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1. Wang ZY, Chen Z: Acute promyelocytic leukemia: from highly fatal to highly curable. Blood; 2008 Mar 1;111(5):2505-15
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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 leukemia: from highly fatal to highly curable.
  • Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia.
  • Morphologically, it is identified as the M3 subtype of acute myeloid leukemia by the French-American-British classification and cytogenetically is characterized by a balanced reciprocal translocation between chromosomes 15 and 17, which results in the fusion between promyelocytic leukemia (PML) gene and retinoic acid receptor alpha (RARalpha).
  • It seems that the disease is the most malignant form of acute leukemia with a severe bleeding tendency and a fatal course of only weeks.
  • Chemotherapy (CT; daunorubicin, idarubicin and cytosine arabinoside) was the front-line treatment of APL with a complete remission (CR) rate of 75% to 80% in newly diagnosed patients.
  • Since the introduction of all-trans retinoic acid (ATRA) in the treatment and optimization of the ATRA-based regimens, the CR rate was raised up to 90% to 95% and 5-year disease free survival (DFS) to 74%.
  • The use of arsenic trioxide (ATO) since early 1990s further improved the clinical outcome of refractory or relapsed as well as newly diagnosed APL.
  • In this article, we review the history of introduction of ATRA and ATO into clinical use and the mechanistic studies in understanding this model of cancer targeted therapy.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18299451.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 111
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2. Testi AM, Al-Hadad SA, Al-Jadiry MF, Moleti ML, Mandelli F, Foà R: Impact of international collaboration on the prognosis of childhood acute promyelocytic leukemia in Iraq. Haematologica; 2006 Apr;91(4):509-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of international collaboration on the prognosis of childhood acute promyelocytic leukemia in Iraq.
  • As a consequence of a collaborative project between the Al Mansour Hospital for Pediatrics in Baghdad and the Pediatric Unit of Hematology of "La Sapienza" University, in Rome, in October 2003 a specific all-trans-retinoic acid-based protocol was designed in order to offer a modern therapeutic program for the management of Iraqi children with acute promyelocytic leukemia, adapted to the severe local difficulties.
  • The preliminary encouraging results represent a substantial improvement over the earlier experience in childhood acute promyelocytic leukemia in Iraq.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / therapy. Tretinoin / administration & dosage

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  • (PMID = 16533724.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
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3. Jul-Larsen A, Grudic A, Bjerkvig R, Bøe SO: Cell-cycle regulation and dynamics of cytoplasmic compartments containing the promyelocytic leukemia protein and nucleoporins. J Cell Sci; 2009 Apr 15;122(Pt 8):1201-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell-cycle regulation and dynamics of cytoplasmic compartments containing the promyelocytic leukemia protein and nucleoporins.
  • Nucleoporins and the promyelocytic leukemia protein (PML) represent structural entities of nuclear pore complexes and PML nuclear bodies, respectively.
  • In addition, these proteins might function in a common biological mechanism, because at least two different nucleoporins, Nup98 and Nup214, as well as PML, can become aberrantly expressed as oncogenic fusion proteins in acute myeloid leukemia (AML) cells.
  • Here we show that PML and nucleoporins become directed to common cytoplasmic compartments during the mitosis-to-G1 transition of the cell cycle.
  • These protein assemblies, which we have termed CyPNs (cytoplasmic assemblies of PML and nucleoporins), move on the microtubular network and become stably connected to the nuclear membrane once contact with the nucleus has been made.
  • The ability of PML to target CyPNs depends on its nuclear localization signal, and loss of PML causes an increase in cytoplasmic-bound versus nuclear-membrane-bound nucleoporins.
  • CyPNs are also targeted by the acute promyelocytic leukemia (APL) fusion protein PML-RARalpha and can be readily detected within the APL cell line NB4.
  • These results provide insight into a dynamic pool of cytoplasmic nucleoporins that form a complex with the tumor suppressor protein PML during the G1 phase of the cell cycle.

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  • (PMID = 19339552.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Nuclear Localization Signals; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Tubulin Modulators; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 143220-95-5 / PML protein, human; EC 2.3.1.48 / CREB-Binding Protein; SH1WY3R615 / Nocodazole
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4. Kogan SC: Curing APL: differentiation or destruction? Cancer Cell; 2009 Jan 6;15(1):7-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Curing APL: differentiation or destruction?
  • In a recent issue of Nature Medicine, Nasr et al. show that the effectiveness of all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia is independent of their ability to cause differentiation.
  • Targeted destruction of the PML-RARalpha oncoprotein appears key to eliminating the cells from which relapse can arise.
  • [MeSH-major] Cell Differentiation / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / pathology. Oncogene Proteins, Fusion / metabolism

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  • [CommentOn] Nat Med. 2008 Dec;14(12):1333-42 [19029980.001]
  • (PMID = 19111876.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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5. Minucci S, Pelicci PG: Determinants of oncogenic transformation in acute promyelocytic leukemia: the hetero-union makes the force. Cancer Cell; 2007 Jul;12(1):1-3
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  • [Title] Determinants of oncogenic transformation in acute promyelocytic leukemia: the hetero-union makes the force.
  • Acute promyelocytic leukemia (APL) is caused by chromosomal translocations that involve the retinoic acid receptor alpha (RAR) and several other genes to yield X-RAR fusion proteins.
  • Unlike wild-type RARs, which require heterodimerization with the retinoid X receptor (RXR) for their function as DNA-binding transcriptional regulators, X-RAR fusion proteins bind DNA and deregulate transcription as homo-oligomers.
  • In this issue of Cancer Cell, however, Zeisig et al. and Zhu et al. show that RXR recruitment is a critical determinant for the transforming potential of oligomeric X-RAR fusion proteins and explore the possibility for targeted interventions in APL with either RAR or RXR ligands.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Humans. Ligands. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors / metabolism

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  • [CommentOn] Cancer Cell. 2007 Jul;12(1):36-51 [17613435.001]
  • [CommentOn] Cancer Cell. 2007 Jul;12(1):23-35 [17613434.001]
  • (PMID = 17613430.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors
  • [Number-of-references] 10
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6. Salomoni P, Bernardi R, Bergmann S, Changou A, Tuttle S, Pandolfi PP: The promyelocytic leukemia protein PML regulates c-Jun function in response to DNA damage. Blood; 2005 May 1;105(9):3686-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The promyelocytic leukemia protein PML regulates c-Jun function in response to DNA damage.
  • The promyelocytic leukemia (PML) gene, a tumor suppressor inactivated in acute promyelocytic leukemia (APL), regulates apoptosis induced by DNA damage.
  • However, the molecular mechanisms by which PML modulates apoptosis following genotoxic stress are only partially elucidated.
  • PML is essential for p53-dependent induction of programmed cell death upon gamma-irradiation through PML-nuclear body (NB)-mediated control of p53 acetylation.
  • Here, we show that PML selectively regulates proapoptotic transcription factors upon different types of DNA damage.
  • We find that Pml inactivation protects fibroblasts from UV-induced apoptosis in a p53-independent manner.
  • We demonstrate that c-Jun is required for UV-induced apoptosis and that PML is essential for both c-Jun transcriptional activation and DNA binding upon UV radiation.
  • We find that PML physically interacts with c-Jun and that upon UV radiation the PML-NBs reorganize into novel nuclear microspeckled structures (UV-NBs), where PML and c-Jun dynamically accumulate.
  • These data identify a novel PML-dependent pathway for c-Jun transcriptional activation and induction of apoptosis in response to DNA damage and shed new light on the role of PML in tumor suppression.


7. Chattopadhyay A, Redner RL: Cryptic insertion of PML-RARA into the 3p25 locus in an acute promyelocytic leukemia with t(3;17)(p25;q21). Cancer Genet Cytogenet; 2010 Aug;201(1):28-31
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  • [Title] Cryptic insertion of PML-RARA into the 3p25 locus in an acute promyelocytic leukemia with t(3;17)(p25;q21).
  • We studied a case of a 72-year-old man with acute promyelocytic leukemia and a t(3;17)(p25;q21).
  • Fluorescence in situ hybridization failed to show rearrangement of the PML (promyelocytic leukemia protein) locus but did demonstrate relocalization of the retinoic acid receptor alpha (RARA) to chromosome 3.
  • Our analysis indicates that the fusion partner is PML.
  • This karyotype therefore results in a cryptic PML-RARA fusion inserted into the 3p25 locus.

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • [Cites] Genet Mol Res. 2009;8(1):1-7 [19224461.001]
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  • (PMID = 20633765.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA067346-09; United States / NCI NIH HHS / CA / R01 CA067346; United States / NCI NIH HHS / CA / R01 CA067346-09
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  • [Other-IDs] NLM/ NIHMS205381; NLM/ PMC2925300
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8. 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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9. Zák P, Korístek Z: [Relapse in acute promyelocytic leukemia and the role of hematopoietic stem cell transplantation in the treatment of APL]. Vnitr Lek; 2008 Jul-Aug;54(7-8):751-6
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  • [Title] [Relapse in acute promyelocytic leukemia and the role of hematopoietic stem cell transplantation in the treatment of APL].
  • [Transliterated title] Relaps akutní promyelocytárni leukemie a role transplantace krvetvorných kmenových bunek v terapii APL.
  • The authors focused on relapses and transplantation treatment in APL.
  • Considering treatment of relapses in APL, arsenic trioxide is now the standard treatment of APL relapse, however, treatment with gentuzumab ozogamicin should be considered when only a molecular relapse is detected.
  • The following part of the issue is focused on the current status of hematopoietic stem cell transplantation in APL and on indications of transplantations from a modern APL therapy point of view.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Promyelocytic, Acute / therapy

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  • (PMID = 18780574.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 36
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10. Matasar MJ, Ritchie EK, Consedine N, Magai C, Neugut AI: Incidence rates of acute promyelocytic leukemia among Hispanics, blacks, Asians, and non-Hispanic whites in the United States. Eur J Cancer Prev; 2006 Aug;15(4):367-70
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  • [Title] Incidence rates of acute promyelocytic leukemia among Hispanics, blacks, Asians, and non-Hispanic whites in the United States.
  • Despite significant improvements in the prognosis of acute promyelocytic leukemia brought about by therapeutic advances, understanding of the epidemiology of acute promyelocytic leukemia remains limited.
  • Earlier reports have suggested that Hispanics may have an increased incidence of acute promyelocytic leukemia, but no systematic analysis of national data has yet been reported.
  • We performed a retrospective cohort study, using data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute from 1992-2001 in order to compare leukemia incidence rates as a function of race and ethnicity.
  • We identified 709 cases of acute promyelocytic leukemia and analyzed incidence rates by race and sex.
  • Hispanics were not found to have greater lifetime incidence rates than whites, with an incidence relative rate (IRR) of 0.86 that of whites (P=0.17).
  • Blacks had lower lifetime incidence rates than non-Hispanic whites (IRR=0.75, P=0.04), Hispanics (IRR=0.64, P=0.007), and Asians (IRR=0.67, P=0.03).
  • These results indicate that while US Hispanics do not have greater lifetime incidence rates of acute promyelocytic leukemia, blacks have lower incidence rates of acute promyelocytic leukemia than Hispanics, non-Hispanic whites, and Asians.
  • [MeSH-major] African Americans / statistics & numerical data. Asian Continental Ancestry Group / statistics & numerical data. European Continental Ancestry Group / statistics & numerical data. Hispanic Americans / statistics & numerical data. Leukemia, Promyelocytic, Acute / epidemiology. Leukemia, Promyelocytic, Acute / ethnology

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  • (PMID = 16835508.001).
  • [ISSN] 0959-8278
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K05 CA89155; United States / NCI NIH HHS / CA / T-32 CA09529; United States / NCI NIH HHS / CA / U54 CA101388
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
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11. Rossi V, Levati L, Biondi A: Diagnosis and monitoring of PML-RARA-positive acute promyelocytic leukemia by qualitative RT-PCR. Methods Mol Med; 2006;125:115-26
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  • [Title] Diagnosis and monitoring of PML-RARA-positive acute promyelocytic leukemia by qualitative RT-PCR.
  • The t(15;17) is the diagnostic hallmark of acute promyelocytic leukemia (APL).
  • As a result, the RARA and the promyelocytic leukemia (PML) genes are fused.
  • The use of reverse-transcription polymerase chain reaction (RT-PCR) for the detection of the PML-RARA and RARA-PML fusion genes is the only technique that defines the PML breakpoint type and that allows the definition of a correct strategy for subsequent minimal residual disease (MRD) monitoring.
  • Standardized conditions for RT-PCR analysis of fusion transcripts from chromosome aberrations in acute leukemia, including APL, have recently been reported in the context of the Biomed-1 Concerted Action, and are described in detail in this chapter.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Gene Expression Profiling / methods. Humans. Monitoring, Physiologic / methods. Neoplasm, Residual / genetics. Translocation, Genetic

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  • (PMID = 16502581.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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12. Quimby BB, Yong-Gonzalez V, Anan T, Strunnikov AV, Dasso M: The promyelocytic leukemia protein stimulates SUMO conjugation in yeast. Oncogene; 2006 May 18;25(21):2999-3005
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  • [Title] The promyelocytic leukemia protein stimulates SUMO conjugation in yeast.
  • The promyelocytic leukemia gene was first identified through its fusion to the gene encoding the retinoic acid receptor alpha (RARalpha) in acute promyelocytic leukemia (APL) patients.
  • The promyelocytic leukemia gene product (PML) becomes conjugated in vivo to the small ubiquitin-like protein SUMO-1, altering its behavior and capacity to recruit other proteins to PML nuclear bodies (PML-NBs).
  • In the NB4 cell line, which was derived from an APL patient and expresses PML:RARalpha, we observed a retinoic acid-dependent change in the modification of specific proteins by SUMO-1.
  • To dissect the interaction of PML with the SUMO-1 modification pathway, we used the budding yeast Saccharomyces cerevisiae as a model system through expression of PML and human SUMO-1 (hSUMO-1).
  • We found that PML stimulated hSUMO-1 modification in yeast, in a manner that was dependent upon PML's RING-finger domain.
  • PML:RARalpha also stimulated hSUMO-1 conjugation in yeast.
  • Interestingly, however, PML and PML:RARalpha differentially complemented yeast Smt3p conjugation pathway mutants.
  • These findings point toward a potential function of PML and PML:RARalpha as SUMO E3 enzymes or E3 regulators, and suggest that fusion of RARalpha to PML may affect this activity.
  • [MeSH-minor] Amino Acid Substitution. Cell Cycle Proteins / metabolism. Cell Line, Tumor / drug effects. Cytoskeletal Proteins / metabolism. Genetic Complementation Test. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Multiprotein Complexes / biosynthesis. Mutagenesis, Site-Directed. Nocodazole / pharmacology. Protein Structure, Tertiary. Recombinant Fusion Proteins / physiology. Repressor Proteins / genetics. Repressor Proteins / physiology. SUMO-1 Protein. Saccharomyces cerevisiae / metabolism. Saccharomyces cerevisiae Proteins / genetics. Saccharomyces cerevisiae Proteins / metabolism. Saccharomyces cerevisiae Proteins / physiology. Species Specificity. Transfection. Tretinoin / pharmacology. Ubiquitin-Protein Ligases / metabolism

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  • (PMID = 16501610.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 HD001902-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDC11 protein, S cerevisiae; 0 / Cell Cycle Proteins; 0 / Cytoskeletal Proteins; 0 / Multiprotein Complexes; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins; 0 / Repressor Proteins; 0 / SMT3 protein, S cerevisiae; 0 / SUMO-1 Protein; 0 / SUMO1 protein, human; 0 / Saccharomyces cerevisiae Proteins; 0 / Siz2 protein, S cerevisiae; 0 / Small Ubiquitin-Related Modifier Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 143220-95-5 / PML protein, human; 5688UTC01R / Tretinoin; EC 6.3.2.19 / Siz1 protein, S cerevisiae; EC 6.3.2.19 / Ubiquitin-Protein Ligases; SH1WY3R615 / Nocodazole
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13. Zhu HH, Liu YR, Qin YZ, Jiang B, Shan FX, Wu SL, Yang PD, Zhao J, Lu DP: Detecting PML-RARalpha transcript in acute promyelocytic leukemia using real-time quantitative RT-PCR. Chin Med J (Engl); 2007 Oct 20;120(20):1803-8
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  • [Title] Detecting PML-RARalpha transcript in acute promyelocytic leukemia using real-time quantitative RT-PCR.
  • BACKGROUND: Real-time quantitative RT-PCR (RQ-PCR) assay has become a vital tool to monitor residual disease of leukemia.
  • However, the complexity and standardization of RQ-PCR should never be overlooked and the results should be interpreted cautiously in clinical conditions.
  • We aimed to assess the methodology of RQ-PCR and its clinical applications in monitoring molecular kinetics of 36 newly diagnosed cases of acute promyelocytic leukemia patients with t (15;.
  • 17) from October 2004 to December 2005.
  • The quantitation of PML-RARalpha transcripts was represented by the normalized quotient, that is, PML-RARalpha transcript copies divided by ABL transcript copies.
  • RESULTS: The sensitivity of RQ-PCR was 1 per 10(5) cells and 5 copies of the PML-RARalpha transcript could be reproducibly detected.
  • No false positive results occurred in 40 non-acute promyelocytic leukemia samples.
  • Compared with pretreatment, median reduction of the PML-RARalpha transcript before first consolidation therapy differed significantly between group 1 and group 2 (log scale, 3.15 vs 2.31, P = 0.024).
  • Interestingly, we found that PML-RARalpha transcript levels temporarily increased in bone marrow (7 patients) and peripheral blood (22 patients) samples of patients during induction therapy in both groups.
  • CONCLUSIONS: The RQ-PCR assay is reliable for the detection of PML-RARalpha transcripts.
  • Arsenics, all-trans retinoic acid and mitoxantrone triad induction treatment of acute promyelocytic leukemia is superior to two-drug combination induction therapy in terms of the molecular response.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18028775.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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14. Yamano T, Yokote T, Akioka T, Hara S, Oka T, Tsuji M, Hanafusa T: [Acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3]. Rinsho Ketsueki; 2006 Jan;47(1):23-5
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  • [Title] [Acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3].
  • A 77-year-old man suffered from acute pancreatitis during the treatment of relapsed acute promyelocytic leukemia with As2O3.
  • Pancreatic enzyme levels were elevated and the computed tomography scan of the abdomen showed swelling of the pancreas.
  • As acute pancreatitis due to As2O3 was suspected, As2O3 was discontinued.
  • Acute pancreatitis should be considered as a possible complication during treatment with As2O3.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Arsenicals / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects. Pancreatitis / chemically induced
  • [MeSH-minor] Acute Disease. Humans. Male. Recurrence

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  • (PMID = 16479979.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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15. Lee GY, Christina S, Tien SL, Ghafar AB, Hwang W, Lim LC, Lim TH: Acute promyelocytic leukemia with PML-RARA fusion on i(17q) and therapy-related acute myeloid leukemia. Cancer Genet Cytogenet; 2005 Jun;159(2):129-36
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  • [Title] Acute promyelocytic leukemia with PML-RARA fusion on i(17q) and therapy-related acute myeloid leukemia.
  • We describe a patient with acute promyelocytic leukemia (APL) and the karyotype 46,XX,i(17)(q10) with PML-RARA fusion gene detected by fluorescence in situ hybridization (FISH) and nested reverse transcriptase-polymerase chain reaction (RT-PCR).
  • FISH using dual-color translocation probes for PML (promyelocytic leukemia) and RARA (retinoic acid receptor-alpha) showed fusion signal for PML-RARA on both arms of i(17q).
  • The patient attained complete remission (CR) with all-trans retinoic acid treatment and became PML-RARA negative.
  • One year later, while PML-RARA negative on FISH and RT-PCR, the patient presented with thrombocytopenia.
  • Bone marrow examination suggested an acute monoblastic leukemia (AML-M5a) including the karyotype 46,XX,t(8;16) (p11.2;p13.3),inv(11)(p15q22 approximately q23)[11]/47,idem,+i(8)(q10)[9].
  • The occurrence of therapy related acute leukemia after successful therapy for APL is an emerging problem.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Chromosomes, Human, Pair 17. Isochromosomes. Leukemia, Monocytic, Acute / chemically induced. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Receptors, Retinoic Acid / genetics. Tretinoin / adverse effects

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  • (PMID = 15899384.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human; 5688UTC01R / Tretinoin
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16. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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17. 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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18. 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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19. 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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20. 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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21. Plummer R, Hayward L, Lorigan P, Soriano V, Moiseyenko V, Szyldergemajn S, Prados R, Smyth J, Calvert H: Plitidepsin alone or with dacarbazine (DTIC) as first-line treatment for advanced unresectable melanoma (AUM). J Clin Oncol; 2009 May 20;27(15_suppl):9059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DTIC alone had a 8-15% response rate (RR), while plitidepsin (Aplidin [APL]) showed a 6% RR and a 14% stable disease (SD) in a Phase (Ph) II study in 35 relapsed/refractory pts after DTIC failure.
  • Furthermore, APL + DTIC has additive activity in preclinical models.
  • METHODS: This multicenter Ph Ib study aim to determine the safe recommended dose (RD) of APL on days 1, 8 & 15 + DTIC only day 1 q4wk.
  • Most pts (96%) had metastasis with a median of 2 sites involved (1-5).
  • Dose levels of APL + DICT (mg/m<sup>2</sup>), were: DL1 (1.8 + 800), 7 pts; DL2 (2.4 + 800), 8 pts; DL 2b (2.4 + 1000), 5 pts; DL3 (3.0 + 800), 8 pts.
  • There were 3 partial responses (PR, 14%) and 4 SD > 3 months (19%); all PR at DL2/3.
  • Five pts were not evaluable, 2 pts had G3 hypersensitivity reactions related to Cremophor oil (APL formulation) and 1 pt had a idiosyncratic reaction to DTIC with prolonged pancytopenia.
  • One pt had a wrong diagnosis and 1 pt had early progressive disease (PD).
  • CONCLUSIONS: APL + DTIC can be safely combined at ≥ 70% of their respective single- agent RD in AUM.
  • Ph Ib showed 14 % PR and 19% clinically meaningful SD.
  • A randomised Ph II study of DTIC + APL vs APL alone is ongoing.

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  • (PMID = 27962154.001).
  • [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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22. Bloomfield CD: Importance of genetic heterogeneity in curing adult acute leukemia (AL). J Clin Oncol; 2009 May 20;27(15_suppl):s1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. Gregory J, Feusner J: Acute promyelocytic leukemia in childhood. Curr Oncol Rep; 2009 Nov;11(6):439-45
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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 leukemia in childhood.
  • Acute promyelocytic leukemia (APL) is a relatively rare form of acute myelogenous leukemia (AML).
  • In the United States, APL in children constitutes only 5% to 10% of AML.
  • Molecularly, the disease is characterized by a fusion protein, promyelocytic leukemia (PML)-retinoic acid receptor (RAR)-alpha that results from a balanced reciprocal translocation between the PML gene on chromosome 15 and the RAR-alpha (RARA) gene on chromosome 17.
  • A major advance in the field of APL treatment has been the use of all-trans-retinoic acid (ATRA).
  • Advances in the treatment of APL have taken this form of AML from a disease with significant morbidity and mortality to one with an excellent outcome.
  • Recent trials have shown a role for arsenic trioxide in both newly diagnosed and relapsed APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Anthracyclines / therapeutic use. Child. Child, Preschool. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Humans. Prognosis. Translocation, Genetic

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  • (PMID = 19840521.001).
  • [ISSN] 1534-6269
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 47
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24. Qiu HR, Li JY, Zhu Y, Hong M, Wang R, Xu W: [A case of acute promyelocytic leukemia with double ider (17q-)]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Dec;15(6):1309-11
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  • [Title] [A case of acute promyelocytic leukemia with double ider (17q-)].
  • This study reported a relapsed case of acute promyelocytic leukemia with complex chromosomal aberrations of double ider (17q-) and explored its laboratory and clinical features.
  • In conclusion, double ider (17q-) is a rare additional abnormality in APL patients; combination of FISH with M-FISH techniques is a reliable way to identify such complicated chromosomal aberrations.

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  • (PMID = 18088491.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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25. Ganzitti L, Fachechi G, Driul L, Marchesoni D: Acute promyelocytic leukemia during pregnancy. Fertil Steril; 2010 Nov;94(6):2330.e5-6
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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 leukemia during pregnancy.
  • OBJECTIVE: To report our experience about a woman with acute promyelocytic leukemia (APL) during pregnancy.
  • PATIENT(S): A 32-year-old-woman, gravida 2, para 1, at the 25th week of pregnancy with a diagnosis of APL.
  • The mother is now undergoing the third and last consolidation step with good results, and APL is in remission.
  • CONCLUSION(S): In cases of APL during the second and third trimesters, the modern chemotherapy associated with close monitoring of maternal and fetal well-being could ensure a good outcome for both the mother and the baby.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Pregnancy Complications, Neoplastic / diagnosis

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  • [Copyright] Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20447623.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 7S5I7G3JQL / Dexamethasone; ZRP63D75JW / Idarubicin
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26. Wei H, Tian Z, Wang XJ, Liu KQ, Zhang CP, Wang HJ, Mi YC, Wang JX: [Acute promyelocytic leukemia with CD59 deficiency]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1105-8
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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 leukemia with CD59 deficiency].
  • The study was aimed to investigate whether CD59 is deficient in acute promyelocytic leukemia (APL) blast cells.
  • Expression of CD59 on APL blast cells was analysed by flow cytometry.
  • The results showed that the deficiency of CD59 expression in 12 out of 19 APL samples was found, its incidence was significantly higher than that in other acute myeloid leukemia (AML) samples (deficiency of CD59 expression in 14 of 40 non-APL AML samples, p=0.042).
  • The expression of CD59 became normal after the patients achieved complete remission (CR), which indicated that the deficient of CD59 expression was only found in APL blast cells, but also found in APL cell line NB4 cells.
  • Sequencing pig-A gene coding region of NB4 cells and one APL patient with deficiency of CD59 displayed that the mutation of pig-A gene was not observed, therefore the deficiency of CD59 expression in APL cells did not result from mutation of pig-A gene.
  • It is concluded that the deficiency of CD59 expression exists in APL blast cells more probably.

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  • (PMID = 21129240.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD59; 0 / Membrane Proteins; 0 / phosphatidylinositol glycan-class A protein; 5688UTC01R / Tretinoin
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27. Worch J, Ritter J, Frühwald MC: Presentation of acute promyelocytic leukemia as granulocytic sarcoma. Pediatr Blood Cancer; 2008 Mar;50(3):657-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Presentation of acute promyelocytic leukemia as granulocytic sarcoma.
  • Granulocytic sarcoma (GS) is a localized tumor composed of immature myeloid cells.
  • This extramedullary tumor can present before, concurrent with or after the diagnosis of acute myeloid leukemia.
  • GS is extremely uncommon in acute promyelocytic leukemia (APL).
  • As a proportion of patients never develop systemic disease, correct and timely diagnosis may be rather difficult, but is a prerequisite for optimal outcome.
  • GS should be considered in the differential diagnosis of children with unusual bone lesions.
  • We describe a patient with GS who presented with symptoms mimicking osteomyelytis or rheumatoid disease.
  • [MeSH-major] Diagnostic Errors. Leukemia, Promyelocytic, Acute / complications. Sarcoma, Myeloid / etiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arthritis, Psoriatic / diagnosis. Biomarkers, Tumor / analysis. Female. Humans. Oncogene Proteins, Fusion / analysis. Osteolysis / etiology. Osteomyelitis / diagnosis. Remission Induction. Shoulder Pain / etiology. Tretinoin / administration & dosage

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17437290.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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28. Xue J, Lin MF: [Expression of survivin gene in NB4 cell line and cells of acute promyelocytic leukemia and its anti-apoptosis and clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):332-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of survivin gene in NB4 cell line and cells of acute promyelocytic leukemia and its anti-apoptosis and clinical significance].
  • The study was aimed to detect expression rate of survivin gene in APL cell and to explore the relationship between its expression and clinical manifestation.
  • PML/RARalpha and survivin mRNA expression were analyzed by using reverse transcriptase polymerase chain reaction (RT-PCR) technique.
  • By treatment with ATRA, survivin mRNA expression in NB4 cell gradually decreased along with time delay and almost could not be detected at the 72th hour. (2) the positive and negative rate of survivin mRNA expression was 67% and 33% respectively, while in all 36 cases of de novo and relapse APL patients, the PML/RAR(alpha) fusion gene expression was positive.
  • In 22 cases at remission stage, the PML/RARalpha fusion gene expression was negative, and the positive and negative rate of survivin mRNA expression was 36% and 64% respectively.
  • The survivin mRNA expression positive rates in the de novo group, relapse group and PML/RARalpha fusion gene L-type positive group were obviously higher than those in remission period group (P < 0.05) and were significantly lower than those in acute leukemia group (P < 0.05, < 0.001). (3) whether the survivin mRNA expression was positive or negative in 36 cases of de novo and relapse APL patients, all the 36 cases could obtain complete remission.
  • 4 APL patients with positive expression of survivin mRNA had DIC and serious infection (one patient died).
  • The clinical symptom showed slight skin or mucosa bleeding, fever and asthenic in the patients with negative expression of survivin mRNA.
  • When 2 APL patients with positive expression of survivin mRNA had been treated with ATRA, induction differentiation sign in their peripheral blood and bone marrow figures was not obvious.
  • It is concluded that the survivin gene positive expression rate is lower in acute promyelocytic leukemia than that in any other types of leukemia and is related to clinical manifestation.

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  • (PMID = 16638209.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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29. Kaito K, Katayama T, Masuoka H, Nishiwaki K, Sano K, Sekiguchi N, Hagino T, Kobayashi M: CD2+ acute promyelocytic leukemia is associated with leukocytosis, variant morphology and poorer prognosis. Clin Lab Haematol; 2005 Oct;27(5):307-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD2+ acute promyelocytic leukemia is associated with leukocytosis, variant morphology and poorer prognosis.
  • The T cell-lineage marker CD2 is sometimes expressed in acute promyelocytic leukemia (APL), and CD2 expression is reported to correlate with some clinical characteristics.
  • However, the significance of CD2 expression in APL has not been fully elucidated.
  • We evaluated CD2 expression in APL treated by the same treatment strategy in a single institute, and whether it had any special characteristics.
  • Among 29 APL, 6 were positive for CD2.
  • Patients with CD2+ APL tended to have a higher leukocyte count than CD2- APL (34.5 +/- 13.1/l vs. 6.8 +/- 2.1/l), morphological characteristics as variant-APL (50 vs. 0%).
  • They also showed poor clinical prognosis.
  • The CR rate of CD2- APL was 87.0% while that of CD2+ APL was 50 %.
  • The mortality was 13.0 and 66.7%, respectively, and the survival rate was significantly lower in CD2+ APL.
  • CD2 expression was proven to be a risk factor associated with death in addition to the morphological characteristics of variant-APL and leukocytosis.
  • These results indicated that CD2 expression might have a significant impact on the prognosis of APL.
  • Whether CD2+ APL should be characterized as a special clinical entity should be discussed in a larger patient population.
  • [MeSH-major] Antigens, CD2 / analysis. Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 16178910.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD2; 0 / Antigens, Neoplasm
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30. Oravcova I, Czako B, Demeckova E, Demitrovicova L, Greksak R, Kotoucek P, Mego M, Mikuskova E, Richterova K, Al Sabti F, Mistrik M: Treatment of newly diagnosed patients with acute promyelocytic leukemia with modified spanish treatment protocol. Neoplasma; 2010;57(3):270-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of newly diagnosed patients with acute promyelocytic leukemia with modified spanish treatment protocol.
  • The results of treatment of acute promyelocytic leukemia, when combination ATRA + chemotherapy is used in induction and maintainance therapy and risk adapted strategy applied in consolidation, improved at present time.
  • Enhanced supportive therapy also contribute to improved outcome of APL patients.
  • 3 - year relapse free, overall survival and clinical and biological presenting features of APL patients were evaluated.
  • 29 (90.6%) patients achieved complete hematologic remission, 2 (6.3 %) molecular relapses were observed, death was observed in 4 patients (12.5%).
  • Survival results correspond with other published clinical studies.
  • Current recommendations for treatment with risk-adapted strategy for patients with newly diagnosed acute promyelocytic leukemia resulted in our patients group to comparable outcome and good compliance like in other published studies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 20353280.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
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31. Hu J, Zhou GB, Wang ZY, Chen SJ, Chen Z: Mutant transcription factors and tyrosine kinases as therapeutic targets for leukemias: from acute promyelocytic leukemia to chronic myeloid leukemia and beyond. Adv Cancer Res; 2007;98:191-220
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutant transcription factors and tyrosine kinases as therapeutic targets for leukemias: from acute promyelocytic leukemia to chronic myeloid leukemia and beyond.
  • Mutations in transcription factors (TFs) and protein tyrosine kinases (PTKs), which result in inhibition of differentiation/apoptosis or enhanced proliferative/survival advantage of hematopoietic stem/progenitor cells, are two classes of the most frequently detected genetic abnormalities in leukemias.
  • The great success of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) in treating acute promyelocytic leukemia through modulation of the causative PML-RARalpha oncoprotein represents the first two paradigms of mutant TFs-targeting therapeutic strategies for leukemia.
  • More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.
  • Thus to further improve clinical outcome of leukemia patients, elucidation of pathogenesis of leukemia, screening for oncoprotein-targeting small molecules, as well as rationally designed combination of drugs with potential synergy are of importance.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Mutation / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Transcription Factors / antagonists & inhibitors


32. Kim M, Lim J, Kim Y, Han K, Lee S, Min CK: Case report: acute promyelocytic leukemia with +der(17)t(15;17) detected by fluorescence in situ hybridization (FISH). Ann Clin Lab Sci; 2005;35(2):195-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case report: acute promyelocytic leukemia with +der(17)t(15;17) detected by fluorescence in situ hybridization (FISH).
  • We describe an unusual case of acute promyelocytic leukemia with +der(17)t(15;17) as the additional cytogenetic abnormality and with t(15;17) defined by fluorescence in situ hybridization (FISH) using a PML/RARA dual color, dual fusion translocation probe.
  • By performing a step-by-step, complementary approach to evaluate unusual chromosomal abnormalities, we detected RARA/PML fusion on a marker chromosome similar to chromosome 17.
  • [MeSH-major] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Leukemia, Promyelocytic, Acute / diagnosis

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  • (PMID = 15943185.001).
  • [ISSN] 0091-7370
  • [Journal-full-title] Annals of clinical and laboratory science
  • [ISO-abbreviation] Ann. Clin. Lab. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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33. Yang D, Hladnik L: Treatment of acute promyelocytic leukemia during pregnancy. Pharmacotherapy; 2009 Jun;29(6):709-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute promyelocytic leukemia during pregnancy.
  • Management of the pregnant patient with acute promyelocytic leukemia (APL) is a challenge.
  • Immediate treatment of APL is critical, as it is an oncologic emergency, with a high risk of morbidity and mortality associated with disseminated intravascular coagulation.
  • In addition, complications associated with APL, including retinoic acid syndrome, add to the complexity of management.
  • To better understand how to manage this complex patient care situation, we searched the PubMed database (January 1972-May 2008) for English-language articles about maternal and fetal outcomes resulting from APL treatment during pregnancy.
  • A total of 42 cases from 35 articles were identified: 12 first-trimester, 21 second-trimester, and 9 third-trimester cases.
  • The overall treatment of the pregnant patient with APL should include a discussion about pregnancy termination, especially if APL is diagnosed in the first trimester.
  • Frequent fetal monitoring, along with aggressive management of potential APL-related complications, is necessary to allow for optimal maternal and fetal outcomes.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Pregnancy Complications, Neoplastic / drug therapy. Tretinoin / administration & dosage

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  • (PMID = 19476422.001).
  • [ISSN] 1875-9114
  • [Journal-full-title] Pharmacotherapy
  • [ISO-abbreviation] Pharmacotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  • [Number-of-references] 71
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34. Lo Coco F, Ammatuna E, Noguera N: Treatment of acute promyelocytic leukemia with gemtuzumab ozogamicin. Clin Adv Hematol Oncol; 2006 Jan;4(1):57-62, 76-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute promyelocytic leukemia with gemtuzumab ozogamicin.
  • Acute promyelocytic leukemia (APL) is a form of acute myeloid leukemia characterized by peculiar biologic features and a unique sensitivity to differentiation therapy with all-trans retinoic acid (ATRA).
  • Modern treatment approaches to APL include simultaneous combination of ATRA and anthracycline-based chemotherapy.
  • Gemtuzumab ozogamicin is a calicheamicin-conjugated monoclonal antibody directed against CD33, a cell surface antigen highly expressed on APL cells.
  • A number of preliminary reports have highlighted the sensitivity of APL to gemtuzumab given alone or in combination with other agents.
  • Several reasons may account for the efficacy of gemtuzumab in APL, including:.
  • (1) CD33 is detectable in virtually 100% of APL cases;.
  • (2) calicheamicin belongs to the anthracycline family, a group of chemotherapeutic agents known to be highly effective in APL; and (3) the APL blast cells lack the multidrug resistance glycoprotein 170.
  • Due to the availability of other highly effective agents (ATRA, arsenic trioxide), relatively few APL patients have been treated thus far with gemtuzumab, and their follow-up is still short.
  • However, it is conceivable that the use of this agent in APL will increase in the near future in light of its capability to induce molecular remission even in advanced disease.
  • This review summarizes the mechanism of action and toxicity profile of gemtuzumab as well as the published experience with this compound in patients with newly diagnosed and relapsed APL.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 16562371.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / gemtuzumab; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 53
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35. Sharma JB, Gupta N, Vimala N, Anand M, Deka D, Mittal S: Acute promyelocytic leukemia: an unusual cause of fatal secondary postpartum hemorrhage. Arch Gynecol Obstet; 2006 Feb;273(5):310-1
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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 leukemia: an unusual cause of fatal secondary postpartum hemorrhage.
  • INTRODUCTION: Postpartum haemorrhage can rarely be associated with an underlying coagulation or haematological disorder.
  • We wish to discuss a case of acute promyelocytic leukemia (APL) presenting as secondary postpartum hemorrhage (PPH), its clinical and pathological features and maternal outcome.
  • Investigations revealed her to be having APL, a diagnosis not suspected by the referring clinic.
  • CONCLUSION: The case emphasizes the importance of suspecting, investigating and energetically treating uncommon causes such as acute leukemia when an unusually severe clinical picture in a postpartum setting suggests such a possibility.
  • This may prove to be life saving, particularly if the leukemia happens to be APL, a cancer with a very high cure rate.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / complications. Postpartum Hemorrhage / etiology

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  • (PMID = 16341866.001).
  • [ISSN] 0932-0067
  • [Journal-full-title] Archives of gynecology and obstetrics
  • [ISO-abbreviation] Arch. Gynecol. Obstet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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36. Fenaux P, Wang ZZ, Degos L: Treatment of acute promyelocytic leukemia by retinoids. Curr Top Microbiol Immunol; 2007;313:101-28
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of acute promyelocytic leukemia by retinoids.
  • We review the role of all-trans retinoic acid (ATRA) in the treatment of acute promyelocytic leukemia (APL).
  • The combination of ATRA and conventional anthracycline-ARA-C chemotherapy (CT) has clearly demonstrated its superiority over CT alone (in terms of relapse and survival) in newly diagnosed APL.
  • With those treatments, the relapse risk appears to be only 10%-15%, although it remains greater in patients who initially have high white blood cell counts (often associated with variant M3 morphology, short bcr3 isoform, etc.) and patients with residual disease detectable by RT-PCR at the end of consolidation courses.
  • ATRA syndrome (now generally called APL differentiation syndrome, as it is also seen with arsenic derivatives) remains the major side effect of ATRA treatment.
  • It occurs in 10%-15% of patients and is currently fatal in at least 10% of them.
  • A sizeable proportion of APL patients who relapse after ATRA and CT can be durably salvaged by the same treatment followed by allogeneic or autologous stem cell transplantation, provided the transplant (in the autologous setting) is RT-PCR-negative.
  • However, in relapsing APL arsenic derivatives (mainly arsenic trioxide) are now considered to be the reference treatment.
  • Some of the current issues with ATRA treatment in newly diagnosed APL include whether ATRA has a role during consolidation treatment and whether arabinoside (AraC) is required in addition to anthracyclines in the chemotherapy combined to ATRA.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Clinical Trials as Topic. Humans. Treatment Outcome

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  • (PMID = 17217041.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  • [Number-of-references] 132
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37. Nagai S, Takahashi T, Kurokawa M: Beneficial and adverse effects of molecularly targeted therapies for acute promyelocytic leukemia in central nervous system. CNS Neurol Disord Drug Targets; 2009 Nov;8(5):387-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beneficial and adverse effects of molecularly targeted therapies for acute promyelocytic leukemia in central nervous system.
  • Acute promyelocytic leukemia (APL) is a distinct subset of acute myeloid leukemia characterized by an abnormal fusion protein, PML/RARA.
  • All-trans retinoic acid (ATRA) and arsenic trioxide, which are the major molecularly targeted therapies in APL, affect or degrade the PML/RARA fusion protein and cause differentiation and apoptosis of APL cells.
  • These therapies have improved the prognosis of APL patients and are now the main therapeutic options in APL.
  • In addition, gemtuzumab ozogamicin is another targeted therapy in APL.
  • On the other hand, the prognosis of patients with central nervous system (CNS) relapses of APL remains poor.
  • In fact, possible active roles of molecularly targeted therapies in CNS relapses of APL have been suggested, and several new approaches with molecularly targeted therapies for CNS relapses have been examined in APL.
  • In this review, we discuss three main topics; the relationship between the incidence of CNS relapses and the introduction of molecularly targeted therapies for APL, new approaches with targeted therapies for CNS relapses of APL, and other complications of targeted therapies in CNS such as pseudotumor cerebri induced by ATRA and subarachnoid hemorrhage.
  • These comprehensive understanding would be helpful for better management of patients with APL.
  • [MeSH-major] Arsenicals / therapeutic use. Central Nervous System Neoplasms / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 19702568.001).
  • [ISSN] 1996-3181
  • [Journal-full-title] CNS & neurological disorders drug targets
  • [ISO-abbreviation] CNS Neurol Disord Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 46
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38. Walker DK, Held-Warmkessel J: Acute promyelocytic leukemia: an overview with implications for oncology nurses. Clin J Oncol Nurs; 2010 Dec;14(6):747-59
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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 leukemia: an overview with implications for oncology nurses.
  • Acute promyelocytic leukemia (APL), once described as the form of leukemia with the highest mortality, is now the most potentially curable subtype of adult acute myeloid leukemia.
  • A brief review of the history of APL will describe the advances in research and clinical practice and their impact on patient outcomes.
  • Oncology nurses should familiarize themselves with the nuances of APL because of the critical role nurses play in providing support for patients.
  • This article provides an overview of APL, including the epidemiology and pathophysiology that distinguishes APL from other types of acute leukemia.
  • Clinical presentation and diagnostic workup for patients suspected of having APL will be reviewed, as will the treatment course.
  • Nursing implications and management will be provided related to potential treatment complications specific to APL, including coagulopathies, differentiation syndrome, and QT prolongation with the use of arsenic trioxide, as will the side effects and complications that can occur in any patient with leukemia, such as infection, hyperleukocytosis, tumor lysis, and increased intracranial pressure.
  • [MeSH-major] Leukemia, Promyelocytic, Acute. Oncology Nursing / manpower

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  • [ReprintIn] ONS Connect. 2010 Dec;25(12):12-3 [21214084.001]
  • (PMID = 21112852.001).
  • [ISSN] 1538-067X
  • [Journal-full-title] Clinical journal of oncology nursing
  • [ISO-abbreviation] Clin J Oncol Nurs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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39. Yoo SJ, Park CJ, Jang S, Seo EJ, Lee KH, Chi HS: Inferior prognostic outcome in acute promyelocytic leukemia with alterations of FLT3 gene. Leuk Lymphoma; 2006 Sep;47(9):1788-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inferior prognostic outcome in acute promyelocytic leukemia with alterations of FLT3 gene.
  • Alterations of the FLT3 gene, in the form of internal tandem duplications (ITD) and D835 point mutations, occur frequently in acute promyelocytic leukemia (APL).
  • We therefore evaluated the frequency and clinical relevance of FLT3 aberrations in a series of Korean APL patients.
  • We assayed FLT3 ITD and D835 mutation status in 75 newly diagnosed APL patients and we correlated the presence of these mutations with clinical parameters and outcomes.
  • Of the 75 patients, fifteen (20.0%) carried FLT3 mutations, nine (12.0%) with FLT3 ITD, seven (9.3%) with D835 mutations and one with both types.
  • There was no association between FLT3 aberrations and other clinicohematologic features including age, gender, M3 variant morphology and PML/RARalpha subtype.
  • Both ITD and D835 mutations were associated with shortened event-free survival (P = 0.048 and P = 0.029, respectively), but there was no correlation between disease-free survival among the 61 patients who achieved complete remission and the presence of FLT3 mutations (P = 0.543 for ITD and P = 0.277 for D835).
  • FLT3 mutations were less frequent in Korean APL patients than in Western APL patients.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Mutation / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17064989.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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40. Wang L, Zhou GB, Liu P, Song JH, Liang Y, Yan XJ, Xu F, Wang BS, Mao JH, Shen ZX, Chen SJ, Chen Z: Dissection of mechanisms of Chinese medicinal formula Realgar-Indigo naturalis as an effective treatment for promyelocytic leukemia. Proc Natl Acad Sci U S A; 2008 Mar 25;105(12):4826-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dissection of mechanisms of Chinese medicinal formula Realgar-Indigo naturalis as an effective treatment for promyelocytic leukemia.
  • To enhance therapeutic efficacy and reduce adverse effects, practitioners of traditional Chinese medicine (TCM) prescribe a combination of plant species/minerals, called formulae, based on clinical experience.
  • In trying to address the possible beneficial effects of formulae with current biomedical approaches, we use Realgar-Indigo naturalis formula (RIF), which has been proven to be very effective in treating human acute promyelocytic leukemia (APL) as a model.
  • Here, we report that the ATI combination yields synergy in the treatment of a murine APL model in vivo and in the induction of APL cell differentiation in vitro.
  • ATI causes intensified ubiquitination/degradation of promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARalpha) oncoprotein, stronger reprogramming of myeloid differentiation regulators, and enhanced G(1)/G(0) arrest in APL cells through hitting multiple targets compared with the effects of mono- or biagents.
  • Furthermore, ATI intensifies the expression of Aquaglyceroporin 9 and facilitates the transportation of A into APL cells, which in turn enhances A-mediated PML-RARalpha degradation and therapeutic efficacy.
  • We therefore suggest that dissecting the mode of action of clinically effective formulae at the molecular, cellular, and organism levels may be a good strategy in exploring the value of traditional medicine.
  • [MeSH-major] Arsenicals / therapeutic use. Drugs, Chinese Herbal / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Medicine, Chinese Traditional. Sulfides / therapeutic use
  • [MeSH-minor] Animals. Aquaporins / genetics. Aquaporins / metabolism. Cell Differentiation / drug effects. Cell Line, Tumor. Disease Models, Animal. Drug Synergism. G0 Phase / drug effects. G1 Phase / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Oncogene Proteins, Fusion / metabolism. Protein Processing, Post-Translational / drug effects. Transcription, Genetic / drug effects. Ubiquitination / drug effects. Up-Regulation / drug effects

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  • (PMID = 18344322.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Drugs, Chinese Herbal; 0 / Oncogene Proteins, Fusion; 0 / Sulfides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / realgar-indigo naturalis; 56320-22-0 / arsenic disulfide
  • [Other-IDs] NLM/ PMC2290784
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41. Kurkjian C, Patel S, Kamble R, Dunn ST, Kern W, Kharfan-Dabaja MA: Acute promyelocytic leukemia and constitutional trisomy 21. Cancer Genet Cytogenet; 2006 Mar;165(2):176-9
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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 leukemia and constitutional trisomy 21.
  • The incidence of acute myelogenous leukemia (AML) in patients with constitutional trisomy 21 is estimated to be 1 in 300; it is usually seen before age four.
  • Clinical and epidemiological data confirm the improved life expectancy of patients with Down syndrome and their increased susceptibility to the development of leukemia, among other cancers.
  • The most frequent subtype of AML associated with Down syndrome is acute megakaryoblastic leukemia (FAB: M7).
  • The description of acute promyelocytic leukemia (APL) in adult patients with Down syndrome is exceedingly rare.
  • Herein, we describe the unusual presentation, treatment, results, and clinical course of an adult patient with APL and constitutional trisomy 21 and provide a brief review of the literature.
  • [MeSH-major] Down Syndrome. Leukemia, Promyelocytic, Acute / genetics

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  • (PMID = 16527614.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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42. Bobé P, Chelbi-Alix MK: [New therapeutic perspectives for arsenic: from acute promyelocytic leukemia to autoimmune diseases]. Med Sci (Paris); 2008 Nov;24(11):967-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [New therapeutic perspectives for arsenic: from acute promyelocytic leukemia to autoimmune diseases].
  • [Transliterated title] De nouvelles perspectives thérapeutiques pour l'arsenic: De la leucémie aiguë promyélocytaire aux maladies auto-immunes.
  • Since 1996, arsenic trioxide (As2O3) is used to treat patients with acute promyelocytic leukemia.
  • This treatment also markedly reduced anti-DNA autoantibodies, rheumatoid factor, IL-18, IFN-gamma, nitric oxide metabolites, TNF-alpha, Fas ligand and IL-10 levels, and immune-complex deposits in glomeruli, leading to significantly prolonged survival rates.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenic / therapeutic use. Autoimmune Diseases / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Animals. Arsenicals / therapeutic use. Disease Models, Animal. Growth Inhibitors / therapeutic use. Humans. Lupus Erythematosus, Systemic / drug therapy. Lymphoproliferative Disorders / drug therapy. Mice. Oxides / therapeutic use


43. Ferrara F: Acute promyelocytic leukemia: what are the treatment options? Expert Opin Pharmacother; 2010 Mar;11(4):587-96
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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 leukemia: what are the treatment options?
  • IMPORTANCE OF THE FIELD: Acute promyelocytic leukemia (APL) represents a paradigm of therapeutic success in clinical hematology.
  • Notwithstanding, various questions concerning the management of APL remain unanswered.
  • AREAS COVERED IN THIS REVIEW: The aim of this article is to focus on still controversial issues in the management of APL, such as the role of arsenic trioxide as front-line therapy, the management of older unfit patients, the potential utility of gemtuzumab-ozogamycin and the effectiveness (if any) of maintenance therapy for patients in molecular remission.
  • WHAT THE READER WILL GAIN: Current and future therapeutic options for the treatment of newly diagnosed and relapsed APL.
  • TAKE HOME MESSAGE: To date, the therapy of APL is the most successful example of differentiation therapy and its scientific history can serve as a model for subsequent development of similar treatments in other leukemias and cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 20163270.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 0 / gemtuzumab; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 75
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44. Ye H, Yang X, Gan L, Sun X, Xu H: Realgar Nanoparticles Induced Cytotoxicity in Promyelocytic Leukemia HL-60 Cells. Conf Proc IEEE Eng Med Biol Soc; 2005;7:7714-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Realgar Nanoparticles Induced Cytotoxicity in Promyelocytic Leukemia HL-60 Cells.
  • Realgar, one of mineral drugs in Chinese traditional medicines has attracted an increasing attention because of its prominent anti-tumor effect.
  • Our previous studies have demonstrated that realgar nanoparticles may provide a less toxic agent for anti-neoplasia by suppressing angiogenesis.
  • In the present study, we improved milling process, prepared raw realgar particles and realgar nanoparticles with the same background As<inf>2</inf>O<inf>3</inf>concentrations and compared their cytoxcity to promyelocytic leukemia HL-60 cells including inhibiting cell growth, inducing oxidative stress.

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  • (PMID = 17282069.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Matsuo T, Sugita T, Shimose S, Kubo T, Ishikawa M, Yasunaga Y, Ochi M: Immunohistochemical expression of promyelocytic leukemia body in soft tissue sarcomas. J Exp Clin Cancer Res; 2008;27:73

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of promyelocytic leukemia body in soft tissue sarcomas.
  • BACKGROUND: The function of promyelocytic leukemia (PML) bodies is not well known but plays an important role in controlling cell proliferation, apoptosis and senescence.
  • This study was undertaken to analyze the clinical significance of PML body expression in primary tumor samples from malignant fibrous histiocytoma (MFH) and liposarcoma patients.
  • METHODS: We studied MFH and liposarcoma samples from 55 patients for PML bodies.
  • Fluorescent immunostaining of PML bodies was performed in the paraffin-embedded tumor sections.
  • RESULTS: PML body immunostaining was identified in 63.9% of MFH and 63.2% of liposarcoma samples.
  • PML body expression rates of all sarcoma cells were 1.5 +/- 1.8% (range: 0-7.0) in MFH and 1.3 +/- 1.4% (0-5.2) in liposarcoma samples.
  • PML body expression (p = 0.0053) and a high rate of PML body expression (p = 0.0012) were significantly greater prognostic risk factors for death than the other clinical factors in MFH patients.
  • All liposarcoma patients without expression of PML were disease free at the end of the study.
  • CONCLUSION: Our study suggests that the presence of PML bodies may indicate a poor prognosis for MFH and liposarcoma patients.

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  • (PMID = 19025608.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
  • [Other-IDs] NLM/ PMC2611968
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46. Kelaidi C, Chevret S, De Botton S, Raffoux E, Guerci A, Thomas X, Pigneux A, Lamy T, Rigal-Huguet F, Meyer-Monard S, Chevallier P, Maloisel F, Deconinck E, Ferrant A, Fegueux N, Ifrah N, Sanz M, Dombret H, Fenaux P, Adès L: Improved outcome of acute promyelocytic leukemia with high WBC counts over the last 15 years: the European APL Group experience. J Clin Oncol; 2009 Jun 1;27(16):2668-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved outcome of acute promyelocytic leukemia with high WBC counts over the last 15 years: the European APL Group experience.
  • PURPOSE: Acute promyelocytic leukemia (APL) with pretreatment WBC counts greater than 10,000/microL is still considered to carry a poorer prognosis than APL with WBC lower than 10,000/mL.
  • PATIENTS AND METHODS: Nine hundred two patients with APL, including 204 patients and 68 patients with WBC counts more than 10,000/microL and more than 50,000/microL, respectively, were enrolled between 1993 and 2005 in two successive randomized trials of the European APL group (APL 93 and APL 2000) that tested, in particular, the modalities of combination of all-trans retinoic acid (ATRA) and chemotherapy, maintenance treatment, escalating doses of cytarabine, early administration of dexamethasone, and CNS prophylaxis.
  • RESULTS: Between the APL 93 and 2000 trials, the complete response (CR) rate increased from 89.6% to 93%, and the 5-year cumulative incidence of relapse (CIR) decreased from 40% to 9.5% in patients with WBC counts of 10,000 to 50,000/microL.
  • Whereas in the APL 93 trial, increased WBC counts were significantly associated with higher CIR and shorter survival, this was not the case in the APL 2000 trial.
  • In patients with increased WBC counts, enrollment onto the APL 2000 trial (v APL 93) and combined maintenance with ATRA and chemotherapy were associated with significantly lower CIR and better survival.
  • CONCLUSION: Outcome of APL with high WBC count has markedly improved over the years as a result of fewer early deaths and fewer relapses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Leukocyte Count. Outcome and Process Assessment (Health Care). Quality of Health Care
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease-Free Survival. Europe. Female. Humans. Infant. Kaplan-Meier Estimate. Male. Middle Aged. Proportional Hazards Models. Recurrence. Risk Assessment. Risk Factors. Time Factors. Treatment Outcome. Young Adult

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  • [CommentIn] J Clin Oncol. 2010 Jan 10;28(2):e21; author reply e22-3 [19949004.001]
  • (PMID = 19414681.001).
  • [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; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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47. Janssen K, Hofmann TG, Jans DA, Hay RT, Schulze-Osthoff K, Fischer U: Apoptin is modified by SUMO conjugation and targeted to promyelocytic leukemia protein nuclear bodies. Oncogene; 2007 Mar 8;26(11):1557-66
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  • [Title] Apoptin is modified by SUMO conjugation and targeted to promyelocytic leukemia protein nuclear bodies.
  • Here, we report for the first time that apoptin interacts directly with the promyelocytic leukemia protein (PML) in tumor cells and accumulates in PML nuclear bodies (NBs), which are involved in apoptosis induction and viral replication.
  • We also demonstrate that apoptin is sumoylated and that a sumoylation-deficient apoptin mutant is no longer recruited to PML-NBs, but localizes in the nuclear matrix.
  • This mutant fails to bind PML, but can still induce apoptosis as efficiently as wild-type apoptin.
  • Moreover, apoptin kills also PML-/- cells and promyelocytic leukemia cells with defective PML expression.
  • Our results therefore suggest that apoptin kills tumor cells independently of PML and sumoylation, however, the interaction of apoptin with PML and small ubiquitin-like modifier (SUMO) proteins might be relevant for CAV replication.

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  • (PMID = 16924230.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / SUMO-1 Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / VP3 protein, Chicken anemia virus; 143220-95-5 / PML protein, human
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48. Oelschlaegel U, Mohr B, Schaich M, Schäkel U, Kroschinsky F, Illmer T, Ehninger G, Thiede C: HLA-DRneg patients without acute promyelocytic leukemia show distinct immunophenotypic, genetic, molecular, and cytomorphologic characteristics compared to acute promyelocytic leukemia. Cytometry B Clin Cytom; 2009 Sep;76(5):321-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-DRneg patients without acute promyelocytic leukemia show distinct immunophenotypic, genetic, molecular, and cytomorphologic characteristics compared to acute promyelocytic leukemia.
  • BACKGROUND: Loss of HLA-DR and CD34 is a well-known characteristic of malignant promyelocytes in acute promyelocytic leukemia (APL).
  • However, this immunophenotype is not specific for APL.
  • The purpose of this study was to investigate whether further biological characterization of the HLA-DR(neg) acute myeloid leukemia patients would allow more clearly define criteria to separate APL from non-APL patients.
  • METHODS: Immunophenotyping, cytogenetics, molecular analyses, and cytomorphology were prospectively performed within routine leukemia diagnostics of 800 patients included in different prospective acute myeloid leukemia multicenter trials.
  • RESULTS: Beside 60 APL, an additional 62 HLA-DR(neg) non-APL patients were identified.
  • The main differential characteristics of HLA-DR(neg) non-APL included high CXCR-4 expression in most patients and almost all leukemia cells, a significantly higher proportion of patients presenting with NPM1 mutations as well as the significant association with cup-like nuclear morphology.
  • The biological distinctness of both leukemia subtypes was further emphasized by the complete absence of aberrant CD2 expression and increased leukocyte and platelet counts in HLA-DR(neg) non-APL patients.
  • Even in the CD34(pos) subgroup of HLA-DR(neg) non-APL all those features contributed in at least the same way to the separation from APL.
  • CONCLUSIONS: The results of the present study show that an immunophenotypic, molecular, and cytomorphologic separation of both HLA-DR(neg) leukemia subgroups is possible indicating that both groups are biologically distinct.
  • [MeSH-major] Flow Cytometry / methods. HLA-DR Antigens / metabolism. Leukemia, Promyelocytic, Acute / metabolism

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  • [Copyright] (c) 2009 Clinical Cytometry Society.
  • (PMID = 19291801.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / CXCR4 protein, human; 0 / DNA, Neoplasm; 0 / HLA-DR Antigens; 0 / Nuclear Proteins; 0 / Receptors, CXCR4; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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49. Ninomiya M, Kajiguchi T, Yamamoto K, Kinoshita T, Emi N, Naoe T: Increased oxidative DNA products in patients with acute promyelocytic leukemia during arsenic therapy. Haematologica; 2006 Nov;91(11):1571-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased oxidative DNA products in patients with acute promyelocytic leukemia during arsenic therapy.
  • Arsenic trioxide (ATO) has been used to treat acute promyelocytic leukemia (APL), but the oxidative DNA damage occurring in patients has not been fully elucidated.
  • We measured 8-hydroxy-2'-deoxyguanosine (8-OHdG), one of the most abundant oxidative products of DNA, by enzyme-linked immunoassay, and reactive oxidative species (ROS), by luminol- and luminol-H2O2 chemiluminescence, in the plasma of four APL patients treated with ATO.
  • After six courses of ATO therapy, the plasma 8-OHdG concentration had increased from 45.6+/-22.8 ng/mL to 310.2+/-239.6 ng/mL.
  • The plasma chemiluminescence level did not change significantly.
  • These findings suggest that ATO generates intracellular oxidative DNA damage, but this is not correlated with the plasma ROS level.
  • The clinical significance of 8-OHdG during and after ATO therapy warrants further study.
  • [MeSH-major] Arsenicals / adverse effects. DNA / blood. Leukemia, Promyelocytic, Acute / blood. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / adverse effects. Reactive Oxygen Species / blood

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  • (PMID = 17082016.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 0 / Reactive Oxygen Species; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; 9007-49-2 / DNA; G9481N71RO / Deoxyguanosine; S7V92P67HO / arsenic trioxide
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50. Chow J, Feusner J: Isolated central nervous system recurrence of acute promyelocytic leukemia in children. Pediatr Blood Cancer; 2009 Jan;52(1):11-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated central nervous system recurrence of acute promyelocytic leukemia in children.
  • The incidence of isolated central nervous system (iCNS) relapse in pediatric acute promyelocytic leukemia (APL) is debated.
  • We analyzed the literature, focusing on clinical trials reported since the advent of ATRA use.
  • This incidence does not support the use of intrathecal CNS prophylaxis for all children with APL.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Child. Clinical Trials as Topic. Humans. Incidence. Premedication. Recurrence

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  • [CommentIn] Pediatr Blood Cancer. 2009 Aug;53(2):235-6; author reply 237 [19353622.001]
  • [CommentIn] Pediatr Blood Cancer. 2010 Feb;54(2):336-7; author reply 338 [19847884.001]
  • (PMID = 18816805.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 27
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51. Ferrara F, Finizio O, D'Arco A, Mastrullo L, Cantore N, Musto P: Acute promyelocytic leukemia in patients aged over 60 years: multicenter experience of 34 consecutive unselected patients. Anticancer Res; 2010 Mar;30(3):967-71
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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 leukemia in patients aged over 60 years: multicenter experience of 34 consecutive unselected patients.
  • Treatment of acute promyelocytic leukemia (APL) has evolved over recent years, resulting in a cure rate of 75-80%.
  • However, the prognosis of older patients with APL remains poorer as compared to young adults because of substantial morbidity of either induction or consolidation therapy.
  • We describe therapeutic results in a series of 34 consecutive APL patients aged over 60 years, with particular emphasis on those patients managed outside of clinical trials because of comorbidities at diagnosis.
  • Six patients (18%) died within two days of diagnosis; among these, only one was on the AIDA protocol.
  • Patients accrued into the GIMEMA AIDA protocol achieved longer survival (median not reached vs. 10 months, p=0.03).
  • In conclusion, our data demonstrate that at least 30% of older APL patients are not eligible to accrual in multicenter trials; furthermore, in this subset, the possibility of early death is substantial.
  • However, when CR is achieved, a personalized consolidation approach can be adopted with the possibility of achieving long-term disease control.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Treatment Outcome

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  • (PMID = 20393021.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Greece
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52. Yang Q, Deng X, Lu B, Cameron M, Fearns C, Patricelli MP, Yates JR 3rd, Gray NS, Lee JD: Pharmacological inhibition of BMK1 suppresses tumor growth through promyelocytic leukemia protein. Cancer Cell; 2010 Sep 14;18(3):258-67
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacological inhibition of BMK1 suppresses tumor growth through promyelocytic leukemia protein.
  • We found that BMK1 interacted with promyelocytic leukemia protein (PML), and inhibited its tumor-suppressor function through phosphorylation.
  • Furthermore, activated BMK1 notably inhibited PML-dependent activation of p21.
  • To further investigate the BMK-mediated inhibition of the tumor suppressor activity of PML in tumor cells, we developed a small-molecule inhibitor of the kinase activity of BMK1, XMD8-92.


53. Korístek Z, Mayer J: [Leukemogenesis and therapy of acute promyelocytic leukemia: from the worse to the most favorable subtype of acute myeloid leukemia]. Vnitr Lek; 2008 Jul-Aug;54(7-8):701-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Leukemogenesis and therapy of acute promyelocytic leukemia: from the worse to the most favorable subtype of acute myeloid leukemia].
  • [Transliterated title] Leukemogeneza a lécba akutní promyelocytární leukemie: cesta od nejhorsího k nejpríznivejsímu typu akutní myeloidní leukemie.
  • The evolution of therapy of acute promyelocytic leukemia (APL) from 1964 to present is reviewed.
  • The paper is focused on the main findings and key studies which formed current and almost standard therapeutic approach to APL.
  • The first important development was the use of anthracyclines for the initial therapy of APL in 1967.
  • The first clinical study which brought information about the effect of ATRA in APL started in China in 1986.
  • A number of the most important subsequent studies focused on pathogenesis and therapy of APL are analyzed and reviewed.
  • The additional considerable finding was the discovery of arsenic trioxide (ATO) therapeutic efficacy in APL and ATO is now in particular used for a therapy of relapsed APL.
  • The publication gives also a recent insight into a leukemogenesis of APL and development of a resistance to ATRA.
  • At the conclusion, the authors emphasize the need of early diagnosis as a one of the main conditions for successful treatment of APL.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18780571.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 166
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54. Kogan SC: Mouse models of acute promyelocytic leukemia. Curr Top Microbiol Immunol; 2007;313:3-29
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mouse models of acute promyelocytic leukemia.
  • Mouse models of acute promyelocytic leukemia have been generated through transgenic, knock-in, retroviral, and xenograft strategies.
  • Among the areas investigated are the role of reciprocal fusions; effects of target cells, expression levels, and mouse strains; cooperating events; and restrictive and permissive factors.
  • Furthermore, preclinical studies utilizing these mice have advanced therapy for myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Disease Models, Animal. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / physiopathology

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  • (PMID = 17217036.001).
  • [ISSN] 0070-217X
  • [Journal-full-title] Current topics in microbiology and immunology
  • [ISO-abbreviation] Curr. Top. Microbiol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 70
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55. Guo XH, Yasen H, Jiang M, Hao JP, Abulaiti D, Chen R: [Retinoic acid in treating acute promyelocytic leukemia with hyperleukocytosis and its therapeutic strategy]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Apr;16(2):439-41
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Retinoic acid in treating acute promyelocytic leukemia with hyperleukocytosis and its therapeutic strategy].
  • In order to investigate the occurrence of hyperleukocytosis in treating acute promyelocytic leukemia (APL) patients with all trans retinoic acid (ATRA) and to explore the influence of the level of leucocyte on curative effect of ATRA, the APL patients were divided into three different groups according to the count of leucocyte in peripheral blood.
  • It is concluded that the ATRA in combination with cytotoxic drugs can efficiently control the occurrence of hyperleukocytosis during ATRA-treating APL and reduce the early mortality.

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  • (PMID = 18426682.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
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56. Dutta P, Sazawal S, Kumar R, Saxena R: Does acute promyelocytic leukemia in Indian patients have biology different from the West? Indian J Pathol Microbiol; 2008 Jul-Sep;51(3):437-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does acute promyelocytic leukemia in Indian patients have biology different from the West?
  • Acute promyelocytic leukemia (APML) is a well-characterized malignancy with typical clinico-hematological and molecular features.
  • This study was conducted to determine the clinico-hematological profile of APML in India.
  • Thirty-five patients with APML presenting to Hematology Department, AIIMS, New Delhi, between July 2003 and June 2005 were evaluated for presenting clinical features, hemogram, peripheral smear, bone marrow morphology and cytochemistry.
  • Reverse transcriptase PCR (RT-PCR) for PML-RARalpha was done in all cases.
  • Male-to-female ratio was 0.9:1 (males--17 and females--18) with median age 25 years (range 11-57 years).
  • RT-PCR showed PML-RARalpha in 33/35 cases with the bcr3 isoform being present in 24/33 positive cases (72.7%).
  • The two cases negative for PML-RARalpha showed typical morphology and responded to ATRA.
  • APML in India has certain unusual features, which may reflect a different biology.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology

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  • (PMID = 18723985.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Azo Compounds; 0 / Naphthalenes; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.- / Esterases
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57. Pagnano KB, de Carvalho Duarte G, Lorand-Metze I, Delamain MT, Miranda EC, De Souza CA: Treatment outcome of acute promyelocytic leukemia with modified aida protocol. Adv Hematol; 2010;2010:672137

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment outcome of acute promyelocytic leukemia with modified aida protocol.
  • We analyzed the outcome of a series of 19 newly diagnosed patients with acute promyelocytic leukemia treated with AIDA modified protocol, using mitoxantrone in place of idarubicin.
  • Eleven patients achieved morphologic CR (58%).
  • The 4-year disease-free survival is 82%.
  • The study showed the antileukemic efficacy of mitoxantrone and that it could be used as a reasonable option in anthracycline-based strategies in APL.

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  • [Cites] Blood. 2008 Oct 15;112(8):3130-4 [18664623.001]
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  • (PMID = 20490274.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2871550
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58. Lee HE, Jee CD, Kim MA, Lee HS, Lee YM, Lee BL, Kim WH: Loss of promyelocytic leukemia protein in human gastric cancers. Cancer Lett; 2007 Mar 8;247(1):103-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of promyelocytic leukemia protein in human gastric cancers.
  • To clarify the clinical implications of promyelocytic leukemia (PML) expression in gastric carcinomas, the expression of PML was analyzed in large series of gastric carcinoma by immunohistochemistry, western blotting and reverse transcription-PCR.
  • PML protein expression was reduced or abolished in gastric carcinomas (31.7 and 10.6%, respectively) by immunohistochemistry.
  • PML protein loss was associated with more lymphatic invasion, higher pTNM stage, and worse patient survival.
  • Only one gastric carcinoma cell line showed loss of PML, and the PML protein re-appeared after the treatment of proteasome inhibitor in this cell line.
  • We conclude that PML protein loss occurs in a minority of gastric carcinomas during carcinogenesis and progression, and suggest the proteasome-dependent pathway as a mechanism of PML protein loss.

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  • (PMID = 16713073.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
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59. Jain D, Singh T, Arora P: Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report. J Med Case Rep; 2007;1:147

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down syndrome with microgranular variant of acute promyelocytic leukemia in a child: a case report.
  • BACKGROUND: Acute promyelocytic leukemia (APL) accounts for less than 10% of pediatric AML.
  • Cases of APL in Down syndrome (DS) have been described in the literature rarely and it is rarer still to find the microgranular variant (M3v) of APL in trisomy 21 patients.
  • CASE PRESENTATION: We present a case of a five-year-old female with Down syndrome diagnosed with acute promyelocytic leukemia (APL).
  • Based on this morphology and cytochemistry, a diagnosis of APL microgranular variant (M3v) was made.
  • CONCLUSION: This case report emphasizes the importance of a high index of suspicion in the diagnosis of acute promyelocytic leukemia microgranular variant in Down syndrome.

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  • (PMID = 18036234.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
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  • [Publication-type] Journal Article
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  • [Other-IDs] NLM/ PMC2211491
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60. Shi J, Vogt PK: Posttranslational regulation of Myc by promyelocytic leukemia zinc finger protein. Int J Cancer; 2009 Oct 1;125(7):1558-65
eagle-i research resources. PMID 19444914 (Special Collections) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Posttranslational regulation of Myc by promyelocytic leukemia zinc finger protein.
  • The promyelocytic leukemia zinc finger (PLZF) protein, a transcriptional repressor, induces cellular resistance to oncogenic transformation by diverse oncoproteins.
  • Two point mutants of PLZF that have lost the antioncogenic activity of the wild-type protein are oncogenic in chicken embryo fibroblasts; this activity is correlated with differential effects on Myc.
  • Wild-type PLZF represses Myc transcription without affecting total Myc protein levels and reduces the levels of phosphorylated Myc.
  • The PLZF mutants do not alter Myc transcription or protein expression but increase the levels of phosphorylated Myc.
  • Wild-type PLZF downregulates the MAPK pathway and activates Akt, resulting in reduced phosphorylation on serine 62 of Myc by Erk and on threonine 58 by glycogen synthase kinase 3beta.
  • We postulate that the 2 PLZF mutants are oncogenic, because they function as dominant negatives of wild-type PLZF, enhancing Myc phosphorylation and increasing Myc transcriptional and oncogenic activity.

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  • (PMID = 19444914.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA078045-07; United States / NCI NIH HHS / CA / R01 CA078230-07; United States / NCI NIH HHS / CA / CA078045-09; United States / NCI NIH HHS / CA / CA078230-07; United States / NCI NIH HHS / CA / R01 CA078230; United States / NCI NIH HHS / CA / R01 CA078230-10; United States / NCI NIH HHS / CA / CA078230-09; United States / NCI NIH HHS / CA / P01 CA078045-10; United States / NCI NIH HHS / CA / R01 CA078230-08; United States / NCI NIH HHS / CA / CA078230-08; United States / NCI NIH HHS / CA / CA078045-07; United States / NCI NIH HHS / CA / P01 CA078045; United States / NCI NIH HHS / CA / CA078045-10; United States / NCI NIH HHS / CA / R01 CA078230-09; United States / NCI NIH HHS / CA / CA078230-10; United States / NCI NIH HHS / CA / P01 CA078045-08; United States / NCI NIH HHS / CA / CA078045-08; United States / NCI NIH HHS / CA / P01 CA078045-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Kruppel-Like Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 147855-37-6 / ZBTB16 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
  • [Other-IDs] NLM/ NIHMS115924; NLM/ PMC2721905
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61. Mokany E, Todd AV, Fuery CJ, Applegate TL: Diagnosis and monitoring of PML-RARalpha-positive acute promyelocytic leukemia by quantitative RT-PCR. Methods Mol Med; 2006;125:127-47
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis and monitoring of PML-RARalpha-positive acute promyelocytic leukemia by quantitative RT-PCR.
  • The last 15 yr have produced dramatic improvements in the survival rate of patients with acute promyelocytic leukemia (APL).
  • These improvements have been due mainly to the introduction of targeted therapies and improved methods for diagnosing and monitoring this disease.
  • The underlying molecular lesion in APL involves a t(15:17) translocation which leads to the generation of PML-RARalpha fusion transcripts and proteins.
  • The PML-RARalpha fusion transcripts have been shown to be useful markers for establishing the diagnosis and for monitoring the response to treatment.
  • This manuscript describes the application of QZyme reverse-transcription polymerase chain reaction (RT-PCR) to the quantification of PML-RARalpha transcripts as a marker of APL.
  • The approach is well suited to monitoring minimal residual disease (MRD) in patients with APL, as a result of its ability to detect low numbers of transcripts and accurately measure differences in concentration over a broad dynamic range.
  • Further, its capacity for duplex analysis has multiple advantages for analysis of clinical specimens.
  • Protocols for duplex, single-tube QZyme RT-PCR assays, which allow simultaneous quantification of PML-RARalpha fusion transcripts (either L-type and V-type, or S-type) and the internal control BCR transcript, are provided.
  • These protocols can be used for analyzing patient RNA specimens and are suitable for clinical trial monitoring.
  • For this type of work, it is recommended that investigators validate the assays to ensure reproducible, accurate, and specific results on the equipment in their own laboratories.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Humans. Monitoring, Physiologic / methods. RNA, Neoplasm / genetics. Translocation, Genetic

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  • (PMID = 16502582.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Neoplasm; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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62. Bowling BL, Adamson AL: Functional interactions between the Epstein-Barr virus BZLF1 protein and the promyelocytic leukemia protein. Virus Res; 2006 May;117(2):244-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional interactions between the Epstein-Barr virus BZLF1 protein and the promyelocytic leukemia protein.
  • The Epstein-Barr virus immediate-early protein BZLF1 (Z) has been shown to alter the cellular localization of the promyelocytic leukemia (PML) protein.
  • PML has important implications for growth control, apoptosis, anti-viral effects and many more processes.
  • Here we further examined the relationship between PML and the Epstein-Barr virus Z protein.
  • We examined the effect of Z expression on PML protein levels, and the effect of increased PML protein levels on Z-mediated dispersion of PML bodies.
  • We found that increased levels of PML protein, such as through interferon treatment, were able to suppress Z-mediated PML body dispersion.
  • We also studied the consequences of PML dispersion by Z, by examining p21 transactivation, A20 transactivation, and MHC Class I presentation levels in Z-expressing cells.
  • We found that, while Z-mediated dispersion of PML did not affect MHC Class I presentation, it did alter p21 and A20 expression.
  • In addition, we found that increased levels of PML were able to prevent Z protein binding to mitotic chromosomes.
  • Our work implies that the balance of PML and Z levels in cells may affect how each protein functions.

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  • (PMID = 16307818.001).
  • [ISSN] 0168-1702
  • [Journal-full-title] Virus research
  • [ISO-abbreviation] Virus Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BZLF1 protein, Herpesvirus 4, Human; 0 / DNA-Binding Proteins; 0 / Histocompatibility Antigens Class I; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Viral Proteins; 143220-95-5 / PML protein, human; EC 1.13.12.- / Luciferases; EC 6.3.2.19 / TNFAIP3 protein, human
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63. Goyal M, Dattatreya PS, Goud I, Murthy SS: Cryptic PML-RARα positive acute promyelocytic leukemia with unusual morphology and cytogenetics. Indian J Pathol Microbiol; 2010 Oct-Dec;53(4):817-9
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  • [Title] Cryptic PML-RARα positive acute promyelocytic leukemia with unusual morphology and cytogenetics.
  • Acute Promyelocytic Leukemia (APL) is different from other forms of acute myeloid leukemia (AML), to the reason being the potential devastating coagulopathy and the sensitivity to all-trans retinoic acid (ATRA) and arsenic trioxide (As 2 O 3 ).
  • We hereby present a case of APL, morphologically distinct from the hypergranular APL; however, the flow cytometry revealed a characteristic phenotype showing dim CD45, bright CD13, bright CD33 and dim CD117 positivity.
  • Conventional cytogenetics revealed a distinct karyotype of a male with translocation t(4;15)(q34.2:q26.3).
  • However, interphase fluorescence-in-situ hybridization (FISH) revealed PML/RARA fusion signal on chromosome 15 in 90% cells.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / pathology. Leukocytes / cytology

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  • (PMID = 21045428.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / HLA Antigens; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human
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64. Kusakabe M, Suzukawa K, Nanmoku T, Obara N, Okoshi Y, Mukai HY, Hasegawa Y, Kojima H, Kawakami Y, Ninomiya H, Nagasawa T: Detection of the STAT5B-RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G-banding. Eur J Haematol; 2008 May;80(5):444-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of the STAT5B-RARA fusion transcript in acute promyelocytic leukemia with the normal chromosome 17 on G-banding.
  • Acute promyelocytic leukemia (APL) is characterized by chromosomal rearrangements of 17q21, leading to fusion of the gene-encoding retinoic acid receptor alpha (RARA) with a number of alternative partner genes.
  • We report a rare case of APL with STAT5B-RARA fusion transcript and the normal chromosome 17 on G-banding.
  • Administration of all trans-retinoic acid improved disseminated intravascular coagulation without decrease of the leukemia cells in his peripheral blood and bone marrow.
  • The molecular mechanism of fusion between STAT5B and RARA by chromosomal rearrangement is discussed based on the data from genome database.
  • Clinical characteristics of APL with STAT5B-RARA are also discussed.
  • [MeSH-major] Chromosomes, Human, Pair 17 / genetics. Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / analysis. Oncogene Proteins, Fusion / genetics. STAT5 Transcription Factor / analysis. STAT5 Transcription Factor / genetics. Transcription, Genetic / genetics

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  • [CommentIn] Eur J Haematol. 2009 Nov;83(5):499-501 [19624718.001]
  • (PMID = 18221386.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / STAT5 Transcription Factor; 0 / STAT5-RARalpha protein, human
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65. Mantadakis E, Samonis G, Kalmanti M: A comprehensive review of acute promyelocytic leukemia in children. Acta Haematol; 2008;119(2):73-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comprehensive review of acute promyelocytic leukemia in children.
  • The outcome of patients with acute promyelocytic leukemia (APL) has substantially improved since the successful introduction of tretinoin, and nowadays combining tretinoin with chemotherapy is potentially curative for at least 70-75% of patients with newly diagnosed APL.
  • In most pediatric series, APL represents < or = 10% of childhood acute myelogenous leukemia.
  • APL in children is more common in girls and in obese children.
  • It is characterized by a higher incidence of hyperleukocytosis, an increased incidence of microgranular morphology and by more frequent occurrence of the PML/RARalpha isoforms bcr 2 and bcr 3 compared to adults.
  • Tretinoin-based therapy is curative for the majority of children with APL.
  • Recent data indicate that > or = 2 negative RT-PCR assays for PML/RARalpha on bone marrow performed at least 1 month apart after completing therapy are strongly associated with long-term remissions, while conversion to PCR positivity for PML/RARalpha during remission is highly predictive of impending relapse.
  • Data from recent studies in adults and limited data from children show that arsenic trioxide is the single most effective agent in APL and deserves immediate study in newly diagnosed children in an effort to further improve prognosis and to limit exposure to conventional cytotoxic chemotherapy.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / therapy

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  • [Copyright] 2008 S. Karger AG, Basel
  • (PMID = 18285695.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 70
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66. Lo-Coco F, Ammatuna E: The biology of acute promyelocytic leukemia and its impact on diagnosis and treatment. Hematology Am Soc Hematol Educ Program; 2006;:156-61, 514
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The biology of acute promyelocytic leukemia and its impact on diagnosis and treatment.
  • Several genetic and phenotypic characteristics of acute promyelocytic leukemia (APL) blasts provide relevant targets and the rationale for tailored treatment.
  • These include the PML/RARalpha fusion and the transcription co-repressor complex recruited at the promoter of target genes by the hybrid protein, the intense and homogeneous expression of the CD33 antigen, absence of multidrug resistance-related phenotype, and a frequently mutated and constitutively activated FLT3 receptor.
  • Such genotypic and phenotypic features are targeted by agents currently in use in front-line therapy or at relapse (i.e., retinoids, arsenic trioxide, anthracyclines and anti-CD33 monoclonal antibodies), and by novel agents that may find a place in future treatments such as histone deacetylase and FLT3 inhibitors.
  • The unique PML/RARalpha aberration serves as a molecular marker for rapid diagnosis and prediction of response to ATRA-and ATO-containing therapies.
  • Methods for prompt and low-cost detection of this genetic abnormality, such as the analysis of PML nuclear staining, are extremely useful in clinical practice and could be adopted in countries with limited resources as a surrogate for rapid genetic diagnosis.
  • Finally, PML/RARalpha monitoring through sensitive RT-PCR can be regarded as an integrating part of the overall treatment strategy in this disease, whereby the treatment type and intensity are modulated in patients at different risk of relapse according to RT-PCR status during follow-up.
  • Because recent clinical studies suggest that most APL patients receiving intensive chemotherapy may be over-treated, longitudinal and stringent RT-PCR monitoring is becoming increasingly important to test the extent to which chemotherapy can be minimized in those presenting with low-risk disease.

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  • (PMID = 17124055.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 41
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67. Dimov ND, Medeiros LJ, Ravandi F, Bueso-Ramos CE: Acute promyelocytic leukemia at time of relapse commonly demonstrates cytogenetic evidence of clonal evolution and variability in blast immunophenotypic features. Am J Clin Pathol; 2010 Mar;133(3):484-90
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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 leukemia at time of relapse commonly demonstrates cytogenetic evidence of clonal evolution and variability in blast immunophenotypic features.
  • Despite the success of the current therapy for patients with acute promyelocytic leukemia (APL), relapse occurs in up to 30% of patients.
  • The characteristics of relapsed APL are not well described.
  • We evaluated a group of APL cases at relapse and compared the clinicopathologic, immunophenotypic, molecular, and cytogenetic findings with those at initial diagnosis.
  • From a group of 207 patients with APL, in 38 patients morphologic evidence of relapse developed.
  • In 30 patients relapse was isolated to bone marrow, and 8 had extramedullary disease.
  • The size of the PML-RARalpha fusion transcript was invariable.
  • We conclude that changes in the immunophenotype and cytogenetic evidence of clonal evolution are common in APL at the time of relapse.
  • [MeSH-major] Cytogenetics. Immunophenotyping. Leukemia, Promyelocytic, Acute / pathology. Neoplasm Proteins / genetics. Neoplasm Proteins / immunology

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  • (PMID = 20154288.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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68. Liang JY, Wu DP, Liu YJ, Ma QF, Gong JX, Zhu MQ, Xue YQ, Chen ZX: [The clinical and laboratory features of acute promyelocytic leukemia: an analysis of 513 cases]. Zhonghua Nei Ke Za Zhi; 2008 May;47(5):389-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The clinical and laboratory features of acute promyelocytic leukemia: an analysis of 513 cases].
  • OBJECTIVE: To investigate the clinical and laboratory features of acute promyelocytic leukemia (APL).
  • METHODS: 513 APL patients in the last two decades were retrospectively analyzed in this research.
  • We investigated the clinical features including age, sex, abnormality of peripheral hemogram before treatment, therapeutic effect and follow-up and laboratory data such as morphology, immunology, cytogenetics and molecular biology (MICM).
  • RESULTS: The median age of the APL patients was 33 years old and the ratio of male and female was 1.21:1.
  • Before treatment, the median level of WBC was 4.3 x 10(9)/L and the detection rate of abnormal promyelocyte on blood film was 85.8%; with immunophenotypic detection, the expression levels of CD117, CD34, HLA-DR, CD7, CD14 and CD19 in APL were found to be lower and the expression levels of CD2, CD33 and MPO higher than those in other subtypes of acute myelocytic leukemia (AML) (both P < 0.01).
  • Specific abnormal chromosome t (15;17) was detected in 91.7% of the patients, of whom 75.9% had standard translocation of t (15;17), being the most common one and 15.8% of the patients had t (15;17) with additional abnormal chromosome.
  • With molecular biological detection, PML/RARalpha fusion gene positive rate was 99.6%.
  • In a relatively long clinical follow-up, we found that the complete remission (CR) rate in APL patients was 84.7%, incidence of DIC was 13.4% and five-year survival rate was 30.7%.
  • CONCLUSIONS: Comprehensive evaluation of MICM could be of important significance in the diagnosis and prognosis judgment for APL patients.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / immunology

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  • (PMID = 18953948.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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69. Ghosh I, Kumar L, Seth R, Thavraj V: Sustained remission achieved with ATRA and chemotherapy in second relapse of acute promyelocytic leukemia in Down syndrome. J Pediatr Hematol Oncol; 2009 Aug;31(8):539-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sustained remission achieved with ATRA and chemotherapy in second relapse of acute promyelocytic leukemia in Down syndrome.
  • Children with Down syndrome (DS) are at an increased risk of developing acute leukemia.
  • Acute myeloid leukemia predominates among DS children below 4 years of age but acute promyelocytic leukemia (APL) has rarely been reported in DS.
  • Acute myeloid leukemia in DS is extremely sensitive to treatment but the optimum treatment of de novo or relapsed APL in DS is not known.
  • We describe a child with DS and APL, who despite having a multiply relapsing course, achieved a third remission with ATRA and chemotherapy, which is sustained with maintenance therapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Down Syndrome / complications. Leukemia, Promyelocytic, Acute / prevention & control. Tretinoin / administration & dosage

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  • (PMID = 19636277.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  • [Number-of-references] 13
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70. Pankiv S, Lamark T, Bruun JA, Øvervatn A, Bjørkøy G, Johansen T: Nucleocytoplasmic shuttling of p62/SQSTM1 and its role in recruitment of nuclear polyubiquitinated proteins to promyelocytic leukemia bodies. J Biol Chem; 2010 Feb 19;285(8):5941-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nucleocytoplasmic shuttling of p62/SQSTM1 and its role in recruitment of nuclear polyubiquitinated proteins to promyelocytic leukemia bodies.
  • It is also suggested to shuttle ubiquitinated proteins for proteasomal degradation. p62 is commonly found in cytosolic protein inclusions in patients with protein aggregopathies, it is up-regulated in several forms of human tumors, and mutations in the gene are linked to classical adult onset Paget disease of the bone.
  • The protein is also found in nuclear promyelocytic leukemia bodies.
  • We found p62 to be essential for accumulation of polyubiquitinated proteins in promyelocytic leukemia bodies upon inhibition of nuclear protein export.

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  • (PMID = 20018885.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATXN1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Ataxin-1; 0 / Ataxins; 0 / Nerve Tissue Proteins; 0 / Nuclear Localization Signals; 0 / Nuclear Proteins; 0 / Peptides; 0 / SQSTM1 protein, human; 26700-71-0 / polyglutamine; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2820819
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71. Cho H, Kim DU, Kehrl JH: RGS14 is a centrosomal and nuclear cytoplasmic shuttling protein that traffics to promyelocytic leukemia nuclear bodies following heat shock. J Biol Chem; 2005 Jan 7;280(1):805-14
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  • [Title] RGS14 is a centrosomal and nuclear cytoplasmic shuttling protein that traffics to promyelocytic leukemia nuclear bodies following heat shock.
  • Mutation of a nuclear export signal or treatment with leptomycin B causes nuclear accumulation of RGS14 and its association with promyelocytic leukemia protein nuclear bodies.
  • Mild heat stress, but not proteotoxic or transcription-linked stresses, re-localizes the RGS14 from the cytoplasm to promyelocytic leukemia nuclear bodies.


72. Jul-Larsen A, Grudic A, Bjerkvig R, Bøe SO: Subcellular distribution of nuclear import-defective isoforms of the promyelocytic leukemia protein. BMC Mol Biol; 2010;11:89
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  • [Title] Subcellular distribution of nuclear import-defective isoforms of the promyelocytic leukemia protein.
  • BACKGROUND: The promyelocytic leukemia (PML) protein participates in a number of cellular processes, including transcription regulation, apoptosis, differentiation, virus defense and genome maintenance.
  • Most PML splice variants target the nucleus where they define sub-nuclear compartments termed PML nuclear bodies (PML NBs).
  • However, PML variants that lack the NLS are also expressed, suggesting the existence of PML isoforms with cytoplasmic functions.
  • In the present study we expressed PML isoforms with a mutated NLS in U2OS cells to identify potential cytoplasmic compartments targeted by this protein.
  • RESULTS: Expression of NLS mutated PML isoforms in U2OS cells revealed that PML I targets early endosomes, PML II targets the inner nuclear membrane (partially due to an extra NLS at its C-terminus), and PML III, IV and V target late endosomes/lysosomes.
  • Clustering of PML at all of these subcellular locations depended on a functional TRIM domain.
  • CONCLUSIONS: This study demonstrates the capacity of PML to form macromolecular protein assemblies at several different subcellular sites.

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  • (PMID = 21092142.001).
  • [ISSN] 1471-2199
  • [Journal-full-title] BMC molecular biology
  • [ISO-abbreviation] BMC Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
  • [Other-IDs] NLM/ PMC2998510
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73. Albano F, Mestice A, Pannunzio A, Lanza F, Martino B, Pastore D, Ferrara F, Carluccio P, Nobile F, Castoldi G, Liso V, Specchia G: The biological characteristics of CD34+ CD2+ adult acute promyelocytic leukemia and the CD34 CD2 hypergranular (M3) and microgranular (M3v) phenotypes. Haematologica; 2006 Mar;91(3):311-6
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  • [Title] The biological characteristics of CD34+ CD2+ adult acute promyelocytic leukemia and the CD34 CD2 hypergranular (M3) and microgranular (M3v) phenotypes.
  • BACKGROUND AND OBJECTIVES: Acute promyelocytic leukemia (APL) is characterized by leukemic cells blocked at the promyelocytic stage of granulocytic differentiation.
  • To date, it is still not clear whether CD34 expression identifies a subset of APL patients with peculiar characteristics.
  • We, therefore, conducted a detailed analysis of CD34 expression at diagnosis in 136 adults with de novo APL.
  • DESIGN AND METHODS: We investigated 136 newly diagnosed APL patients from four Italian Institutions.
  • All 136 cases were tested for CD34 and CD2 expression: 124 (91%) cases were classified as hypergranular (M3) and 12 (9%) as the hyporgranular M3 variant (M3v).
  • The parameters considered were white blood cell (WBC) and platelet counts, hemoglobin levels, percentage of peripheral blood leukemic promyelocytes (PBLP), CD15, CD56 and HLA-DR expression, and the PML/RARalpha isoform, to assess their relationship with CD34 and CD2 expression.
  • Moreover, compared with CD34- APL patients, CD34+ APL patients had a significantly higher percentage of PBLP at presentation, were more frequently female and had a higher proportion of bcr3 expression.
  • Among the 136 APL cases, 24 (17.6%) and 80 (58.8%) were identified as CD34+CD2+ and CD34-CD2-, respectively.
  • There were no differences between the two groups in terms of complete remission, overall survival and disease-free survival.
  • INTERPRETATION AND CONCLUSIONS: Our findings suggest that immunophenotypic analysis can distinguish a subset of APL patients with different biological characteristics.
  • [MeSH-major] Antigens, CD2 / genetics. Antigens, CD34 / biosynthesis. Leukemia, Promyelocytic, Acute / genetics. Phenotype

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  • [CommentIn] Haematologica. 2006 Mar;91(3):289C [16531246.001]
  • (PMID = 16531253.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD2; 0 / Antigens, CD34
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74. Wrede JE, Sundram U, Kohler S, Cherry AM, Arber DA, George TI: Fluorescence in situ hybridization investigation of cutaneous lesions in acute promyelocytic leukemia. Mod Pathol; 2005 Dec;18(12):1569-76
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  • [Title] Fluorescence in situ hybridization investigation of cutaneous lesions in acute promyelocytic leukemia.
  • Cutaneous manifestations of acute promyelocytic leukemia are rare but well documented.
  • Skin biopsies of leukemia can be difficult to confirm using morphology alone, and paraffin section immunophenotyping is not specific in separating acute promyelocytic leukemia from other acute myeloid leukemias involving the skin or inflammatory conditions, such as Sweet's syndrome and all-trans retinoic acid-associated genital ulcers, which may mimic leukemia cutis.
  • Fluorescence in situ hybridization has been shown to be a fast and effective method of detecting the PML/RARA fusion gene characteristic of acute promyelocytic leukemia in fresh blood and bone marrow samples.
  • This retrospective study of cutaneous lesions from four patients with acute promyelocytic leukemia evaluates the utility of performing fluorescence in situ hybridization to confirm the presence of cutaneous manifestations of acute promyelocytic leukemia in formalin-fixed, paraffin-embedded skin biopsies.
  • All patients had previous bone marrow findings of acute promyelocytic leukemia with characteristic morphology, immunophenotype, and cytogenetic studies, which detailed the presence of the t(15;17)(q22;q12) rearrangement.
  • The fourth case, involving the scrotum, showed a predominant neutrophilic infiltrate diffusely involving the dermis and epidermis with a subset of blastic cells.
  • Nuclei were extracted from core biopsies of the formalin-fixed paraffin-embedded tissue and fluorescence in situ hybridization was performed using a dual color, dual fusion PML / RARA probe.
  • All cases showed evidence of the t(15;17) rearrangement, with 90, 79, 51 and 16% positive signal patterns, each well above background limits.
  • Fluorescence in situ hybridization appears to be a robust technique to detect cutaneous manifestations of acute promyelocytic leukemia in formalin-fixed paraffin-embedded skin biopsies.
  • [MeSH-major] In Situ Hybridization, Fluorescence. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Skin Neoplasms / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Cells / pathology. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Female. Humans. Infant. Interphase / genetics. Male. Middle Aged. Paraffin Embedding. Retrospective Studies

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  • (PMID = 16056248.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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75. Tang J, Xie W, Yang X: Association of caspase-2 with the promyelocytic leukemia protein nuclear bodies. Cancer Biol Ther; 2005 Jun;4(6):645-9
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  • [Title] Association of caspase-2 with the promyelocytic leukemia protein nuclear bodies.
  • One such complex is the plasma membrane-bound death-inducing signaling complex (DISC), formed upon engagement of death receptors, which recruits and activates caspase-8 and -10.
  • Here we present evidence that caspase-2 is localized to the promyelocytic leukemia protein nuclear bodies (PML-NBs), nuclear macro-molecular complexes that are involved in many scenarios of apoptosis including DNA damage.
  • These data suggest the existence of a nuclear apoptosis pathway that involves both caspase-2 and the PML-NBs.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Apoptosis. CRADD Signaling Adaptor Protein. Caspase 2. HeLa Cells. Humans. Kidney / metabolism. Promyelocytic Leukemia Protein

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  • (PMID = 15917662.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA88868
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CRADD Signaling Adaptor Protein; 0 / CRADD protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Promyelocytic Leukemia Protein; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; EC 3.4.22.- / CASP2 protein, human; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Cysteine Endopeptidases
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76. Felicetti F, Errico MC, Bottero L, Segnalini P, Stoppacciaro A, Biffoni M, Felli N, Mattia G, Petrini M, Colombo MP, Peschle C, Carè A: The promyelocytic leukemia zinc finger-microRNA-221/-222 pathway controls melanoma progression through multiple oncogenic mechanisms. Cancer Res; 2008 Apr 15;68(8):2745-54
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  • [Title] The promyelocytic leukemia zinc finger-microRNA-221/-222 pathway controls melanoma progression through multiple oncogenic mechanisms.
  • We have identified the promyelocytic leukemia zinc finger (PLZF) transcription factor as a repressor of miR-221 and miR-222 by direct binding to their putative regulatory region.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cyclin-Dependent Kinase Inhibitor p27. Disease Progression. Down-Regulation. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Nude. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism

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  • (PMID = 18417445.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Kruppel-Like Transcription Factors; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs; 0 / Oligonucleotides, Antisense; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 147855-37-6 / ZBTB16 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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77. Samochatova EV, Maschan AA, Aleĭnikova OV, Bespalova AV, Baĭdil'dina DD, Dubrovina ME, Fleĭshman EV, Nasedkina TV, Rumiantsev SA, Rumiantsev AG: [Long-term results of combined treatment of acute promyelocytic leukemia in children and adolescents with gene therapy]. Ter Arkh; 2007;79(7):26-30
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  • [Title] [Long-term results of combined treatment of acute promyelocytic leukemia in children and adolescents with gene therapy].
  • AIM: To analyse the results of treatment of children and adolescents with acute promyelocytic leukemia (APL) including polychemotherapy and ATRA (protocols APL 93, 98 and 2003).
  • MATERIAL AND METHODS: The course of the disease, modification of the treatment protocols with reduction of anthracyclines and ATRA doses, results of molecular monitoring of PML/RARalpha transcript have been analysed for 107 APL patients.
  • RESULTS: For prognosis of the disease important are initial characteristics of the patient and the time of the tumor regress assessed by molecular methods--establishment of molecular remission and molecular recurrence.
  • CONCLUSIONS: In APL it is necessary to conduct molecular monitoring especially in patients at high risk and with poor prognosis in a decrease of treatment intensity for toxicity relief.
  • To raise efficacy of APL recurrence therapy it is necessary to design a special updated protocol.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Receptors, Retinoic Acid / genetics. Transcription, Genetic / drug effects

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  • (PMID = 17802786.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha
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78. Yang S, Jeong JH, Brown AL, Lee CH, Pandolfi PP, Chung JH, Kim MK: Promyelocytic leukemia activates Chk2 by mediating Chk2 autophosphorylation. J Biol Chem; 2006 Sep 8;281(36):26645-54
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  • [Title] Promyelocytic leukemia activates Chk2 by mediating Chk2 autophosphorylation.
  • Here we elucidate one such alternative mechanism regulated by PML (promyelocytic leukemia) that is involved in acute promyelocytic leukemia (APL).
  • Although p53-inactivating mutations are extremely rare in APL, t(15;17) chromosomal translocation which fuses retinoic acid receptor (RARalpha) to PML is almost always present in APL, while the other PML allele is intact.
  • We demonstrate that PML interacts with Chk2 and activates Chk2 by mediating its autophosphorylation step, an essential step for Chk2 activity that occurs after phosphorylation by the upstream kinase ATM (ataxia telangiectasia-mutated).
  • PML/RARalpha in APL suppresses Chk2 by dominantly inhibiting the auto-phosphorylation step, but inactivation of PML/RARalpha with alltrans retinoic acid (ATRA) restores Chk2 autophosphorylation and activity.
  • Thus, by fusing PML with RARalpha, the APL cells appear to have achieved functional suppression of Chk2 compromising the Chk2-p53 apoptotic pathway.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Protein-Serine-Threonine Kinases / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 16835227.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Pml protein, mouse; 0 / Receptors, Retinoic Acid; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Atm protein, mouse; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Chek2 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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79. 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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80. Plevova P, Walczyskova S, Jeziskova I, Jurckova N, Krepelova A, Puchmajerova A, Pavlikova K, Foretova L, Zapletalova J, Silhanova E: Germline variants of the promyelocytic leukemia tumor suppressor gene in patients with familial cancer. Neoplasma; 2009;56(6):500-7
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  • [Title] Germline variants of the promyelocytic leukemia tumor suppressor gene in patients with familial cancer.
  • The promyelocytic leukemia (PML) gene is an important tumor suppressor gene.
  • We tested the hypothesis that germline disruption of the PML gene may be associated with a cancer predisposition syndrome.
  • Mutation analysis of the PML gene was performed in 111 patients with familial adult cancer or young age-onset adult cancer.
  • Frequency of the c.2260G>C (p.Ala754Pro) variant in isoform IV of the PML gene was higher in patients with colon polyposis and cancer than in the control group (P = 0.029).
  • In conclusion, germline disruption of the PML gene is probably not associated with a highly penetrant susceptibility to adult-onset breast and colon cancer.
  • Pathogenicity of c.83C>T and c.1558C>T variants in the PML gene is uncertain.
  • [MeSH-minor] Adult. Aged. DNA Mutational Analysis. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Young Adult

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  • (PMID = 19728758.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human
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81. Hasan SK, Lo-Coco F: Utilization of molecular phenotypes to detect relapse and optimize the management of acute promyelocytic leukemia. Clin Lymphoma Myeloma Leuk; 2010 Oct;10 Suppl 3:S139-43
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  • [Title] Utilization of molecular phenotypes to detect relapse and optimize the management of acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (APL) is characterized by a unique genetic aberration, the t(15;17) chromosome translocation.
  • Translocation breakpoints are located within the promyelocytic leukemia (PML) locus on chromosome 15 and the retinoic acid receptor alpha (RARA) locus on chromosome 17.
  • In the past 2 decades, critical advances have been made in understanding the molecular pathogenesis of APL.
  • APL represents a paradigm for molecularly targeted therapy in cancer and an extraordinary model for translational research in medicine.
  • In fact, the release of differentiation block upon treatment of APL with all-trans-retinoic acid (ATRA) has represented the first example of targeted therapy in human cancer.
  • More recently, the advent of arsenic trioxide (ATO) has allowed further progress in the management of this disease through improved outcomes in patients receiving this agent in combination with ATRA.
  • Finally, optimization of therapy and minimization of toxicity is feasible in this disease through careful monitoring of residual disease using polymerase chain reaction-based approaches targeting the PML-RARA fusion gene.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / drug therapy. Molecular Targeted Therapy. Phenotype

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  • (PMID = 21115433.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Arsenicals; 0 / Oxides; 0 / PRAM1 protein, human; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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82. Taguchi A, Takahashi T, Harima Y, Takemoto Y, Ando T, Nomiyama J, Matsubara A, Yujiri T, Tanizawa Y: [All-trans retinoic acid-induced erythema nodosum in acute promyelocytic leukemia]. Rinsho Ketsueki; 2005 Mar;46(3):202-5
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  • [Title] [All-trans retinoic acid-induced erythema nodosum in acute promyelocytic leukemia].
  • A 24-year-old woman with acute promyelocytic leukemia was treated with all-trans retinoic acid (ATRA) as a remission induction therapy.
  • Although the administration of ATRA was continued until complete remission of the leukemia, the erythema nodosum rapidly disappeared following short-term steroid therapy and no recurrence was observed.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Erythema Nodosum / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects

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  • (PMID = 16447715.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin; 9PHQ9Y1OLM / Prednisolone
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83. Iki S, Yokota S, Okabayashi T, Yokosawa N, Nagata K, Fujii N: Serum-dependent expression of promyelocytic leukemia protein suppresses propagation of influenza virus. Virology; 2005 Dec 5;343(1):106-15

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  • [Title] Serum-dependent expression of promyelocytic leukemia protein suppresses propagation of influenza virus.
  • Basal and interferon (IFN)-induced levels of typical IFN-inducible anti-viral proteins, such as 2',5'-oligoadenylate synthetase, dsRNA-activated protein kinase and MxA, were unaffected by variation in FBS concentrations.
  • But promyelocytic leukemia protein (PML) was expressed in a serum-dependent manner.
  • In particular, the 65 to 70 kDa isoform of PML was markedly upregulated following the addition of serum.
  • Immunofluorescence microscopy indicated that PML was mainly formed nuclear bodies in Caco-2 cells at various FBS concentrations, and the levels of the PML-nuclear bodies were upregulated by FBS.
  • Overexpression of PML isoform consisting of 560 or 633 amino acid residues by transfection of expression plasmid results in significantly delayed viral replication rate in Caco-2 cells.
  • On the other hand, downregulation of PML expression by RNAi enhanced viral replication.
  • These results indicate that PML isoforms which are expressed in a serum-dependent manner suppress the propagation of influenza virus at an early stage of infection.

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  • (PMID = 16154611.001).
  • [ISSN] 0042-6822
  • [Journal-full-title] Virology
  • [ISO-abbreviation] Virology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media; 0 / MX1 protein, human; 0 / Myxovirus Resistance Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; 9008-11-1 / Interferons; EC 2.7.11.1 / eIF-2 Kinase; EC 2.7.7.- / 2',5'-Oligoadenylate Synthetase; EC 3.6.1.- / GTP-Binding Proteins
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84. Dvorak CC, Sanders RP, Dahl GV, Donaldson SS, Razzouk BI: Reinduction of relapsed acute promyelocytic leukemia with ATRA and low dose antimetabolite-based chemotherapy. Pediatr Blood Cancer; 2007 May;48(5):582-5
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  • [Title] Reinduction of relapsed acute promyelocytic leukemia with ATRA and low dose antimetabolite-based chemotherapy.
  • While the disease-free survival of acute promyelocytic leukemia (APML) now approaches 75%, some children continue to experience relapses, and questions remain as to the optimal management of these patients.
  • These cases demonstrate that there is a role for ATRA plus differentiating chemotherapy other than arsenic trioxide in the treatment of relapsed APML.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / administration & dosage

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  • (PMID = 16123994.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA 21765
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 5688UTC01R / Tretinoin; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate
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85. Drilon AD, Gamboa EO, Koolaee R, Goel A: Acute promyelocytic leukemia in HIV-infected adults: a case report and review of therapeutic considerations. Clin Lymphoma Myeloma Leuk; 2010 Oct;10(5):E47-52
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  • [Title] Acute promyelocytic leukemia in HIV-infected adults: a case report and review of therapeutic considerations.
  • The incidence of acute promyelocytic leukemia (APL) in patients with HIV is exceedingly rare, making the establishment of therapeutic approaches challenging and often individualized.
  • We report the case of a 43-year-old female who presented with fatigue and malaise, and was concurrently diagnosed with APL and HIV.
  • Induction and consolidation with all-trans-retinoic acid (ATRA), idarubicin, and mitoxantrone were initiated in conjunction with highly active anti-retroviral therapy (HAART) consisting of tenofovir/emtricitabine, fosamprenavir, and raltegravir.
  • A complete morphologic, cytogenetic, and molecular response was achieved post-induction.
  • ATRA has been found to induce apoptosis in HIV-infected leukemic cells, and protease inhibitor therapy has furthermore been reported to be synergistic with ATRA in inducing differentiation of APL cell lines.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiretroviral Therapy, Highly Active. HIV Infections / complications. HIV Infections / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / virology


86. Ghavamzadeh A, Alimoghaddam K, Ghaffari SH, Rostami S, Jahani M, Hosseini R, Mossavi A, Baybordi E, Khodabadeh A, Iravani M, Bahar B, Mortazavi Y, Totonchi M, Aghdami N: Treatment of acute promyelocytic leukemia with arsenic trioxide without ATRA and/or chemotherapy. Ann Oncol; 2006 Jan;17(1):131-4
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  • [Title] Treatment of acute promyelocytic leukemia with arsenic trioxide without ATRA and/or chemotherapy.
  • INTRODUCTION: Arsenic trioxide is effective and approved for treatment of relapsed or refractory acute promyelocytic leukemia (APL) cases resistant to all-trans retinoic acid (ATRA), but its effect on new cases of APL is not clear.
  • MATERIALS AND METHODS: We studied 111 patients with APL.
  • Arsenic trioxide was infused at 0.15 mg/kg daily dose, until complete remission was achieved.
  • We studied minimal residual disease (MRD) by semi-sensitive reverse transcription polymerase chain reaction (RT-PCR) on peripheral blood samples.
  • With the median (range) follow-up period of 16.5 (1-57) months, 1- and 2-year disease-free survival was 88.3% and 63.7%, respectively; 24 patients relapsed, 19 of whom achieved a second complete remission, again by arsenic trioxide.
  • CONCLUSIONS: Arsenic trioxide is effective as first-line treatment for APL.

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  • (PMID = 16227315.001).
  • [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] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; S7V92P67HO / arsenic trioxide
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87. Lang L, Li HM, Liu H, Wang YM, Zhang XM: [Detection of PML/RARa transcripts in acute promyelocytic leukemia by real-time quantitative reverse transcription polymerase chain reaction]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):714-9
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  • [Title] [Detection of PML/RARa transcripts in acute promyelocytic leukemia by real-time quantitative reverse transcription polymerase chain reaction].
  • This study was purposed to establish a real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) for detection of PML/RARa fusion gene in patients with acute promyelocytic leukemia (APL) and to explore the relationship between the expression level of PML/RARa fusion gene transcript and the clinical status or efficacy of the therapy in APL.
  • The conventional RT-PCR was used to amplify PML/RARa gene from cultured NB4 cells.
  • The PML/RARa gene transcripts of bone marrows in 4 APL patients before and after treatment and in 1 APL patient relapsed after complete remission were dynamically detected by modified real-time quantitative RT-PCR.
  • The results indicated that the sensitivity of real-time quantitative RT-PCR for detecting PML/RARa fusion gene was about 10(-5) microg cDNA from NB4 cells, the repeatability and reproducibility of this method were satisfactory, intra-and inter-assay coefficients of variation were 2.1% and 3.8%.
  • The copy numbers of PML/RARa transcripte reflecting PML/RARa fusion gene expression level in 4 newly diagnosed patients with APL were 1884, 5533, 1803, 4677 and the median was 3 475.
  • After ATRA + chemotherapy copy numbers of PML/RARa transcript decreased to 40, 135, 79, 29, and mean was 121.
  • Another patient's PML/RARa gene copy number was 8600 at diagnosis, the gene copy number was 730 after therapy for 4 months, although he was in complete remission, but copy number increased to 11 000 when APL relapsed 3 months later.
  • The efficiency of method was finally tested for patient samples, showing a PML/RARa transcript copy number in APL patients significantly decrease after therapy, and increase at the time of relapse which indicate that changes of fusion gene expression levels coincide with clinical progress of disease.
  • This method can be used to detect the minimal residual disease, assess response to treatment and evaluate prognosis of disease.

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  • (PMID = 17708789.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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88. Yamauchi T, Arai H, Taga M, Amaya N, Lee JD, Ueda T: [Adams-Stokes attack due to complete atrioventricular block in a patient with acute promyelocytic leukemia during remission induction therapy using all-trans retinoic acid]. Rinsho Ketsueki; 2005 Mar;46(3):206-10
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  • [Title] [Adams-Stokes attack due to complete atrioventricular block in a patient with acute promyelocytic leukemia during remission induction therapy using all-trans retinoic acid].
  • Remission induction therapy was performed for a 46-year-old Japanese man with acute promyelocytic leukemia using ATRA (45 mg/m2), enocitabine (170 mg/m2, 5 days), and mitoxantrone (4 mg/m2, 3 days).
  • The normal sinus rhythm was restored 15 days thereafter, and the patient eventually reached remission.
  • [MeSH-major] Heart Block / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / adverse effects

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  • (PMID = 16447716.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 9YVR68W306 / enocitabine; BZ114NVM5P / Mitoxantrone
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89. Lin J, Han LX, Qian J, Wang YL, Qian Z, Yang XF, Sheng XJ: [Quantification of PML/RAR alpha fusion gene transcripts in patients with acute promyelocytic leukemia by using real-time quantitative PCR]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2008 Jun;25(3):319-21
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  • [Title] [Quantification of PML/RAR alpha fusion gene transcripts in patients with acute promyelocytic leukemia by using real-time quantitative PCR].
  • OBJECTIVE: To establish and evaluate a real time quantitative PCR (RQ-PCR) method for detection and quantification the PML/RAR alpha fusion gene transcripts in patients with acute promyelocytic leukemia (APL).
  • METHODS: Three pairs of primers and TaqMan probe were designed for detecting the most frequent PML/RAR alpha transcripts (L-form, S-form and V-form) and normal ABL was used as an internal control.
  • A real time PCR condition was established to detect PML/RAR alpha and ABL positive templates with a series of dilutions.
  • To evaluate this assay, bone marrow samples from 6 APL patients were detected.
  • The median absolute and normalized amount of PML/RAR alpha fusion gene transcripts were 4.27 x 10(3)-3.36 x 10(5) copies/50 ng (median 4.33 x 10(4)copies/50 ng) and 29.38%-600.53% (median 48.12%) respectively.
  • One case showed significant decrease of PML/RAR alpha fusion gene transcripts after induction therapy compared to that at the time of diagnosis, while the fusion transcripts significantly increased after relapsed.
  • CONCLUSION: RQ-PCR is a sensitive, reliable quantitative assay and can be used in the diagnosis of APL and measurement of MRD.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 18543226.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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90. Tallman MS: The expanding role of arsenic in acute promyelocytic leukemia. Semin Hematol; 2008 Jul;45(3 Suppl 2):S25-9
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  • [Title] The expanding role of arsenic in acute promyelocytic leukemia.
  • Ten percent to 15% of adults in the United States with acute myeloid leukemia (AML) are diagnosed with acute promyelocytic leukemia (APL) each year, which amounts to approximately 1,200 newly diagnosed patients.
  • In almost all APL patients, the retinoic acid receptor-alpha (RARalpha) gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, denoted as t(15;17)(q22;q12).
  • All patients have the PML/RAR-alpha fusion transcript.
  • Identification of this fusion transcript is important for both diagnosis and for detection of minimal residual disease.
  • Overall, more than 80% of APL patients are curable using current strategies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Arsenicals / administration & dosage. Clinical Trials as Topic. Cytarabine / administration & dosage. Humans. Oxides / administration & dosage. Treatment Outcome. Tretinoin / administration & dosage

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  • (PMID = 18760708.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 32
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91. Guidez F, Howell L, Isalan M, Cebrat M, Alani RM, Ivins S, Hormaeche I, McConnell MJ, Pierce S, Cole PA, Licht J, Zelent A: Histone acetyltransferase activity of p300 is required for transcriptional repression by the promyelocytic leukemia zinc finger protein. Mol Cell Biol; 2005 Jul;25(13):5552-66
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  • [Title] Histone acetyltransferase activity of p300 is required for transcriptional repression by the promyelocytic leukemia zinc finger protein.
  • Promyelocytic leukemia zinc finger (PLZF), originally identified as a fusion with retinoic acid receptor alpha in rare cases of all-trans-retinoic acid-resistant acute promyelocytic leukemia, is a transcriptional repressor that recruits histone deacetylase-containing corepressor complexes to specific DNA binding sites.

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  • (PMID = 15964811.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA059936; United States / NCI NIH HHS / CA / CA59936; United States / NIGMS NIH HHS / GM / R37 GM062437; United States / NIGMS NIH HHS / GM / GM62437; United States / NIGMS NIH HHS / GM / R01 GM062437; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Fluorescent Dyes; 0 / Kruppel-Like Transcription Factors; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 147855-37-6 / ZBTB16 protein, human; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.48 / Histone Acetyltransferases; I223NX31W9 / Fluorescein-5-isothiocyanate
  • [Other-IDs] NLM/ PMC1156991
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92. Wang LH, Yang JY, Cui W, Shin YK, Wu CF: Involvement of promyelocytic leukemia protein in the ethanol-induced apoptosis in mouse embryo fibroblasts. Yakugaku Zasshi; 2008 Jul;128(7):1067-71
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  • [Title] Involvement of promyelocytic leukemia protein in the ethanol-induced apoptosis in mouse embryo fibroblasts.
  • The promyelocytic leukemia (PML) gene is a tumor suppressor gene associated with cell apoptosis, cell proliferation, and senescence.
  • However, the role of PML in the ethanol-induced apoptosis is not fully-known.
  • In this study, using wild-type mouse embryo fibroblasts (MEF) and PML null MEF cells, we found that (1) ethanol (100 mM and 200 mM) could obviously induce apoptosis of wild-type MEF cells, whereas, in PML null MEF cells, the pro-apoptotic function of ethanol was partially blocked;.
  • (2) the expression levels of phosphorylated p53 and two of its target genes, p21 and Bax, could be significantly up-regulated by ethanol (200 mM) in wild-type MEF cells in a time-dependent manner, but not in PML null MEF cells.
  • These results indicate that PML plays an important role in ethanol-induced apoptosis, and p53-dependent apoptotic pathway may be involved in this process.

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  • (PMID = 18591875.001).
  • [ISSN] 0031-6903
  • [Journal-full-title] Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
  • [ISO-abbreviation] Yakugaku Zasshi
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Pml protein, mouse; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 3K9958V90M / Ethanol
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93. Tarkanyi I, Dudognon C, Hillion J, Pendino F, Lanotte M, Aradi J, Ségal-Bendirdjian E: Retinoid/arsenic combination therapy of promyelocytic leukemia: induction of telomerase-dependent cell death. Leukemia; 2005 Oct;19(10):1806-11
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  • [Title] Retinoid/arsenic combination therapy of promyelocytic leukemia: induction of telomerase-dependent cell death.
  • Acute promyelocytic leukemia (APL) is efficiently treated with a cell differentiation inducer, all-trans retinoic acid (ATRA).
  • Recently, arsenic trioxide (As2O3), alone or in combination with ATRA, has been identified as an alternative therapy in patients with both ATRA-sensitive and ATRA-resistant APL.
  • Previous investigations restricted the mechanism of this synergism to the modulation and/or degradation of PML-RARalpha oncoprotein through distinct pathways.
  • In this study, using several ATRA maturation-resistant APL cell lines, we demonstrate in vitro that the success of ATRA/As2O3 treatment in APL pathology can be explained, at least in part, by a synergistic effect of these two drugs in triggering downregulation of telomerase efficient enough to cause telomere shortening and subsequent cell death.
  • Such long-term low-dose combinatorial therapy strategies, developed also to avoid acute side effects, reinforce the notion that the antitelomerase strategy, based on a combination of active agents, should now be considered and evaluated not only in APL but also in other malignancies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. DNA-Binding Proteins / metabolism. Drug Resistance, Neoplasm. Leukemia, Promyelocytic, Acute / drug therapy. Telomerase / metabolism

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  • (PMID = 16107885.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arsenicals; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; EC 2.7.7.49 / Telomerase; S7V92P67HO / arsenic trioxide
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94. Schwarz J, Korístek Z, Starý J, Zák P, Kozák T, Marková J, Michalová K, Dvoráková D, Mayer J, Cetkovský P: [Therapy of acute promyelocytic leukemia in Czechia: results and analysis of prognostic factors]. Vnitr Lek; 2008 Jul-Aug;54(7-8):757-70
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  • [Title] [Therapy of acute promyelocytic leukemia in Czechia: results and analysis of prognostic factors].
  • [Transliterated title] Lécba akutní promyelorytárni leukemie v Cesku: výsledky a analýza prognostických faktorů.
  • We have retrospectively evaluated a cohort of 144 patients (including 17 pediatric ones) with de novo acute promyelocytic leukemia registered in databases of institutions cooperating within the CELL group (The Czech Leukemia Study Group for Life).
  • The aim was to check how well fared the patients, the majority of whom was not included into clinical trials, in real life.
  • The projected overall survival (OS) 4 years after diagnosis was 58.9%, and 55.3% at 6 years.
  • In 8 patients (6.0%), no antileukemic therapy at all was given (either they died shortly after admission to the ward or therapy was not feasible due to their clinical status).
  • Of 102 patients with induction treatment with a combination of anthracycline and tretinoin (ATRA), 84 individuals (82.4%) attained CR (typically, this cohort might have been subjected to clinical trials).
  • This result was better than that of patients treated by chemotherapy only (n = 15; CR 46.7%; P = 0.003) or by ATRA monotherapy (n = 13; CR 62.5%; P = 0.17).
  • Another parameter with a significant impact on attaining CR was the leukocyte (WBC) count at diagnosis: its median values in patients achieving and not achieving CR were 2.1 and 24.0 x 10(9)/l, respectively (P < 0.0001).
  • FAB M3v morphology, LDH serum level, fibrinogen level, presence of internal tandem duplication (ITD) of the FLT3 gene (which was strongly associated with leukocytosis and also with the short PML/RARalpha transcript resulting from the bcr3 break in the PML gene).
  • The platelet counts at diagnosis had no impact on entering CR.
  • Our study points to a significant difference of the results obtained in real life and of the results that could be achieved in patients who were fit to enter clinical trials.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18780575.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
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95. Chen J, Gu LJ, Tang JY, Xue HL, Pan C, Ye QD, Jiang H, Dong L, Zhou M, Wang YP: [Effectiveness of the AML-XH-99-M3 protocol for treatment of acute promyelocytic leukemia in children]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Jun;10(3):329-32
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  • [Title] [Effectiveness of the AML-XH-99-M3 protocol for treatment of acute promyelocytic leukemia in children].
  • OBJECTIVE: To evaluate the effectiveness of AML-XH-99-M3 protocol for treatment of acute promyelocytic leukemia (APL) in children.
  • METHODS: Thirty-three children with APL received AML-XH-99-M3 protocol treatment.
  • The event-free survival (EFS), disease-free survival (DFS), and overall survival (OS) were evaluated by the Kaplan-Meier medthod with SPSS13.0 software.
  • Six patients (18.2%) relapsed in an average of 29.17 months (16-38 months).
  • CONCLUSIONS: The AML-XH-99-M3 protocol for the treatment of APL produced a higher CR rate and higher EFS, DFS and OS rates in children.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy

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  • (PMID = 18554461.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; ZS7284E0ZP / Daunorubicin
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96. Sharma P, Murillas R, Zhang H, Kuehn MR: N4BP1 is a newly identified nucleolar protein that undergoes SUMO-regulated polyubiquitylation and proteasomal turnover at promyelocytic leukemia nuclear bodies. J Cell Sci; 2010 Apr 15;123(Pt 8):1227-34
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  • [Title] N4BP1 is a newly identified nucleolar protein that undergoes SUMO-regulated polyubiquitylation and proteasomal turnover at promyelocytic leukemia nuclear bodies.
  • Consistent with this, endogenous N4BP1 is stabilized in primary embryonic fibroblasts from mutants of the desumoylating enzyme SENP1, which show increased steady-state sumoylation levels.
  • However, a small fraction is found at promyelocytic leukemia (PML) nuclear bodies (NBs).
  • In cells deficient for SENP1 or in wild-type cells treated with the proteasome inhibitor MG132, there is considerable accumulation of N4BP1 at PML NBs.
  • [MeSH-major] Carrier Proteins / metabolism. Intranuclear Inclusion Bodies / metabolism. Leukemia, Promyelocytic, Acute / metabolism. Nuclear Proteins / metabolism. Polyubiquitin / metabolism. Proteasome Endopeptidase Complex / metabolism. Small Ubiquitin-Related Modifier Proteins / metabolism

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  • (PMID = 20233849.001).
  • [ISSN] 1477-9137
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / N4BP1 protein, mouse; 0 / Nuclear Proteins; 0 / Proteasome Inhibitors; 0 / Small Ubiquitin-Related Modifier Proteins; 120904-94-1 / Polyubiquitin; EC 3.4.- / Endopeptidases; EC 3.4.- / Senp1 protein, mouse; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC2848111
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97. Au WY, Tam S, Fong BM, Kwong YL: Determinants of cerebrospinal fluid arsenic concentration in patients with acute promyelocytic leukemia on oral arsenic trioxide therapy. Blood; 2008 Nov 1;112(9):3587-90
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  • [Title] Determinants of cerebrospinal fluid arsenic concentration in patients with acute promyelocytic leukemia on oral arsenic trioxide therapy.
  • Elemental arsenic levels in 67 paired cerebrospinal fluid (CSF) and plasma samples from 9 patients with acute promyelocytic leukemia (APL) on oral arsenic trioxide (As2O3), obtained during intrathecal chemotherapy (treatment of CNS APL, n = 6; prophylaxis, n = 3) were measured.
  • Median arsenic levels of CSF and plasma were 95.8 nmol/L (range, 3.5-318.9 nmol/L) and 498.9 nmol/L (range, 36.3-1892.8 nmol/L).
  • As a group, CSF and plasma arsenic was linearly correlated (P < .001), with CSF at 17.7% the plasma level.
  • The CSF/plasma arsenic ratio, which reflected the arsenic CSF penetration efficiency, varied significantly in individual patients (P < .001).
  • Repeated intrathecal chemotherapy and presence of blasts in CSF did not affect the CSF/plasma arsenic ratio.
  • Plasma arsenic was the only significant determinant of CSF arsenic levels.
  • CSF arsenic was present at therapeutically meaningful levels, implying that As2O3 therapy might be beneficial in CNS APL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenic / cerebrospinal fluid. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / cerebrospinal fluid. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • (PMID = 18703707.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; 04079A1RDZ / Cytarabine; N712M78A8G / Arsenic; S7V92P67HO / arsenic trioxide; YL5FZ2Y5U1 / Methotrexate
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98. Morimatsu Y, Matsubara S, Hirose N, Ohkuchi A, Izumi A, Ozaki K, Ozawa K, Suzuki M: Acute promyelocytic leukemia: an unusual cause showing prolonged disseminated intravascular coagulation after placental abruption. Arch Gynecol Obstet; 2008 Mar;277(3):267-70
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  • [Title] Acute promyelocytic leukemia: an unusual cause showing prolonged disseminated intravascular coagulation after placental abruption.
  • BACKGROUND: Disseminated intravascular coagulation (DIC) caused by placental abruption usually improves rapidly after prompt delivery and adequate anti-DIC treatment.
  • She exhibited DIC, which continued even after termination of the pregnancy and anti-DIC treatment.
  • We closely observed her, and at the 58th day postpartum, blast cells appeared in the peripheral blood and she was diagnosed with acute promyelocytic leukemia (APL).
  • The close observation after delivery enabled us to make the prompt diagnosis/treatment, leading to the complete remission.
  • CONCLUSION: APL should be added to the list of differential diagnosis when DIC persists even after prompt delivery and appropriate anti-DIC treatment after placental abruption.
  • [MeSH-major] Abruptio Placentae / etiology. Disseminated Intravascular Coagulation / etiology. Leukemia, Promyelocytic, Acute / diagnosis. Pregnancy Complications, Neoplastic / diagnosis

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  • (PMID = 17713776.001).
  • [ISSN] 0932-0067
  • [Journal-full-title] Archives of gynecology and obstetrics
  • [ISO-abbreviation] Arch. Gynecol. Obstet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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99. Mandegary A, Hosseini R, Ghaffari SH, Alimoghaddam K, Rostami S, Ghavamzadeh A, Ghahremani MH: The expression of p38, ERK1 and Bax proteins has increased during the treatment of newly diagnosed acute promyelocytic leukemia with arsenic trioxide. Ann Oncol; 2010 Sep;21(9):1884-90
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  • [Title] The expression of p38, ERK1 and Bax proteins has increased during the treatment of newly diagnosed acute promyelocytic leukemia with arsenic trioxide.
  • BACKGROUND: Promising reports exist regarding the use of arsenic trioxide (ATO) as first-line treatment in acute promyelocytic leukemia (APL).
  • PATIENTS AND METHODS: Newly diagnosed APL patients were involved and received ATO (0.15 mg.kg/day) for 28 days as induction followed by consolidation therapy.
  • Clinical findings and white blood cell counts were recorded as well.
  • RESULTS: Complete remission was observed in 17 (85%) patients with the median duration of 28 days (18-38) and cumulative dosage of median 280 mg (180-350).
  • Hyperleukocytosis and APL differentiation syndrome (63%), gastrointestinal disorders (30%), liver enzyme elevation and night sweating (50%) were the most prevalent side-effects.

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  • (PMID = 20164150.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / BAX protein, human; 0 / Oxides; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; S7V92P67HO / arsenic trioxide
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100. Baĭdil'dina DD, Maschan MA, Skorobogatova EV, Dubrovina ME, Rumiantseva IuV, Maschan AA, Rumiantsev AG, Samochatova EV: [Recurrences of acute promyelocytic leukemia in children: experience with arsenic trioxide therapy and autologous hematopoietic cell transplantation]. Ter Arkh; 2010;82(7):20-5
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  • [Title] [Recurrences of acute promyelocytic leukemia in children: experience with arsenic trioxide therapy and autologous hematopoietic cell transplantation].
  • AIM: To analyze the specific features of recurrences of acute promyelocytic leukemia (APL) in children after standard therapy with daunorubicin, cytosine arabinoside (Ara-C), all-trans retinoic acid (ATRA) and to develop further programmed treatment policy.
  • SUBJECTS AND METHODS: The study included 9 patients with recurrent APL.
  • The recurrences developed significantly more frequently in a very high-risk group (patients with minimal residual disease being preserved after the intensive therapy phase).
  • Following autoHSCT, another patient with a developed repeat recurrence died from complications due to related partially compatible transplantation.
  • In the APL-2003 protocol, overall and event-free survival rates were 93 +/- 3 and 76 +/- 6%, respectively.
  • CONCLUSION; The application of ATO and autoHSCT in recurrent APL makes it possible to achieve and preserve the second molecular remission in case of insignificant extrahematological toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Promyelocytic, Acute / prevention & control. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Arsenicals / administration & dosage. Arsenicals / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Disease-Free Survival. Humans. Infant. Oxides / administration & dosage. Oxides / therapeutic use. Remission Induction. Secondary Prevention. Transplantation, Autologous

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  • (PMID = 20853604.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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