISA) (coating buffer, microplate brand, blocking buffer, dilution buffer, and conjugate) were analyzed to evaluate how they affect variability in test results.
  • Thirty-two samples from patients with antiphospholipid syndrome (APS) positive for abeta(2)GPI IgG antibodies and three calibrators (a pool of abeta(2)GPI-positive patients, the monoclonal HCAL antibody, and a home-made calibrator) were tested.

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  • (PMID = 17785337.001).
  • [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 / Buffers; 0 / beta 2-Glycoprotein I
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19. Everett RD, Chelbi-Alix MK: PML and PML nuclear bodies: implications in antiviral defence. Biochimie; 2007 Jun-Jul;89(6-7):819-30
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  • [Title] PML and PML nuclear bodies: implications in antiviral defence.
  • Several pathways have been implicated in resistance to viral infection in IFN-treated cells, one of which implicates the ProMyelocytic Leukaemia (PML) protein and PML nuclear bodies (NBs, also known as ND10).
  • PML NBs are dynamic intranuclear structures that require PML for their formation and which harbour numerous other transiently or permanently localised proteins.
  • PML is expressed as a family of isoforms (PML I-VII) as a result of alternative splicing, most of which are found in the nucleus.
  • IFN treatment directly induces transcription of the genes encoding both PML and Sp100, (another major component of PML NBs), resulting in higher levels of expression of these proteins and increases in both the size and number of PML NBs.
  • These and other observations have encouraged the hypothesis that PML, PML NBs and a number of other constituents of these structures are involved in host antiviral defences.
  • For example, exogenous expression of PML III or PML VI can impede infection by a number of RNA and DNA viruses, and certain viral proteins accumulate in PML NBs then cause their disruption by a variety of mechanisms.
  • Although there are many other functions of PML NBs in a wide range of cellular pathways, there is accumulating evidence that they represent preferential targets for viral infections and that PML plays a role in the mechanism of the antiviral action of IFN.
  • This article reviews the potential antiviral activities of PML NB constituent proteins, how RNA and DNA viruses overcome these defences, and the connections between these events and IFN pathways.
  • [MeSH-major] Antiviral Agents / pharmacology. Intranuclear Inclusion Bodies / metabolism. Leukemia, Promyelocytic, Acute / metabolism

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  • (PMID = 17343971.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U130169966
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Antiviral Agents; 0 / Autoantigens; 0 / Nuclear Proteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 135844-47-2 / Sp100 protein, human; 63231-63-0 / RNA; 9007-49-2 / DNA; 9008-11-1 / Interferons
  • [Number-of-references] 137
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20. Pierangeli SS, Vega-Ostertag M, Liu X, Girardi G: Complement activation: a novel pathogenic mechanism in the antiphospholipid syndrome. Ann N Y Acad Sci; 2005 Jun;1051:413-20
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  • [Title] Complement activation: a novel pathogenic mechanism in the antiphospholipid syndrome.
  • Antiphospholipid antibodies (aPLs) have been shown to induce thrombosis, activate endothelial cells, and induce fetal loss.
  • The pathogenesis of aPL-induced thrombosis is incompletely understood, but it is thought to involve platelet and endothelial cell activation as well as pro-coagulant effects of aPL antibody directly on clotting pathway components.
  • Recent studies have shown that uncontrolled complement activation leads to fetal death in aPL-antibody treated mice.
  • We hypothesized that aPL antibodies activate complement, generating split products that induce thrombosis.
  • To test this hypothesis, we used an in vivo model of thrombosis in which aPL antibodies induce a significant increase in thrombus size and a mouse model of endothelial cell activation in which aPLs induce significant adhesion of leukocytes (WBCs) to endothelial cells.
  • We found that mice deficient in complement components C3 and C5 were resistant to enhanced thrombosis and endothelial cell activation induced by aPL antibodies.
  • Furthermore, inhibition of C5 activation using anti-C5 mAb prevented thrombophilia induced by aPL antibodies.
  • Our data show that complement activation mediates two important effectors of aPL antibodies: induction of thrombosis and endothelial activation.
  • [MeSH-major] Antiphospholipid Syndrome / etiology. Complement Activation
  • [MeSH-minor] Animals. Antibodies, Antiphospholipid / blood. Complement C3 / physiology. Complement C5 / physiology. Humans. Mice. Thrombosis / prevention & control

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  • (PMID = 16126983.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / G12 RR 03034; United States / NIGMS NIH HHS / GM / S02 GM M 08248
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Complement C3; 0 / Complement C5
  • [Number-of-references] 39
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21. Meng R, Zhou J, Sui M, Li Z, Feng G, Yang B: Arsenic trioxide promotes mitochondrial DNA mutation and cell apoptosis in primary APL cells and NB4 cell line. Sci China Life Sci; 2010 Jan;53(1):87-93
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  • [Title] Arsenic trioxide promotes mitochondrial DNA mutation and cell apoptosis in primary APL cells and NB4 cell line.
  • This study aimed to investigate the effects of arsenic trioxide (As(2)O(3)) on the mitochondrial DNA (mtDNA) of acute promyelocytic leukemia (APL) cells.
  • The NB4 cell line was treated with 2.0 micromol/L As(2)O(3) in vitro, and the primary APL cells were treated with 2.0 micromol/L As(2)O(3) in vitro and 0.16 mg kg(-1) d(-1) As(2)O(3) in vivo.
  • Mitochondrial DNA mutation in the D-loop region was found in NB4 and APL cells before As(2)O(3) use, but the mutation spots were remarkably increased after As(2)O(3) treatment, which was positively correlated to the rates of cellular apoptosis, the correlation coefficient: r (NB4-As2O3)=0.973818, and r (APL-As2O3)=0.934703.
  • It is revealed that As(2)O(3) aggravates mtDNA mutation in the D-loop region of acute promyelocytic leukemia cells both in vitro and in vivo.
  • Mitochondrial DNA might be one of the targets of As(2)O(3) in APL treatment.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Base Sequence. Cell Line, Tumor. DNA Mutational Analysis. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology. Molecular Sequence Data. Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 20596959.001).
  • [ISSN] 1869-1889
  • [Journal-full-title] Science China. Life sciences
  • [ISO-abbreviation] Sci China Life Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / DNA, Mitochondrial; 0 / Oxides; S7V92P67HO / arsenic trioxide
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22. Son SH, Yu E, Choi EK, Lee H, Choi J: Promyelocytic leukemia protein-induced growth suppression and cell death in liver cancer cells. Cancer Gene Ther; 2005 Jan;12(1):1-11
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  • [Title] Promyelocytic leukemia protein-induced growth suppression and cell death in liver cancer cells.
  • The promyelocytic leukemia protein (PML), involved in the pathogenesis of acute promyelocytic leukemia, is a coactivator of p53 tumor suppressive functions.
  • The ability of PML to inhibit growth and induce cell death in solid tumor cells, however, has not been determined.
  • We therefore assayed the tumor suppressor activities of PML and compared them with those of p53 in four liver cancer cell lines.
  • Following infection of cells with replication-deficient recombinant PML adenovirus, the exogenous PML localized in the nucleus and formed abnormally enlarged PML-nuclear bodies after 24 hours.
  • In vitro growth curve analysis showed that the overexpressed PML initially induced a substantial G1 cell cycle arrest and triggered massive cell death in all tested cell lines, irrespective of their p53 status.
  • PML-induced cell death decreased by about 30% in the presence of a broad caspase inhibitor, zVAD.
  • The cell death effect of PML was higher than that induced by p53 over a longer period of time.
  • As with p53, overexpression of PML was closely related to upregulation of p21 and decrease of cyclin D1 expression.
  • Unexpectedly, retinoic acid (RA) antagonized rather than enhanced PML-triggered cell death.
  • RA enhanced the expression of adenovirus-cytomegalovirus-promoted PML at both transcription and protein levels within 12 hours after treatment; however, the PML protein was significantly degraded in the presence of RA at days 3-5 postinfection.
  • PML degradation was also observed in SK-BR3 breast cancer cells treated with RA.
  • Taken together, our findings strongly support the hypothesis that PML acts as a strong independent cell death inducer and that RA conversely abolishes the therapeutic effects of the PML proteins through proteasomal degradation of the protein.


23. Stasi R: Gemtuzumab ozogamicin: an anti-CD33 immunoconjugate for the treatment of acute myeloid leukaemia. Expert Opin Biol Ther; 2008 Apr;8(4):527-40
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  • [Title] Gemtuzumab ozogamicin: an anti-CD33 immunoconjugate for the treatment of acute myeloid leukaemia.
  • BACKGROUND: Gemtuzumab ozogamicin consists of a semisynthetic derivative of calicheamicin, a potent cytotoxic antibiotic, linked to a humanized anti-CD33 monoclonal antibody.
  • OBJECTIVES: To describe the pharmacology of gemtuzumab ozogamicin and to provide an overview of clinical trials in acute myeloid leukaemia.
  • RESULTS/CONCLUSIONS: Gemtuzumab ozogamicin has shown moderate activity as a single agent in patients with CD33-positive refractory or relapsed acute myeloid leukaemia, with more promising results in acute promyelocytic leukaemia.
  • The side effect profile may be an improvement on conventional chemotherapy, except for a higher frequency of veno-occlusive disease or sinusoidal obstructive syndrome, especially after a subsequent haematopoietic stem cell transplantation.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunotoxins / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Clinical Trials as Topic. Humans. Middle Aged. Recurrence. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 18352855.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  • [Number-of-references] 78
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24. He J, Luster TA, Thorpe PE: Radiation-enhanced vascular targeting of human lung cancers in mice with a monoclonal antibody that binds anionic phospholipids. Clin Cancer Res; 2007 Sep 1;13(17):5211-8
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  • [Title] Radiation-enhanced vascular targeting of human lung cancers in mice with a monoclonal antibody that binds anionic phospholipids.
  • We recently showed that anionic phospholipids, principally phosphatidylserine, are specifically exposed on the luminal surface of tumor blood vessels.
  • Here we tested the hypothesis that radiation therapy can increase phosphatidylserine exposure on lung tumor vasculature, thereby enhancing the antitumor properties of the anti-phosphatidylserine antibody 2aG4.
  • Bavituximab, a chimeric version of 2aG4 in clinical trials, has the potential to enhance the therapeutic efficacy of radiation therapy in lung cancer patients.

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  • (PMID = 17785577.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Phosphatidylserines; 0 / bavituximab
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25. Yamauchi T, Arai H, Taga M, Amaya N, Lee JD, Ueda T: [Adams-Stokes attack due to complete atrioventricular block in a patient with acute promyelocytic leukemia during remission induction therapy using all-trans retinoic acid]. Rinsho Ketsueki; 2005 Mar;46(3):206-10
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  • [Title] [Adams-Stokes attack due to complete atrioventricular block in a patient with acute promyelocytic leukemia during remission induction therapy using all-trans retinoic acid].
  • Remission induction therapy was performed for a 46-year-old Japanese man with acute promyelocytic leukemia using ATRA (45 mg/m2), enocitabine (170 mg/m2, 5 days), and mitoxantrone (4 mg/m2, 3 days).
  • The normal sinus rhythm was restored 15 days thereafter, and the patient eventually reached remission.
  • [MeSH-major] Heart Block / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects

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  • (PMID = 16447716.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 9YVR68W306 / enocitabine; BZ114NVM5P / Mitoxantrone
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26. Vasse M: Protein Z, a protein seeking a pathology. Thromb Haemost; 2008 Oct;100(4):548-56
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  • Protein Z (PZ) is a vitamin K-dependent factor identified in human plasma in 1984 characterized by an homology with other vitamin K-dependent factors (factor VII, IX, X, protein C).
  • ZPI inhibits the activated factor X (FXa) on phospholipid surface.
  • In humans, PZ is characterized by an unusual wide distribution in plasma, and a major decrease induced by warfarin.
  • Unexpectedly, a relationship between PZ deficiency and ischemic arterial diseases such as stroke, acute coronary syndromes or peripheral arterial disease was described but not confirmed by all studies.
  • PZ deficiency could be also a risk factor for early fetal losses, and increases the arterial risk in antiphospholipid syndrome.

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  • (PMID = 18841275.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / plasma protein Z; 12001-79-5 / Vitamin K
  • [Number-of-references] 98
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27. Kim TM, Kim JS, Han SW, Hong YS, Kim I, Ha J, Kim SJ, Chung JW, Park JH, Lee D, Park S, Kim BK, Kim NK, Yoon SS: Clinical predictors of recurrent venous thromboembolism: a single institute experience in Korea. Thromb Res; 2009;123(3):436-43
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  • [Title] Clinical predictors of recurrent venous thromboembolism: a single institute experience in Korea.
  • Independent predictors for recurrent VTE were presence of residual thrombosis (hazard ratio [HR]=3.1, 95% confidence interval [CI] 1.0-9.3; p=0.044), antiphospholipid syndrome (APS) (HR=4.3, 95% CI 1.0-19.0; p=0.052), and age 50 years or younger (HR=2.5, 95% CI 1.0-6.6; p=0.053) by multivariate analysis.

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  • [CommentIn] Thromb Res. 2009 Jun;124(2):236 [18849061.001]
  • (PMID = 18579181.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants
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28. Yamaguchi Y, Usui N, Dobashi N, Yano S, Yahagi Y, Takei Y, Sugiyama K, Ogasawara Y, Saito T, Minami J, Kobayashi T, Katsube A, Kamiyama Y, Machishima T, Morikawa N, Otsubo H, Kaito K, Asai O, Aiba K: Gemtuzumab ozogamicin (GO) in relapsed/refractory patients with acute myeloid leukemia. Gan To Kagaku Ryoho; 2009 Jul;36(7):1105-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemtuzumab ozogamicin (GO) in relapsed/refractory patients with acute myeloid leukemia.
  • OBJECTIVE: Gemtuzumab ozogamicin (GO) is a humanized anti-CD33 antibody, linked to calicheamicin, which has been approved in Japan recently.
  • We conducted to evaluate the efficacy and toxicity of GO in our patients with relapsed or refractory AML retrospectively.
  • PATIENTS AND METHODS: Data were collected between March 1, 2000, and March 1, 2006, on 10 patients with relapsed or refractory AML(excluding FAB: M3).
  • No patient developed hepatic veno-occlusive disease including 2 patients who underwent HSCT.
  • CONCLUSION: GO is a valuable new treatment option for relapsed or refractory AML patients, however, the benefit from single agent appears insufficient.
  • On going clinical trials including combination with other antileukemic agents might better define the role of GO.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19620797.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
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29. Liu ZM, Huang HS: As2O3-induced c-Src/EGFR/ERK signaling is via Sp1 binding sites to stimulate p21WAF1/CIP1 expression in human epidermoid carcinoma A431 cells. Cell Signal; 2006 Feb;18(2):244-55
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  • Arsenic has been effectively used to treat acute promyelocytic leukemia, and can induce cell cycle arrest or apoptosis in human solid tumors.

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  • (PMID = 15961274.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Oxides; 0 / Sp1 Transcription Factor; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src); EC 2.7.11.24 / Extracellular Signal-Regulated MAP 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 / Mitogen-Activated Protein Kinase 8; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; S7V92P67HO / arsenic trioxide
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30. Asherson RA, Gómez-Puerta JA, Marinopoulos G: Recurrent pulmonary thromboembolism in a patient with systemic lupus erythematosus and HIV-1 infection associated with the presence of antibodies to prothrombin: a case report. Clin Infect Dis; 2005 Nov 15;41(10):e89-92
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  • [Title] Recurrent pulmonary thromboembolism in a patient with systemic lupus erythematosus and HIV-1 infection associated with the presence of antibodies to prothrombin: a case report.
  • Antiphospholipid antibodies are demonstrable in patients with both conditions, but clinical manifestations of the antiphospholipid syndrome (APS) in HIV-infected patients, although reported, are uncommon.
  • METHODS: We describe a patient with HIV infection and SLE who manifested 4 episodes of deep vein thrombosis (DVT) complicated by pulmonary embolism.
  • Enzyme-linked immunosorbant assay was used to test for the presence of antiphospholipid antibodies, including anticardiolipin antibodies, anti- beta 2-glycoprotein 1 antibodies, and antiprothrombin antibodies (anti-PT).
  • RESULTS: We document the case of 35-year-old African woman with HIV infection and SLE who developed recurrent episodes of DVT and pulmonary embolism in the presence of anti-PT and discuss in depth the pathogenic role of these antibodies and the clinical challenges posed to clinicians by the coexistence of HIV and SLE in the same patient.
  • [MeSH-major] Antibodies / immunology. HIV Infections / complications. Lupus Erythematosus, Systemic / complications. Prothrombin / immunology. Pulmonary Embolism / etiology
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Adult. Anti-HIV Agents / therapeutic use. Anticoagulants / therapeutic use. Female. Humans. Venous Thrombosis / etiology. Warfarin / therapeutic use


31. Lindhoff-Last E, Luxembourg B: Evidence-based indications for thrombophilia screening. Vasa; 2008 Feb;37(1):19-30
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  • The knowledge about the clinical relevance of thrombophilic defects is increasing, and evidence-based indications for thrombophilia screening are therefore discussed in this review.
  • In the majority of patients with acute venous thrombosis, the results of thrombophilia screening do not influence the duration of oral anticoagulation.
  • The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population.
  • Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis or a positive family history.
  • While antiphospholipid antibodies are known to be associated with arterial thrombosis, screening for heritable thrombophilias is not useful in arterial thrombosis, although subgroup analysis indicates that they may play a role particularly in young patients and children.
  • [MeSH-major] Anticoagulants / therapeutic use. Blood Coagulation / drug effects. Mass Screening. Patient Selection. Thrombophilia / diagnosis
  • [MeSH-minor] Abortion, Spontaneous / blood. Abortion, Spontaneous / etiology. Arterial Occlusive Diseases / blood. Arterial Occlusive Diseases / etiology. Contraceptives, Oral, Hormonal / adverse effects. Estrogen Replacement Therapy / adverse effects. Evidence-Based Medicine. Female. Genetic Predisposition to Disease. Humans. Male. Pedigree. Pre-Eclampsia / blood. Pre-Eclampsia / etiology. Pregnancy. Pregnancy Complications, Cardiovascular / blood. Pregnancy Complications, Cardiovascular / etiology. Risk Factors. Thromboembolism / blood. Thromboembolism / etiology. Venous Thrombosis / blood. Venous Thrombosis / etiology

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  • [CommentIn] Vasa. 2008 May;37(2):189; author reply 190-2 [18622971.001]
  • (PMID = 18512539.001).
  • [ISSN] 0301-1526
  • [Journal-full-title] VASA. Zeitschrift für Gefässkrankheiten
  • [ISO-abbreviation] VASA
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Contraceptives, Oral, Hormonal
  • [Number-of-references] 74
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32. Mulkiewicz E, Jastorff B, Składanowski AC, Kleszczyński K, Stepnowski P: Evaluation of the acute toxicity of perfluorinated carboxylic acids using eukaryotic cell lines, bacteria and enzymatic assays. Environ Toxicol Pharmacol; 2007 May;23(3):279-85
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  • [Title] Evaluation of the acute toxicity of perfluorinated carboxylic acids using eukaryotic cell lines, bacteria and enzymatic assays.
  • The acute biological activity of a homologous series of perfluorinated carboxylic acids - perfluorohexanoic acid (PFHxA), perfluoroheptanoic acid (PFHpA), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA) and perfluorodecanoic acid (PFDA) - was studied.
  • The viability of cells from the promyelocytic leukemia rat cell line (IPC-81) and the rat glioma cell line (C6) was assayed calorimetrically with WST-1 reagent.
  • The evaluation was combined with the Vibrio fischeri acute bioluminescence inhibition assay.
  • The biological activity of the compounds was also determined at the molecular level with acetylcholinesterase and glutathione reductase inhibition assays.
  • The results show these compounds have a very low acute biological activity.

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  • [Copyright] Copyright © 2006 Elsevier B.V. All rights reserved.
  • (PMID = 21783770.001).
  • [ISSN] 1382-6689
  • [Journal-full-title] Environmental toxicology and pharmacology
  • [ISO-abbreviation] Environ. Toxicol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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33. Bérubé NG, Healy J, Medina CF, Wu S, Hodgson T, Jagla M, Picketts DJ: Patient mutations alter ATRX targeting to PML nuclear bodies. Eur J Hum Genet; 2008 Feb;16(2):192-201
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  • [Title] Patient mutations alter ATRX targeting to PML nuclear bodies.
  • ATRX associates with the nuclear matrix, pericentromeric heterochromatin, and promyelocytic leukemia nuclear bodies (PML-NBs) in a speckled nuclear staining pattern.
  • One of the latter domains is responsible for targeting ATRX to PML-NBs.
  • More importantly, four different patient mutations within this domain resulted in an approximately 80% reduction in the number of transfected cells with ATRX nuclear speckles and PML colocalization.
  • These results demonstrate that patient mutations have a dramatic effect on subnuclear targeting to PML-NBs.
  • Moreover, these findings support the hypothesis that ATRX patient mutations represent functional hypomorphs and suggest that loss of proper targeting to PML-NBs is an important contributor to the pathogenesis of the ATR-X syndrome.

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  • (PMID = 17957225.001).
  • [ISSN] 1018-4813
  • [Journal-full-title] European journal of human genetics : EJHG
  • [ISO-abbreviation] Eur. J. Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / ATRX protein, human
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34. Liu Y, Shevchenko A, Shevchenko A, Berk AJ: Adenovirus exploits the cellular aggresome response to accelerate inactivation of the MRN complex. J Virol; 2005 Nov;79(22):14004-16
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  • During adenovirus infection, the viral protein E4orf3 associates with MRN in promyelocytic leukemia protein nuclear bodies before MRN is bound by E1B-55K.

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  • (PMID = 16254336.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA064799; United States / NCI NIH HHS / CA / CA64799
  • [Publication-type] 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 / 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; EC 6.5.1.- / DNA Repair Enzymes
  • [Other-IDs] NLM/ PMC1280221
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35. Puccetti E, Zheng X, Brambilla D, Seshire A, Beissert T, Boehrer S, Nürnberger H, Hoelzer D, Ottmann OG, Nervi C, Ruthardt M: The integrity of the charged pocket in the BTB/POZ domain is essential for the phenotype induced by the leukemia-associated t(11;17) fusion protein PLZF/RARalpha. Cancer Res; 2005 Jul 15;65(14):6080-8
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  • [Title] The integrity of the charged pocket in the BTB/POZ domain is essential for the phenotype induced by the leukemia-associated t(11;17) fusion protein PLZF/RARalpha.
  • Acute myeloid leukemia is characterized by a differentiation block as well as by an increased self-renewal of hematopoietic precursors in the bone marrow.
  • This phenotype is induced by specific acute myeloid leukemia-associated translocations, such as t(15;17) and t(11;17), which involve an identical portion of the retinoic acid receptor alpha (RARalpha) and either the promyelocytic leukemia (PML) or promyelocytic zinc finger (PLZF) genes, respectively.
  • [MeSH-minor] Acute Disease. Animals. COS Cells. Dimerization. Female. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / physiology. Histone Deacetylase Inhibitors. Histone Deacetylases / metabolism. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Mice. Mice, Inbred C57BL. Molecular Weight. Mutagenesis, Site-Directed. Point Mutation. Promoter Regions, Genetic. Protein Binding. Protein Folding. Protein Structure, Tertiary. Structure-Activity Relationship. Transcription, Genetic. Zinc Fingers

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  • (PMID = 16024608.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / PLZF-RARalpha fusion protein, human; EC 3.5.1.98 / Histone Deacetylases
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36. Parks J, Gyeltshen T, Prachyawarakorn V, Mahidol C, Ruchirawat S, Kittakoop P: Glutarimide alkaloids and a terpenoid benzoquinone from Cordia globifera. J Nat Prod; 2010 May 28;73(5):992-4
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  • Cordiarimide B (4) exhibited radical scavenging activity, as it inhibited superoxide anion radical formation in the xanthine/xanthine oxidase (XXO) assay, and also suppressed superoxide anion generation in differentiated HL-60 human promyelocytic leukemia cells when induced by 12-O-tetradecanoylphorbol-13-acetate (TPA).

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  • (PMID = 20384317.001).
  • [ISSN] 1520-6025
  • [Journal-full-title] Journal of natural products
  • [ISO-abbreviation] J. Nat. Prod.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Benzoquinones; 0 / Free Radical Scavengers; 0 / Piperidones; 0 / Terpenes; 0 / cordiarimide A; 0 / cordiarimide B; 0 / globiferane; 11062-77-4 / Superoxides; 3T006GV98U / benzoquinone; EC 1.17.3.2 / Xanthine Oxidase; NI40JAQ945 / Tetradecanoylphorbol Acetate
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37. Ishimaru C, Yonezawa Y, Kuriyama I, Nishida M, Yoshida H, Mizushina Y: Inhibitory effects of cholesterol derivatives on DNA polymerase and topoisomerase activities, and human cancer cell growth. Lipids; 2008 Apr;43(4):373-82
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  • Compounds 2, 3 and 6 inhibited the activity of human topo II, with IC50 values of 5.0, 12.5 and 120 microM, respectively.
  • Compounds 2, 3 and 6 also suppressed human cancer cell (promyelocytic leukemia cell line, HL-60) growth, and LD50 values were 8.8, 20.2 and 72.3 microM, respectively, suggesting that cell growth inhibition had the same tendency as the inhibition of topos rather than pols.
  • From these findings, the action mode of cholesterol derivatives as anti-cancer compounds is discussed.

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  • (PMID = 18214566.001).
  • [ISSN] 0024-4201
  • [Journal-full-title] Lipids
  • [ISO-abbreviation] Lipids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Nucleic Acid Synthesis Inhibitors; 0 / Topoisomerase Inhibitors; 97C5T2UQ7J / Cholesterol; EC 2.7.7.7 / DNA-Directed DNA Polymerase; EC 5.99.1.- / DNA Topoisomerases
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38. Ma Z, Saluta G, Kucera GL, Bierbach U: Effect of linkage geometry on biological activity in thiourea- and guanidine-substituted acridines and platinum-acridines. Bioorg Med Chem Lett; 2008 Jul 1;18(13):3799-801
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  • Novel thiourea- and guanidine-modified acridine-4-carboxamides (4, 7) and a corresponding platinum-intercalator conjugate (4') have been synthesized and evaluated as cytotoxic agents in human promyelocytic leukemia, HL-60, and a non-small cell lung cancer, NCI-H460.
  • Modification of thiourea sulfur in derivative 4 with a DNA platinating moiety, giving 4', resulted in a pronounced cytotoxic enhancement, and the conjugate proved to be the most active of the newly synthesized compounds in NCI-H460 cells.

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  • (PMID = 18515101.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101880-04; United States / NCI NIH HHS / CA / R01 CA101880; United States / NCI NIH HHS / CA / CA101880; United States / NCI NIH HHS / CA / R01 CA101880-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acridines; 0 / Antineoplastic Agents; 141-83-3 / guanidine carboxamide; 49DFR088MY / Platinum; 8W8T17847W / Urea; GYV9AM2QAG / Thiourea; JU58VJ6Y3B / Guanidine
  • [Other-IDs] NLM/ NIHMS57183; NLM/ PMC2474763
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39. Wang YA, Shen K, Ishida Y, Wang Y, Kakizuka A, Brooks SC: Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha. Mol Carcinog; 2005 Dec;44(4):252-61
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  • [Title] Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha.
  • Acute promyelocytic leukemia (APL) is invariably associated with chromosomal translocation to retinoic acid receptor alpha (RARalpha) locus.
  • In a vast majority of cases, RARalpha translocates to and fuses with the promyelocytic leukemia (PML) gene.
  • It was thought that the fusion protein PML-RARalpha acts as a double dominant negative mutant to inhibit the PML and RARalpha signaling.
  • Here we showed that dominant negative RARalpha induced acute lymphoblastic leukemia and lymphoma development in the transgenic mice.
  • Thus, our results suggested that disruption of RARalpha signaling was the first essential step in the development of APL in vivo.
  • [MeSH-major] Gene Expression Regulation / physiology. Genes, Dominant. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Receptors, Retinoic Acid / genetics
  • [MeSH-minor] Acute Disease. Animals. Apoptosis. Cell Proliferation. Female. Humans. Male. Mammary Tumor Virus, Mouse / genetics. Mice. Mice, Transgenic. Survival Rate. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 16273555.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA89526
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
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40. Leymarie V, Galoisy AC, Falkenrodt A, Natarajan-Ame S, Dufour P, Lessard M: Latent acute promyelocytic leukemia t(15;17)(q22;q12-21) and sarcoidosis: long-term cohabitation. Eur J Intern Med; 2005 Dec;16(8):598-600
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  • [Title] Latent acute promyelocytic leukemia t(15;17)(q22;q12-21) and sarcoidosis: long-term cohabitation.
  • To our knowledge, we report the first case involving sarcoidosis and acute promyelocytic leukemia (APL) t(15;17)(q22;q12-21).
  • The major interest lies in the chronology of the two diseases: the APL demonstrated an unusual smoldering evolution, suggesting that pre-existing sarcoidosis may have a non-fortuitous immunological impact on leukemic clone proliferation.

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  • (PMID = 16314244.001).
  • [ISSN] 0953-6205
  • [Journal-full-title] European journal of internal medicine
  • [ISO-abbreviation] Eur. J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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41. Mahadeo KM, Dhall G, Ettinger LJ, Kurer CC: Exacerbation of anthracycline-induced early chronic cardiomyopathy with ATRA: role of B-type natriuretic peptide as an indicator of cardiac dysfunction. J Pediatr Hematol Oncol; 2010 Mar;32(2):134-6
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  • [Title] Exacerbation of anthracycline-induced early chronic cardiomyopathy with ATRA: role of B-type natriuretic peptide as an indicator of cardiac dysfunction.
  • Cardiac disease is a significant complication of childhood oncologic therapy.
  • We report the case of a 14-year-old female with acute promyelocytic leukemia who developed symptomatic cardiomyopathy only 4 months into treatment with a combination of daunomycin and all-trans retinoic acid (ATRA).
  • Improvement and deterioration in systolic function on echocardiogram and serum B-natriuretic peptide levels were seen while receiving ATRA 1 week on and 1 week off, respectively, during the maintenance phase of therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / adverse effects. Cardiomyopathies / chemically induced. Daunorubicin / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Natriuretic Peptide, Brain / blood. Tretinoin / adverse effects
  • [MeSH-minor] Adolescent. Chronic Disease. Female. Humans

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  • (PMID = 20098333.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 114471-18-0 / Natriuretic Peptide, Brain; 5688UTC01R / Tretinoin; ZS7284E0ZP / Daunorubicin
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42. Luo RQ, Lei YX, Zhang X, Liang F: [Clinical analysis of patients with systemic lupus erythematosus and concomitant pulmonary hypertension]. Nan Fang Yi Ke Da Xue Xue Bao; 2008 Oct;28(10):1860-3
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  • [Title] [Clinical analysis of patients with systemic lupus erythematosus and concomitant pulmonary hypertension].
  • OBJECTIVE: To investigate the clinical manifestations, diagnosis and interventions of pulmonary hypertension (PAH) in patients with systemic lupus erythematosus (SLE).
  • METHODS: From January 2001 to December 2007, 798 SLE patients without prior diagnosis were admitted in our hospital, among whom 39 were identified to have concomitant PAH defined by echocardiography.
  • The clinical data of the 39 cases were analyzed retrospectively.
  • The 39 SLE patients with concomitant PAH included 5 men and 34 women with a mean age of 34-/+12 years.
  • Positive correlations were found between the occurrence of PAH and the Raynaud phenomenon, fingertip vasculitis, anti-u1RNP antibody positivity, antiphospholipid antibody positivity, pericardial effusion, and interstitial pneumonia (P < 0.05).
  • Patients with higher scores for SLE Disease Activity Index were liable to PAH.
  • The presence of Raynaud phenomenon, fingertip vasculitis, anti-u1RNP antibody positivity, antiphospholipid antibody positivity, pericardial effusion, and interstitial pneumonia is correlated to greater severity PAH with poor prognosis.
  • CONCLUSION: PAH is not a rare concomitant disease in SLE patients.
  • The presence of Raynaud phenomenon, fingertip vasculitis, anti-u1RNP antibody positivity, antiphospholipid antibody positivity, pericardial effusion, and interstitial pneumonia all suggest the likeliness of PAH in SLE patients, and echocardiographic examination may help derive an early diagnosis.
  • [MeSH-major] Hypertension, Pulmonary / complications. Hypertension, Pulmonary / diagnosis. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. China / epidemiology. Early Diagnosis. Echocardiography. Female. Humans. Male. Middle Aged. Raynaud Disease / complications. Retrospective Studies


43. Gouider E, Ben Salah N, Jeddi R, Belakhal F, Meddeb B, Hafsia R: [Cytology and immunophenotyping of acute promyelocytary leukaemia]. Arch Inst Pasteur Tunis; 2006;83(1-4):49-52
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  • [Title] [Cytology and immunophenotyping of acute promyelocytary leukaemia].
  • Acute promyelocytic leukaemia (AML3) is characterized by particular clinical and biological features.
  • A double negativity of HLA-DR and CD34 is found in 12 cases and aberrant expression of CD2 in 2AML3v.
  • Cytological diagnosis is often evident, although in some cases, it is not typical and immunophenotype will contribute to the diagnosis.
  • [MeSH-major] Cytological Techniques / methods. Immunophenotyping / methods. Leukemia, Promyelocytic, Acute / diagnosis

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  • (PMID = 19388597.001).
  • [ISSN] 0020-2509
  • [Journal-full-title] Archives de l'Institut Pasteur de Tunis
  • [ISO-abbreviation] Arch Inst Pasteur Tunis
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Validation Studies
  • [Publication-country] Tunisia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, CD2; 0 / Antigens, CD34; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD65s antigen, human; 0 / HLA-DR Antigens; 0 / Sialic Acid Binding Ig-like Lectin 2; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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44. Doudican NA, Bowling B, Orlow SJ: Enhancement of arsenic trioxide cytotoxicity by dietary isothiocyanates in human leukemic cells via a reactive oxygen species-dependent mechanism. Leuk Res; 2010 Feb;34(2):229-34
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  • Although clearly effective in acute promyelocytic leukemia (APL), arsenic trioxide (ATO) demonstrates little clinical benefit as a single agent in the treatment of non-APL hematological malignancies.
  • Cellular exposure to sulforaphane in combination with ATO resulted in a dramatic increase in levels of reactive oxygen species (ROS) compared to treatment with either agent alone.
  • Combinatorial treatment with isothiocyanates and ATO might provide a promising therapeutic approach for a variety of myeloid malignancies.

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
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  • (PMID = 19540589.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR041880; United States / NIAMS NIH HHS / AR / R01 AR041880-12; United States / NIAMS NIH HHS / AR / R21 AR050645-02; United States / NIAMS NIH HHS / AR / AR041880-12; United States / NIAMS NIH HHS / AR / AR041880-11; United States / NIAMS NIH HHS / AR / AR041880-14; United States / NIAMS NIH HHS / AR / R01 AR041880-13; United States / NIAMS NIH HHS / AR / AR41880; United States / NIAMS NIH HHS / AR / R21 AR050645; United States / NIAMS NIH HHS / AR / R01 AR041880-14; United States / NIAMS NIH HHS / AR / AR050645-02; United States / NIAMS NIH HHS / AR / AR041880-13; United States / NIAMS NIH HHS / AR / R01 AR041880-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Isothiocyanates; 0 / Oxides; 0 / Reactive Oxygen Species; 0 / Sulfides; 0 / Sulfones; 0 / Thiocyanates; 4478-93-7 / sulforafan; 504-84-7 / erysolin; CTE370DL3U / erucin; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ NIHMS131574; NLM/ PMC2815001
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45. Dvorak CC, Agarwal R, Dahl GV, Gregory JJ, Feusner JH: Hematopoietic stem cell transplant for pediatric acute promyelocytic leukemia. Biol Blood Marrow Transplant; 2008 Jul;14(7):824-30
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  • [Title] Hematopoietic stem cell transplant for pediatric acute promyelocytic leukemia.
  • The optimal form of treatment for children with relapsed or refractory acute promyelocytic leukemia (APL) is unclear.
  • We retrospectively analyzed the results of 32 (11 autologous, 21 allogeneic) hematopoietic stem cell transplants (HSCT) performed for children originally treated on either the Eastern Cooperative Group E2491 Trial or the Cancer and Leukemia Group B C9710 Trial and subsequently diagnosed with relapsed or refractory APL.
  • This data demonstrates that autologous and allogeneic HSCT are both effective therapies for treatment of children with relapsed or refractory APL.
  • Autologous HSCT is associated with a low incidence of TRM, whereas allogeneic HSCT is associated with a low incidence of relapse, suggesting a strong GVL effect against residual APL.

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  • (PMID = 18541203.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098543-06; United States / NCI NIH HHS / CA / U10 CA098543-06
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS162635; NLM/ PMC2796449
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46. Narita T, Suga A, Kobayashi M, Hashimoto K, Sakagami H, Motohashi N, Kurihara T, Wakabayashi H: Tumor-specific cytotoxicity and type of cell death induced by benzo[b]cyclohept[e][1,4]oxazine and 2-aminotropone derivatives. Anticancer Res; 2009 Apr;29(4):1123-30
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  • [Title] Tumor-specific cytotoxicity and type of cell death induced by benzo[b]cyclohept[e][1,4]oxazine and 2-aminotropone derivatives.
  • The highly active derivatives, 7-bromo-2-(4-hydroxyanilino)tropone [16] and 4-isopropyl-2-(2-hydroxyanilino)tropone [20], induced internucleosomal DNA fragmentation and caspase-3, -8 and -9 activation in human promyelocytic leukemia HL-60 cells, but only at concentrations twice or four times higher than CC(50) values.

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  • (PMID = 19414354.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 2-aminotropone; 0 / 4-isopropyl-2-(2-hydroxyanilino)tropone; 0 / 7-bromo-2-(4-hydroxyanilino)tropone; 7L6DL16P1T / Tropolone; EC 3.4.22.- / Caspases
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47. Hwang J, Kalejta RF: Human cytomegalovirus protein pp71 induces Daxx SUMOylation. J Virol; 2009 Jul;83(13):6591-8
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  • A component of promyelocytic leukemia nuclear bodies, Daxx is a transcriptional corepressor that silences the expression of viral immediate-early (IE) genes at the start of both lytic and quiescent HCMV infections. pp71 is a tegument component delivered directly to cells by infecting HCMV virions.
  • Here we report that pp71 also substantially increases the basal level of SUMOylated Daxx observed in cells.
  • Thus, while pp71 enhances the basal level of SUMOylated Daxx, the role that this modification plays in regulating Daxx activity in uninfected or HCMV-infected cells remains an enigma.

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  • (PMID = 19369322.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI074984; United States / NIAID NIH HHS / AI / R56 AI064703; United States / NIAID NIH HHS / AI / R01-AI074984; United States / NIAID NIH HHS / AI / R56-AI064703
  • [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 / Adaptor Proteins, Signal Transducing; 0 / DAXX protein, human; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / Viral Proteins; 107852-97-1 / cytomegalovirus phosphoprotein 71kDa
  • [Other-IDs] NLM/ PMC2698545
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48. Johnson JE, Varkonyi RJ, Schwalm J, Cragle R, Klein-Szanto A, Patchefsky A, Cukierman E, von Mehren M, Broccoli D: Multiple mechanisms of telomere maintenance exist in liposarcomas. Clin Cancer Res; 2005 Aug 1;11(15):5347-55
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  • EXPERIMENTAL DESIGN: Tumor samples were analyzed with respect to telomerase activity, telomere length, and the presence of ALT-specific subcellular structures, ALT-associated promyelocytic leukemia nuclear bodies.
  • In addition, telomere length was always shorter in recurrent disease, regardless of the telomere maintenance mechanism.

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  • (PMID = 16061847.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA006927; United States / NCI NIH HHS / CA / CA098087-03; United States / NCI NIH HHS / CA / CA109442-01; United States / NCI NIH HHS / CA / T32 CA09035-29
  • [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 / Nucleoproteins; 0 / RNA, Messenger; EC 2.7.7.49 / Telomerase
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49. de Thé H, Chen Z: Acute promyelocytic leukaemia: novel insights into the mechanisms of cure. Nat Rev Cancer; 2010 Nov;10(11):775-83
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  • [Title] Acute promyelocytic leukaemia: novel insights into the mechanisms of cure.
  • The fusion oncogene, promyelocytic leukaemia (PML)-retinoic acid receptor-α (RARA), initiates acute promyelocytic leukaemia (APL) through both a block to differentiation and increased self-renewal of leukaemic progenitor cells.
  • The current standard of care is retinoic acid (RA) and chemotherapy, but arsenic trioxide also cures many patients with APL, and an RA plus arsenic trioxide combination cures most patients.
  • This Review discusses the recent evidence that reveals surprising new insights into how RA and arsenic trioxide cure this leukaemia, by targeting PML-RARα for degradation.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 20966922.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
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50. Donadini MP, Crowther M: Antiphospholipid syndrome: a challenging hypercoagulable state with systemic manifestations. Hematol Oncol Clin North Am; 2010 Aug;24(4):669-76, vii
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  • [Title] Antiphospholipid syndrome: a challenging hypercoagulable state with systemic manifestations.
  • Antiphospholipid syndrome (APS) is a systemic disease that causes venous and arterial thrombosis in virtually any organ and is responsible for fetal losses and pregnancy disorders.
  • The spectrum of clinical manifestations is wide, because the thrombotic process may involve arterial and venous vessels of any size in any organ.
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Thrombophilia / diagnosis

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20659651.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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51. Makhoul BF, Guralnik L, Azzam ZS: Catastrophic antiphospholipid syndrome presented with abdominal, pulmonary, and bone marrow complications. Rheumatol Int; 2010 Jan;30(3):401-4
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  • [Title] Catastrophic antiphospholipid syndrome presented with abdominal, pulmonary, and bone marrow complications.
  • We are presenting a case of catastrophic antiphospholipid syndrome in an adult female manifesting with abdominal thrombosis, pancytopenia, and alveolar hemorrhage.
  • The diagnosis should be made promptly based on clinical symptoms coupled with radiological features.
  • Once this diagnosis is suspected, treatment with corticosteroids and anticoagulation must be initiated as soon as possible in order to reduce severe morbidity and high mortality.
  • [MeSH-major] Antiphospholipid Syndrome / complications. Hemorrhage / etiology. Lung Diseases / etiology. Pancytopenia / etiology. Thrombosis / etiology
  • [MeSH-minor] Abdominal Pain / etiology. Acute Disease / therapy. Anticoagulants / therapeutic use. Dyspnea / etiology. Dyspnea / physiopathology. Female. Humans. Lung / diagnostic imaging. Lung / pathology. Lung / physiopathology. Middle Aged. Pleural Effusion / diagnostic imaging. Pleural Effusion / etiology. Pleural Effusion / pathology. Portal Vein / pathology. Portal Vein / physiopathology. Pulmonary Alveoli / pathology. Pulmonary Alveoli / physiopathology. Steroids / therapeutic use. Tomography, X-Ray Computed. Treatment Outcome


52. 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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53. Ieko M, Naito S, Yoshida M: [Laboratory examinations in antiphospholipid syndrome]. Rinsho Byori; 2010 Apr;58(4):343-51
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  • [Title] [Laboratory examinations in antiphospholipid syndrome].
  • Antiphospholipid syndrome (APS), formerly detected by the association between clinical events (venous/arterial thrombosis or pregnancy morbidity) and positivity in at least one of the laboratory tests used to detect antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), IgG- or IgM-class anticardiolipin antibodies (aCL), and IgG or IgM-class anti-beta2GPI antibodies (abeta2GPI), is now diagnosed using revised APS classification criteria.
  • However, there are a number of problems with the methods used to detect aPL.
  • According to the guidelines for detection of LA recently published by ISTH-SSC, APTT reagents with silica as an activator and double centrifugation-treated samples (including control plasma) are recommended to detect LA, while 50% patient plasma mixed with control plasma is recommended for a cross-mixing test.
  • In the present study, we obtained favorable results for LA detection with cross-mixing tests by measuring APTT in mixtures of control plasma with 0%, 10%, 20%, 50%, and 100% concentrations of patient plasma treated with a 0.2 microm filter.
  • In the future, laboratory examinations for APS will change with diagnostic criteria, as APS has not yet been established as a distinct disease concept.
  • [MeSH-major] Antibodies, Anticardiolipin / blood. Antibodies, Antiphospholipid / blood. Antiphospholipid Syndrome / diagnosis

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  • (PMID = 20496762.001).
  • [ISSN] 0047-1860
  • [Journal-full-title] Rinsho byori. The Japanese journal of clinical pathology
  • [ISO-abbreviation] Rinsho Byori
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Biomarkers; 0 / Lupus Coagulation Inhibitor; 0 / Reagent Kits, Diagnostic; 0 / beta 2-Glycoprotein I
  • [Number-of-references] 27
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54. Carmona F, Lázaro I, Reverter JC, Tàssies D, Font J, Cervera R, Balasch J: Impaired factor XIIa-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications. Am J Obstet Gynecol; 2006 Feb;194(2):457-65
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  • [Title] Impaired factor XIIa-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
  • OBJECTIVE: The objective of the study was to investigate the potential role of impaired factor XII-dependent activation of fibrinolysis in treated antiphospholipid syndrome gestations developing late-pregnancy complications.
  • STUDY DESIGN: This was a prospective study in a third-level teaching hospital, including 75 patients: 25 pregnant patients having the antiphospholipid syndrome and carrying their pregnancies until 26 weeks' gestation or later (group 1); 25 pregnant patients having normal term pregnancies and delivery and no previous miscarriage (group 2); and 25 pregnant patients being diagnosed as having severe pre-eclampsia and/or intrauterine growth restriction but testing negative for antiphospholipid antibodies (group 3).
  • RESULTS: Patients in group 1 were characterized by increased factor VIIa levels, increased prothrombin fragment 1+2 levels, reduced factor XIIa levels, diminished functional urokinase-type plasminogen activator levels, and decreased levels of plasmin/alpha-2-plasmin inhibitor complexes.
  • CONCLUSIONS: Impaired factor XIIa-dependent activation of fibrinolysis seems to be a key mechanism related to late-pregnancy complications in patients with the antiphospholipid syndrome.
  • [MeSH-major] Antiphospholipid Syndrome / physiopathology. Factor XIIa / physiology. Fibrinolysis / physiology. Pregnancy Complications / physiopathology

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  • (PMID = 16458646.001).
  • [ISSN] 1097-6868
  • [Journal-full-title] American journal of obstetrics and gynecology
  • [ISO-abbreviation] Am. J. Obstet. Gynecol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Coagulation Factors; EC 3.4.21.38 / Factor XIIa
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55. Pu YS, Jan KY, Wang TC, Wang AS, Gurr JR: 8-Oxoguanine DNA glycosylase and MutY homolog are involved in the incision of arsenite-induced DNA adducts. Toxicol Sci; 2007 Feb;95(2):376-82
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  • Treatment of human promyelocytic leukemia NB4 cells with 0.5muM As(2)O(3) for 30 min induced no DNA breaks, as analyzed by a standard comet assay.

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  • (PMID = 17101720.001).
  • [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 / Arsenicals; 0 / DNA Adducts; 0 / Environmental Pollutants; 0 / Ferrous Compounds; 0 / Oxides; 39R4TAN1VT / ferrous sulfate; BBX060AN9V / Hydrogen Peroxide; EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase; EC 3.2.2.- / oxoguanine glycosylase 1, human; S7V92P67HO / arsenic trioxide
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56. Rainaldi G, Romano R, Indovina P, Ferrante A, Motta A, Indovina PL, Santini MT: Metabolomics using 1H-NMR of apoptosis and Necrosis in HL60 leukemia cells: differences between the two types of cell death and independence from the stimulus of apoptosis used. Radiat Res; 2008 Feb;169(2):170-80
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  • [Title] Metabolomics using 1H-NMR of apoptosis and Necrosis in HL60 leukemia cells: differences between the two types of cell death and independence from the stimulus of apoptosis used.
  • High-resolution proton nuclear magnetic resonance ((1)H-NMR) spectroscopy was used to examine and compare the metabolic variations that occur in cells of the HL60 promyelocytic leukemia cell line after induction of apoptosis by ionizing radiation and the antineoplastic drug doxorubicin as well as after induction of necrosis by heating.

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  • (PMID = 18220461.001).
  • [ISSN] 0033-7587
  • [Journal-full-title] Radiation research
  • [ISO-abbreviation] Radiat. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cytotoxins; 0 / Proteome; 0 / Protons; 80168379AG / Doxorubicin
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57. Lindhoff-Last E, Luxembourg B, Pabinger I: [Update thrombophilia]. Hamostaseologie; 2008 Dec;28(5):365-75
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  • A survey on definitions, epidemiology, clinical manifestations of congenital and acquired thrombophilias is given with focus on evidence-based data.
  • The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population.
  • Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis to be able to decide whether anticoagulation is necessary when these patients become pregnant.

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  • (PMID = 19132167.001).
  • [ISSN] 0720-9355
  • [Journal-full-title] Hämostaseologie
  • [ISO-abbreviation] Hamostaseologie
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / factor V Leiden; 9001-24-5 / Factor V; 9001-26-7 / Prothrombin; 9001-27-8 / Factor VIII; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 3.4.21.5 / Thrombin
  • [Number-of-references] 136
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58. Lopes AA: Pathophysiological basis for anticoagulant and antithrombotic therapy in pulmonary hypertension. Cardiovasc Hematol Agents Med Chem; 2006 Jan;4(1):53-9
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  • [Title] Pathophysiological basis for anticoagulant and antithrombotic therapy in pulmonary hypertension.
  • In pulmonary hypertension (PH), thrombosis and thromboembolism may occur as primary events associated with inherited or acquired thrombophilia.
  • Alternatively, in situ thrombosis may develop as a complication of pre-existing vasculopathy as in the case of idiopathic PH and related disorders (so called pulmonary arterial hypertension).
  • These abnormalities are suggestive of a shift of pulmonary vascular microenvironment toward a procoagulant, prothrombotic and antifibrinolytic pattern.
  • The abnormalities described so far include circulating antiphospholipid antibodies, increased plasma levels of platelet aggregating agents (serotonin, thromboxane), adhesion molecules (P-selectin, von Willebrand factor), antifibrinolytic enzymes (plasminogen activator inhibitor 1) and cytokines.
  • The present review is focused on the procoagulant, prothrombotic and antifibrinolytic mechanisms so far identified in PH, in both clinical setting and animal models.
  • [MeSH-major] Anticoagulants / therapeutic use. Fibrinolytic Agents / therapeutic use. Hypertension, Pulmonary / drug therapy. Hypertension, Pulmonary / physiopathology

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  • (PMID = 16529549.001).
  • [ISSN] 1871-5257
  • [Journal-full-title] Cardiovascular & hematological agents in medicinal chemistry
  • [ISO-abbreviation] Cardiovasc Hematol Agents Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Fibrinolytic Agents
  • [Number-of-references] 88
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59. Harder J, Thürmel K, Maier M, Lanzl I: [Bilateral recurrent retinal thrombosis in a young man]. Ophthalmologe; 2009 Oct;106(10):924-7
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  • An antiphospholipid antibody syndrome was diagnosed which was treated with anticoagulants.
  • [MeSH-major] Anticoagulants / therapeutic use. Antiphospholipid Syndrome / diagnosis. Antiphospholipid Syndrome / drug therapy. Retinal Diseases / diagnosis. Retinal Diseases / therapy. Thrombosis / diagnosis. Thrombosis / drug therapy
  • [MeSH-minor] Adult. Humans. Macular Edema / diagnosis. Macular Edema / drug therapy. Male. Secondary Prevention. Treatment Outcome

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  • [Cites] Semin Thromb Hemost. 1999;25(3):333-50 [10443963.001]
  • [Cites] Ophthalmology. 2002 Jan;109(1):126-31 [11772591.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1827-32 [12393574.001]
  • [Cites] JAMA. 2006 Mar 1;295(9):1050-7 [16507806.001]
  • (PMID = 19495773.001).
  • [ISSN] 1433-0423
  • [Journal-full-title] Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft
  • [ISO-abbreviation] Ophthalmologe
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anticoagulants
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60. Qin H, Liu T, Yang JL, Huang X, Liu B, Song X, Zhao X, Wei YQ: [Screening proteins related to retinoic acid resistance by proteomic analysis]. Zhonghua Yi Xue Za Zhi; 2007 Feb 27;87(8):520-5
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  • METHODS: The total cellular proteins from the RA sensitive cells of the line NB4 and the RA resistant cells of the line MR2 obtained from a patient with acute promyelocytic leukemia (APL) were separated by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and analyzed by PDQuest v7.1 analysis software to screen the differential protein spots.
  • Differentially expressed spots were analyzed by mass spectrometry for peptide mass finger (PMF) data and identified by Mascot software and SWISS-PROT protein database.
  • RESULTS: 2-DE patterns of APL cell lines with high-resolution and reproducibility were obtained.
  • 25 differential protein spots were identified by mass spectrometry and 17 proteins were successfully assigned to 13 gene-reading frames, of which one was unknown function protein (FLJ00279) and the others were included in the categories of oncoprotein (DJ-1), transcription factor (MYC promoter-binding protein 1), molecule chaperone (HSP70, HSP60 and protein disulfide isomerase), metabolism protein (prohibitin, triosephosphate isomerase 1, and calreticulin), signal transduction (Rho GDP dissociation inhibitor), and cytoskeleton (ACTG1 protein, Beta 5-tubulin, and keratin 10).
  • Semi-quantification RT-PCR analysis showed that there was no correlation between the protein expression changes and mRNA levels of HSP70 or HSP60.

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  • (PMID = 17459200.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi 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 / Antineoplastic Agents; 0 / Calreticulin; 0 / Intracellular Signaling Peptides and Proteins; 5688UTC01R / Tretinoin
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61. Li L, He DL: Transfection of promyelocytic leukemia in retrovirus vector inhibits growth of human bladder cancer cells. Acta Pharmacol Sin; 2005 May;26(5):610-5
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  • [Title] Transfection of promyelocytic leukemia in retrovirus vector inhibits growth of human bladder cancer cells.
  • AIM: To construct a recombinant retrovirus vector carrying human promyelocytic leukemia (PML) cDNA and identify its expression and biology role in bladder cancer UM-UC-2 cells for future gene therapy.
  • METHODS: PML full-length cDNA was inserted into the EcoR I and BamH I site of pLXSN vector containing the long terminal repeat (LTR) promoter.
  • PML cDNA was detected by polymerase chain reaction (PCR) and the protein was identified by laser confocal microscopy and Western blot in bladder cancer cells, respectively.
  • RESULTS: Restriction enzyme digestion proved that a 2.1 kb PML cDNA was inserted into the pLXSN vector.
  • CONCLUSION: The retrovirus pLPMLSN vector was successfully constructed and could generate high effective expression of human PML in bladder cancer cell UM-UC-2, suggesting that PML recombinant retrovirus have potential utility in the gene therapy for bladder cancer.
  • [MeSH-major] Cell Proliferation. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Retroviridae / genetics. Transcription Factors / genetics. Tumor Suppressor Proteins / genetics. Urinary Bladder Neoplasms / pathology

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  • (PMID = 15842782.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
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62. Chim CS, Kwong YL: Adverse prognostic impact of CDKN2B hyper-methylation in acute promyelocytic leukemia. Leuk Lymphoma; 2006 May;47(5):815-25
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  • [Title] Adverse prognostic impact of CDKN2B hyper-methylation in acute promyelocytic leukemia.
  • The use of all-trans retinoic acid (ATRA) has markedly improved the survival of patients with acute promyelocytic leukemia (APL), making it potentially curable.
  • High presentation leucocyte count has been found to correlate with inferior disease-free-survival (DFS).
  • The CpG island inside the CDKN2B promoter is hyper-methylated in approximately 50 - 60% of APL patients.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p15 / genetics. DNA Methylation. Leukemia, Promyelocytic, Acute / genetics

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  • (PMID = 16753865.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15
  • [Number-of-references] 71
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63. 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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64. Quenby S, Mountfield S, Cartwright JE, Whitley GS, Chamley L, Vince G: Antiphospholipid antibodies prevent extravillous trophoblast differentiation. Fertil Steril; 2005 Mar;83(3):691-8
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  • [Title] Antiphospholipid antibodies prevent extravillous trophoblast differentiation.
  • OBJECTIVE: We investigated the hypothesis that antiphospholipid antibodies (aPL) have a detrimental effect on human extravillous trophoblast (EVT) differentiation into giant multinucleated cells "in vitro."
  • MAIN OUTCOME MEASURE(S): This model was then used to investigate the effect of two different monoclonal aPL to beta2-glycoprotein 1 (IIC5 and ID2), and control mouse IgG antibody on EVT differentiation.
  • The aPL, IIC5, and ID2 significantly inhibited GMC formation, whereas the mouse IgG control had no effect.
  • CONCLUSION(S): Antiphospholipid antibodies can inhibit EVT differentiation and GMC formation "in vitro" suggesting that a failure of trophoblast differentiation and subsequent uteroplacental development may be an underlying pathology in antiphospholipid syndrome-associated pregnancy loss.
  • [MeSH-major] Antibodies, Antiphospholipid / pharmacology. Trophoblasts / cytology. Trophoblasts / immunology

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  • (PMID = 15749499.001).
  • [ISSN] 0015-0282
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Antibodies, Monoclonal
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65. Suvajac G, Stojanovich L, Milenkovich S: Ocular manifestations in antiphospholipid syndrome. Autoimmun Rev; 2007 Jun;6(6):409-14
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  • [Title] Ocular manifestations in antiphospholipid syndrome.
  • Antiphospholipid syndrome (APS) is characterized by increased hypercoagulability and divergent symptoms including ocular manifestations.
  • In APS patients arterial and/or venous thromboses and repeated fetal loss are diagnosed in presence of antiphospholipid (aPL) antibodies.
  • Antiphospholipid antibodies are heterogeneous group of immunoglobulins with different antigenic structure.
  • Primary APS is defined in the absence of underlying disease, while secondary APS is seen within another pathological condition.
  • In secondary APS occlusion of central retinal artery and vein (OACR, OVCR) is the most common finding, thus when found in younger patients it should be considered indicative of APS.
  • [MeSH-major] Antibodies, Antiphospholipid / immunology. Antiphospholipid Syndrome / complications. Antiphospholipid Syndrome / immunology. Eye Diseases / etiology
  • [MeSH-minor] Anterior Eye Segment. Humans. Lupus Erythematosus, Systemic / complications. Lupus Erythematosus, Systemic / immunology. Thrombosis

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  • (PMID = 17537387.001).
  • [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 / Antibodies, Antiphospholipid
  • [Number-of-references] 26
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66. Martinuc Porobic J, Avcin T, Bozic B, Kuhar M, Cucnik S, Zupancic M, Prosenc K, Kveder T, Rozman B: Anti-phospholipid antibodies following vaccination with recombinant hepatitis B vaccine. Clin Exp Immunol; 2005 Nov;142(2):377-80
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  • [Title] Anti-phospholipid antibodies following vaccination with recombinant hepatitis B vaccine.
  • This study was undertaken to evaluate the possible role of hepatitis B recombinant vaccine inducing the synthesis of IgG and IgM anti-cardiolipin antibodies (aCL), antibodies against beta(2)GPI (anti-beta(2)GPI), lupus anti-coagulant (LA), anti-nuclear antibodies and antibodies against extractable nuclear antigens (anti-ENA).
  • One month after vaccination with the first dose of hepatitis B vaccine a minority of vaccinated individuals showed changes in IgG or IgM aCL or anti-beta(2)GPI or LA activity (P < 0.001).
  • Among subjects in whom changes of IgG anti-beta(2)GPI were observed, a significantly higher number of increased (8/85) than decreased (2/85) values were found (P < 0.01).
  • Analyses of paired data showed that differences in aCL or anti-beta(2)GPI levels before vaccination or 1 month later did not reach statistical significance.
  • In two people aCL transitorily reached medium positivity after the first dose of hepatitis B vaccine with a drop 5 months later.
  • Similar evident anti-beta(2)GPI fluctuation was also observed in one person.
  • Another participant was initially low positive for IgG anti-beta2GPI and the levels were increasing after vaccination.
  • Two participants became positive for anti-nuclear antibodies during 6 months' follow-up.
  • There were no sex-dependent differences in tested antibodies observed and no associations between levels of aPL and levels of anti-HBV antibodies.
  • We conclude that HBV can induce aPL, although rarely.
  • [MeSH-major] Antibodies, Antiphospholipid / biosynthesis. Hepatitis B Vaccines / immunology. Vaccines, Synthetic / immunology

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  • (PMID = 16232227.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Antiphospholipid; 0 / Engerix-B; 0 / Glycoproteins; 0 / Hepatitis B Vaccines; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor; 0 / Vaccines, Synthetic; 0 / beta 2-Glycoprotein I
  • [Other-IDs] NLM/ PMC1809502
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67. Gopal M, Cohn CD, McEntire MR, Alperin JB: Thrombotic thrombocytopenic purpura and adult onset Still's disease. Am J Med Sci; 2009 May;337(5):373-6
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  • [Title] Thrombotic thrombocytopenic purpura and adult onset Still's disease.
  • Although recent literature supports the role of ADAMTS13 (a disintegrin-like metalloproteinase with thrombospondin type 1 repeats), the von Willebrand factor cleaving protease, in the pathogenesis of the disease, many aspects of the disease remain a mystery.
  • Various drugs and autoimmune conditions, such as systemic lupus erythematosus and the antiphospholipid syndrome, have been observed in association with TTP.
  • Adult onset Still's disease (AOSD) has been reported less frequently in association with TTP.
  • He responded initially to plasma exchange, but never achieved complete remission.
  • DISCUSSION: Literature review shows that the autoimmune diseases usually associated with TTP include systemic lupus erythematosus and the antiphospholipid syndrome.
  • Interestingly, the patient's AOSD-associated arthritis responded to plasma exchange, but did not resolve after splenectomy.
  • [MeSH-major] Purpura, Thrombotic Thrombocytopenic / complications. Purpura, Thrombotic Thrombocytopenic / diagnosis. Still's Disease, Adult-Onset / complications. Still's Disease, Adult-Onset / diagnosis
  • [MeSH-minor] ADAM Proteins / blood. ADAM Proteins / immunology. Adult. Antigens, CD36 / blood. Antigens, CD36 / immunology. Hematology / methods. Humans. Male. Plasma Exchange. Remission Induction. Splenectomy. Treatment Outcome

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  • (PMID = 19322066.001).
  • [ISSN] 0002-9629
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAMTS13 protein, human
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68. Atienza MR, Respaldiza N, De La Santa E, Martín-Garrido I, Medrano FJ, Varela JM, Calderón E: Antiphospholipid antibodies investigation in Pneumocystis jirovecii carriers. Scand J Infect Dis; 2008;40(10):840-2
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  • [Title] Antiphospholipid antibodies investigation in Pneumocystis jirovecii carriers.
  • It is well documented that antiphospholipid antibodies are increased in patients with HIV-1 infection and these are most commonly seen in those with Pneumocystis jirovecii pneumonia.
  • We report here our experience concerning the possible relationship between P. jirovecii infection in non-immunocompromized adults and the production of antiphospholipid antibodies.
  • IgG anticardiolipin antibodies were positive in 2 out of 5 (40%) P. jirovecii carriers and 2 out of 10 (20%) subjects with no evidence of pulmonary infection by this microorganism (p=0.4).

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  • (PMID = 18609205.001).
  • [ISSN] 0036-5548
  • [Journal-full-title] Scandinavian journal of infectious diseases
  • [ISO-abbreviation] Scand. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Immunoglobulin M; 0 / Lupus Coagulation Inhibitor
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69. Jerga A, Miller DJ, White SW, Rock CO: Molecular determinants for interfacial binding and conformational change in a soluble diacylglycerol kinase. J Biol Chem; 2009 Mar 13;284(11):7246-54
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  • Anionic phospholipids, like phosphatidylglycerol (PtdGro), were required for DgkB to recognize diacylglycerol embedded in a phospholipid bilayer.
  • DgkB interaction with phospholipid vesicles was not influenced by the presence of ATP, but anionic vesicles decreased the Km of the enzyme for ATP.
  • The key residues responsible for the structural Mg2+ binding site, the conformational changes that increase ATP affinity, and interfacial recognition of anionic phospholipids were identical in DgkB and the mammalian diacylglycerol kinase catalytic cores.
  • This sequence conservation suggests that the mammalian enzymes also require a structural divalent cation and surface positively charged residues to bind phospholipid bilayers and trigger conformational changes that accelerate catalysis.

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  • (PMID = 19112175.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NIGMS NIH HHS / GM / GM34496
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Proteins; 0 / Lipid Bilayers; 0 / Phosphatidylglycerols; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.1.107 / Diacylglycerol Kinase; I38ZP9992A / Magnesium
  • [Other-IDs] NLM/ PMC2652325
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70. Szewczyk M, Wielkoszyński T, Zakliczyński M, Zembala M, Szumska-Kostrzewska M: Anti-ox-LDL and anticardiolipin autoantibodies in patients after cardiac transplantation. Transplant Proc; 2007 Nov;39(9):2870-2
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  • [Title] Anti-ox-LDL and anticardiolipin autoantibodies in patients after cardiac transplantation.
  • INTRODUCTION: Among cardiac transplantation (OHT) of coronary arterial disease, the pathogenesis can be associated with autoimmunologic effects due to oxidative lipoprotein modification and their change in antigenicity.
  • These factors may lead to lipoprotein vascular changes observed in antiphospholipid syndrome or systemic lupus erythematosus.
  • The aim of the presented study was to evaluate anticardiolipin autoantibodies (ACA) and anti-ox-LDL (antibodies against oxidized LDL) levels in the plasma immunoglobulin IgG class.
  • RESULTS: OHT patients showed significantly higher ACA concentrations compared with the control group (3.53 vs 1.10 GPL U/mL), whereas anti-ox-LDL levels did not differ considerably (494 vs 385 mU/mL).
  • Significant differences between the 2 OHT patient groups regarding anti-ox-LDL concentration were demonstrated among samples taken in 2002.
  • It is necessary to focus further research on the possibilities of developing secondary antiphospholipid syndrome.


71. Khalifa M, Ghannouchi N, Kaabia N, BenJazia E, Hachfi W, Krifa A, Letaief A, Bahri F: Primary antiphospholipid syndrome and Evan's syndrome: 2 case reports. Acta Clin Belg; 2009 Jan-Feb;64(1):65-7
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  • [Title] Primary antiphospholipid syndrome and Evan's syndrome: 2 case reports.
  • The main clinical features of primary antiphospholipid syndrome are recurrent foetal loss, arterial or venous thrombosis and thrombocytopaenia.
  • Evan's syndrome is characterized by simultaneous or sequential association of autoimmune anaemia and thombocytopaenia, rarely reported in primary antiphospholipid syndrome.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / complications. Antiphospholipid Syndrome / complications. Thrombocytopenia / complications

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  • (PMID = 19317244.001).
  • [ISSN] 1784-3286
  • [Journal-full-title] Acta clinica Belgica
  • [ISO-abbreviation] Acta Clin Belg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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72. Cuong NM, Tai BH, Hoan DH, Huong TT, Kim YH, Hyun JH, Kang HK: Inhibitory effects of indirubin derivatives on the growth of HL-60 leukemia cells. Nat Prod Commun; 2010 Jan;5(1):103-6
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  • [Title] Inhibitory effects of indirubin derivatives on the growth of HL-60 leukemia cells.
  • Six indirubin derivatives have been synthesized and their inhibitory effects on the growth of HL-60 human promyelocytic leukemia cells investigated.
  • Indirubin-3'-oxime (I-1) inhibited the growth of HL-60 cells with a GI50 value of 36.6 microM, whereas I-0, I-2, I-3, I-4 and I-6 showed only weak cytotoxic activities against HL-60 cancer cells with GI50 values in the range of 97.3 to over 100 microM.

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  • (PMID = 20184032.001).
  • [ISSN] 1934-578X
  • [Journal-full-title] Natural product communications
  • [ISO-abbreviation] Nat Prod Commun
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Indoles; V86L8P74GI / indirubin
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73. Hertig A, Ridel C, Rondeau E: [Hemolytic uremic syndrome in adults]. Nephrol Ther; 2010 Jul;6(4):258-71
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  • [Transliterated title] Syndromes hémolytiques et urémiques de l'adulte.
  • Hemolytic uremic syndrome (HUS) is related to a renal thrombotic microangiopathy, inducing hypertension and acute renal failure (ARF).
  • HUS may also occur after various treatments such as mitomycin C, gemcitabine, ciclosporin A, or tacrolimus, and as reported more recently bevacizumab, an anti VEGF antibody.
  • In adults, several HUS are encountered in the course of chronic nephropathies: nephroangiosclerosis, chronic glomerulonephritis, post irradiation nephropathy, scleroderma, disseminated lupus erythematosus, antiphospholipid syndrome.
  • Overall the prognosis of HUS has improved, with a patient survival greater than 85% at 1 year.
  • Plasma infusions and plasma exchanges are effective in most of the cases to treat hemolysis and thrombocytopenia.
  • A new monoclonal anti-C5 antibody is tested, and seems to be effective in atypical HUS with abnormal complement alternate pathway activation.
  • [MeSH-minor] Acute Kidney Injury / etiology. Adult. Escherichia coli Infections / complications. Humans. Hypertension / etiology. Kidney Failure, Chronic / complications. Risk Factors. Thrombotic Microangiopathies / complications

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  • [Copyright] Copyright 2010 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.
  • (PMID = 20399168.001).
  • [ISSN] 1872-9177
  • [Journal-full-title] Néphrologie & thérapeutique
  • [ISO-abbreviation] Nephrol. Ther.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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74. Robinson PJ, Pinheiro TJ: Phospholipid composition of membranes directs prions down alternative aggregation pathways. Biophys J; 2010 Apr 21;98(8):1520-8
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  • [Title] Phospholipid composition of membranes directs prions down alternative aggregation pathways.
  • Atomic force microscopy is used to image the aggregation of prions on supported lipid bilayers composed of mixtures of the zwitterionic lipid, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) and the anionic lipid, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoserine (POPS).
  • Prion aggregation is observed on both zwitterionic and anionic membranes, and the morphology of the aggregates formed is dependent on the anionic phospholipid content of the membrane.
  • The presence of POPS results in larger aggregates with a distinctive sponge-like morphology that are disruptive to membranes.

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  • [Copyright] Copyright 2010 Biophysical Society. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20409471.001).
  • [ISSN] 1542-0086
  • [Journal-full-title] Biophysical journal
  • [ISO-abbreviation] Biophys. J.
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / 88/DTA19176; United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D524516/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipid Bilayers; 0 / Phosphatidylcholines; 0 / Phosphatidylserines; 0 / Phospholipids; 0 / Prions; 0 / Solutions; 40290-44-6 / 1-palmitoyl-2-oleoylglycero-3-phosphoserine; TE895536Y5 / 1-palmitoyl-2-oleoylphosphatidylcholine
  • [Other-IDs] NLM/ PMC2856143
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75. Lormeau C, Falgarone G, Roulot D, Boissier MC: Rheumatologic manifestations of chronic hepatitis C infection. Joint Bone Spine; 2006 Dec;73(6):633-8
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  • Tests are usually negative for antibodies to cyclic citrullinated peptides (anti-CCP), which may help to differentiate the two conditions.
  • HCV-associated vasculitis is usually related to cryoglobulinemia, although a few cases of polyarteritis nodosa-like disease affecting the medium-sized vessels have been reported.
  • Other conditions reported in patients with chronic HCV infection include fibromyalgia, systemic lupus erythematosus (SLE), antiphospholipid syndrome, and osteosclerosis.

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  • (PMID = 17056293.001).
  • [ISSN] 1778-7254
  • [Journal-full-title] Joint, bone, spine : revue du rhumatisme
  • [ISO-abbreviation] Joint Bone Spine
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 59
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76. Zabek J, Noworyta J, Brasse-Rumin M, Rell-Bakalarska M: [Inhibition of cardiolipin binding antibodies from synovial fluids of patients with arthritis by endotoxin]. Pol Arch Med Wewn; 2006 May;115(5):447-51
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  • In the presented study was prooven that aCl antibodies cross-reacting with LPS (endotoxin) from arthritic synovial fluids are part of the aPL antibodies pool and correlated with presence in joints bacterial cell wall components like LPS-showing endotoxin presence in synovial fluids and they may be usefull in differential diagnosis of the different kind of arthritis and also in explanation of their aetiology at all--especially in cases of early, undifferentiated arthritis.
  • [MeSH-major] Antibodies, Anticardiolipin / immunology. Arthritis / diagnosis. Arthritis / immunology. Lipopolysaccharides / metabolism. Synovial Fluid / immunology
  • [MeSH-minor] Antibodies, Bacterial / analysis. Antigens, Bacterial / analysis. Arthritis, Rheumatoid / diagnosis. Biomarkers / metabolism. Cross Reactions. Diagnosis, Differential. Humans. Immunologic Tests. Osteoarthritis / diagnosis. Osteoarthritis / immunology

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  • (PMID = 17195359.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antibodies, Anticardiolipin; 0 / Antibodies, Bacterial; 0 / Antigens, Bacterial; 0 / Biomarkers; 0 / Lipopolysaccharides
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77. Kraemer L, Wajid M, Shimomura Y, Christiano AM: Mutations in the hairless gene underlie APL in three families of Pakistani origin. J Dermatol Sci; 2008 Apr;50(1):25-30
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  • [Title] Mutations in the hairless gene underlie APL in three families of Pakistani origin.
  • BACKGROUND: Atrichia with papular lesions (APL) (OMIM#209500) is a rare autosomal recessively inherited form of irreversible alopecia characterized by papular lesions of keratin-filled cysts on various regions of the body.
  • Males and females are equally affected and present with a distinct pattern of total hair loss on scalp, axilla and body.
  • Mutations in the hairless (HR) gene have been previously shown to be responsible for APL.
  • OBJECTIVE: In this study, we studied the molecular basis of APL in three unrelated families of Pakistani origin.
  • In family B, we identified a novel homozygous deletion of a G nucleotide at the exon 15-intron 15 boundary, termed 3097delG.

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  • (PMID = 18164595.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR047338; United States / NIAMS NIH HHS / AR / R01 AR047338-06A2S1; United States / NIAMS NIH HHS / AR / R01 AR47338
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / HR protein, human; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS125830; NLM/ PMC2914536
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78. Guo Y, Dolinko AV, Chinyengetere F, Stanton B, Bomberger JM, Demidenko E, Zhou DC, Gallagher R, Ma T, Galimberti F, Liu X, Sekula D, Freemantle S, Dmitrovsky E: Blockade of the ubiquitin protease UBP43 destabilizes transcription factor PML/RARα and inhibits the growth of acute promyelocytic leukemia. Cancer Res; 2010 Dec 1;70(23):9875-85
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  • [Title] Blockade of the ubiquitin protease UBP43 destabilizes transcription factor PML/RARα and inhibits the growth of acute promyelocytic leukemia.
  • More effective treatments for acute promyelocytic leukemia (APL) are needed.
  • APL cell treatment with all-trans-retinoic acid (RA) degrades the chimeric, dominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARα, which is generated in APL by chromosomal translocation.
  • The E1-like ubiquitin-activating enzyme (UBE1L) associates with interferon-stimulated gene ISG15 that binds and represses PML/RARα protein.
  • In this study, we explored how RA regulates UBP43 expression and the effects of UBP43 on PML/RARα stability and APL growth, apoptosis, or differentiation.
  • RA treatment induced UBE1L, ISG15, and UBP43 expression in RA-sensitive but not RA-resistant APL cells.
  • Similar in vivo findings were obtained in a transgenic mouse model of transplantable APL, and in the RA response of leukemic cells harvested directly from APL patients.
  • UBP43 knockdown repressed PML/RARα protein levels and inhibited RA-sensitive or RA-resistant cell growth by destabilizing the PML domain of PML/RARα.
  • This inhibitory effect promoted apoptosis but did not affect the RA differentiation response in these APL cells.
  • In contrast, elevation of UBP43 expression stabilized PML/RARα protein and inhibited apoptosis.
  • Taken together, our findings define the ubiquitin protease UBP43 as a novel candidate drug target for APL treatment.

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  • (PMID = 20935222.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01-CA087546; United States / NCI NIH HHS / CA / R01 CA062275-16; United States / NCI NIH HHS / CA / R01 CA111422; United States / NHLBI NIH HHS / HL / R01 HL074175; United States / NCI NIH HHS / CA / R01 CA062275; United States / NCI NIH HHS / CA / R01-CA111422; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / CA062275-16; United States / NCI NIH HHS / CA / R01 CA056771; United States / NCI NIH HHS / CA / R01 CA087546; United States / NHLBI NIH HHS / HL / R00 HL098342; United States / NCI NIH HHS / CA / R01-CA56771; United States / NCI NIH HHS / CA / R01-CA062275
  • [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 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; EC 3.4.- / Endopeptidases; EC 3.4.99.- / USP18 protein, human
  • [Other-IDs] NLM/ NIHMS242702; NLM/ PMC2999664
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79. Furlow B: Fallon leukaemia cluster findings, research plans announced. Lancet Oncol; 2007 Jan;8(1):9
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  • [Title] Fallon leukaemia cluster findings, research plans announced.
  • [MeSH-major] Disease Outbreaks. Leukemia, Promyelocytic, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 17348115.001).
  • [ISSN] 1470-2045
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] News
  • [Publication-country] England
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80. Gopal S, Marcussen S, Dobin SM, Koss W, Donner LR: Primary myeloid sarcoma of the testicle with t(15;17). Cancer Genet Cytogenet; 2005 Mar;157(2):148-50
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  • [Title] Primary myeloid sarcoma of the testicle with t(15;17).
  • The first case of acute promyelocytic leukemia presenting as a solitary testicular mass (myeloid sarcoma) that relapsed in the contralateral testicle is described.
  • Translocation (15;17)(q22;q21.1) was revealed by cytogenetics and was verified by fluorescence in situ hybridization.
  • Contralateral testicle is a favorite site for recurrence in a subset of testicular myeloid sarcomas.
  • Subclassification of all cases of myeloid sarcoma ought to be attempted.
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Leukemia, Promyelocytic, Acute / diagnosis. Sarcoma, Myeloid / genetics. Testicular Neoplasms / genetics. Translocation, Genetic

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  • (PMID = 15721636.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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81. Vora S, Shetty S, Salvi V, Satoskar P, Ghosh K: A comprehensive screening analysis of antiphospholipid antibodies in Indian women with fetal loss. Eur J Obstet Gynecol Reprod Biol; 2008 Apr;137(2):136-40
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  • [Title] A comprehensive screening analysis of antiphospholipid antibodies in Indian women with fetal loss.
  • STUDY DESIGN: Four hundred and thirty women (median age 26 years, range 18-39 years) with unexplained fetal loss (median number of abortions 3, range 1-13) were screened for the presence of antiphospholipid antibodies (APA), i.e. lupus anticoagulant (LA), IgG/M antibodies for cardiolipin (ACA), beta 2 glycoprotein 1 (beta2 GP1) and annexin V.
  • The overall prevalence of IgG and/or IgM antibodies for cardiolipin, beta 2 GP1 and annexin V were as follows-ACA 27.9% (OR 18.9; 95% CI, 5-70; P<0.05), beta 2 GP1 12.2% (OR 6.8; 95% CI, 1.8-25; P<0.05) and annexin V 14.6% (OR 17; 95% CI, 2.9-98; P<0.05).
  • [MeSH-major] Abortion, Spontaneous / immunology. Antibodies, Antiphospholipid / blood. Mass Screening / methods

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  • (PMID = 17644242.001).
  • [ISSN] 0301-2115
  • [Journal-full-title] European journal of obstetrics, gynecology, and reproductive biology
  • [ISO-abbreviation] Eur. J. Obstet. Gynecol. Reprod. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies; 0 / Antibodies, Antiphospholipid; 0 / Cardiolipins; 0 / Lupus Coagulation Inhibitor; 0 / beta 2-Glycoprotein I
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82. Gallien S, Milea D, Thiebaut MM, Bricaire F, Le Hoang P: Brain and optic nerve ischemia in malaria with immune disorders. J Infect; 2007 Jan;54(1):e1-3
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  • We report an unusual case of Plasmodium falciparum malaria in a European returning from tropical regions associating an anterior ischemic optic neuropathy and an asymptomatic centropontine myelinolysis.
  • The transient antiphospholipid antibodies detected in the patient may have played a role in the ischemic process at the origin of this unusual clinical association.
  • [MeSH-minor] Antibodies, Antiphospholipid / blood. France. Humans. Male. Middle Aged. Travel

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  • (PMID = 16647756.001).
  • [ISSN] 1532-2742
  • [Journal-full-title] The Journal of infection
  • [ISO-abbreviation] J. Infect.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid
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83. von Scheven E, Elder ME: Association between beta2-glycoprotein I gene polymorphisms and pediatric SLE and antiphospholipid antibodies. Lupus; 2005;14(6):440-4
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  • [Title] Association between beta2-glycoprotein I gene polymorphisms and pediatric SLE and antiphospholipid antibodies.
  • Antibodies against phospholipids (PL) and PL-binding proteins have been causally implicated in antiphospholipid syndrome (APS).
  • The purpose of this study was to identify associations between beta2GPI mutations and both antiphospholipid antibodies (aPL) and their associated clinical manifestations in a pediatric and adolescent cohort and to search for novel mutations.
  • Genetic analysis of beta2GPI was performed in 58 youths with systemic lupus erythematosus (SLE) and/or aPL, to identify known polymorphisms at amino acids 247 and 306 as well as novel mutations in exon 7 of the beta2GPI gene, and their association with aPL-associated clinical manifestations.
  • Our results demonstrate an association between substitution of Val for Leu at AA247 (L247V) of beta2GPI and both the development of aPL (P = 0.05) and aPL-associated clinical manifestations (P = 0.03) among pediatric patients.
  • The odds ratio associated with risk of aPL-associated clinical manifestations for the homozygous VV polymorphism was 5.5 (CI 1.3-23, P = 0.03) for the overall cohort, and 4.75 (CI 0.66-55.49, P = 0.06) after adjusting for ethnicity.
  • Association between the VV genotype at amino acid 247 of beta2GPI and clinical disease supports a genetic cause for APS among children and adolescents.
  • [MeSH-major] Antibodies, Antiphospholipid / blood. Glycoproteins / genetics. Lupus Erythematosus, Systemic / genetics. Lupus Erythematosus, Systemic / immunology
  • [MeSH-minor] Adolescent. Adult. Alleles. Amino Acid Substitution. Antiphospholipid Syndrome / genetics. Antiphospholipid Syndrome / immunology. Base Sequence. Child. Child, Preschool. Cohort Studies. DNA, Complementary / genetics. Female. Humans. Male. Polymorphism, Genetic. beta 2-Glycoprotein I

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  • (PMID = 16038107.001).
  • [ISSN] 0961-2033
  • [Journal-full-title] Lupus
  • [ISO-abbreviation] Lupus
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR 20684; United States / NCRR NIH HHS / RR / M01 RR01271
  • [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] England
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / DNA, Complementary; 0 / Glycoproteins; 0 / beta 2-Glycoprotein I
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84. Bao SH, Wang XP, Lin QD, Di W, Xu L, Ding CW: The investigation on the value of repeat and combination test of ACA and anti-beta2-GPI antibody in women with recurrent spontaneous abortion. Am J Reprod Immunol; 2008 Oct;60(4):372-8
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  • [Title] The investigation on the value of repeat and combination test of ACA and anti-beta2-GPI antibody in women with recurrent spontaneous abortion.
  • PROBLEM: In order to investigate the value of anticardiolipin antibodies (ACA) and anti-beta2-GPI antibodies detection in screening autoimmune type recurrent spontaneous abortion and its clinic application in antiphospholipid syndrome diagnosis, we adopt repeat combined ACA and anti-beta2-GPI antibodies detection in this study.
  • METHOD OF STUDY: Sera were collected from patients and work-up was done for detection of ACA and anti-beta2-GPI antibodies by enzyme-linked immunosorbent assay (ELISA).
  • RESULTS: The repeated and combined detection of ACA and anti-beta2-GPI antibodies detection could raise the positivity rate up to 21.8% (P < 0.05) in comparison with positive for ACA alone (14.1%), positive for anti-beta2-GPI alone (3.1%), and concurrently positive for both ACA and anti-beta2-GPI antibodies (4.6%).
  • In 91 confirmed positive antiphospholipid antibodies (APA) patients, with more frequent screening for ACA and anti-beta2-GPI antibodies, more patients with APA were found.
  • CONCLUSION: Our data implied that it would be appropriate to take over five or more screenings of combined ACA and anti-beta2-GPI antibodies detection in suspect patients to facilitate the positive diagnostic rate for autoimmune type RSA.
  • [MeSH-major] Abortion, Habitual / diagnosis. Abortion, Spontaneous / diagnosis. Antibodies, Anticardiolipin / blood. Autoimmune Diseases / diagnosis. beta 2-Glycoprotein I / blood


85. Moran DM, Shen H, Maki CG: Puromycin-based vectors promote a ROS-dependent recruitment of PML to nuclear inclusions enriched with HSP70 and Proteasomes. BMC Cell Biol; 2009 May 01;10:32
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  • [Title] Puromycin-based vectors promote a ROS-dependent recruitment of PML to nuclear inclusions enriched with HSP70 and Proteasomes.
  • BACKGROUND: Promyelocytic Leukemia (PML) protein can interact with a multitude of cellular factors and has been implicated in the regulation of various processes, including protein sequestration, cell cycle regulation and DNA damage responses.
  • Previous studies reported that misfolded proteins or proteins containing polyglutamine tracts form aggregates with PML, chaperones, and components of the proteasome, supporting a role for PML in misfolded protein degradation.
  • RESULTS: In the current study, we have identified a reactive oxygen species (ROS) dependent aggregation of PML, small ubiquitin-like modifier 1 (SUMO-1), heat shock protein 70 (HSP70) and 20S proteasomes in human cell lines that have been transiently transfected with vectors expressing the puromycin resistance gene, puromycin n-acetyl transferase (pac).
  • Immunofluorescent studies demonstrated that PML, SUMO-1, HSP70 and 20S proteasomes aggregated to form nuclear inclusions in multiple cell lines transfected with vectors expressing puromycin (puro) resistance in regions distinct from nucleoli.

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  • (PMID = 19409099.001).
  • [ISSN] 1471-2121
  • [Journal-full-title] BMC cell biology
  • [ISO-abbreviation] BMC Cell Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108843; United States / NCI NIH HHS / CA / R01 CA 108843
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HSP70 Heat-Shock Proteins; 0 / Nuclear Proteins; 0 / Reactive Oxygen Species; 0 / SUMO-1 Protein; 0 / SUMO1 protein, human; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; 4A6ZS6Q2CL / Puromycin; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2685373
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86. Asherson RA, Davidge-Pitts MC, Wypkema E: "Primary" antiphospholipid syndrome evolving into Waldenstrom's macroglobulinaemia: a case report. Clin Rheumatol; 2007 Feb;26(2):278-80
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  • [Title] "Primary" antiphospholipid syndrome evolving into Waldenstrom's macroglobulinaemia: a case report.
  • A 57-year-old woman with a history of transient ischaemic attacks and six recurrent foetal losses accompanied by elevations of antiphospholipid antibodies was diagnosed as having a "primary" antiphospholipid syndrome.
  • A false positive serological test for syphilis was demonstrated and apparently had been noted in her second pregnancy more than 20 years prior to her presentation with an antiphospholipid syndrome.
  • This case illustrates the importance of this investigation in any middle-aged patient presenting with an antiphospholipid syndrome and a monoclonal gammopathy This finding might presage the development of a more serious condition, even years later (as in our patient).
  • [MeSH-major] Antiphospholipid Syndrome / complications. Waldenstrom Macroglobulinemia / complications

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  • (PMID = 16547696.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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87. Glasnović M, Bosnjak I, Vcev A, Kosuta M, Lenz B, Glasnović-Horvatić E: [Diagnostic and therapeutic approach to pregnant women suspect on antiphospholipid syndrome]. Reumatizam; 2008;55(1):10-5
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  • [Title] [Diagnostic and therapeutic approach to pregnant women suspect on antiphospholipid syndrome].
  • Antiphospholipid syndrome includes the presence of antiphospholipid antibodies, vascular thrombosis and reproductive function disturbances.
  • 62 women were included in study, 32 with primary antiphospholipd syndrome (PAPS), and 30 with secondary antiphospholipid syndrome (SAPS).
  • In SAPS group anticardiolipin antibodies (aCL) was positive in 8 patients (26.6%) compared to PAPS group with 3 aCL positive patients (9.4%).
  • [MeSH-major] Antiphospholipid Syndrome / diagnosis. Pregnancy Complications / diagnosis


88. Chung RH, Hauser ER, Martin ER: Interpretation of simultaneous linkage and family-based association tests in genome screens. Genet Epidemiol; 2007 Feb;31(2):134-42
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  • Linkage tests and family-based tests of association are often applied in the same data to help fine-map disease loci or validate results.
  • We used computer simulations and theoretical statements to estimate the correlation between linkage statistics (affected sib pair maximum LOD scores) and family-based association statistics (pedigree disequilibrium test (PDT) and association in the pressure of linkage (APL)) under various hypotheses.
  • We concluded that when linkage and association tests are applied in the same data, the type I error rate of neither test will be affected and that power can be increased by applying tests conditionally.

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  • (PMID = 17123303.001).
  • [ISSN] 0741-0395
  • [Journal-full-title] Genetic epidemiology
  • [ISO-abbreviation] Genet. Epidemiol.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / MH59528; United States / NINDS NIH HHS / NS / NS51355
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers
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89. Nilsson A, Liljensten E, Bergström C, Sollerman C: Results from a degradable TMC joint Spacer (Artelon) compared with tendon arthroplasty. J Hand Surg Am; 2005 Mar;30(2):380-9
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  • Fibers of the polymer were woven into a T-shaped device in which the vertical portion separates the bone edges of the TMC joint and the horizontal portion stabilizes the joint.
  • Ten patients received the spacer device and the remaining 5 (control group) were treated with a trapezium resection arthroplasty with abductor pollicis longus (APL) stabilization.
  • The median values for both key pinch and tripod pinch increased compared with before surgery in the spacer group but not in the APL group.
  • CONCLUSIONS: This study showed significantly better pinch strength after Artelon TMC Spacer implantation into the TMC joint compared with APL arthroplasty.

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  • (PMID = 15781363.001).
  • [ISSN] 0363-5023
  • [Journal-full-title] The Journal of hand surgery
  • [ISO-abbreviation] J Hand Surg Am
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biocompatible Materials; 0 / Polymers; 0 / Polyurethanes; 97343-15-2 / polyetherurethane urea
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90. Schinke C, Goel S, Bhagat TD, Zhou L, Mo Y, Gallagher R, Kabalka GW, Platanias LC, Verma A, Das B: Design and synthesis of novel derivatives of all-trans retinoic acid demonstrate the combined importance of acid moiety and conjugated double bonds in its binding to PML-RAR-alpha oncogene in acute promyelocytic leukemia. Leuk Lymphoma; 2010 Jun;51(6):1108-14
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  • [Title] Design and synthesis of novel derivatives of all-trans retinoic acid demonstrate the combined importance of acid moiety and conjugated double bonds in its binding to PML-RAR-alpha oncogene in acute promyelocytic leukemia.
  • The binding of all-trans retinoic acid (ATRA) to retinoid receptor-alpha (RAR-alpha) relieves transcriptional repression induced by the promyelocytic leukemia-retinoic acid receptor (PML-RAR) oncoprotein.
  • To determine the contributions of these structural components of ATRA to its clinical efficacy, we synthesized three novel retinoids.
  • Reporter assays demonstrated that compound 13a successfully relieved transcriptional repression by RAR-alpha, while 13b and 13c could not, demonstrating the critical role of the acid moiety in this binding.
  • However, only ATRA was able to significantly inhibit the proliferation of APL cells while 13a, 13b, or 13c was not.
  • Our results demonstrate that both the acid moiety and conjugated double bonds present in the ATRA molecule are important for its biological activity in APL and have important implications for the design of future novel retinoids.
  • [MeSH-minor] Antigens, CD11 / analysis. Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Drug Design. Flow Cytometry. Gene Expression Regulation / drug effects. Humans. Infant. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Luciferases / genetics. Luciferases / metabolism. Molecular Structure. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Response Elements / genetics. Transfection

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  • (PMID = 20536349.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA121192; United States / NCI NIH HHS / CA / R01 CA121192-04; United States / NCI NIH HHS / CA / T32 CA009173; United States / NHLBI NIH HHS / HL / 1R01HL082946-01; United States / NCI NIH HHS / CA / P30 CA060553; United States / NCI NIH HHS / CA / R01 CA121192-03; United States / NHLBI NIH HHS / HL / R01 HL082946; United States / NHLBI NIH HHS / HL / R01 HL082946-04; United States / NCI NIH HHS / CA / CA121192
  • [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.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ NIHMS590806; NLM/ PMC4104194
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91. Chan MY, Becker RC: Identification and treatment of arterial thrombophilia. Curr Treat Options Cardiovasc Med; 2008 Feb;10(1):3-11
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  • Once the diagnosis of a thrombophilic state has been established, management must include one or more strategies designed to attenuate thrombotic risk and the likelihood of clinical events.
  • Other specific therapies should be directed at the underlying thrombophilic disorder.
  • These treatments include direct thrombin inhibitors such as argatroban for heparin-induced thrombocytopenia (HIT), myelosuppressive drugs such as hydroxyurea for essential thrombocytosis, plasma exchange for thrombotic thrombocytopenic purpura, and phlebotomy for polycythemia vera.
  • Additionally, the treating physician must seek input early from a hematologist or rheumatologist when managing patients with known or suspected HIT, TTP, and myeloproliferative disorders, or the antiphospholipid syndrome, respectively.

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  • (PMID = 18325302.001).
  • [ISSN] 1092-8464
  • [Journal-full-title] Current treatment options in cardiovascular medicine
  • [ISO-abbreviation] Curr Treat Options Cardiovasc Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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92. Cole SM, Patterson MB, Cupp CL: Tonsillectomy in the anticoagulated patient. Ann Otol Rhinol Laryngol; 2007 Aug;116(8):589-93
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  • A case report is detailed of a 28-year-old woman with antiphospholipid syndrome on warfarin for high risk of venous thrombosis who underwent tonsillectomy.
  • [MeSH-major] Anticoagulants / adverse effects. Antiphospholipid Syndrome / drug therapy. Blood Loss, Surgical / prevention & control. Peritonsillar Abscess / surgery. Postoperative Hemorrhage / chemically induced. Tonsillectomy / methods. Venous Thrombosis / prevention & control. Warfarin / adverse effects

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  • (PMID = 17847726.001).
  • [ISSN] 0003-4894
  • [Journal-full-title] The Annals of otology, rhinology, and laryngology
  • [ISO-abbreviation] Ann. Otol. Rhinol. Laryngol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Enoxaparin; 0 / Heparin, Low-Molecular-Weight; 5Q7ZVV76EI / Warfarin; 9005-49-6 / Heparin
  • [Number-of-references] 21
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93. Melnick A: Predicting the effect of transcription therapy in hematologic malignancies. Leukemia; 2005 Jul;19(7):1109-17
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  • As a consequence, the three-dimensional structure of the target gene is altered and its potential to support transcription is increased or decreased.
  • The success of all-trans retinoic acid in the treatment of acute promyelocytic leukemia indicates that transcription therapy can be highly effective and safe.
  • A classification scheme of these therapeutic strategies is proposed herein, which allows predictions to be made regarding specificity, efficacy, disease spectrum and side effects.
  • This framework could help facilitate discussion of the mechanisms of action of transcription therapy drugs as well as the design of preclinical and clinical trials in the future.

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  • (PMID = 15858614.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01CA104348
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Transcription Factors
  • [Number-of-references] 114
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94. Chang YC, Huang HP, Hsu JD, Yang SF, Wang CJ: Hibiscus anthocyanins rich extract-induced apoptotic cell death in human promyelocytic leukemia cells. Toxicol Appl Pharmacol; 2005 Jun 15;205(3):201-12
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  • [Title] Hibiscus anthocyanins rich extract-induced apoptotic cell death in human promyelocytic leukemia cells.
  • [MeSH-minor] Androstadienes / pharmacology. Anthracenes / pharmacology. BH3 Interacting Domain Death Agonist Protein. Carrier Proteins / genetics. Carrier Proteins / metabolism. Caspases / genetics. Caspases / metabolism. Cell Survival / drug effects. Cytochromes c / drug effects. Cytochromes c / metabolism. DNA, Mitochondrial / drug effects. DNA, Mitochondrial / metabolism. Dose-Response Relationship, Drug. Fas Ligand Protein. Flavonoids / pharmacology. Flowers / chemistry. Humans. Imidazoles / pharmacology. Membrane Glycoproteins / genetics. Membrane Glycoproteins / metabolism. Proto-Oncogene Proteins c-jun / genetics. Proto-Oncogene Proteins c-jun / metabolism. Pyridines / pharmacology. RNA, Messenger. Time Factors. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors. p38 Mitogen-Activated Protein Kinases / drug effects. p38 Mitogen-Activated Protein Kinases / pharmacology

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  • (PMID = 15922006.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Androstadienes; 0 / Anthocyanins; 0 / Anthracenes; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / Carrier Proteins; 0 / DNA, Mitochondrial; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Flavonoids; 0 / Imidazoles; 0 / Membrane Glycoproteins; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-jun; 0 / Pyridines; 0 / RNA, Messenger; 0 / SB 203580; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; 9007-43-6 / Cytochromes c; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; XVA4O219QW / wortmannin
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95. Di Simone N, Luigi MP, Marco D, Fiorella DN, Silvia D, Clara DM, Alessandro C: Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature. Ann N Y Acad Sci; 2007 Jun;1108:505-14
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  • [Title] Pregnancies complicated with antiphospholipid syndrome: the pathogenic mechanism of antiphospholipid antibodies: a review of the literature.
  • There are several possible mechanisms by which antiphospholipid antibodies (aPL) may have adverse effects on placental functions.
  • Examination of placentas and first-trimester decidua from antiphospholipid syndrome-complicated pregnancies has found little evidence of specific thrombotic placental pathology.
  • It is now generally accepted that the clinically relevant aPL bind to proteins with affinity for phospholipids.
  • The most important epitope for antiphospholipid syndrome-related aPL resides on beta2-glycoprotein-I (beta2GPI).
  • aPL detected by anti-beta2GPI assays are associated with fetal loss.
  • During differentiation to syncytium, trophoblasts express cell membrane anionic phospholipids that can bind beta2GPI.
  • It might reduce the binding of aPL, inflammation by inhibiting complement activation, and might facilitate implantation.
  • Further investigations are needed to better understand how aPL induce obstetric complications and to better clarify the functional role of heparin in the human placenta, leading to more successful therapeutic options.
  • [MeSH-major] Antibodies, Antiphospholipid / immunology. Antiphospholipid Syndrome / immunology. Pregnancy Complications / etiology. Trophoblasts / immunology

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  • (PMID = 17894016.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Antiphospholipid; 0 / Autoantigens; 0 / beta 2-Glycoprotein I; 9005-49-6 / Heparin
  • [Number-of-references] 55
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96. Shanmugam VK, Price P, Attinger CE, Steen VD: Lower extremity ulcers in systemic sclerosis: features and response to therapy. Int J Rheumatol; 2010;2010
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  • Patients with diffuse scleroderma had shorter disease duration at the time of ulcer development (mean 4.05 years ± 0.05) compared to those with limited disease (mean 22.83 years ± 5.612, P value .0078).
  • In the 10 patients with ulcers, antiphospholipid antibodies were positive in 50%, and genetic prothrombotic screen was positive in 70% which is higher than expected based on prevalence reports from the general scleroderma population.
  • Of patients with biopsy specimens available (n = 5), fibrin occlusive vasculopathy was seen in 100%, and all of these patients had either positive antiphospholipid antibody screen, or positive genetic prothrombotic profile.
  • We recommend screening scleroderma patients with lower extremity ulcers for the presence of anti-phospholipid antibodies and genetic prothrombotic states.

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  • (PMID = 20827313.001).
  • [ISSN] 1687-9279
  • [Journal-full-title] International journal of rheumatology
  • [ISO-abbreviation] Int J Rheumatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2933896
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97. Yu W, Burns CM: All-trans retinoic acid-induced focal myositis, synovitis, and mononeuritis. J Clin Rheumatol; 2009 Oct;15(7):358-60
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  • All-trans retinoic acid has revolutionized the treatment of acute promyelocytic leukemia, but this therapy is often complicated by the all-trans retinoic acid syndrome.
  • Here we report a patient with newly diagnosed acute promyelocytic leukemia who developed acute focal myositis, synovitis, and possible vasculitis, after receiving all-trans retinoic acid therapy.
  • We review the existing literature on this rare clinical entity, all-trans retinoic acid-induced myositis.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Female. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Middle Aged. Treatment Outcome. Withholding Treatment


98. Patterson AM, Ford I, Graham A, Booth NA, Greaves M: The influence of anti-endothelial/antiphospholipid antibodies on fibrin formation and lysis on endothelial cells. Br J Haematol; 2006 May;133(3):323-30
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  • [Title] The influence of anti-endothelial/antiphospholipid antibodies on fibrin formation and lysis on endothelial cells.
  • The prothrombotic mechanisms associated with antiphospholipid antibodies remain incompletely defined.
  • Antibody binding to endothelial cells in vitro is a feature of antiphospholipid antibody-positive sera.
  • We hypothesised that impairment of endothelium-dependent fibrinolysis by antiphospholipid/anti-endothelial antibodies is a contributory factor in the pathogenesis of thrombosis.
  • Binding of immunoglobulin (Ig) from antiphospholipid antibody-positive sera to endothelial cells was examined using a cell-based enzyme-linked immunosorbent assay.
  • With four of 14 antiphospholipid antibody-positive sera there was some prolongation of fibrin clot lysis time, consistent with impairment of endothelial fibrinolytic activity.
  • Secretion of PAI-1 was significantly correlated with clot lysis time on endothelial cell monolayers incubated with antiphospholipid/anti-endothelial antibody-positive sera, but not with control sera.
  • IgG from antiphospholipid antibody-positive sera had little effect on endothelial cell surface annexin-V expression.
  • We conclude that impaired endothelial fibrinolysis is a potential prothrombotic mechanism in subjects with antiphospholipid antibodies.
  • We were unable to confirm enhanced displacement of annexin-V from endothelium by antiphospholipid antibodies.
  • [MeSH-minor] Annexin A5 / metabolism. Antibodies, Antiphospholipid / immunology. Blood Coagulation / immunology. Cells, Cultured. Endothelial Cells / immunology. Humans. Immunoenzyme Techniques. Plasminogen Activator Inhibitor 1 / metabolism

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  • (PMID = 16643435.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Antiphospholipid; 0 / Autoantibodies; 0 / Plasminogen Activator Inhibitor 1; 9001-31-4 / Fibrin
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99. Wampfler J, Tschan MP, Shan D, Laemmle A, Leibundgut EO, Baerlocher GM, Stroka D, Fey MF, Britschgi C: SIRT1 is downregulated during neutrophil differentiation of acute promyelocytic leukaemia cells. Br J Haematol; 2009 Aug;146(3):337-41
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  • [Title] SIRT1 is downregulated during neutrophil differentiation of acute promyelocytic leukaemia cells.
  • [MeSH-major] Hematopoietic Stem Cells / metabolism. Leukemia, Promyelocytic, Acute / metabolism. Sirtuins / metabolism

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  • (PMID = 19466968.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.5.1.- / SIRT1 protein, human; EC 3.5.1.- / Sirtuin 1; EC 3.5.1.- / Sirtuins
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100. Minucci S, Pelicci PG: Determinants of oncogenic transformation in acute promyelocytic leukemia: the hetero-union makes the force. Cancer Cell; 2007 Jul;12(1):1-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Determinants of oncogenic transformation in acute promyelocytic leukemia: the hetero-union makes the force.
  • Acute promyelocytic leukemia (APL) is caused by chromosomal translocations that involve the retinoic acid receptor alpha (RAR) and several other genes to yield X-RAR fusion proteins.
  • Unlike wild-type RARs, which require heterodimerization with the retinoid X receptor (RXR) for their function as DNA-binding transcriptional regulators, X-RAR fusion proteins bind DNA and deregulate transcription as homo-oligomers.
  • In this issue of Cancer Cell, however, Zeisig et al. and Zhu et al. show that RXR recruitment is a critical determinant for the transforming potential of oligomeric X-RAR fusion proteins and explore the possibility for targeted interventions in APL with either RAR or RXR ligands.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Humans. Ligands. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors / metabolism

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  • [CommentOn] Cancer Cell. 2007 Jul;12(1):36-51 [17613435.001]
  • [CommentOn] Cancer Cell. 2007 Jul;12(1):23-35 [17613434.001]
  • (PMID = 17613430.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors
  • [Number-of-references] 10
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