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1. Talbot S, Nelson R, Self WT: Arsenic trioxide and auranofin inhibit selenoprotein synthesis: implications for chemotherapy for acute promyelocytic leukaemia. Br J Pharmacol; 2008 Jul;154(5):940-8
Hazardous Substances Data Bank. AURANOFIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide and auranofin inhibit selenoprotein synthesis: implications for chemotherapy for acute promyelocytic leukaemia.
  • BACKGROUND AND PURPOSE: Arsenicals have been used medicinally for decades to treat both infectious disease and cancer.
  • Arsenic trioxide (As2O3) is effective for treatment of acute promyelocytic leukaemia (APL), yet the mechanism of action of this drug is still widely debated.
  • The level of mRNA encoding cytosolic TrxR (TrxR1) was determined using real-time reverse transcriptase-PCR.
  • Because As2O3 is used to treat APL, our findings may reveal the mechanism of this therapeutic action and lead to further research targeting selenium metabolism to find novel chemotherapeutic agents for the treatment of APL.

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  • Hazardous Substances Data Bank. SODIUM SELENITE .
  • Hazardous Substances Data Bank. METHANEARSONIC ACID .
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  • (PMID = 18587442.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / ES014354-01; United States / NIEHS NIH HHS / ES / R15 ES014354; United States / NIEHS NIH HHS / ES / ES01434; United States / NIEHS NIH HHS / ES / R15 ES014354-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Arsenites; 0 / Enzyme Inhibitors; 0 / Oxides; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Selenium Radioisotopes; 0 / Selenoproteins; 0 / Sodium Compounds; 3H04W2810V / Auranofin; 48OVY2OC72 / sodium arsenite; EC 1.8.1.9 / TXNRD1 protein, human; EC 1.8.1.9 / Thioredoxin Reductase 1; HIW548RQ3W / Sodium Selenite; J37VJ5709S / monomethylarsonic acid; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC2451042
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2. Wassenaar T, Black J, Kahl B, Schwartz B, Longo W, Mosher D, Williams E: Acute promyelocytic leukaemia and acquired alpha-2-plasmin inhibitor deficiency: a retrospective look at the use of epsilon-aminocaproic acid (Amicar) in 30 patients. Hematol Oncol; 2008 Dec;26(4):241-6
Hazardous Substances Data Bank. HEPARIN .

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  • [Title] Acute promyelocytic leukaemia and acquired alpha-2-plasmin inhibitor deficiency: a retrospective look at the use of epsilon-aminocaproic acid (Amicar) in 30 patients.
  • Bleeding diathesis and a hyper-fibrinolytic state often accompany a diagnosis of Acute Promyelocytic Leukaemia (APML).
  • This complication can have grave effects if not successfully treated, with a 10-20% incidence of haemorrhagic death.
  • We hypothesized that alpha-2-antiplasmin levels would correlate with the risk for bleeding, and that administration of epsilon-aminocaproic acid (EACA) would attenuate that risk.
  • To assess this, we conducted a retrospective chart review analyzing 30 APML patients, 17 of whom were treated with EACA.
  • Patients with low alpha-2-antiplasmin levels were treated with a coagulopathy protocol consisting of low-dose heparin, EACA and blood product support.
  • The presence and grade of haemorrhage appeared to be associated with the alpha-2-antiplasmin level.
  • One episode of central venous catheter associated thromboembolism and three deaths from infection during chemotherapy were observed. alpha-2-Antiplasmin levels are a reliable surrogate for fibrinolysis and haemorrhagic risk in patients with APML.
  • Treatment with EACA is a rational way to pharmacologically inhibit fibrinolysis, is associated with a low incidence of severe haemorrhagic events, and appears to be safe with a low risk of thrombosis.
  • Randomized clinical trials further assessing the efficacy and potential toxicity of EACA in inhibiting fibrinolysis in patients with APML are needed.
  • [MeSH-major] Aminocaproic Acid / therapeutic use. Antifibrinolytic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / complications. alpha-2-Antiplasmin / deficiency

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  • [Copyright] Copyright (c) 2008 John Wiley & Sons, Ltd.
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  • (PMID = 18613223.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA014520
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifibrinolytic Agents; 0 / alpha-2-Antiplasmin; 9005-49-6 / Heparin; U6F3787206 / Aminocaproic Acid
  • [Other-IDs] NLM/ NIHMS398867; NLM/ PMC3496178
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3. Zhou GB, Zhang J, Wang ZY, Chen SJ, Chen Z: Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy. Philos Trans R Soc Lond B Biol Sci; 2007 Jun 29;362(1482):959-71
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

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  • [Title] Treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide: a paradigm of synergistic molecular targeting therapy.
  • To turn a disease from highly fatal to highly curable is extremely difficult, especially when the disease is a type of cancer.
  • However, we can gain some insight into how this can be done by looking back over the 50-year history of taming acute promyelocytic leukaemia (APL).
  • APL is the M3 type of acute myeloid leukaemia characterized by an accumulation of abnormal promyelocytes in bone marrow, a severe bleeding tendency and the presence of the chromosomal translocation t(15;17) or variants.
  • APL was considered the most fatal type of acute leukaemia five decades ago and the treatment of APL was a nightmare for physicians.
  • Great efforts have been made by scientists worldwide to conquer this disease.
  • A rational and intriguing hypothesis, to induce differentiation of APL cells rather than killing them, was raised in the 1970s.
  • Laudably, the use of all-trans retinoic acid (ATRA) in treating APL resulted in terminal differentiation of APL cells and a 90-95% CR rate of patients, turning differentiation therapy in cancer treatment from hypothesis to practice.
  • When arsenic trioxide (ATO) was used to treat relapsed APL not only the patients but also the ancient drug were revived.
  • ATO exerts dose-dependent dual effects on APL cells: at low concentration, ATO induces partial differentiation, while at relatively high concentration, it triggers apoptosis.
  • Of note, both ATRA and ATO trigger catabolism of the PML-RARalpha fusion protein which is the key player in APL leukaemogenesis generated from t(15;17), targeting the RARalpha (retinoic acid receptor alpha) or promyelocytic leukaemia (PML) moieties, respectively.
  • Hence, in treating APL both ATRA and ATO represent paradigms for molecularly targeted therapy.
  • At molecular level, ATRA and ATO synergistically modulate multiple downstream pathways/cascades.
  • Strikingly, a clearance of PML-RARalpha transcript in an earlier and more thorough manner, and a higher quality remission and survival in newly diagnosed APL are achieved when ATRA is combined with ATO, as compared to either monotherapy, making APL a curable disease.
  • Thus, the story of APL can serve as a model for the development of curative approaches for disease; it suggests that molecularly synergistic targeted therapies are powerful tools in cancer, and dissection of disease pathogenesis or anatomy of the cancer genome is critical in developing molecular target-based therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use

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  • (PMID = 17317642.001).
  • [ISSN] 0962-8436
  • [Journal-full-title] Philosophical transactions of the Royal Society of London. Series B, Biological sciences
  • [ISO-abbreviation] Philos. Trans. R. Soc. Lond., B, Biol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 90
  • [Other-IDs] NLM/ PMC2435563
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4. Chandesris MO, Ghez D, Besson C, Suarez F, Delarue R, Rubio MT, Bazarbachi A, Varet B, Hermine O: Complete remission of a relapsing adult T cell leukaemia following treatment of a secondary acute promyelocytic leukaemia: towards a reappraisal of arsenic trioxide and all-transretinoic acid? BMJ Case Rep; 2009;2009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remission of a relapsing adult T cell leukaemia following treatment of a secondary acute promyelocytic leukaemia: towards a reappraisal of arsenic trioxide and all-transretinoic acid?
  • Despite improvements in therapeutic options, human T cell lymphotropic virus type 1 (HTLV-1)-related adult T cell leukaemia/lymphoma (ATLL) has a dismal prognosis.
  • The present report concerns the case of a multirelapsing ATLL that reached a complete remission following the treatment of a secondary acute promyelocytic leukaemia with cytarabine, anthracyclin, all-transretinoic acid and arsenic trioxide.
  • This unexpected result with a multitreated/chemorefractory disease led us to reconsider the potential therapeutic benefits of arsenic trioxide, which has demonstrated efficacy against ATLL cells.

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  • (PMID = 21829417.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3030139
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5. Castagnola C, Elena C, Merli M: Central nervous system relapse occurs in about 5% of cases of acute promyelocytic leukaemia. Haematologica; 2008 Feb;93(2):e28
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  • [Title] Central nervous system relapse occurs in about 5% of cases of acute promyelocytic leukaemia.
  • In this report, we present images from a patient with acute promyelocytic leukemia who experienced several central nervous system relapses.
  • [MeSH-major] Cell Nucleus / pathology. Central Nervous System Neoplasms / pathology. Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 18245644.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; ZRP63D75JW / Idarubicin; AIDA protocol
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6. Gupta V, Yi QL, Brandwein J, Lipton JH, Messner HA, Schuh AC, Wells RA, Minden MD: Role of all-trans-retinoic acid (ATRA) in the consolidation therapy of acute promyelocytic leukaemia (APL). Leuk Res; 2005 Jan;29(1):113-4
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  • [Title] Role of all-trans-retinoic acid (ATRA) in the consolidation therapy of acute promyelocytic leukaemia (APL).
  • The role of all-trans-retinoic acid (ATRA) in the consolidation therapy of acute promyelocytic leukaemia (APL) is undefined at present.
  • Between 1994 and 1999, we treated 38 newly diagnosed APL patients with ATRA and chemotherapy during the induction and consolidation.
  • The 5-year overall and leukaemia-free survival of study patients was 82% (95% C.I.
  • The role of ATRA during consolidation therapy of APL merits further investigation as this may allow shortening the overall duration of APL treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / administration & dosage

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  • (PMID = 15541484.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
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7. Stein E, McMahon B, Kwaan H, Altman JK, Frankfurt O, Tallman MS: The coagulopathy of acute promyelocytic leukaemia revisited. Best Pract Res Clin Haematol; 2009 Mar;22(1):153-63
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  • [Title] The coagulopathy of acute promyelocytic leukaemia revisited.
  • Since the initial description of the disease, the life-threatening coagulopathy associated with acute promyelocytic leukaemia (APL) has been the defining clinical characteristic.
  • Historically, this uncommon subtype of acute myeloid leukaemia has been associated with a high mortality rate during induction therapy, most frequently attributable to haemorrhage.
  • Since the introduction of all-trans retinoic acid (ATRA) into the therapy of all patients with APL, disease-free survival and overall survival have improved dramatically, such that the disease is now highly curable.
  • As a result, while the predominant clinical manifestation of the coagulopathy is haemorrhage, thromboembolic events may occur both at presentation and during therapy.
  • A major recent finding is the high expression of annexin II in the leukaemic cells from patients with APL.
  • Annexin II is a protein with high affinity for plasminogen and tissue-type plasminogen activator (tPA), and also acts as a cofactor for plasminogen activation by tPA.
  • Annexin II is expressed in high amounts in cerebral microvascular endothelial cells, perhaps accounting for the relatively high incidence of intracranial haemorrhage in APL compared with other sites.
  • Recent studies have found that microparticles containing tissue factor, tPA, plasminogen activator inhibitor-1 and annexin II have been found in the plasma of APL patients, suggesting a role in pathogenesis of the coagulopathy.
  • The most important factor may be the early introduction of ATRA at the first suspicion of a diagnosis of APL, before it is confirmed genetically.
  • [MeSH-major] Blood Coagulation Disorders / complications. Hemorrhage / complications. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 19285282.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009207
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Annexin A2; 5688UTC01R / Tretinoin; 9001-91-6 / Plasminogen; EC 3.4.21.68 / Tissue Plasminogen Activator
  • [Number-of-references] 64
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8. Barbarroja N, Siendones E, Torres LA, Luque MJ, Martinez JM, Dorado G, Velasco F, Torres A, López-Pedrera C: MEK inhibition induces caspases activation, differentiation blockade and PML/RARalpha degradation in acute promyelocytic leukaemia. Br J Haematol; 2008 Jul;142(1):27-35
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  • [Title] MEK inhibition induces caspases activation, differentiation blockade and PML/RARalpha degradation in acute promyelocytic leukaemia.
  • The hallmark of acute promyelocytic leukaemia (APL) is the reciprocal translocation t(15;17), which leads to the expression of the promyelocytic leukaemia/retinoic acid receptor alpha (PML/RARalpha) fusion protein and a cell differentiation blockade at the promyelocytic stage.
  • PML/RARalpha is directly targeted by all-trans-retinoic acid (ATRA), which degrades the oncoprotein and induces complete remission of malignancies.
  • The aberrant function of PML/RARalpha, together with the constitutive activation of the mitogen-activated protein/extracellular signal-regulated kinase (MEK/ERK) signalling pathway, regulates the ability of haematopoietic cells to proliferate, differentiate, and escape from apoptotic episodes.
  • The role of the MEK/ERK pathway in PML/RARalpha expression, differentiation, proliferation and apoptosis in APL cells was analysed using specific MEK inhibitors.
  • The blockade of MEK/ERK pathway resulted in caspase-dependent degradation of PML/RARalpha, and attenuation of the cell differentiation induction.
  • To our knowledge, this is the first report to show that PML/RARalpha was suppressed by MEK/ERK inhibition, through a mechanism dependent on caspase activation.
  • ATRA co-operated with MEK inhibitor to increase degradation of PML/RARalpha and exhibited a convergence point in caspase activation with MEK inhibitors.
  • Taken together, our data suggest a new role of MEK/ERK pathway in the pathogenesis of APL, thus supporting the use of MEK/ERK inhibitors as an efficient therapeutic strategy for this haematological malignancy.
  • [MeSH-major] Caspases / metabolism. Cell Transformation, Neoplastic / metabolism. Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors. Leukemia, Promyelocytic, Acute / metabolism. Oncogene Proteins, Fusion / metabolism. Protein Kinase Inhibitors / pharmacology

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  • (PMID = 18445086.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.22.- / Caspases
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9. Agarwal NK, Mueller GA, Mueller C, Streich JH, Asif AR, Dihazi H: Expression proteomics of acute promyelocytic leukaemia cells treated with methotrexate. Biochim Biophys Acta; 2010 Apr;1804(4):918-28
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  • [Title] Expression proteomics of acute promyelocytic leukaemia cells treated with methotrexate.
  • To understand the molecular mechanism by which methotrexate induces apoptosis, we analyzed the resulting intracellular protein changes in methotrexate-treated acute promyelocytic leukaemia (HL-60) cells by cysteine-labeled differential in-gel electrophoresis (CL-DIGE) combined with mass spectrometry.
  • Initial CL-DIGE analysis revealed that 24 proteins were differentially expressed (p<0.05) in the HL-60 cell proteome after treatment with 2.5microM methotrexate for 72h.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Methotrexate / pharmacology

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20097313.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Protein Subunits; EC 3.4.25.1 / Proteasome Endopeptidase Complex; YL5FZ2Y5U1 / Methotrexate
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10. Matsui W, Smith BD, Vala M, Beal N, Huff CA, Diehl LF, Jones RJ: Requirement for myeloid growth factors in the differentiation of acute promyelocytic leukaemia. Br J Haematol; 2005 Mar;128(6):853-62
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  • [Title] Requirement for myeloid growth factors in the differentiation of acute promyelocytic leukaemia.
  • It is well known that the differentiation of acute promyelocytic leukaemia (APL) cells by all-trans-retinoic acid (ATRA) may be enhanced by myeloid growth factors, but the requirement for growth factors in this process is unclear.
  • Our previous studies in multiple myeloma and non-APL acute myeloid leukaemia demonstrated that lineage-specific growth factors are required for the maximal activity of many pharmacologic differentiating agents in vitro.
  • Thus, we studied whether the differentiation of APL is similarly dependent on growth factors.
  • We found that the myeloid growth factors granulocyte colony-stimulating factor or granulocyte-macrophage colony-stimulating factor markedly increased the differentiation of NB4 cells or APL blasts from clinical samples treated with ATRA, arsenic trioxide (ATO), or bryostatin-1 as evidenced by the enhanced expression of myeloid surface antigens and the inhibition of clonogenic growth.
  • Furthermore, myeloid growth factors were necessary for the differentiation of APL cells since the activity of each pharmacologic agent could be blocked by specific growth factor-neutralizing antibodies.
  • These data demonstrate that both pharmacologic differentiating agents and myeloid growth factors are required, but neither sufficient, for the differentiation of APL cells.
  • The combined use of pharmacologic differentiating agents and growth factors may improve the clinical efficacy of differentiation therapy in APL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Granulocyte Colony-Stimulating Factor / pharmacology. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Growth Inhibitors / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Myelopoiesis / drug effects

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  • (PMID = 15755292.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5P30CA06973; United States / NCI NIH HHS / CA / P01CA15396
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Bryostatins; 0 / Growth Inhibitors; 0 / Macrolides; 0 / Oxides; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 37O2X55Y9E / bryostatin 1; 5688UTC01R / Tretinoin; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; S7V92P67HO / arsenic trioxide
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11. Bartley PA, Martin-Harris MH, Budgen BJ, Ross DM, Morley AA: Rapid isolation of translocation breakpoints in chronic myeloid and acute promyelocytic leukaemia. Br J Haematol; 2010 Apr;149(2):231-6
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  • [Title] Rapid isolation of translocation breakpoints in chronic myeloid and acute promyelocytic leukaemia.
  • Isolation and sequencing of the translocation breakpoint in chronic myeloid leukaemia-(CML) and acute promyelocytic leukaemia (APML) may help to elucidate the mechanism of translocation and provide a molecular marker for monitoring of minimal residual disease.
  • Amplification across the translocation breakpoint was performed in samples from 91 patients with CML and 15 patients with APML using single-tube multiplex polymerase chain reaction (PCR) involving 308 primers for CML and 40 primers for APML.
  • The strategy of highly multiplexed PCR followed by SHP-PCR is thus an effective method for isolating the translocation breakpoint in CML and APML.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Promyelocytic, Acute / genetics. Translocation, Genetic

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  • (PMID = 20067557.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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12. Luesink M, Jansen JH: Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia. Br J Haematol; 2010 Nov;151(3):209-20

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  • [Title] Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia.
  • In acute promyelocytic leukaemia (APL), differentiation therapy can be complicated by the development of a differentiation syndrome (DS).
  • Pulmonary infiltration of differentiating leukaemic cells is a key event in the development of DS.
  • Several mediators have been identified that may promote migration and extravasation of differentiating APL cells from the bloodstream into the tissue.
  • Adhesion of APL cells to each other and to the endothelium is induced by upregulation of the expression of adhesion molecules and constitutively active β2-integrins during differentiation therapy.
  • Pulmonary chemokine production can trigger transendothelial migration of differentiating APL cells from the bloodstream into the underlying tissue (initiation phase of DS).
  • Massive production of chemokines by infiltrated APL cells can further enhance transendothelial migration of differentiating APL cells, causing an uncontrollable hyperinflammatory reaction in the lung (aggravation phase), which is not efficiently switched-off by corticosteroids.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology. Leukemic Infiltration / pathology. Lung / pathology

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20735400.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chemokines
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13. Battistelli S, Stefanoni M, Petrioli R, Genovese A, Dell'Avanzato R, Donati G, Vittoria V, Roviello F: Antiphospholipid antibodies and acute-phase response in non-metastatic colorectal cancer patients. Int J Biol Markers; 2008 Jan - Mar;23(1):31-35
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  • [Title] Antiphospholipid antibodies and acute-phase response in non-metastatic colorectal cancer patients.
  • AIM: To investigate the plasma levels and prevalence of the most common antiphospholipid antibodies, as well as their relationships with several plasma markers of inflammation, in order to characterize some aspects of cancer thrombophilia.
  • MATERIALS AND METHODS: Eighty-three cancer patients with non-metastatic colorectal solid tumors and 94 control subjects were tested for the presence of IgG/IgM/IgA anti-cardiolipin and anti-Beta2-glycoprotein I antibodies and of several acutephase reactants, i.e., fibrinogen, factor VIII:C and C4b-binding protein.
  • RESULTS: In cancer patients the plasma levels of the acute-phase reactants and the IgA/IgG anti-cardiolipin and IgA anti-Beta2- glycoprotein I antibodies were significantly higher; the acute-phase reactants were significantly correlated with anti-cardiolipin antibodies; the prevalence of antiphospholipid antibodies was not significantly higher.
  • CONCLUSIONS: In patients with non-metastatic colorectal cancer the acute-phase response is associated with antiphospholipid generation.

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  • (PMID = 28207104.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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14. Clavio M, Ghiso A, Ghiggi C, Spriano M, Colombo N, Grasso R, Varaldo R, Miglino M, Pierri I, Olcese F, Aquino S, Biasco S, Balleari E, Carella AM, Sessarego M, Gobbi M: Seventeen years of experience with ATRA-based therapy for acute promyelocytic leukaemia: long-term follow-up of patients treated at S. Martino Hospital, Genoa. Oncol Rep; 2009 Apr;21(4):1045-52
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  • [Title] Seventeen years of experience with ATRA-based therapy for acute promyelocytic leukaemia: long-term follow-up of patients treated at S. Martino Hospital, Genoa.
  • We conducted a long-term follow-up retrospective study on 91 consecutive newly diagnosed acute promyelocytic leukaemia (APL) patients.
  • After a median follow-up of 100 months (12-192), 10 of the 75 patients who achieved complete remission (13%) relapsed.
  • Seventy-eight percent of the patients were expected to be alive at 14 years from diagnosis, i.e., 90 and 48% of patients of intermediate-low risk and high risk at presentation, respectively (p=0.0009).
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / administration & dosage

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  • (PMID = 19288007.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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15. Robertson KA, Colvin ES, Kelley MR, Fishel ML: APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS). J Clin Oncol; 2009 May 20;27(15_suppl):e14613

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] APX3330 inhibition of the redox function of ape-1/ref-1 (Ref-1) in promyelocytic leukemia cells enhances retinoic acid (ATRA) induced myeloid differentiation and limits cell proliferation as an approach to the prevention of the retinoic acid syndrome (RAS).
  • : e14613 Background: ATRA + chemotherapy has improved the treatment of promyelocytic leukemia(APL).
  • However, 25% of ATRA treated APL patients experience toxicities that comprise the RAS (life-threatening respiratory distress, edema, renal failure, hypotension, coagulopathy and rising blast count).
  • One approach to prevent RAS is to limit blast proliferation and enhance myeloid differentiation.
  • HL60 myeloid leukemia cells are promyeloblasts that respond to ATRA with granulocytic differentiation/growth arrest.
  • These finding may provide a therapeutic approach for prevention of the RAS.

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  • (PMID = 27964118.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Kuchenbauer F, Schoch C, Kern W, Hiddemann W, Haferlach T, Schnittger S: Impact of FLT3 mutations and promyelocytic leukaemia-breakpoint on clinical characteristics and prognosis in acute promyelocytic leukaemia. Br J Haematol; 2005 Jul;130(2):196-202
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  • [Title] Impact of FLT3 mutations and promyelocytic leukaemia-breakpoint on clinical characteristics and prognosis in acute promyelocytic leukaemia.
  • In the present study 170 newly diagnosed acute promyelocytic leukaemia patients (M3: n = 121; M3v: n = 49) were molecularly characterised with respect to PML breakpoint and additional molecular mutations.
  • Bcr3 was more frequent in M3v (65.3%) compared with M3 (41.3%) (P = 0.005).
  • Cases with bcr3 showed a significantly higher white blood cell count (median: 3.65 x 10(9)/l vs. 1.59 x 10(9)/l, P = 0.003), as well as a higher PML-RARAABL expression ratio (14.8% vs. 72.7%, P < 0.005) compared with bcr1.
  • FLT3-length-mutations were detected more frequently together with bcr3 compared with bcr1 (56.5% vs. 19.4%, P < 0.001) and in M3v compared with M3 (64.5% vs. 24.1%, P < 0.005).
  • FLT3-mutations were detected in 62 of 139 cases (44.6%) and associated with a significant lower overall survival (P = 0.0339).
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Mutation. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Disease-Free Survival. Female. Humans. Leukocyte Count. Male. Middle Aged. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Polymerase Chain Reaction / methods. Prognosis. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-bcr. Survival Rate. fms-Like Tyrosine Kinase 3

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  • (PMID = 16029447.001).
  • [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 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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17. Olwill SA, McGlynn H, Gilmore WS, Alexander HD: All-trans retinoic acid-induced downregulation of annexin II expression in myeloid leukaemia cell lines is not confined to acute promyelocytic leukaemia. Br J Haematol; 2005 Oct;131(2):258-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] All-trans retinoic acid-induced downregulation of annexin II expression in myeloid leukaemia cell lines is not confined to acute promyelocytic leukaemia.
  • Most acute promyelocytic leukaemia (APL) patients suffer from disordered haemostasis.
  • APL can be treated successfully in most instances by all-trans retinoic acid (ATRA) therapy, which induces endpoint maturation of the leukaemic promyelocytes with the characteristic t(15;17).
  • Annexin II (AnII), a profibrinolytic protein, has been implicated in the bleeding manifestation seen in APL.
  • Our group has shown previously that high levels of AnII are expressed on other acute myeloid leukaemia subtypes that are sometimes associated with disordered haemostasis, albeit less frequently than APL.
  • This study examined the effects of ATRA on AnII expression and cell differentiation, on myeloid leukaemia cell lines to determine whether a regulatory influence on AnII may contribute to the return of haemostatic stability in APL following treatment.
  • The results confirmed that AnII expression in the APL cell line (NB4) was significantly downregulated in response to ATRA (P < 0.01), with associated morphological and immunophenotypical evidence of myeloid differentiation.
  • ATRA also downregulated AnII expression on other myeloid cell lines, albeit to a lesser extent than observed on NB4 cells.
  • The results provide evidence that ATRA may resolve the hyperfibrinolysis in APL by downregulation of AnII expression.
  • [MeSH-major] Annexin A2 / metabolism. Leukemia, Myeloid / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Analysis of Variance. Cell Differentiation. Cell Line, Tumor. Down-Regulation. Fibrinolysis / drug effects. Flow Cytometry. Hemostasis. Humans. Leukemia, Promyelocytic, Acute / drug therapy. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [ErratumIn] Br J Haematol. 2006 Jan;132(1):119
  • (PMID = 16197459.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / RNA, Messenger; 5688UTC01R / Tretinoin
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18. Ghaffari SH, Rostami S, Bashash D, Alimoghaddam K, Ghavamzadeh A: Real-time PCR analysis of PML-RAR alpha in newly diagnosed acute promyelocytic leukaemia patients treated with arsenic trioxide as a front-line therapy. Ann Oncol; 2006 Oct;17(10):1553-9
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  • [Title] Real-time PCR analysis of PML-RAR alpha in newly diagnosed acute promyelocytic leukaemia patients treated with arsenic trioxide as a front-line therapy.
  • BACKGROUND: Recently, patients with acute promyelocytic leukaemia (APL) have experienced significant clinical gains after treatment with arsenic trioxide.
  • PATIENTS AND METHODS: Of 95 newly diagnosed APL patients, 85 patients who achieved complete remission (CR) were sequentially evaluated during a 4-60 month period by conventional RT-PCR.
  • The PML-RARalpha fusion transcripts values were normalised to every 10(6) copies of G6PDH transcripts (NQ).
  • RESULTS: RQ-PCR analyses showed a rapid rate of clearance of NQ levels during the courses of arsenic therapy.
  • In the majority of patients in CR, the NQ levels were below 5 x 10(2) in peripheral blood (PB) samples.
  • In all the relapsed cases with follow-up intervals of 1-6 months (median 3 months) clinical relapse was predictable by increasing NQ level above this threshold.
  • CONCLUSIONS: Our study highlights the usefulness of PB and the definition of threshold level for early prediction of relapse.
  • The threshold level correlates well with risk of relapse; therefore, transcript ratio below the level should be regarded as a goal in the clinical management of this disease.

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  • (PMID = 16831853.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / Protein Isoforms; 0 / Recombinant Fusion Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 1.1.1.49 / Glucosephosphate Dehydrogenase; S7V92P67HO / arsenic trioxide
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19. Bloomfield CD: Importance of genetic heterogeneity in curing adult acute leukemia (AL). J Clin Oncol; 2009 May 20;27(15_suppl):s1

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  • [Title] Importance of genetic heterogeneity in curing adult acute leukemia (AL).
  • Publication of the French-American-British classification 34 years ago resulted in acceptance that morphology and cytochemistry separated AL into two different diseases, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), that required separate treatment.
  • During the next 15-20 years the importance of cytogenetics in dissecting ALL and AML into entities requiring different therapies became widely accepted, resulting in 2001 in their first incorporation into the World Health Organization (WHO) classification of AL.
  • The most striking example of increased curability of AL is acute promyelocytic leukemia, in which targeted therapy combined with chemotherapy has increased survival from a 2-week median to an 80% cure rate.
  • Recognition of increased sensitivity of a genetic subtype of AML to high-dose cytarabine (HiDAC) has increased the cure rate of core-binding factor (CBF) AML from <10%-25% to 55%-60%.
  • Recent discovery of the adverse impact of KIT mutations in CBF AML may allow the addition of tyrosine kinase inhibitors to HiDAC to substantially further increase cure.
  • Among adult de novo AML 40%-45% are cytogenetically normal (CN); the striking molecular heterogeneity of CN-AML is now being recognized and promises to allow individualized approaches that improve substantially upon the current cure rate of 40%.
  • New approaches to studying the leukemia genome and epigenome should improve our understanding of AL heterogeneity, identify new therapeutic targets, and allow the cure of most patients.

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  • (PMID = 27962366.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Martini V, Minotti C, Breccia M, De Angelis G, Buffolino S, Mariella M, Lo-Coco F, Avvisati G, Cimino G: Prolonged molecular remission in a newly diagnosed acute promyelocytic leukaemia with a severe cardiomyopathy using low-dose gemtuzumab ozogamicin and all-trans retinoic acid. Ann Hematol; 2007 Apr;86(4):295-7
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  • [Title] Prolonged molecular remission in a newly diagnosed acute promyelocytic leukaemia with a severe cardiomyopathy using low-dose gemtuzumab ozogamicin and all-trans retinoic acid.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Cardiomyopathies / complications. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use

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  • (PMID = 17136541.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / gemtuzumab; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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21. Gallipoli P, Drummond MW: Pseudotumour cerebri as a manageable side effect of prolonged all-trans retinoic acid therapy in an adult patient with acute promyelocytic leukaemia. Eur J Haematol; 2009 Mar;82(3):242-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudotumour cerebri as a manageable side effect of prolonged all-trans retinoic acid therapy in an adult patient with acute promyelocytic leukaemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Pseudotumor Cerebri / chemically induced. Pseudotumor Cerebri / therapy. Tretinoin / adverse effects. Tretinoin / therapeutic use

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  • [ErratumIn] Eur J Haematol. 2009 May;82(5):411. Drummond, M W [added]
  • (PMID = 19018859.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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22. Tabagari D, Nemsadze G, Jincharadze M, Janjalia M, Shan JS: Phase II study of bavituximab plus docetaxel in patients with locally advanced or metastatic breast cancer. J Clin Oncol; 2009 May 20;27(15_suppl):3005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3005 Background: Phosphatidylserine (PS) is an anionic phospholipid normally present on the inside surface of cell membranes.
  • Bavituximab (B) is a novel anti-PS monoclonal antibody and has demonstrated preclinical synergistic antitumor activity when used in combination with docetaxel.
  • METHODS: This Simon 2-stage trial is designed to determine the overall response rate (CR+PR) in patients with locally advanced or metastatic breast cancer to a combination of weekly bavituximab (3 mg/kg) plus docetaxel (35 mg/m2) on days 1, 8, 15 of a 28-day cycle for up to 6 cycles.
  • If ≥ 6 responses are observed in the 15 pt enrolled to Stage A, an additional 31 pts will be enrolled to Stage B.
  • RESULTS: Data are available for the 15 female pts enrolled in Stage A of the trial.
  • Using RECIST, the overall response rate in these 15 pt is 67% (95% confidence interval, 38-88%) for the intent-to-treat group and 71% (95% CI, 42-92%) for the 14 evaluable patients.

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  • (PMID = 27962047.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Machner B, Neppert B, Paulsen M, Hofmann C, Sander T, Helmchen C: Pseudotumor cerebri as a reversible side effect of all-trans retinoic acid treatment in acute promyelocytic leukaemia. Eur J Neurol; 2008 Jul;15(7):e68-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pseudotumor cerebri as a reversible side effect of all-trans retinoic acid treatment in acute promyelocytic leukaemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Pseudotumor Cerebri / chemically induced. Tretinoin / adverse effects

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  • (PMID = 18452541.001).
  • [ISSN] 1468-1331
  • [Journal-full-title] European journal of neurology
  • [ISO-abbreviation] Eur. J. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; O3FX965V0I / Acetazolamide; ZRP63D75JW / Idarubicin
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24. Pemmaraju N, Kantarjian H, Ravandi F, O'Brien S, Wierda W, Thomas D, Garcia-Manero G, Borthakur G, Pierce S, Cortes J: Acute myeloid leukemia (AML) in adolescents and young adults (AYA): The M. D. Anderson Cancer Center (MDACC) experience. J Clin Oncol; 2009 May 20;27(15_suppl):7051

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML) in adolescents and young adults (AYA): The M. D. Anderson Cancer Center (MDACC) experience.
  • : 7051 Background: AML is a heterogeneous group of hematopoietic neoplasms demonstrating clonal proliferation of myeloid precursors and is typically a disease of older adults.
  • Little is known about outcomes of AYA with AML.
  • METHODS: We retrospectively analyzed all patients (pts) with AML treated at MDACC from 1965 to 2008.
  • RESULTS: Among 3,934 adult AML pts treated during this period, 163 pts (4%) were AYA with median age of 19 yrs.
  • This cohort included 27 (17%) pts with Core Binding Factor (CBF)-AML [inv(16), t(8:21)] and 19 pts (12%) with acute promyelocytic leukemia (APL).
  • Complete remission (CR) rates were 89% for CBF AML, 79% for APL, and 75% for all other pts.
  • Outcome is better for pts with CBF leukemia (3 yr survival 56%, sustained CR 49%) and APL (3 yr survival 51%, sustained CR 36%) compared to other AML (3 yr survival 28%, sustained CR 24%).
  • To compare outcomes of AYA with older adults, we focused on those with diploid cytogenetics.CR for pts ages 16-21 was 81%, with 3 yr survival of 46%; for ages 22-45, CR was 75% and 3 yr survival 36%; for ages 46-60 CR was 68% with 3 yr survival 28%; and for pts age greater than 60, CR was 54% with 3 yr survival of 22%.
  • CONCLUSIONS: The outcome of AYA pts with AML is significantly better than for older adults with AML.
  • Despite the advances in treatments over time, there is still significant room for improvement, particularly among those AYA with AML other than CBF and APL.

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  • (PMID = 27961415.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Guo YL, Zhou J, Huang Y, Bao M: Modeling of Photoinduced Deformation in Silicon Microcantilever. Sensors (Basel); 2007 Sep 03;7(9):1713-1719

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The results from our model much more closely approximate the experimental values than the former model built up by Datskos, Rajic and Datskou [1](APL, Vol.73 (1998) No.16, pp 3219-2321), represented by the reduction of the error between calculation and measurement from 25 times to 0.85 times.

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  • (PMID = 28903192.001).
  • [ISSN] 1424-8220
  • [Journal-full-title] Sensors (Basel, Switzerland)
  • [ISO-abbreviation] Sensors (Basel)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Keywords] NOTNLM ; Photostriction / deformation / microcantilever / silicon
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26. Murrin RJ, Harrison P, Neilson JR: A highly unusual cluster of acute promyelocytic leukaemia: an environmental aetiology? Clin Lab Haematol; 2005 Feb;27(1):71-3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A highly unusual cluster of acute promyelocytic leukaemia: an environmental aetiology?
  • We report three consecutive cases of acute promyelocytic leukaemia (APML) that were diagnosed within a 4-month period.
  • Our data strongly suggests that environmental agents may play a greater role in the aetiology of APML than is commonly perceived.
  • [MeSH-major] Environmental Exposure. Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / epidemiology

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  • (PMID = 15686512.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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27. 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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28. Chalam KV, Gupta SK, Agarwal S: Rituximab effectively reverses papilledema associated with cerebral venous sinus thrombosis in antiphospholipid antibody syndrome. Eur J Ophthalmol; 2007 Sep-Oct;17(1):867-870

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab effectively reverses papilledema associated with cerebral venous sinus thrombosis in antiphospholipid antibody syndrome.
  • PURPOSE: A case of bilateral papilledema secondary to cerebral venous sinus thrombosis treated with Rituximab, an anti-CD20 monoclonal antibody.
  • METHODS: A 23 year old obese female with a one week history of blurred vision, headaches and vomiting presented with bilateral papilledema.
  • Laboratory investigations revealed thrombocytopenia, prolonged prothrombin time (not reversed when mixed with normal plasma) and anticardiolipin antibodies.
  • The patient to have anti phospholipid antibody syndrome and treated with rituximab I.V.
  • CONCLUSIONS: Rituximab was effective in reversing papilledema and cerebral sinus thrombosis, while preserving the vision in patient with antiphospholipid antibody syndrome.
  • It is efficacious in treating papilledema in patients refractory to treatment with systemic steroids and immunoglobulin, with better clinical compliance and no side effects.

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  • (PMID = 28221537.001).
  • [ISSN] 1724-6016
  • [Journal-full-title] European journal of ophthalmology
  • [ISO-abbreviation] Eur J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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29. Wong KF, Chow E, Siu LL, Wong WS: Acute promyelocytic leukaemia with cryptic PML-RARA fusion. Br J Haematol; 2009 Apr;145(1):2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukaemia with cryptic PML-RARA fusion.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Aged. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Cytogenetic Analysis. Female. Humans. Translocation, Genetic

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  • (PMID = 19036120.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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30. Au WY, Fung AT, Ma ES, Chan CH, Wong KF, Chim CS, Liang RH, Kwong YL: Serial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide. Br J Haematol; 2005 Dec;131(5):632-5
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  • [Title] Serial studies of methylation of CDKN2B and CDKN2A in relapsed acute promyelocytic leukaemia treated with arsenic trioxide.
  • Ninety consecutive patients with acute promyelocytic leukaemia were investigated for promoter methylation of CDKN2B (alias p15) and CDKN2A (alias p16) in disease relapse and progression.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Cyclin-Dependent Kinase Inhibitor p15 / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Leukemia, Promyelocytic, Acute / metabolism. Neoplasm, Residual / metabolism. Oxides / therapeutic use

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  • (PMID = 16351640.001).
  • [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 / Antineoplastic Agents; 0 / Arsenicals; 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Oxides; S7V92P67HO / arsenic trioxide
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31. Ibrahim FA, Yassin MA, El-Ayoubi HR, Alhiji IA, Albinali AS, Almansour SM, Qafoud FM: Clinico-pathological profile of acute promyelocytic leukaemia at Al-Amal Oncology-Haematology Centre, Qatar. East Mediterr Health J; 2010 Sep;16(9):958-65

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinico-pathological profile of acute promyelocytic leukaemia at Al-Amal Oncology-Haematology Centre, Qatar.
  • This cases series describes the profile of adult patients with acute promyelocytic leukaemia (APt) at a referral hospital in Qatar.
  • Of 34 acute myeloid leukaemia (AML) cases diagnosed, 11(32%) were classified as APt.
  • Only 2 patients were of the classic hypergranular type.
  • Translocation t(15;17) was detected in 63% of cases.
  • APL constitutes a high proportion of AML cases in Qatar, with considerable morphological heterogeneity and a oredominance of APL variants with unfavourable oresenting features.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / epidemiology. Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 21218723.001).
  • [ISSN] 1020-3397
  • [Journal-full-title] Eastern Mediterranean health journal = La revue de santé de la Méditerranée orientale = al-Majallah al-ṣiḥḥīyah li-sharq al-mutawassiṭ
  • [ISO-abbreviation] East. Mediterr. Health J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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32. Marasca R, Maffei R, Zucchini P, Castelli I, Saviola A, Martinelli S, Ferrari A, Fontana M, Ravanetti S, Torelli G: Gene expression profiling of acute promyelocytic leukaemia identifies two subtypes mainly associated with flt3 mutational status. Leukemia; 2006 Jan;20(1):103-14
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  • [Title] Gene expression profiling of acute promyelocytic leukaemia identifies two subtypes mainly associated with flt3 mutational status.
  • Acute promyelocytic leukaemia (APL) is a well-defined disease characterized by a typical morphology of leukaemic cells, the presence of t(15;17) translocation and the unique sensitivity to the differentiating effect of all-trans retinoic acid.
  • Nevertheless, some aspects are variable among APL patients, with differences substantially related to morphological variants, peripheral leukocytes count, the presence of a disseminated intravascular coagulopathy, different PML/RARalpha isoforms (long, variable or short) and Fms-like tyrosine kinase 3 (Flt3) mutations.
  • In order to better define this variability, we investigated the gene expression profiles of 18 APL cases revealing, besides a high uniformity in gene expression pattern, the presence of few robust differences among patients able to identify, by an unsupervised analysis, two major clusters of patients characterized by different phenotypes (hypogranular M3v vs classical M3) and by the presence or absence of Flt3 internal tandem duplications (ITDs).
  • Further supervised analysis confirmed that Flt3 status was the APL parameter best associated with these two subgroups.
  • We identified, between Flt3 wild-type and Flt3-ITDs subsets, 147 differentially expressed genes that were involved in the cytoskeleton organization, in the cell adhesion and migration, in the proliferation and the coagulation/inflammation pathways as well as in differentiation and myeloid granules constitution suggesting a role of Flt3 mutations in the pathogenesis and clinical manifestations of APL.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Promyelocytic, Acute / genetics. Multigene Family. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16270043.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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33. Creutzig U, Zimmermann M, Dworzak M, Urban C, Henze G, Kremens B, Lakomek M, Bourquin JP, Stary J, Reinhardt D: Favourable outcome of patients with childhood acute promyelocytic leukaemia after treatment with reduced cumulative anthracycline doses. Br J Haematol; 2010 May;149(3):399-409
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Favourable outcome of patients with childhood acute promyelocytic leukaemia after treatment with reduced cumulative anthracycline doses.
  • Acute promyelocytic leukaemia (APL) treatment often includes high cumulative doses of anthracyclines, which can cause long-term cardiotoxicity.
  • Here, we report the favourable outcome in 81 paediatric APL patients treated according to the consecutive acute myeloid leukaemia-Berlin/Frankfurt/Muenster (AML-BFM) trials -93/-98/-2004 with an anthracycline-cytarabine regimen in combination with all-trans-retinoid acid (ATRA).
  • Outcomes achieved by treatment with a reduced cumulative anthracycline dose (350 mg/m(2)) were comparable to those reported for studies with higher doses.
  • Overall survival was similar when comparing AML-BFM trial periods (trial 93: 88 +/- 8%, 98: 85 +/- 7% and 2004: 94 +/- 8%, P((logrank)) = 0.63).
  • Salvage treatment was effective in 7/9 patients (78%) with relapsed APL, who now are long-term survivors after second line combination treatment with arsenic trioxide (4/7 patients) and stem cell transplantation (5/7 patients).
  • Our results demonstrate that - combined with ATRA - a lower cumulative anthracycline dose can be used safely to maintain high cure rates and promote the reduction of long-term sequelae, such as cardiotoxicity in APL patients.
  • [MeSH-major] Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 20230404.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin
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34. Lopez-Enriquez AT: Acute promielocytic leukemia: 14 years experience at the University Hospital, San Juan, Puerto Rico. J Clin Oncol; 2009 May 20;27(15_suppl):e18006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promielocytic leukemia: 14 years experience at the University Hospital, San Juan, Puerto Rico.
  • : e18006 Background: Acute promielocytic leukemias (APL) are a unique example in carcinogenesis, of maturation arrest at the promielocytic stage, associated with a chromosomal reciprocal translocation of a portion of chromosome 15 and 17 with the formation of fusion proteins between the PML gene and the alpha-retinoic acid receptor site.
  • METHODS: Since 1994 when transretinoic acid (ATRA) became available to us, we developed a protocol incorporating this drug to the standard regime of induction chemotherapy for acute leukemias used in our institution of 7 days of continuous infusion of cytosine arabinoside (Ara-C) and three days of daunorubicine (7+3), starting the ATRA on day 14 at 45 mg/m2 and continued daily for 120 days.
  • RESULTS: We have treated 91 patients with APL since 1994 up to November 2008.
  • Four patients developed ATRA syndrome; three early pulmonary syndromes with one death, and the other two responded to steroids and went into remission.
  • Fifty-three (53) has remained in complete remission with a range of 6months to 14 years, for a rate of 76%.
  • Seventeen (17) patients or 25% (17/70) relapsed within the first 2 years of treatment.
  • Thirteen of 17 (13/17) relapsed after receiving Dauno x3 x3 as consolidation chemotherapy for a 76% relapsed rate.
  • CONCLUSIONS: The initial high early mortality needs to be addressed with a more aggressive support system.

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  • (PMID = 27963993.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Gupta SK, Sazawal S, Mahapatra M, Saxena R: Evaluation of PG-M3 antibody in the diagnosis of acute promyelocytic leukaemia. Eur J Clin Invest; 2010 Oct;40(10):960-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of PG-M3 antibody in the diagnosis of acute promyelocytic leukaemia.
  • BACKGROUND & OBJECTIVES: Acute promyelocytic leukaemia (APL) is a distinct subtype of acute myeloid leukaemia (AML) characterized by a reciprocal translocation, t(15;17) and a high incidence of life-threatening coagulopathy.
  • APL diagnosis is considered a medical emergency.
  • As reverse transcription-polymerase chain reaction (RT-PCR) for PML-RAR fusion oncoprotein is time consuming, there is a need for a rapid and accurate diagnostic test for APL.
  • This study evaluates the role of PG-M3 monoclonal antibody using immunofluorescence (IF) in the early diagnosis of APL.
  • MATERIALS AND METHODS: Thirty-six new untreated APL cases diagnosed with RT-PCR for PML-RAR as the gold standard and 38 non-APL controls (28 non-APL AMLs and 10 non-leukaemic samples) were evaluated by routine morphology and cytochemistry, RT-PCR and IF using PG-M3 monoclonal antibody.
  • RESULTS: Using IF, 34 of 36 (94·4%) APL cases showed a microgranular pattern suggestive of APL and two cases (5·6%) showed a speckled pattern typical of wild-type PML protein (False negative).
  • By comparison, two of 28 (7·1%) non-APL AMLs showed microgranular pattern (false positive).
  • Hence, IF as a diagnostic test for APL resulted in a sensitivity of 94·4%, specificity of 92·9% and positive and negative predictive values of 94·4% and 92·9% respectively.
  • CONCLUSIONS: IF using PG-M3 antibodies can be used as a rapid (takes 2 h), cheap, sensitive and specific method to identify APL.
  • It can be a useful adjunct for diagnosis of APL especially if facilities for RT-PCR are not available, particularly in resource-limited settings.
  • [MeSH-major] Antibodies, Monoclonal. Leukemia, Promyelocytic, Acute / diagnosis

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  • [Copyright] © 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation.
  • (PMID = 20701624.001).
  • [ISSN] 1365-2362
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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36. Suárez-Cuenca JA, Arellano-Sánchez JL, Scherling-Ocampo AA, Sánchez-Hernández G, Pérez-Guevara D, Chalapud-Revelo JR: Rapidly progressing, fatal and acute promyelocytic leukaemia that initially manifested as a painful third molar: a case report. J Med Case Rep; 2009;3:102

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapidly progressing, fatal and acute promyelocytic leukaemia that initially manifested as a painful third molar: a case report.
  • INTRODUCTION: Acute promyelocytic leukaemia, an uncommon and devastating subtype of leukaemia, is highly prevalent in Latin American populations.
  • The disease may be detected by a dentist since oral signs are often the initial manifestation.
  • However, despite several cases describing oral manifestations of acute promyelocytic leukaemia and genetic analysis, reports of acute promyelocytic leukaemia in Hispanic populations are scarce.
  • The identification of third molar pain as an initial clinical manifestation is also uncommon.
  • Peripheral blood and bone marrow analyses revealed a hypercellular infiltrate of atypical promyelocytic cells.
  • Cytogenetic analysis showing genetic translocation t(15;17) further confirmed acute promyelocytic leukaemia.
  • CONCLUSION: The description of this unusual presentation of acute promyelocytic leukaemia, the diagnostic difficulties and the fatal outcome are particularly directed toward dental surgery practitioners to emphasise the importance of clinical assessment and preoperative evaluation as a minimal clinically-oriented routine.
  • This case may also be of particular interest to haematologists, since the patient's cytogenetic analysis, clinical course and therapeutic response are well documented.

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  • [Cites] Blood. 1999 Jul 1;94(1):12-22 [10381493.001]
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  • (PMID = 19946580.001).
  • [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/ PMC2783043
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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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38. Lunghi M, Castagnola C, Calatroni S, Bernasconi P, Lazzarino M: Central nervous system relapse in acute promyelocytic leukaemia. Haematologica; 2006 Jun;91(6 Suppl):ECR24

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central nervous system relapse in acute promyelocytic leukaemia.
  • [MeSH-major] Central Nervous System Neoplasms / etiology. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 16785127.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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39. Altwegg SC, Altwegg LA, Maier W: Intracoronary thrombus with tissue factor expression heralding acute promyelocytic leukaemia. Eur Heart J; 2007 Nov;28(22):2731
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intracoronary thrombus with tissue factor expression heralding acute promyelocytic leukaemia.
  • [MeSH-major] Bone Marrow / pathology. Coronary Thrombosis / etiology. Leukemia, Promyelocytic, Acute / pathology. Myocardial Infarction / etiology. Thromboplastin / metabolism
  • [MeSH-minor] Angioplasty, Balloon, Coronary / methods. Biopsy. Blood Cell Count. Coronary Occlusion / etiology. Coronary Occlusion / radiography. Humans. Incidental Findings. Male. Middle Aged. Pancytopenia / diagnosis

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  • (PMID = 17561495.001).
  • [ISSN] 0195-668X
  • [Journal-full-title] European heart journal
  • [ISO-abbreviation] Eur. Heart J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9035-58-9 / Thromboplastin
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40. Masamoto Y, Nannya Y, Arai S, Koike Y, Hangaishi A, Yatomi Y, Kurokawa M: Evidence for basophilic differentiation of acute promyelocytic leukaemia cells during arsenic trioxide therapy. Br J Haematol; 2009 Mar;144(5):798-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evidence for basophilic differentiation of acute promyelocytic leukaemia cells during arsenic trioxide therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Basophils / pathology. Leukemia, Promyelocytic, Acute / pathology. Oxides / therapeutic use

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  • (PMID = 19036092.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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41. Ammatuna E, Cavaliere A, Divona M, Amadori S, Scambia G, Lo-Coco F: Successful pregnancy after arsenic trioxide therapy for relapsed acute promyelocytic leukaemia. Br J Haematol; 2009 Aug;146(3):341
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful pregnancy after arsenic trioxide therapy for relapsed acute promyelocytic leukaemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Pregnancy Complications, Neoplastic

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  • (PMID = 19545283.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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42. Fabbiano F, Magrin S, Cangialosi C, Felice R, Mirto S, Pitrolo F: All-trans retinoic acid induced cardiac and skeletal myositis in induction therapy of acute promyelocytic leukaemia. Br J Haematol; 2005 May;129(3):444-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] All-trans retinoic acid induced cardiac and skeletal myositis in induction therapy of acute promyelocytic leukaemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Myositis / chemically induced. Tretinoin / adverse effects

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  • (PMID = 15842672.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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43. Candoni A, Pizzolitto S, Boscutti G, Fanin R: Atypical haemolytic-uraemic syndrome at the onset of acute promyelocytic leukaemia. Br J Haematol; 2005 Feb;128(3):274

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical haemolytic-uraemic syndrome at the onset of acute promyelocytic leukaemia.
  • [MeSH-major] Hemolytic-Uremic Syndrome / etiology. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 15667528.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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44. Brown C, Opat S: An unusual case of indigestion: persistence of phagocytosed Auer rods in acute promyelocytic leukaemia. Br J Haematol; 2006 Apr;133(2):112

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An unusual case of indigestion: persistence of phagocytosed Auer rods in acute promyelocytic leukaemia.
  • [MeSH-major] Inclusion Bodies / pathology. Leukemia, Promyelocytic, Acute / pathology. Phagocytosis

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  • (PMID = 16611301.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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45. Manikam SD, Stanslas J: Andrographolide inhibits growth of acute promyelocytic leukaemia cells by inducing retinoic acid receptor-independent cell differentiation and apoptosis. J Pharm Pharmacol; 2009 Jan;61(1):69-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Andrographolide inhibits growth of acute promyelocytic leukaemia cells by inducing retinoic acid receptor-independent cell differentiation and apoptosis.
  • OBJECTIVES: The growth inhibiting potential of andrographolide was evaluated in three acute promyelocytic leukaemia cell line models (HL-60, NB4 and all-trans retinoic acid (ATRA)-resistant NB4-R2).
  • METHODS: In elucidating the mechanisms of growth inhibition, a special emphasis was placed on assessing the induction of differentiation and apoptosis by andrographolide in the primary acute promyelocytic leukaemia NB4 cells.
  • CONCLUSIONS: Taken together, these results suggest andrographolide and its derivatives, apparently with a novel cell differentiating mechanism and with ability to induce apoptosis, might be beneficial in the treatment of primary and ATRA-resistant acute promyelocytic leukaemia.
  • [MeSH-minor] Andrographis / chemistry. Anti-Inflammatory Agents, Non-Steroidal / chemistry. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. HL-60 Cells. Humans. Inhibitory Concentration 50. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Microscopy, Fluorescence. Molecular Structure. Naphthalenes / chemistry. Naphthalenes / pharmacology. Plant Extracts / chemistry. Plant Extracts / isolation & purification. Plant Extracts / pharmacology. Tretinoin / chemistry. Tretinoin / pharmacology

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  • [ErratumIn] J Pharm Pharmacol. 2009 May;61(5):687. Manikam, Shiamala T [corrected to Manikam, Shiamala T]
  • (PMID = 19126299.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AGN 193109; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Diterpenes; 0 / Naphthalenes; 0 / Plant Extracts; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 410105JHGR / andrographolide; 5688UTC01R / Tretinoin
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46. Chan KH, Yuen SL, Joshua D: A case of all-trans retinoic acid-induced myositis in the treatment of acute promyelocytic leukaemia. Clin Lab Haematol; 2005 Dec;27(6):399-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of all-trans retinoic acid-induced myositis in the treatment of acute promyelocytic leukaemia.
  • The use of all-trans retinoic acid (ATRA) is now standard therapy for the treatment of acute promyelocytic leukaemia (APML).
  • We report a case of a young man with APML who developed ATRA-induced myositis characterized by unexplained fevers, bilateral leg swelling and a non-painful purpuric, petechial rash, with prompt resolution of symptoms and signs with high-dose steroids and cessation of ATRA.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / complications. Myositis / chemically induced. Tretinoin / adverse effects

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  • (PMID = 16307543.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Steroids; 5688UTC01R / Tretinoin
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47. Arbuthnot C, Wilde JT: Haemostatic problems in acute promyelocytic leukaemia. Blood Rev; 2006 Nov;20(6):289-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haemostatic problems in acute promyelocytic leukaemia.
  • Despite the development of highly effective treatment strategies for acute promyelocytic leukaemia around 10% of patients die in the presentation period as a consequence of the associated bleeding diathesis.
  • The cause of the coagulopathy is complex resulting from a combination of tissue factor (TF) and cancer procoagulant (CP) induced disseminated intravascular coagulation, exaggerated fibrinolysis due predominantly to enhanced expression of annexin II on APL blast cell membranes and blast cell production of cytokines.
  • All-trans retinoic acid (ATRA) has revolutionised the treatment of APL.
  • Commencement of ATRA induces APL blast cell differentiation and is associated with a rapid resolution of the bleeding tendency through a combination of effects which include up regulation of thrombomodulin and down regulation of TF and CP production and cell surface expression of annexin II.
  • [MeSH-major] Hemorrhagic Disorders / etiology. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 16757074.001).
  • [ISSN] 0268-960X
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  • [Number-of-references] 90
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48. Breccia M, Cimino G, Diverio D, Gentilini F, Mandelli F, Lo Coco F: Sustained molecular remission after low dose gemtuzumab-ozogamicin in elderly patients with advanced acute promyelocytic leukemia. Haematologica; 2007 Sep;92(9):1273-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sustained molecular remission after low dose gemtuzumab-ozogamicin in elderly patients with advanced acute promyelocytic leukemia.
  • We report here a preliminary experience with gemtuzumab ozogamicin (GO) used at low dosage (3 mg/m (2)) in 3 elderly patients with acute promyelocytic leukaemia (APL) who presented molecular relapse and were unfit for intensive chemotherapy.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 17768126.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
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49. Shipra P, Srijit D: Variant Abductor Pollicis Longus Muscle: a Case Report. Acta Medica (Hradec Kralove); 2007;50(3):213-215

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Abductor pollicis longus (APL) muscle is known to exhibit different variations with respect to its attachments.
  • Various studies have reported the splitting of the APL muscle.
  • Comparative anatomical findings of split insertion of APL is commonly found in chimpanzees, gorillas and gibbons.
  • In the present study, we describe an anomalous APL muscle, which originated from the posterior surface of the shaft of the radius and ulna and traversed a course deep to the extensor retinaculum.
  • Interestingly, immediately after emerging form the deeper aspect of extensor retinaculum, the thin tendon of the APL muscle continued again as a muscular belly in relation to the dorsolateral part of the 1st metacarpal bone, to end as a tendon with its attachment to the base of the proximal phalanx.
  • Such an unusual variation of APL with its attachment into proximal phalanx is a rare finding and may be of importance in altering the mechanics of the thumb during abduction.
  • The clinical significance of such an anatomical variation of APL may be important during reconstructive surgeries involving thumb and also of academic interest.

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  • (PMID = 28795947.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Abductor pollicis longus / Anomaly / Attachment / Muscle / Tendon / Variation
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50. Thomas X, Troncy J: Arsenic: a beneficial therapeutic poison - a historical overview. Adler Mus Bull; 2009 Jun;35(1):3-13
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  • Fowler's potassium bicarbonate-based solution of arsenic trioxide (As2O3)solution was the main treatment of chronic myeloid leukaemia until the 1930s.
  • After a decline in the use of arsenic during the mid-20th century, arsenic trioxide was reintroduced as an anticancer agent after reports emerged from China of the success of an arsenic trioxide-containing herbal mixture for the treatment of acute promyelocytic leukaemia.
  • Arsenic trioxide was first purified and used in controlled studies in China in the 1970s.Subsequently, randomised clinical trials performed in the United States led to FDA approval of arsenic trioxide in the treatment of patients with relapsed or refractory acute promyelocytic leukaemia.
  • [MeSH-major] Arsenic. Clinical Trials as Topic. Materia Medica. Medicine, Traditional. Poisons. Therapeutics
  • [MeSH-minor] Arsenic Poisoning / ethnology. Arsenic Poisoning / history. Herbal Medicine / education. Herbal Medicine / history. History, 19th Century. History, 20th Century. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / ethnology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / history. Plant Preparations / history

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  • (PMID = 20052806.001).
  • [ISSN] 0258-2058
  • [Journal-full-title] Adler Museum bulletin
  • [ISO-abbreviation] Adler Mus Bull
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article
  • [Publication-country] South Africa
  • [Chemical-registry-number] 0 / Materia Medica; 0 / Plant Preparations; 0 / Poisons; N712M78A8G / Arsenic
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51. Bain BJ: Clinical applications of molecular haematology: an overview. J Assoc Physicians India; 2007 Jul;55:503-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical applications of molecular haematology: an overview.
  • The molecular understanding has helped in fine-tuning the diagnosis, prognosis and management.
  • Following is an overview of clinical applications of molecular haematology, especially in the field of chronic myeloid leukaemia, chronic eosinophilic leukaemia, bcr abl negative chronic myeloproliferative disorders and acute promyelocytic leukaemia.
  • [MeSH-minor] Humans. Hypereosinophilic Syndrome / diagnosis. Janus Kinase 2 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Promyelocytic, Acute. Molecular Biology. Myeloproliferative Disorders / diagnosis. Prognosis

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  • (PMID = 17907501.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 16
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52. Iversen PO, Sørensen DR, Sioud M: A combined immunostimulatory and immunoinhibitory short interference RNA reduces hypercoagulability in a rat model of acute promyelocytic leukaemia. Thromb Haemost; 2010 Aug;104(2):350-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A combined immunostimulatory and immunoinhibitory short interference RNA reduces hypercoagulability in a rat model of acute promyelocytic leukaemia.
  • Acute promyelocytic leukaemia (APL) confers an increased risk of thrombosis and bleeding.
  • We recently showed that a combined immunoinhibitory and immunostimulatory short interference (si) RNA effectively inhibited leukaemic growth and metastasis in rats with APL.
  • We now asked if the reported anti-leukaemic effects of siRNA treatment could be explained by inhibition of hypercoagulability.
  • We measured markers of coagulation and fibrinolysis in plasma collected from APL rats with overt leukaemia using conventional assays.
  • Treatment of leukaemic rats with the siRNA reduced (p < 0.05) the concentration of thrombin-anti-thrombin complex (a marker of coagulation) by 40% compared with rats treated with an inactive, control siRNA.
  • Substantial reductions (p < 0.05) were also obtained for two markers of fibrinolysis: D-dimer (72%) and plasminogen activator inhibitor type 1 (51%).
  • The bifunctional siRNA reduces the hypercoagulable state in APL in addition to its direct anti-leukaemic properties, supporting testing of this small molecule in human APL.
  • [MeSH-major] Blood Coagulation. Dendritic Cells / transplantation. Genetic Therapy / methods. Interleukin-10 / metabolism. Leukemia, Promyelocytic, Acute / therapy. RNA Interference. RNA, Small Interfering / biosynthesis. Thrombophilia / therapy
  • [MeSH-minor] Animals. Antithrombin III. Biomarkers / blood. Cells, Cultured. Disease Models, Animal. Fibrin Fibrinogen Degradation Products / metabolism. Fibrinogen / metabolism. Male. Peptide Hydrolases / blood. Plasminogen Activator Inhibitor 1 / blood. Rats. Rats, Inbred BN. Thromboplastin / metabolism. Transfection

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  • (PMID = 20539915.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Fibrin Fibrinogen Degradation Products; 0 / Plasminogen Activator Inhibitor 1; 0 / RNA, Small Interfering; 0 / antithrombin III-protease complex; 0 / fibrin fragment D; 130068-27-8 / Interleukin-10; 9000-94-6 / Antithrombin III; 9001-32-5 / Fibrinogen; 9035-58-9 / Thromboplastin; EC 3.4.- / Peptide Hydrolases
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53. Fuchs O, Provazníková D, Peslová G: [Promyelocytic leukaemia protein and defect in transforming growth factor-beta signal pathway in acute promyelocytic leukaemia]. Cas Lek Cesk; 2005;144(2):90-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Promyelocytic leukaemia protein and defect in transforming growth factor-beta signal pathway in acute promyelocytic leukaemia].
  • Chromosome translocations are detected in 50-70% of human leukaemia.
  • The promyelocytic leukaemia (PML) gene is involved in the t(15;17) chromosomal translocation of acute promyelocytic leukaemia (APL).
  • PML gene encodes a protein, which was shown to be concentrated in PML-nuclear bodies.
  • Histone acetyltransferases and deacetylases, and chromatin-modifying proteins are accumulated in complexes with PML protein in these nuclear bodies giving the evidence of their role in transcription regulation.
  • Physical interactions of PML protein with transcription factors, co-activators and co-repressors of transcription correspond with the role of PML in transcription regulation.
  • PML plays an important role in apoptosis, proliferation and senescence of cells.
  • PML gene is a tumour-suppressor gene and a product of its expression acts as a potent cell growth suppressor.
  • All these activities of PML protein are ascribed to its nuclear functions.
  • Cytoplasmic form of PML (cPML) is also very important and it is critical for transforming growth factor-beta (TGF-beta) signalling.
  • Cytoplasmic PML interacts with two TGF-beta receptors (TbetaBRI and TbetaRII) and acts as a bridging factor between protein called Smad anchor of receptor activation (SARA) and Smad proteins and it plays a role in the transport of whole complex into the early endosomes in TGF-beta signalling.
  • The loss of functional cPML induces not only APL but it might influence behaviour of cancer cells and their resistance to TGF-beta.
  • [MeSH-minor] Cell Nucleus / metabolism. Cytoplasm / metabolism. DNA-Binding Proteins / metabolism. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Leukemia, Promyelocytic, Acute. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm Proteins / physiology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Nuclear Proteins / physiology. Receptors, Transforming Growth Factor beta / metabolism. Serine Endopeptidases / metabolism. Smad Proteins. Trans-Activators / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism. Transcription Factors / physiology. Tumor Suppressor Proteins

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  • (PMID = 15807293.001).
  • [ISSN] 0008-7335
  • [Journal-full-title] Casopís lékar̆ů c̆eských
  • [ISO-abbreviation] Cas. Lek. Cesk.
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Smad Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 3.4.21- / ZFYVE16 protein, human; EC 3.4.21.- / Serine Endopeptidases
  • [Number-of-references] 40
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54. Resche-Rigon M, Chevret S: Local influence for the subdistribution of a competing risk. Stat Med; 2006 Jun 15;25(11):1937-47
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  • This was illustrated on a real data set from a randomized clinical trial in acute promyelocytic leukaemia and on a simulation study.
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Clinical Trials, Phase III as Topic / methods. Computer Simulation. Humans. Leukemia, Promyelocytic, Acute / therapy. Models, Biological. Recurrence. Risk Factors. Tretinoin / administration & dosage. Tretinoin / therapeutic use

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  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd.
  • (PMID = 16158402.001).
  • [ISSN] 0277-6715
  • [Journal-full-title] Statistics in medicine
  • [ISO-abbreviation] Stat Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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55. Jayshree RS, Shafiulla M, George J, David JK, Bapsy PP, Chakrabarti A: Microscopic, cultural and molecular evidence of disseminated invasive aspergillosis involving the lungs and the gastrointestinal tract. J Med Microbiol; 2006 Jul;55(Pt 7):961-4
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  • A patient with acute promyelocytic leukaemia developed invasive aspergillosis post chemotherapy during a pancytopenic episode, clinically involving the lungs and the gastrointestinal tract.
  • Cultures of the samples yielded Aspergillus flavus, which were identical by RFLP and random amplification of polymorphic DNA analyses and antifungal MICs, proving disseminated disease.
  • [MeSH-minor] Adolescent. Antifungal Agents / therapeutic use. DNA, Fungal / chemistry. DNA, Fungal / genetics. Feces / microbiology. Humans. Leukemia, Promyelocytic, Acute / microbiology. Male. Random Amplified Polymorphic DNA Technique. Sputum / microbiology

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  • (PMID = 16772427.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / DNA, Fungal
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56. Salomoni P, Bellodi C: New insights into the cytoplasmic function of PML. Histol Histopathol; 2007 08;22(8):937-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights into the cytoplasmic function of PML.
  • PML is a tumour suppressor inactivated in Acute Promyelocytic Leukaemia (APL).
  • PML is the essential component of a subnuclear structure called the PML nuclear body (PML-NB), which is disrupted in APL.
  • By targeting different cellular proteins to this structure, PML can either hamper or potentiate their functions.
  • The PML transcript undergoes alternative splicing to generate both nuclear and cytoplasmic isoforms.
  • Most of the research in this field has focused its attention on studying nuclear PML.
  • Nevertheless, new exciting studies show that cytoplasmic PML may control essential cellular functions, thus opening new avenues for investigation.
  • [MeSH-major] Cytoplasm / metabolism. Gene Expression Regulation, Neoplastic. Leukemia, Promyelocytic, Acute / metabolism. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Signal Transduction. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus. Adaptor Proteins, Signal Transducing / metabolism. Alternative Splicing. Animals. Cell Cycle. Cell Nucleus / metabolism. Humans. Interferons / metabolism. Membrane Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Promyelocytic Leukemia Protein. Protein Isoforms / metabolism. Transforming Growth Factor beta / metabolism. Virus Diseases / metabolism

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  • (PMID = 17503350.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670601
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Promyelocytic Leukemia Protein; 0 / Protein Isoforms; 0 / TRIM protein, human; 0 / Transcription Factors; 0 / Transforming Growth Factor beta; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 143220-95-5 / PML protein, human; 9008-11-1 / Interferons
  • [Number-of-references] 80
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57. Tsai WH, Shih CH, Lin CC, Ho CK, Hsu FC, Hsu HC: Monocyte chemotactic protein-1 in the migration of differentiated leukaemic cells toward alveolar epithelial cells. Eur Respir J; 2008 May;31(5):957-62
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  • All-trans retinoic acid (ATRA) can induce acute respiratory distress syndrome in patients with acute promyelocytic leukaemia (APL).
  • The current study investigated the role of monocyte chemotactic protein (MCP)-1 in the chemotactic transmigration of ATRA-treated NB4 (ATRA-NB4) APL cells toward A549 alveolar epithelial cells.
  • Monocyte chemotactic protein-1 secreted from alveolar epithelial cells plays an important role in the cell-cell interaction involved in the chemotactic transmigration of all-trans retinoic acid-treated acute promyelocytic leukaemia cells toward alveolar epithelial cells.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Chemotaxis / drug effects. Epithelial Cells / drug effects. Granulocyte Precursor Cells / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects
  • [MeSH-minor] Cell Differentiation / drug effects. Cells, Cultured. Chemokine CCL2 / drug effects. Coculture Techniques. Humans. Pulmonary Alveoli / cytology. Pulmonary Alveoli / drug effects. Receptors, CCR2

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  • (PMID = 18216048.001).
  • [ISSN] 1399-3003
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCR2 protein, human; 0 / Chemokine CCL2; 0 / Receptors, CCR2; 5688UTC01R / Tretinoin
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58. Pascual AM, Téllez N, Boscá I, Mallada J, Belenguer A, Abellán I, Sempere AP, Fernández P, Magraner MJ, Coret F, Sanz MA, Montalbán X, Casanova B: Revision of the risk of secondary leukaemia after mitoxantrone in multiple sclerosis populations is required. Mult Scler; 2009 Nov;15(11):1303-10
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  • [Title] Revision of the risk of secondary leukaemia after mitoxantrone in multiple sclerosis populations is required.
  • The objective in this paper is to compare the cumulative incidence and incidence density of therapy-related acute myeloid leukaemia in two cohorts of patients with multiple sclerosis treated with mitoxantrone, and with previously reported data in the literature.
  • Six new cases of acute myeloid leukaemia were observed by prospectively following two Spanish series of 142 and 88 patients with worsening relapsing multiple sclerosis and secondary-progressive disease treated with mitoxantrone.
  • A literature review shows 32 further cases of acute myeloid leukaemia reported, 65.6% of which are therapy-related acute promyelocytic leukaemia.
  • Five cases in the cohorts fulfilled the diagnostic criteria for acute promyelocytic leukaemia, and one patient was diagnosed with pre-B-acute lymphoblastic leukaemia.
  • Acute myeloid leukaemia latency after mitoxantrone discontinuation was 1 to 45 months.
  • In the only seven previously reported series, the accumulated incidence varied from 0.15% to 0.80%.
  • The real incidence of acute myeloid leukaemia after mitoxantrone therapy in the multiple sclerosis population could be higher as evidenced by the growing number of cases reported.
  • These data stress the necessity of re-evaluating this risk.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Mitoxantrone / adverse effects. Multiple Sclerosis / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Anti-Inflammatory Agents / therapeutic use. Child. Cohort Studies. Female. Humans. Interferon Type I / therapeutic use. Male. Mediterranean Region / epidemiology. Methylprednisolone / therapeutic use. Middle Aged. Multiple Sclerosis, Chronic Progressive / complications. Multiple Sclerosis, Chronic Progressive / drug therapy. Multiple Sclerosis, Relapsing-Remitting / complications. Multiple Sclerosis, Relapsing-Remitting / drug therapy. Prospective Studies. Recombinant Proteins. Risk Assessment. Young Adult

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  • (PMID = 19825889.001).
  • [ISSN] 1477-0970
  • [Journal-full-title] Multiple sclerosis (Houndmills, Basingstoke, England)
  • [ISO-abbreviation] Mult. Scler.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents; 0 / Interferon Type I; 0 / Recombinant Proteins; BZ114NVM5P / Mitoxantrone; X4W7ZR7023 / Methylprednisolone
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59. Oliveira AC, Domingo-Domenech E, Arnan M, Gallardo D, Puig I, González-Barca E: All-trans retinoic acid-induced myositis in a case of acute promyelocytic leukaemia. Int J Lab Hematol; 2008 Jun;30(3):254-5
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  • [Title] All-trans retinoic acid-induced myositis in a case of acute promyelocytic leukaemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Myositis / chemically induced. Tretinoin / adverse effects

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  • (PMID = 18205843.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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60. Di Veroli A, Ramadan SM, Divona M, Cudillo L, Giannì L, Wieland S, Giannotti F, Mirabile M, Arcese W, Lo-Coco F: Molecular remission in advanced acute promyelocytic leukaemia after treatment with the oral synthetic retinoid Tamibarotene. Br J Haematol; 2010 Oct;151(1):99-101
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  • [Title] Molecular remission in advanced acute promyelocytic leukaemia after treatment with the oral synthetic retinoid Tamibarotene.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzoates / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Tetrahydronaphthalenes / therapeutic use

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  • (PMID = 20618325.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoates; 0 / Tetrahydronaphthalenes; 08V52GZ3H9 / tamibarotene
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61. Dalal BI, Bruyere H, Barnett MJ: Significance of persistent Auer rods and cytogenetic abnormality after first cycle of therapy for acute promyelocytic leukaemia. Br J Haematol; 2007 Jun;137(5):385
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  • [Title] Significance of persistent Auer rods and cytogenetic abnormality after first cycle of therapy for acute promyelocytic leukaemia.
  • [MeSH-major] Bone Marrow Examination. Chromosome Aberrations. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Humans. In Situ Hybridization, Fluorescence. Male. Oncogene Proteins, Fusion / genetics. Remission Induction. Translocation, Genetic. Tretinoin / therapeutic use

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  • [CommentIn] Br J Haematol. 2008 Sep;142(6):998-1000 [18544082.001]
  • (PMID = 17374141.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; ZS7284E0ZP / Daunorubicin
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62. Mohamedbhai S, Pule M, Conn B, Hopper C, Ramsay A, Khwaja A: Acute promyelocytic leukaemia presenting with a myeloid sarcoma of the tongue. Br J Haematol; 2008 May;141(5):565
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promyelocytic leukaemia presenting with a myeloid sarcoma of the tongue.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology. Sarcoma, Myeloid / pathology. Tongue Neoplasms / pathology

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  • (PMID = 18373707.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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63. Knipp S, Gattermann N, Schapira M, Käferstein H, Germing U: Arsenic in the cerebrospinal fluid of a patient receiving arsenic trioxide for relapsed acute promyelocytic leukemia with CNS involvement. Leuk Res; 2007 Nov;31(11):1585-7
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  • [Title] Arsenic in the cerebrospinal fluid of a patient receiving arsenic trioxide for relapsed acute promyelocytic leukemia with CNS involvement.
  • We report on a 42-year-old patient whose relapse of acute promyelocytic leukaemia (APL) included meningeal infiltration.
  • Arsenic showed a peak CSF concentration of 0.008 mg/l (0.11 micromol/l) and a nadir of 0.002 mg/l (0.027 micromol/l), both representing about 14% of blood levels.
  • ATO thus crosses the blood-CSF-barrier when administered intravenously, but the concentration in CSF is probably not sufficient for treatment of meningeal leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenic / cerebrospinal fluid. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 17416415.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; N712M78A8G / Arsenic; S7V92P67HO / arsenic trioxide
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64. Liu W, Zhu YS, Guo M, Yu Y, Chen GQ: Therapeutic efficacy of NSC606985, a novel camptothecin analog, in a mouse model of acute promyelocytic leukemia. Leuk Res; 2007 Nov;31(11):1565-74
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  • [Title] Therapeutic efficacy of NSC606985, a novel camptothecin analog, in a mouse model of acute promyelocytic leukemia.
  • Nanomolar concentrations of NSC606985, a novel camptothecin (CPT) analog, effectively induces apoptosis in vitro in acute myeloid leukemic (AML) cells.
  • Here we investigated the potential therapeutic effects of NSC606985 on the mice model with acute promyelocytic leukaemia (APL), a unique subtype of AML.
  • These results propose that NSC606985 warrants further preclinical and clinical investigations for AML treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Camptothecin / analogs & derivatives. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Disease Models, Animal. Mice

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  • (PMID = 17428537.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NSC606985; XT3Z54Z28A / Camptothecin
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65. Salomoni P, Ferguson BJ, Wyllie AH, Rich T: New insights into the role of PML in tumour suppression. Cell Res; 2008 Jun;18(6):622-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New insights into the role of PML in tumour suppression.
  • The PML gene is involved in the t(15;17) translocation of acute promyelocytic leukaemia (APL), which generates the oncogenic fusion protein PML (promyelocytic leukaemia protein)-retinoic acid receptor alpha.
  • The PML protein localises to a subnuclear structure called the PML nuclear domain (PML-ND), of which PML is the essential structural component.
  • In APL, PML-NDs are disrupted, thus implicating these structures in the pathogenesis of this leukaemia.
  • Unexpectedly, recent studies indicate that PML and the PML-ND play a tumour suppressive role in several different types of human neoplasms in addition to APL.
  • Because of PML's extreme versatility and involvement in multiple cellular pathways, understanding the mechanisms underlying its function, and therefore role in tumour suppression, has been a challenging task.

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  • (PMID = 18504460.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670601
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 187
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66. Oku E, Imamura R, Nagata S, Takata Y, Seki R, Otsubo K, Hashiguchi M, Osaki K, Yakushiji K, Yoshimoto K, Ogata H, Sata M, Okamura T: Promyelocytic crisis of chronic myelogenous leukaemia during imatinib mesylate treatment. Acta Haematol; 2007;117(4):191-6
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  • [Title] Promyelocytic crisis of chronic myelogenous leukaemia during imatinib mesylate treatment.
  • An untreated 66-year-old woman with chronic myelogenous leukaemia (CML) in the chronic phase was initially given imatinib mesylate, rapidly achieving a good cytogenetic response with treatment.
  • However, acute promyelocytic leukaemia complicated by a disseminated intravascular coagulation occurred 9 months after beginning imatinib treatment.
  • Promyelocytic crisis of CML was diagnosed by demonstration of both BCR/ABL and PML/RAR alpha chimeric genes in leukaemic cells by karyotypic and fluorescence in situ hybridization analysis.
  • Clonal evolution with addition of the PML/RAR alpha translocation may have arisen in the early chronic phase of CML, with expansion of this clone during imatinib treatment.
  • Promyelocytic crisis of CML is rare; furthermore, we know of no previous report of promyelocytic crisis occurring during treatment with imatinib.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • [Copyright] 2007 S. Karger AG, Basel
  • [CommentIn] Acta Haematol. 2007;117(4):236-7 [17308370.001]
  • (PMID = 17170522.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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67. Ajana I, Astier A, Gibaud S: Arsthinol nanosuspensions: pharmacokinetics and anti-leukaemic activity on NB4 promyelocytic leukaemia cells. J Pharm Pharmacol; 2009 Oct;61(10):1295-301
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  • [Title] Arsthinol nanosuspensions: pharmacokinetics and anti-leukaemic activity on NB4 promyelocytic leukaemia cells.
  • The aim of this work was to study its anti-leukaemic activity and to develop nanosuspensions of the drug, thereby limiting brain concentrations and the risk of encephalopathy.
  • The anti-leukaemic activity was assessed on NB4 acute promyelocytic leukaemia cells (vs solutions of arsthinol, As(2)O(3) and melarsoprol).
  • This formulation also reduced the drug's access to the brain (C(max) = 0.03 micromol/g) whereas bone marrow concentrations remained very high (C(max) = 2 micromol/g).
  • CONCLUSIONS: Nanosuspensions of arsthinol could be proposed for further studies in the treatment of acute promyelocytic leukaemia.

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  • (PMID = 19814860.001).
  • [ISSN] 2042-7158
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / Suspensions; QNT09A162Y / arsthinol; S7V92P67HO / arsenic trioxide; ZF3786Q2E8 / Melarsoprol
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68. Altucci L, Leibowitz MD, Ogilvie KM, de Lera AR, Gronemeyer H: RAR and RXR modulation in cancer and metabolic disease. Nat Rev Drug Discov; 2007 Oct;6(10):793-810
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  • [Title] RAR and RXR modulation in cancer and metabolic disease.
  • Retinoic acid receptors (RARs) are ligand-controlled transcription factors that function as heterodimers with retinoid X receptors (RXRs) to regulate cell growth and survival.
  • The success of RAR modulation in the treatment of acute promyelocytic leukaemia (APL) has stimulated considerable interest in the development of RAR and RXR modulators.
  • Here, we discuss the challenges and opportunities for therapeutic strategies based on RXR and RAR modulators, with a focus on cancer and metabolic diseases such as diabetes and obesity.
  • [MeSH-minor] Clinical Trials as Topic. Humans. Ligands. Retinoid X Receptors / agonists. Retinoid X Receptors / antagonists & inhibitors. Retinoid X Receptors / metabolism

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  • (PMID = 17906642.001).
  • [ISSN] 1474-1784
  • [Journal-full-title] Nature reviews. Drug discovery
  • [ISO-abbreviation] Nat Rev Drug Discov
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Retinoids
  • [Number-of-references] 184
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69. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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70. Jeddi R, Kacem K, Ben Lakhal R, Aissaoui L, Ben Abid H, Belhadj Ali Z, Meddeb B: [Pseudotumor cerebri with all-trans retinoic acid. A case report]. Tunis Med; 2006 Dec;84(12):827-9
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  • The diagnosis of pseudotumor cerebri (PC) is based on the triad of:.
  • (1) papilledema, (2) elevated intracranial pressure with a normal cerebrospinal constituency and (3) normal central nervous system imaging studies.
  • It is an uncommon complication of all-trans-retinoic acid (ATRA) therapy in children treated for acute promyelocytic leukaemia (APL).
  • Its occurrence is rare among adult patients with APL and treated with ATRA .
  • We report a case of an adult with APL who developed PC during induction therapy with ATRA-PC was managed with repeated lumbar punctures and corticotherapy.

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  • (PMID = 17288291.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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71. Leupin N, Kuhn A, Hügli B, Grob TJ, Jaggi R, Tobler A, Delorenzi M, Fey MF: Gene expression profiling reveals consistent differences between clinical samples of human leukaemias and their model cell lines. Br J Haematol; 2006 Nov;135(4):520-3
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  • [Title] Gene expression profiling reveals consistent differences between clinical samples of human leukaemias and their model cell lines.
  • Microarray gene expression profiles of fresh clinical samples of chronic myeloid leukaemia in chronic phase, acute promyelocytic leukaemia and acute monocytic leukaemia were compared with profiles from cell lines representing the corresponding types of leukaemia (K562, NB4, HL60).
  • In a hierarchical clustering analysis, all clinical samples clustered separately from the cell lines, regardless of leukaemic subtype.
  • Gene ontology analysis showed that cell lines chiefly overexpressed genes related to macromolecular metabolism, whereas in clinical samples genes related to the immune response were abundantly expressed.
  • [MeSH-major] Leukemia / genetics. Tumor Cells, Cultured / metabolism
  • [MeSH-minor] Gene Expression. Gene Expression Profiling / methods. Humans. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid / genetics. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Up-Regulation

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  • [Cites] Bioinformatics. 2004 Feb 12;20(3):307-15 [14960456.001]
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  • [CommentIn] Br J Haematol. 2008 Jul;142(1):137-8; author reply 138-41 [18445085.001]
  • (PMID = 17061979.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1654200
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72. Sedlacek P, Vavra V, Masova I, Codl D, Laznickova T, Malaskova L, Nyc O, Stary J: Successful therapy with ABLC, surgery and posaconazole for Rhizopus microsporus var. rhizopodiformis liver eumycetoma in a child with acute leukaemia. Mycoses; 2009 May;52(3):276-9
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  • [Title] Successful therapy with ABLC, surgery and posaconazole for Rhizopus microsporus var. rhizopodiformis liver eumycetoma in a child with acute leukaemia.
  • Diagnosis of non-Aspergillus mould infections remains challenging despite application of a wide spectrum of non-culture-based microbiological techniques.
  • In this article, we present the case of a 15-month-old boy diagnosed with Rhizopus microsporus var. rhizopodiformis liver mycetoma during induction chemotherapy for acute promyelocytic leukaemia.
  • Following surgery, he was effectively treated with a combination of ABLC and posaconazole during ongoing intensive chemotherapy.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Leukemia, Myeloid, Acute / complications. Liver Diseases / therapy. Mycetoma / therapy. Rhizopus / isolation & purification. Triazoles / therapeutic use

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  • (PMID = 18643916.001).
  • [ISSN] 1439-0507
  • [Journal-full-title] Mycoses
  • [ISO-abbreviation] Mycoses
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 0 / liposomal amphotericin B; 6TK1G07BHZ / posaconazole; 7XU7A7DROE / Amphotericin B
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73. Zhou J, Meng R, Sui X, Li W, Yang B: Various tolerances to arsenic trioxide between human cortical neurons and leukemic cells. Sci China C Life Sci; 2006 Dec;49(6):567-72
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  • Arsenic trioxide (As2O3) is very effective for treatment of acute promyelocytic leukaemia (APL) but little can pass through the blood-brain-barrier (BBB), which limits its use in the prevention and treatment of central nervous system leukaemia (CNSL).
  • The changes of apoptosis biomarkers, [Ca2+]i and PKC activity of both leukaemia cells and human cortical neurons, were monitored before and after being treated with As2O3 in vitro with laser confocal microscopy and Western blot.

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  • (PMID = 17312995.001).
  • [ISSN] 1006-9305
  • [Journal-full-title] Science in China. Series C, Life sciences
  • [ISO-abbreviation] Sci. China, C, Life Sci.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide; SY7Q814VUP / Calcium
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74. Chim CS, Chan WW, Kwong YL: Epigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemias. J Clin Pathol; 2008 Jul;61(7):844-7
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  • [Title] Epigenetic dysregulation of the DAP kinase/p14/HDM2/p53/Apaf-1 apoptosis pathway in acute leukaemias.
  • AIM AND METHODS: To analyse the potential inactivation of the DAP kinase/p14/HDM2/p53/Apaf-1 pathway by aberrant promoter methylation in acute leukaemias.
  • At diagnosis, DAP kinase methylation occurred in eight (25%) APL patients and none of the other AML patients (8/32 vs 0/50, p = 0.001).
  • DAP kinase methylation was detected in four (16%) ALL patients. p14 and Apaf-1 methylation was not detected in any of the 32 cases of acute promyelocytic leukaemia (APL), 50 cases of other subtypes of acute myeloid leukaemia (AML), and 25 cases of acute lymphoblastic leukaemia.
  • CONCLUSION: Among AML subtypes, DAP kinase is preferentially hypermethylated in APL.
  • [MeSH-major] Apoptosis / genetics. Death-Associated Protein Kinases / genetics. Epigenesis, Genetic. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Adult. Apoptotic Protease-Activating Factor 1 / genetics. Apoptotic Protease-Activating Factor 1 / metabolism. Base Sequence. DNA Methylation. Humans. Molecular Sequence Data. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Polymerase Chain Reaction / methods. Proto-Oncogene Proteins c-mdm2 / genetics. Proto-Oncogene Proteins c-mdm2 / metabolism. Signal Transduction. Tumor Cells, Cultured. Tumor Suppressor Protein p14ARF / genetics. Tumor Suppressor Protein p14ARF / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18587015.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ J04238
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APAF1 protein, human; 0 / Apoptotic Protease-Activating Factor 1; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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75. Hayes MJ, Longbottom RE, Evans MA, Moss SE: Annexinopathies. Subcell Biochem; 2007;45:1-28
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  • Annexins comprise a conserved family of proteins characterised by their ability to bind and order charged phospholipids in membranes, often in response to elevated intracellular calcium.
  • The family members (there are at least 12 in humans) have become specialised over evolutionary time and are involved in a diverse range of cellular functions both inside the cell and extracellularly Although a mutation in an annexin has never been categorically proven to be the cause of a disease state, they have been implicated in pathologies as diverse as autoimmunity, infection, heart disease, diabetes and cancer.
  • Rand to describe the pathological sequelae in two disease states, the overexpression of annexin 2 in a patients with a haemorrhagic form of acute promyelocytic leukaemia, and the under-expression of annexin 5 on placental trophoblasts in the antiphospholipid syndrome.
  • [MeSH-minor] Animals. Annexin A2 / physiology. Antiphospholipid Syndrome / physiopathology. Bacterial Infections / physiopathology. Cystic Fibrosis / physiopathology. Diabetes Mellitus / physiopathology. Genetic Diseases, X-Linked / physiopathology. Heart Diseases / physiopathology. Humans. Inflammation / physiopathology. Kidney Diseases / physiopathology. Leukemia, Promyelocytic, Acute / blood. Leukemia, Promyelocytic, Acute / physiopathology. Neoplasms / physiopathology. Virus Diseases / physiopathology

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  • (PMID = 18193632.001).
  • [ISSN] 0306-0225
  • [Journal-full-title] Sub-cellular biochemistry
  • [ISO-abbreviation] Subcell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Annexins
  • [Number-of-references] 149
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76. Arruda WO, Montú MB, de Oliveira Mde S, Ramina R: Acute myeloid leukaemia induced by mitoxantrone: case report. Arq Neuropsiquiatr; 2005 Jun;63(2A):327-9
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  • [Title] Acute myeloid leukaemia induced by mitoxantrone: case report.
  • It has a leukemogenesis potential induced by cytogenetic abnormalities, though with a low incidence.
  • Promyelocitic leukaemia (type M3) and other forms of acute myeloblastic leukaemias (M4 and M5) have been described in a few MS patients who received MX during their treatment.
  • We describe a white female patient, 47 year-old, with SPMS (EDSS = 4) with 14 years of disease.
  • She received MX during her disease and developed acute promyelocytic leukaemia (M3), with severe thrombocytopenia 30 months later.
  • Other cases of treatment related to AML are reviewed and discussed.
  • [MeSH-major] Immunosuppressive Agents / adverse effects. Leukemia, Promyelocytic, Acute / chemically induced. Mitoxantrone / adverse effects

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  • (PMID = 16100984.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; BZ114NVM5P / Mitoxantrone
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77. Stapnes C, Gjertsen BT, Reikvam H, Bruserud Ø: Targeted therapy in acute myeloid leukaemia: current status and future directions. Expert Opin Investig Drugs; 2009 Apr;18(4):433-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapy in acute myeloid leukaemia: current status and future directions.
  • BACKGROUND: The limit of acceptable toxicity for standard chemotherapeutic drugs used in acute myeloid leukaemia (AML) therapy has been reached.
  • OBJECTIVE: This review summarizes development in new strategies, and gives an overview of the clinical status on new drugs for non-promyelocytic AML in adults.
  • RESULTS/CONCLUSION: The major improvements in AML treatment during the last two decades has not been the introduction of new therapeutic agents, but rather the more optimal use of well-known drugs (e.g., high-dose cytarabine therapy, the use of ATRA in maintenance therapy of acute promyelocytic leukaemia) and improvement in the diagnosis and treatment of potentially life-threatening complications in patients treated with allogeneic stem cell transplantation.
  • However, further investigations based on specific targeted therapy and stratification of patients according to knowledge of the individual disease and health status will probably be necessary in future studies of new targeted therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Design. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 19335274.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors
  • [Number-of-references] 234
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78. da Silva J, Lautenschläger F, Sivaniah E, Guck JR: The cavity-to-cavity migration of leukaemic cells through 3D honey-combed hydrogels with adjustable internal dimension and stiffness. Biomaterials; 2010 Mar;31(8):2201-8
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  • This paper presents a method for fabricating periodic hydrogel scaffolds with a 3D honeycomb-like structure from colloidal crystal templates.
  • Acute promyelocytic leukaemia (APL) cells were differentiated with all-trans retinoic acid (ATRA) and treated with paclitaxel.
  • [MeSH-major] Cell Movement / physiology. Hydrogels / chemistry. Leukemia, Promyelocytic, Acute / pathology. Tissue Scaffolds

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20015545.001).
  • [ISSN] 1878-5905
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Biocompatible Materials; 0 / Hydrogels; 5688UTC01R / Tretinoin; P88XT4IS4D / Paclitaxel
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79. Soriano C, Creus A, Marcos R: Arsenic trioxide mutational spectrum analysis in the mouse lymphoma assay. Mutat Res; 2008 Nov 10;646(1-2):1-7
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  • Nevertheless, arsenic has also demonstrated to have anticancer activity; thus, arsenic trioxide (ATO, As2O3) is an inorganic trivalent arsenic form, currently used in the treatment against acute promyelocytic leukaemia (APL).
  • Our results show that, in mouse lymphoma cells, ATO is a strong clastogenic compound inducing large deletions, at chromosomal level, covering the Tk gene, as well as other regions of chromosome 11.
  • [MeSH-minor] Animals. Arsenicals. Biological Assay. Cell Line, Tumor. Leukemia L5178 / genetics. Leukemia, Promyelocytic, Acute / genetics. Mice. Spectrum Analysis. Thymidine Kinase / genetics

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  • (PMID = 18822301.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; EC 2.7.1.21 / Thymidine Kinase; S7V92P67HO / arsenic trioxide
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80. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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81. Tsimberidou AM, Estey E: Relevance of clinical trials in acute myeloid leukaemia. Hematol Oncol; 2008 Sep;26(3):182-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relevance of clinical trials in acute myeloid leukaemia.
  • Patients with newly diagnosed acute myeloid leukaemia (AML) are increasingly being enrolled in clinical trials sponsored by pharmaceutical companies or the National Cancer Institute.
  • These trials routinely exclude patients who are less likely to respond (LLTR), e.g. those with Zubrod performance status >2 and levels of bilirubin or creatinine >/=2.0 mg/dL.
  • Here we examine rates of enrollment of LLTR patients in clinical trials over the past 16 years.
  • Overall, 2323 adults with newly diagnosed AML (excluding acute promyelocytic leukaemia) were registered on clinical trials from 1991 to 2006.
  • Our results suggest that newer clinical trials may be less applicable to LLTR patients than previous trials.
  • There is a need for clinical trials specific to the LLTR population, the group most in need of novel therapies.
  • [MeSH-major] Clinical Trials as Topic / methods. Leukemia, Myeloid, Acute / drug therapy

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  • [Copyright] Copyright (c) 2008 John Wiley & Sons, Ltd.
  • (PMID = 18381703.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] England
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82. Suzuki R, Onizuka M, Kojima M, Shimada M, Fukagawa S, Tsuboi K, Kobayashi H, Shintani A, Ogawa Y, Kawada H, Hotta T, Ando K: Preferential hypermethylation of the Dickkopf-1 promoter in core-binding factor leukaemia. Br J Haematol; 2007 Sep;138(5):624-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preferential hypermethylation of the Dickkopf-1 promoter in core-binding factor leukaemia.
  • Here, we investigated hypermethylation of the DKK1 promoter in patients with acute myeloid leukaemia (AML), especially core-binding factor (CBF) leukaemia.
  • The methylation status of DKK1 was analysed using methylation-specific polymerase chain reaction in 47 patients with AML.
  • DKK1 methylation was found in 14 (29.8%) patients, and more frequently in those with CBF leukaemia (6 of 12 patients), than in those with acute promyelocytic leukaemia (APL) (0 of 6 patients) (P = 0.03).
  • In contrast, Wnt inhibitory factor-1 methylation was found in APL (4 of 6 patients) but not in CBF leukaemia (0 of 12 patients) (P = 0.001).
  • Sequential analysis using four paired samples obtained at diagnosis and relapse suggested that DKK1 methylation was involved in the progression of leukaemia.
  • Therefore, DKK1 methylation may be involved in leukaemogenesis, especially in CBF leukaemia, and may be a useful prognostic marker in AML.
  • [MeSH-major] Biomarkers, Tumor / genetics. DNA Methylation. Intercellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow Cells / metabolism. Core Binding Factors / metabolism. DNA, Neoplasm / genetics. Disease Progression. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Prognosis. Promoter Regions, Genetic / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Survival Analysis. Tumor Cells, Cultured

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  • (PMID = 17686056.001).
  • [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 / Biomarkers, Tumor; 0 / Core Binding Factors; 0 / DKK1 protein, human; 0 / DNA, Neoplasm; 0 / Intercellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins
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83. Patatanian E, Thompson DF: Retinoic acid syndrome: a review. J Clin Pharm Ther; 2008 Aug;33(4):331-8
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  • The retinoic acid syndrome (RAS) is an unpredictable but frequent complication which may develop after administration of all-trans retinoic acid (ATRA) most commonly in patients with acute promyelocytic leukaemia (APL).
  • In this review, we describe the incidence, predictive factors, clinical course, outcome and treatment of RAS in patients with APL treated with ATRA.
  • Prophylactic steroids are not recommended but prompt administration of steroids at the first sign of unexplained dyspnea, fever, weight gain or pulmonary infiltrate, is critical.
  • Liposomal ATRA is being investigated to induce haematological cure in APL without chemotherapy and to reduce the incidence of RAS but further validation of its usefulness is necessary.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects

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  • (PMID = 18613850.001).
  • [ISSN] 1365-2710
  • [Journal-full-title] Journal of clinical pharmacy and therapeutics
  • [ISO-abbreviation] J Clin Pharm Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids; 5688UTC01R / Tretinoin; EC 3.4.11.2 / Antigens, CD13
  • [Number-of-references] 42
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84. Vizzardi E, Zanini G, Antonioli E, D'Aloia A, Raddino R, Cas LD: QT prolongation: a case of arsenical pericardial and pleural effusion. Cardiovasc Toxicol; 2008 Mar;8(1):41-4
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  • Arsenic trioxide is an effective treatment for patients with acute promyelocytic leukaemia (APL) who have relapsed from or are refractory to all trans-retinoic acid and anthracycline chemotherapy.
  • Cardiac effects observed include electrocardiographic changes such as QTc prolongation, T-wave abnormalities, torsades de pointes and sudden death.
  • We describe a case of a man, 76 years old, who was admitted to our department for dyspnoea in APL in treatment with arsenic trioxide.
  • [MeSH-minor] Aged. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Male. Recovery of Function. Withholding Treatment

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  • (PMID = 18084726.001).
  • [ISSN] 1559-0259
  • [Journal-full-title] Cardiovascular toxicology
  • [ISO-abbreviation] Cardiovasc. Toxicol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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85. Britschgi A, Simon HU, Tobler A, Fey MF, Tschan MP: Epigallocatechin-3-gallate induces cell death in acute myeloid leukaemia cells and supports all-trans retinoic acid-induced neutrophil differentiation via death-associated protein kinase 2. Br J Haematol; 2010 Apr;149(1):55-64
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  • [Title] Epigallocatechin-3-gallate induces cell death in acute myeloid leukaemia cells and supports all-trans retinoic acid-induced neutrophil differentiation via death-associated protein kinase 2.
  • Acute promyelocytic leukaemia (APL) patients are successfully treated with all-trans retinoic acid (ATRA).
  • We aimed at deciphering the molecular mechanism of EGCG-induced cell death in acute myeloid leukaemia (AML).
  • A significant increase of death-associated protein kinase 2 (DAPK2) levels was found in AML cells upon EGCG treatment paralleled by increased cell death that was significantly reduced upon silencing of DAPK2.
  • EGCG toxicity of primary AML blasts correlated with 67 kDa laminin receptor (67LR) expression.
  • Pretreatment of AML cells with ATRA, causing downregulation of 67LR, rendered these cells resistant to EGCG-mediated cell death.
  • In summary, it was found that (i) DAPK2 is essential for EGCG-induced cell death in AML cells, (ii) ATRA and EGCG cotreatment significantly boosted neutrophil differentiation, and 67LR expression correlates with susceptibility of AML cells to EGCG.
  • We thus suggest that EGCG, by selectively targeting leukaemic cells, may improve differentiation therapies for APL and chemotherapy for other AML subtypes.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Catechin / analogs & derivatives. Leukemia, Myeloid, Acute / pathology. Neutrophils / drug effects. Tretinoin / pharmacology

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  • (PMID = 20096012.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 5688UTC01R / Tretinoin; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; EC 2.7.11.1 / DAPK2 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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86. Siderov J, Duggan J: Arsenic trioxide associated toothache. J Oncol Pharm Pract; 2010 Jun;16(2):127-8
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  • Arsenic trioxide in the treatment of acute promyelocytic leukaemia is relatively safe with minimal side effects.
  • A 45-year-old male with relapsed APL was commenced on a treatment schedule of all-trans-retinoic acid 20mg four times a day for 14 days concurrent with a 10mg intravenous infusion of arsenic trioxide for 28 days.
  • After 14 doses of the 6th cycle of treatment he experienced severe acute pain in various parts of the oral cavity.
  • [MeSH-major] Arsenicals / administration & dosage. Arsenicals / adverse effects. Oxides / administration & dosage. Oxides / adverse effects. Toothache / chemically induced. Toothache / diagnosis
  • [MeSH-minor] Humans. Infusions, Intravenous. Leukemia, Promyelocytic, Acute / drug therapy. Male. Middle Aged. Tretinoin / administration & dosage

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  • (PMID = 19525303.001).
  • [ISSN] 1477-092X
  • [Journal-full-title] Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners
  • [ISO-abbreviation] J Oncol Pharm Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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87. Bellodi C, Kindle K, Bernassola F, Cossarizza A, Dinsdale D, Melino G, Heery D, Salomoni P: A cytoplasmic PML mutant inhibits p53 function. Cell Cycle; 2006 Nov;5(22):2688-92
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  • [Title] A cytoplasmic PML mutant inhibits p53 function.
  • The promyelocytic leukaemia gene (Pml) is a tumor suppressor identified in acute promyelocytic leukaemia (APL), where it is fused to RAR alpha gene as a result of the chromosomal translocation t(15;17).
  • Pml encodes both nuclear and cytoplasmic isoforms.
  • While nuclear PML has been intensively investigated, cytoplasmic PML proteins are less characterized.
  • PML nuclear isoforms (nPML) are the essential components of subnuclear structures referred to as PML nuclear bodies (PML-NB).
  • Two missense mutations resulting in truncated PML cytoplasmic proteins (Mut PML) have been identified in aggressive APL cases.
  • Here we report that cytoplasmic PML is able to induce the relocation of nPML to the cytoplasm, thus reducing the number of PML-NBs.
  • Remarkably, Mut PML inhibits p53 transcriptional, growth suppressive, and apoptotic functions, thus suggesting that cytoplasmic expression of PML has an impact on survival through inhibition of nuclear PML.
  • Overall our findings shed new light on the role of PML cytoplasmic proteins in the regulation of p53.
  • [MeSH-minor] Apoptosis. Cells, Cultured. Gene Expression Regulation, Neoplastic. HL-60 Cells. Humans. Leukemia, Promyelocytic, Acute / metabolism. Microscopy, Fluorescence. Promyelocytic Leukemia Protein. Transfection

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  • (PMID = 17172828.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670600; United Kingdom / Medical Research Council / / MC/ U132670601
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Promyelocytic Leukemia Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
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88. Lallemand-Breitenbach V, Jeanne M, Benhenda S, Nasr R, Lei M, Peres L, Zhou J, Zhu J, Raught B, de Thé H: Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway. Nat Cell Biol; 2008 May;10(5):547-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic degrades PML or PML-RARalpha through a SUMO-triggered RNF4/ubiquitin-mediated pathway.
  • In acute promyelocytic leukaemia (APL), arsenic trioxide induces degradation of the fusion protein encoded by the PML-RARA oncogene, differentiation of leukaemic cells and produces clinical remissions.
  • SUMOylation of its PML moiety was previously implicated, but the nature of the degradation pathway involved and the role of PML-RARalpha catabolism in the response to therapy have both remained elusive.
  • Here, we demonstrate that arsenic-induced PML SUMOylation triggers its Lys 48-linked polyubiquitination and proteasome-dependent degradation.
  • When exposed to arsenic, SUMOylated PML recruits RNF4, the human orthologue of the yeast SUMO-dependent E3 ubiquitin-ligase, as well as ubiquitin and proteasomes onto PML nuclear bodies.
  • Arsenic-induced differentiation is impaired in cells transformed by a non-degradable PML-RARalpha SUMOylation mutant or in APL cells transduced with a dominant-negative RNF4, directly implicating PML-RARalpha catabolism in the therapeutic response.
  • We thus identify PML as the first protein degraded by SUMO-dependent polyubiquitination.
  • As PML SUMOylation recruits not only RNF4, ubiquitin and proteasomes, but also many SUMOylated proteins onto PML nuclear bodies, these domains could physically integrate the SUMOylation, ubiquitination and degradation pathways.

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  • [CommentIn] Nat Cell Biol. 2008 May;10(5):507-9 [18454129.001]
  • (PMID = 18408733.001).
  • [ISSN] 1476-4679
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R37 CA49152
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Small Interfering; 0 / RNF4 protein, human; 0 / Recombinant Fusion Proteins; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 120904-94-1 / Polyubiquitin; 143220-95-5 / PML protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex; N712M78A8G / Arsenic
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89. Tatham MH, Geoffroy MC, Shen L, Plechanovova A, Hattersley N, Jaffray EG, Palvimo JJ, Hay RT: RNF4 is a poly-SUMO-specific E3 ubiquitin ligase required for arsenic-induced PML degradation. Nat Cell Biol; 2008 May;10(5):538-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RNF4 is a poly-SUMO-specific E3 ubiquitin ligase required for arsenic-induced PML degradation.
  • In acute promyelocytic leukaemia (APL), the promyelocytic leukaemia (PML) protein is fused to the retinoic acid receptor alpha (RAR).
  • This disease can be treated effectively with arsenic, which induces PML modification by small ubiquitin-like modifiers (SUMO) and proteasomal degradation.
  • PML protein accumulated in RNF4-depleted cells and was ubiquitinated by RNF4 in a SUMO-dependent fashion in vitro.
  • In the absence of RNF4, arsenic failed to induce degradation of PML and SUMO-modified PML accumulated in the nucleus.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Molecular Sequence Data. Proteasome Endopeptidase Complex / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Rats. Sequence Alignment. Ubiquitin / metabolism


90. Ourique AF, Azoubel S, Ferreira CV, Silva CB, Marchiori MC, Pohlmann AR, Guterres SS, Beck RC: Lipid-core nanocapsules as a nanomedicine for parenteral administration of tretinoin: development and in vitro antitumor activity on human myeloid leukaemia cells. J Biomed Nanotechnol; 2010 Jun;6(3):214-23
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  • [Title] Lipid-core nanocapsules as a nanomedicine for parenteral administration of tretinoin: development and in vitro antitumor activity on human myeloid leukaemia cells.
  • In addition, the effect of nanoencapsulation on the antiproliferative and differentiation properties of tretinoin was studied on human myeloid leukemia cells (HL60 cells) showing that tretinoin-loaded lipid-core nanocapsules presents a longer antitumor efficiency compared to the free tretinoin.
  • These results allow us to propose the current formulation (tretinoin-loaded lipid-core nanocapsules) as a promising parenteral nanomedicine for the treatment of acute promyelocytic leukaemia.

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  • (PMID = 21179938.001).
  • [ISSN] 1550-7033
  • [Journal-full-title] Journal of biomedical nanotechnology
  • [ISO-abbreviation] J Biomed Nanotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lipids; 0 / Nanocapsules; 5688UTC01R / Tretinoin
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91. Benjazia E, Khalifa M, Benabdelkader A, Laatiri A, Braham A, Letaief A, Bahri F: Granulocytic sarcoma of the rectum: Report of one case that presented with rectal bleeding. World J Gastrointest Pathophysiol; 2010 Oct 15;1(4):144-6

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  • It may present in association with acute myeloid leukaemia, myelodysplastic syndrome and chronic myelogenous leukaemia.
  • We report on the case of a 17 year old female who presented with rectal bleeding, abdominal pain and weight loss one mo prior to admission.
  • Bone marrow examination was compatible with acute promyelocytic leukaemia (FAB type M3).
  • This case report is a reminder of this peculiar sign of tumoral syndrome in acute myeloid leukaemia.
  • We also discuss diagnostic methods and analyze the disease course.

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  • [Cites] Gastroenterol Clin Biol. 1999 Jun-Jul;23(6-7):779-82 [10470535.001]
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  • (PMID = 21607155.001).
  • [ISSN] 2150-5330
  • [Journal-full-title] World journal of gastrointestinal pathophysiology
  • [ISO-abbreviation] World J Gastrointest Pathophysiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC3097956
  • [Keywords] NOTNLM ; Acute myeloid leukaemia / Chemotherapy / Gastrointestinal bleeding / Granulocytic sarcoma / Rectum
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92. Goebeler V, Ruhe D, Gerke V, Rescher U: Annexin A8 displays unique phospholipid and F-actin binding properties. FEBS Lett; 2006 May 1;580(10):2430-4
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  • [Title] Annexin A8 displays unique phospholipid and F-actin binding properties.
  • Initially only identified at the cDNA level it had been tentatively linked to acute promyelocytic leukaemia (APL) due to its high and regulated expression in APL-derived cells.
  • [MeSH-major] Actins / metabolism. Annexins / metabolism. Phospholipids / metabolism

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  • (PMID = 16638567.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Actins; 0 / Annexins; 0 / Phospholipids; SY7Q814VUP / Calcium
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93. Pession A, Rondelli R, Basso G, Rizzari C, Testi AM, Fagioli F, De Stefano P, Locatelli F, AML Strategy & Study Committee of the Associazione Italiana di Ematologia e Oncologia Pediatrica (AIEOP): Treatment and long-term results in children with acute myeloid leukaemia treated according to the AIEOP AML protocols. Leukemia; 2005 Dec;19(12):2043-53
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  • [Title] Treatment and long-term results in children with acute myeloid leukaemia treated according to the AIEOP AML protocols.
  • Since 1982, four consecutive studies on childhood acute myeloid leukaemia (AML) (namely LAM-82, -87, -87M and -92) have been conducted in Italy by the Associazione Italiana di Ematologia e Oncologia Pediatrica (AIEOP) group.
  • The induction therapy of the first three studies consisted of daunorubicin and cytarabine structured in a 3+7 backbone.
  • Patients with acute promyelocytic leukaemia (20% of diagnoses) were included in LAM-87 and 87M studies.
  • The long-term outcome of patients enrolled in the LAM-82, 87 and 87M studies was comparable, whereas that of children treated according to LAM-92 study was significantly better (P<0.005).
  • Patients enrolled in the LAM-92 study were stratified in standard and high-risk groups with different outcome (67 vs 47%, respectively, P=0.04).
  • Altogether, the results obtained in these four studies have permitted a progressive refinement of treatment, contributing to the structure of the ongoing LAM-2002 protocol that stratifies patients according to the presence of definite genetic anomalies and response to induction therapy.
  • [MeSH-major] Antineoplastic Protocols / standards. Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Infant. Infant, Newborn. Male. Remission Induction / methods. Survival Analysis. Treatment Outcome

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  • (PMID = 16107897.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
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94. Proietti L, Visalli R, Cultrera M, Romeo G, Libra M, Travali S, Duscio D: [In vitro exposure of U937 cells to potassium dichromate: study of apoptosis]. G Ital Med Lav Ergon; 2005 Jan-Mar;27(1):35-8
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  • For this reason we have utilised U937 cells, a cellular line derived from acute promyelocytic leukaemia.
  • Our results show that the minimum concentration of potassium dichromate induces apoptosis in the U937 cells and is of 600 microM, already after 12 hours, the cells treated with potassium dichromate with a concentration of 500 microM presented an apoptosis of 27% while the respective control showed a base apoptosis of 9.5%.

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  • (PMID = 15915672.001).
  • [ISSN] 1592-7830
  • [Journal-full-title] Giornale italiano di medicina del lavoro ed ergonomia
  • [ISO-abbreviation] G Ital Med Lav Ergon
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] T4423S18FM / Potassium Dichromate
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95. Jeddi R, Hdiji S, Kacem K, Ben Lakhal R, Aissaoui L, Ben Abid H, Belhadj Ali Z, Meddeb B: [Therapeutic results with apl 93 protocol in acute promyelocytic leukemia (34 cases)]. Tunis Med; 2006 Nov;84(11):717-20
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  • [Title] [Therapeutic results with apl 93 protocol in acute promyelocytic leukemia (34 cases)].
  • BACKGROUND: Acute promyelocytic leukaemia (APL) account for approximately 10% to 15% of all AML in most reports.
  • Clinical features includes the presence in 80% to 90% of patients of a severe hemorrhagic syndrome, a specific balanced translocation between chromosomes 15 and 17 with a fusion of a large pert of the retinoic acid receptor a gene (RARa) on chromosome 17 to a part of the promyelocytic leukaemia (PML) gene on chromosome 15.
  • AIM: of the study was to assess of the therapeutic management of APL 93 protocol in acute promyelocytic leukemia.
  • METHODS: We present here the results of a retrospective study concerning 34 patients with APL included between 1998 and 2004 in the APL 93 protocol : 20 in group B and 14 in group C.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Anthracyclines / administration & dosage. Child. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Female. Humans. Male. Middle Aged. Pilot Projects. Receptors, Retinoic Acid. Remission Induction. Retrospective Studies. Survival Analysis. Translocation, Genetic. Tretinoin / administration & dosage. Tunisia

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  • (PMID = 17294898.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Multicenter Study
  • [Publication-country] Tunisia
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
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96. Fischer S, Kohlhase J, Böhm D, Schweiger B, Hoffmann D, Heitmann M, Horsthemke B, Wieczorek D: Biallelic loss of function of the promyelocytic leukaemia zinc finger (PLZF) gene causes severe skeletal defects and genital hypoplasia. J Med Genet; 2008 Nov;45(11):731-7
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  • [Title] Biallelic loss of function of the promyelocytic leukaemia zinc finger (PLZF) gene causes severe skeletal defects and genital hypoplasia.
  • We present a patient with similar clinical findings, in addition to absence of the thumbs, hypoplasia of the radii and ulnae, additional vertebrae and ribs, retarded bone age and genital hypoplasia.
  • RESULTS: The patient has an approximately 8 Mbp de novo deletion on the paternal chromosome 11, which includes the promyelocytic leukaemia zinc-finger gene (PLZF, ZBTB16; OMIM 176797).
  • Taking into account specific alpha-helical propensities of Val and Met, this mutation is likely to destabilise the alpha helix of the zinc finger that forms the contact with the DNA duplex, thus affecting the biological function as shown by reporter-gene assays.
  • DISCUSSION: The PLZF gene is one of five partners fused to the retinoic acid receptor alpha in acute promyelocytic leukaemia.
  • We describe the first patient, to our knowledge, with a germline mutation of PLZF.
  • Furthermore, this case highlights the importance of searching for a recessive mutation on the non-deleted chromosome in patients with a microdeletion and atypical clinical findings.


97. Park SJ, Kim M, Kim NH, Oh MK, Cho JK, Jin JY, Kim IS: Auranofin promotes retinoic acid- or dihydroxyvitamin D3-mediated cell differentiation of promyelocytic leukaemia cells by increasing histone acetylation. Br J Pharmacol; 2008 Jul;154(6):1196-205
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  • [Title] Auranofin promotes retinoic acid- or dihydroxyvitamin D3-mediated cell differentiation of promyelocytic leukaemia cells by increasing histone acetylation.
  • BACKGROUND AND PURPOSE: To investigate the molecular mechanism for the effect of auranofin on the induction of cell differentiation, the cellular events associated with differentiation were analysed in acute promyelocytic leukaemia (APL) cells.
  • EXPERIMENTAL APPROACH: The APL blasts from leukaemia patients and NB4 cells were cotreated with auroanofin and all-trans-retinoic acid (ATRA) at suboptimal concentration.
  • KEY RESULTS: Treatment with auroanofin and ATRA cooperatively induced granulocytic differentiation of fresh APL blasts isolated from patients and NB4 cells.
  • The combined treatment also increased reorganization of nuclear PML bodies and histone acetylation at the promoter of the RARbeta2 gene.
  • Consistent with this, the expressions of p21, p27 and PTEN were increased and the levels of cyclin A, Cdk2 and Cdk4 were decreased.
  • CONCLUSIONS AND IMPLICATIONS: These findings indicate that auroanofin in combination with low doses of either ATRA or 1,25(OH)2 vit D3 promotes APL cell differentiation by enhancing histone acetylation and the expression of differentiation-associated genes.

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  • (PMID = 18500361.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Chromatin; 0 / Histones; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 0 / retinoic acid receptor beta; 3H04W2810V / Auranofin; 5688UTC01R / Tretinoin; EC 3.6.5.2 / Oncogene Protein p21(ras); FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ PMC2483395
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98. Glynn RW, Miller N, Kerin MJ: 17q12-21 - the pursuit of targeted therapy in breast cancer. Cancer Treat Rev; 2010 May;36(3):224-9
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  • Research has since focused on the area of chromosome 17 in which HER2/neu is located in order to identify other genes in the vicinity.
  • EXPERIMENTAL DESIGN: This review discusses the evidence in relation to 4 genes located at the HER2/neu amplicon, namely TOP2A, GRB7, STARD3 and RARA.
  • STARD3 and RARA also hold clinical relevance, the former having been shown to function in steroidogenesis and therefore implicated in hormone-receptor-positive breast cancer.
  • Finally, RARA may be the key to unlocking the problem of resistance to all-trans retinoic acid (ATRA) in breast cancer sufferers; this treatment has previously been demonstrated to induce remission in over 80% of patients with acute promyelocytic leukaemia (APML).
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / therapy. Chromosomes, Human, Pair 17 / genetics. Gene Targeting
  • [MeSH-minor] Antigens, Neoplasm / physiology. Carrier Proteins / physiology. DNA Topoisomerases, Type II / physiology. DNA-Binding Proteins / physiology. Female. GRB7 Adaptor Protein / physiology. Humans. Membrane Proteins / physiology. Receptors, Retinoic Acid / physiology

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  • [Copyright] Copyright 2009. Published by Elsevier Ltd.
  • (PMID = 20100636.001).
  • [ISSN] 1532-1967
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Carrier Proteins; 0 / DNA-Binding Proteins; 0 / GRB7 protein, human; 0 / Membrane Proteins; 0 / Receptors, Retinoic Acid; 0 / STARD3 protein, human; 0 / retinoic acid receptor alpha; 149058-53-7 / GRB7 Adaptor Protein; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Number-of-references] 58
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99. Olwill SA, McGlynn H, Gilmore WS, Alexander HD: Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines. Thromb Res; 2005;115(1-2):109-14
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  • [Title] Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines.
  • INTRODUCTION: Acute promyelocytic leukaemia (APL) (M3) is associated with both a characteristic t(15;17) and severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • MATERIALS AND METHODS: This study examined the level of annexin II cell surface and mRNA expression in a range of acute myeloid leukaemia (AML) cell lines.
  • The evidence that annexin II levels are higher in APL would lend support to the hypothesis that the bleeding disorder seen in APL is caused by hyperfibrinolysis.
  • RESULTS: Cell surface annexin II was found to be expressed at higher levels on NB4 (promyelocytic) cells than on either KG1a (early myeloid) or HL60 (myelocytic) cells.
  • However, even higher levels were found on U937 and MM6 (histo-monocytic) and HEL (erythroid) cells (p<0.01).
  • CONCLUSIONS: These findings do not fully support the concept of the coagulopathy associated with APL being caused by hyperfibrinolysis alone.
  • Further investigations are required to identify the significance of annexin II expression and regulation in leukaemia.
  • [MeSH-major] Annexin A2 / genetics. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / complications. RNA, Messenger / analysis

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  • (PMID = 15567461.001).
  • [ISSN] 0049-3848
  • [Journal-full-title] Thrombosis research
  • [ISO-abbreviation] Thromb. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANXA2 protein, human; 0 / Annexin A2; 0 / Membrane Proteins; 0 / RNA, Messenger
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100. Ellis R, Boggild M: Therapy-related acute leukaemia with Mitoxantrone: what is the risk and can we minimise it? Mult Scler; 2009 Apr;15(4):505-8
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute leukaemia with Mitoxantrone: what is the risk and can we minimise it?
  • BACKGROUND: Therapy-related acute leukaemia (TRAL) is a concern for neurologists and patients when considering treatment with Mitoxantrone for multiple sclerosis (MS).
  • RESULTS: Case-series including 5472 patients were identified; mean dose of Mitoxantrone was 74.2 mg/m(2) (range:12-120 mg/m(2)).
  • Acute Myelocytic Leukaemia and Acute Promyelocytic Leukaemia represented 46.4% each of the leukaemia subtypes.
  • Over 80% of cases occurred in patients exposed to >60 mg/m(2), with a relative risk of 1.44 (CI95%:1.18-1.70) when comparing total dose >60 mg/m(2) against <60 mg/m(2) strongly suggesting a relationship between risk of TRAL and total dose.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / epidemiology. Mitoxantrone / adverse effects. Multiple Sclerosis / drug therapy. Multiple Sclerosis / epidemiology
  • [MeSH-minor] Acute Disease. Adult. Databases, Factual. Female. Humans. Leukemia, Promyelocytic, Acute / chemically induced. Leukemia, Promyelocytic, Acute / epidemiology. Male. Middle Aged. Risk Factors

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
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  • (PMID = 19251838.001).
  • [ISSN] 1352-4585
  • [Journal-full-title] Multiple sclerosis (Houndmills, Basingstoke, England)
  • [ISO-abbreviation] Mult. Scler.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone
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