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

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  • (PMID = 18352855.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  • [Number-of-references] 78
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2. Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E: Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia. Tohoku J Exp Med; 2008 Jan;214(1):11-6
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  • [Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia is the most common form of cancer in children.
  • Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.
  • In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.
  • We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
  • By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.
  • As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
  • In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.
  • The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.
  • Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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3. Lightfoot T: Aetiology of childhood leukemia. Bioelectromagnetics; 2005;Suppl 7:S5-S11
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  • [Title] Aetiology of childhood leukemia.
  • Leukemia is the most common cancer to affect children, accounting for approximately a third of all childhood cancers.
  • The major morphological subtypes of leukemia, acute lymphoblastic leukemia (ALL), and acute myeloblastic leukemia (AML), are characterized by chromosomal translocations involving over 200 genes including mixed lineage leukemia (MLL), TEL, and AML1.
  • Chromosomal translocations involving the MLL gene at 11q23 are a common feature of infant acute leukemia, found in up to 80% of all cases, and there is strong evidence that rearrangements involving the MLL gene or the TEL-AML1 gene fusion can originate in utero.
  • As with most other cancers, the mechanism by which leukemia arises is likely to involve gene-environment interactions.
  • Accordingly, it is important to identify exposures that cause DNA damage and induce chromosome breaks which are inadequately repaired, ultimately leading to the initiation and disease progression.
  • Exposures acting before birth and early in life has long been thought to be important determinants of leukemia, and the list of suspected chemical, physical, and biological agents continues to increase.
  • Unfortunately, the evidence regarding the majority of suggested exposures is limited and often contradictory, and there are areas, which clearly warrant further investigation in order to further our understanding of the aetiology of childhood leukemia.
  • [MeSH-major] Electromagnetic Fields / adverse effects. Environmental Exposure / adverse effects. Leukemia, Radiation-Induced / etiology. Leukemia, Radiation-Induced / physiopathology. Prenatal Exposure Delayed Effects / etiology. Prenatal Exposure Delayed Effects / physiopathology

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 16059922.001).
  • [ISSN] 0197-8462
  • [Journal-full-title] Bioelectromagnetics
  • [ISO-abbreviation] Bioelectromagnetics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 54
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4. Italia KY, Colah R, Mohanty D: Evaluation of F cells in sickle cell disorders by flow cytometry -- comparison with the Kleihauer-Betke's slide method. Int J Lab Hematol; 2007 Dec;29(6):409-14
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  • Adult F cell numbers are raised in inherited haemoglobin disorders, such as beta-thalassaemia and sickle cell anaemia, hereditary persistence of foetal haemoglobin, and some acquired conditions, such as juvenile myelomonocytic leukaemia, during acute erythropoietic stress and pregnancy.
  • [MeSH-minor] Adult. Erythropoiesis. Female. Fetomaternal Transfusion / blood. Fetomaternal Transfusion / pathology. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / pathology. Male. Pregnancy. Sensitivity and Specificity

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  • (PMID = 17988294.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9034-63-3 / Fetal Hemoglobin
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5. Shen M, Yen A: Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D(3) to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells. Oncology; 2009;76(2):91-100
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  • [Title] Nicotinamide cooperates with retinoic acid and 1,25-dihydroxyvitamin D(3) to regulate cell differentiation and cell cycle arrest of human myeloblastic leukemia cells.
  • Nicotinamide, the amide derivative of vitamin B(3), cooperates with retinoic acid (RA), a form of vitamin A, and 1,25-dihydroxyvitamin D(3) (D3), to regulate cell differentiation and proliferation of human myeloblastic leukemia cells.
  • In human myeloblastic leukemia cells, RA or D3 are known to cause MAPK signaling leading to myeloid or monocytic differentiation and G0 cell cycle arrest.
  • [MeSH-major] Calcitriol / metabolism. Leukemia, Myelomonocytic, Acute / drug therapy. Niacinamide / administration & dosage. Tretinoin / administration & dosage

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  • (PMID = 19127080.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA033505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD14; 25X51I8RD4 / Niacinamide; 5688UTC01R / Tretinoin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.2.2.5 / Antigens, CD38; FXC9231JVH / Calcitriol
  • [Other-IDs] NLM/ PMC2826433
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6. Chan WK, Cheung CC, Law HK, Lau YL, Chan GC: Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function. J Hematol Oncol; 2008;1:9
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  • [Title] Ganoderma lucidum polysaccharides can induce human monocytic leukemia cells into dendritic cells with immuno-stimulatory function.
  • The question of how leukemic cells especially in monocytic lineage respond to GL-PS stimuli remains unclear.
  • RESULTS: In this study, we used in vitro culture model with leukemic monocytic cell-lines THP-1 and U937 as monocytic effectors cells for proliferation responses and DCs induction.
  • CONCLUSION: Our findings suggested that GL-PS could induce selected monocytic leukemic cell differentiation into DCs with immuno-stimulatory function.
  • The possible clinical impact of using this commonly used medicinal mushroom in patients with monocytic leukemia (AML-M4 and M5) deserved further investigation.
  • [MeSH-major] Adjuvants, Immunologic / pharmacology. Dendritic Cells / immunology. Leukemia / immunology. Monocytes / immunology. Polysaccharides / immunology. Reishi / chemistry

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  • (PMID = 18644156.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Polysaccharides; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2517069
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7. Cuiffo B, Ren R: Palmitoylation of oncogenic NRAS is essential for leukemogenesis. Blood; 2010 Apr 29;115(17):3598-605
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  • Activating mutations of NRAS are common in acute myeloid leukemia, chronic myelomonocytic leukemia, and myelodysplastic syndrome.
  • We have previously shown that expression of oncogenic NRAS using a bone marrow transduction and transplantation model efficiently induces a chronic myelomonocytic leukemia- or acute myeloid leukemia-like disease in mice.

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  • (PMID = 20200357.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL083515; United States / NHLBI NIH HHS / HL / R01HL083515
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 2V16EO95H1 / Palmitic Acid; EC 2.5.1.29 / Farnesyltranstransferase; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2867268
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8. Draper NL, Conley C, Smith C, Benson K: Dispermic chimerism identified during HLA typing for stem cell transplantation. Transfusion; 2008 Jul;48(7):1398-402
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  • CASE REPORT: A 32-year-old man was diagnosed with acute myelomonocytic leukemia.
  • Molecular HLA typing may increase the accurate identification of phenotypically normal chimeras and aid in selecting proper donors for transplantation to reduce graft-versus-host disease and transplant rejection in these patients.
  • [MeSH-minor] Adult. HLA-B Antigens / genetics. HLA-C Antigens / genetics. Haplotypes / genetics. Humans. Leukemia, Myelomonocytic, Acute / surgery. Male. Microsatellite Repeats / genetics. Sequence Analysis, DNA

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  • (PMID = 18422842.001).
  • [ISSN] 0041-1132
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-B Antigens; 0 / HLA-C Antigens
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9. Trachsler J, Gaspert A, Previsdomini M, Wüthrich RP, Fehr T: Massive uric acid nephrolithiasis with progressive renal failure due to spontaneous tumour lysis syndrome. NDT Plus; 2008 Oct;1(5):307-9
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  • Here, we present a case of spontaneous TLS in a patient with chronic myelomonocytic leukaemia (CMML) with massive uric acid stone and crystal formation and rapidly worsening renal failure.

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  • (PMID = 25983919.001).
  • [ISSN] 1753-0784
  • [Journal-full-title] NDT plus
  • [ISO-abbreviation] NDT Plus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4421287
  • [Keywords] NOTNLM ; acute renal failure / therapy / tumour lysis syndrome / uric acid nephrolithiasis
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10. Mayayo E, Landeyro J, Stchigel AM, Gazzoni A, Capilla J: [Perineural spread by fungal cells. Case report and literature review]. Rev Iberoam Micol; 2010 Jun 30;27(2):94-7
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  • [Transliterated title] Infiltración perineural por células fúngicas. Presentación de un caso y revisión de la literatura.
  • We present a clinical case of a 73-year-old male, with diabetes and acute myelomonocytic leukaemia that began with tumefaction on the left side of his face, spreading to the sinus with invasion of the soft tissues and fistulae in the oral cavity.
  • Clinical examination showed cerebral involvement.
  • [MeSH-minor] Aged. Blast Crisis / complications. Diabetes Mellitus, Type 2 / complications. Disease Progression. Fatal Outcome. Humans. Immunocompromised Host. Leukemia, Myelomonocytic, Chronic / complications. Lung Diseases, Fungal / microbiology. Male

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  • [Copyright] Copyright 2009 Revista Iberoamericana de Micología. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20347372.001).
  • [ISSN] 1130-1406
  • [Journal-full-title] Revista iberoamericana de micología
  • [ISO-abbreviation] Rev Iberoam Micol
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Spain
  • [Number-of-references] 18
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11. Johan MF, Bowen DT, Frew ME, Goodeve AC, Reilly JT: Aberrant methylation of the negative regulators RASSFIA, SHP-1 and SOCS-1 in myelodysplastic syndromes and acute myeloid leukaemia. Br J Haematol; 2005 Apr;129(1):60-5
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  • [Title] Aberrant methylation of the negative regulators RASSFIA, SHP-1 and SOCS-1 in myelodysplastic syndromes and acute myeloid leukaemia.
  • Mutations in the receptor tyrosine kinase (RTK/RAS) signalling pathway frequently provide a proliferative signal in myeloid malignancies.
  • However, the role of RASSF1A, SHP-1 and SOCS-1, negative regulators of RTK/RAS signalling, has not been extensively investigated in the myelodysplastic syndromes (MDS) or acute myeloid leukaemia (AML).
  • This study employed methylation-specific polymerase chain reaction (MS-PCR) to determine if aberrant promotor methylation of RASSF1A, SHP-1 and SOCS-1 is involved in the pathogenesis of myeloid malignancies.
  • Patients with MDS (n = 107), AML (n = 154) and juvenile myelomonocytic leukaemia (JMML, n = 5) were investigated, together with 15 normal controls.
  • Methylation of RASSF1A was found in five of 55 (9%) MDS cases, but not in any of 57 AML cases studied.
  • SHP-1 methylation was present in 13 of 121 (11%) AML cases but was not found in MDS or JMML.
  • SOCS-1 promoter methylation was present in eight of 74 (11%) MDS patients but was not seen in JMML or AML.
  • [MeSH-minor] Acute Disease. DNA, Neoplasm / genetics. Humans. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Polymerase Chain Reaction / methods. Protein Tyrosine Phosphatase, Non-Receptor Type 6. Protein Tyrosine Phosphatases / genetics. Repressor Proteins / genetics. Sensitivity and Specificity. Sequence Analysis, DNA / methods. Suppressor of Cytokine Signaling Proteins. Tumor Suppressor Proteins / genetics

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  • (PMID = 15801956.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / RASSF1 protein, human; 0 / Repressor Proteins; 0 / SOCS1 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Tumor Suppressor Proteins; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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12. Wang TY, Huang XO, Xu CG, Chen XC, Wang H: [Acute myelomonocytic leukemia occurred after multiple myeloma treated: a case report]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2007 Mar;38(2):347-9
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  • [Title] [Acute myelomonocytic leukemia occurred after multiple myeloma treated: a case report].
  • We reported a case of multiple myeloma, who suffered from the acute myelomonocytic leukemia (AML-M4) after the chemotherapy of alkylating agent.
  • Thus, the diagnosis of multiple myeloma in remission and secondary AML-M4 was established.
  • When the chemotherapy regimen to AML was being planned for this patient, she died of massive hemorrhage of gastrointestinal tract due to thrombocytopenia and ineffectiveness.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / diagnosis. Multiple Myeloma / drug therapy


13. Sakagami H, Kishino K, Kobayashi M, Hashimoto K, Iida S, Shimetani A, Nakamura Y, Takahashi K, Ikarashi T, Fukamachi H, Satoh K, Nakashima H, Shimizu T, Takeda K, Watanabe S, Nakamura W: Selective antibacterial and apoptosis-modulating activities of mastic. In Vivo; 2009 Mar-Apr;23(2):215-23
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  • Among a total of thirteen human cell types, promyelocytic leukemia HL-60 was the most sensitive to the cytotoxicity of mastic, followed by myeloblastic leukemia (ML-1, KG-1), erythroleukemia (K-562), oral squamous cell carcinoma (HSC-2, HSC-3, HSC-4), hepatocellular carcinoma (HepG2), glioblastoma (T98G, U87MG) and normal oral cells (gingival fibroblast, pulp cell, periodontal ligament fibroblast, most resistant).

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  • (PMID = 19414406.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Resins, Plant; 61789-92-2 / gum mastic; EC 3.4.22.- / Caspase 3; V10TVZ52E4 / Putrescine
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14. Corazza F, Hermans C, D'Hondt S, Ferster A, Kentos A, Benoît Y, Sariban E: Circulating thrombopoietin as an in vivo growth factor for blast cells in acute myeloid leukemia. Blood; 2006 Mar 15;107(6):2525-30
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  • [Title] Circulating thrombopoietin as an in vivo growth factor for blast cells in acute myeloid leukemia.
  • We studied patients with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML) and used TPO-induced c-fos protein up-regulation as a marker of c-mpl functionality and observed that c-mpl-presenting blast cells were present in 62% (37 of 60) of patients with ALL but that c-mpl was nonfunctional in 0 of 28 patients and that they were present in 56% (22 of 39) of patients with AML and were functional in 43% (12 of 28).
  • Adequate increases in serum TPO level in response to thrombocytopenia were seen in patients with ALL and with c-mpl-deficient (c-mpl-) AML.
  • In contrast, in patients with c-mpl-proficient (c-mpl+) AML, TPO levels were found to be inappropriately low but increased to expected values during induction chemotherapy as blasts disappeared.
  • In vitro significant TPO-associated blast cell proliferation or decreased apoptosis was observed only in patients with c-mpl+ AML compared with ALL or c-mpl- AML and was highly correlated with low in vivo TPO levels (P < .001).
  • These data suggest that, in patients with AML, inadequate TPO levels are secondary to TPO clearing by functional c-mpl receptor myeloid blast cells and that TPO may serve as an in vivo myeloid leukemic growth factor in a significant number of patients.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Thrombopoietin / blood
  • [MeSH-minor] Acute Disease. Apoptosis. Cell Proliferation. Growth Substances / blood. Humans. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins / physiology. Receptors, Cytokine / analysis. Receptors, Cytokine / physiology. Receptors, Thrombopoietin. Thrombocytopenia / blood

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  • (PMID = 16317100.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Growth Substances; 0 / Proto-Oncogene Proteins; 0 / Receptors, Cytokine; 0 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; 9014-42-0 / Thrombopoietin
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15. Flotho C, Paulun A, Batz C, Niemeyer CM: AKAP12, a gene with tumour suppressor properties, is a target of promoter DNA methylation in childhood myeloid malignancies. Br J Haematol; 2007 Sep;138(5):644-50
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  • [Title] AKAP12, a gene with tumour suppressor properties, is a target of promoter DNA methylation in childhood myeloid malignancies.
  • We hypothesized that epigenetic repression of the AKAP12 gene might occur in malignant myeloid disorders.
  • Re-expression of AKAP12 in Kasumi-1 and SKNO-1 cells was accomplished by treatment with MS275 alone or in combination with zebularine, indicating epigenetic mechanisms of gene repression.
  • AKAP12 hypermethylation was found in one case of refractory anaemia with excess blasts (RAEB) and two cases of acute myeloid leukaemia (AML) in a panel of 21 blood or bone marrow samples from children with malignant myeloid disorders including refractory cytopenia, RAEB, juvenile myelomonocytic leukaemia and AML.
  • While AKAP12 function has not been previously linked to leukaemogenesis, our results raise the possibility that epigenetic silencing of AKAP12 is involved in myeloid malignancies.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA Methylation. DNA, Neoplasm / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] A Kinase Anchor Proteins. Adolescent. Anemia, Refractory, with Excess of Blasts / genetics. Anemia, Refractory, with Excess of Blasts / metabolism. Child. Child, Preschool. Epigenesis, Genetic. Female. Gene Silencing. Humans. Infant. Infant, Newborn. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Male. Neoplasm Proteins / metabolism. Promoter Regions, Genetic. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured

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  • (PMID = 17686059.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / A Kinase Anchor Proteins; 0 / AKAP12 protein, human; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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16. Liu LB, Li WM, He W, Zhang M, Xiao J, Zhong ZD, Li L, Zou P: [Blocking the escape of leukemic cells from killing of T cell by combining anti-Fas ribozyme and CD80-IgG fusion protein]. Zhonghua Yi Xue Za Zhi; 2005 Dec 28;85(49):3469-74
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  • OBJECTIVE: To study Fas expression regulation of cytotoxic T lymphocyte(CTL)via anti-Fas ribozyme, increasing of CD80 epitope on the surface of acute myelomonocytic leukemia cells by CD80-IgG fusion protein and their effects on the apoptosis and killing ability against acute myelomonocytic leukemia cells of CTL.
  • Then allogeneic mixed lymphocytes culture between the mouse spleen T cells transfected with pEGFP-RZ596 and WEHI-3 cells (mouse acute myelomonocyte leukemia cell line) incubated with CD80-IgG fusion protein was performed.
  • [MeSH-minor] Animals. Antigens, CD80 / genetics. Antigens, CD80 / immunology. Antigens, CD80 / metabolism. Antigens, CD95 / genetics. Antigens, CD95 / immunology. Antigens, CD95 / metabolism. Blotting, Western. CHO Cells. Cell Line, Tumor. Coculture Techniques. Cricetinae. Cricetulus. Female. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Immunoglobulin G / genetics. Immunoglobulin G / immunology. Immunoglobulin G / metabolism. Leukemia, Myelomonocytic, Acute / immunology. Leukemia, Myelomonocytic, Acute / metabolism. Leukemia, Myelomonocytic, Acute / pathology. Mice. Mice, Inbred BALB C. Reverse Transcriptase Polymerase Chain Reaction. Transfection. Tumor Escape

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  • (PMID = 16686062.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD95; 0 / Immunoglobulin G; 0 / RNA, Catalytic; 0 / Recombinant Fusion Proteins; 147336-22-9 / Green Fluorescent Proteins
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17. Gervais C, Murati A, Helias C, Struski S, Eischen A, Lippert E, Tigaud I, Penther D, Bastard C, Mugneret F, Poppe B, Speleman F, Talmant P, VanDen Akker J, Baranger L, Barin C, Luquet I, Nadal N, Nguyen-Khac F, Maarek O, Herens C, Sainty D, Flandrin G, Birnbaum D, Mozziconacci MJ, Lessard M, Groupe Francophone de Cytogénétique Hématologique: Acute myeloid leukaemia with 8p11 (MYST3) rearrangement: an integrated cytologic, cytogenetic and molecular study by the groupe francophone de cytogénétique hématologique. Leukemia; 2008 Aug;22(8):1567-75
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  • [Title] Acute myeloid leukaemia with 8p11 (MYST3) rearrangement: an integrated cytologic, cytogenetic and molecular study by the groupe francophone de cytogénétique hématologique.
  • Thirty cases of acute myeloid leukaemia (AML) with MYST histone acetyltransferase 3 (MYST3) rearrangement were collected in a retrospective study from 14 centres in France and Belgium.
  • The mean age at diagnosis was 59.4 years and 67% of the patients were females.
  • Most cases (77%) were secondary to solid cancer (57%), haematological malignancy (35%) or both (8%), and appeared 25 months after the primary disease.
  • AMLs were myelomonocytic (7%) or monocytic (93%), with erythrophagocytosis (75%) and cytoplasmic vacuoles (75%).
  • Immunophenotype showed no particularity compared with monocytic leukaemia without MYST3 abnormality.
  • Type I (MYST3 exon 16-CREBBP exon 3) was the most frequent MYST3-CREBBP fusion transcript (65%).
  • All those particular clinical, cytologic, cytogenetic, molecular and prognostic characteristics of AML with MYST3 rearrangement may have allowed an individualization into the World Health Organization classification.
  • [MeSH-major] Chromosomes, Human, Pair 8. Gene Rearrangement. Histone Acetyltransferases / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18528428.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  • [Investigator] Vial JP; Guerin E; Micheau M; Treille-Ritouet D; Callat MP; Buchonnet G; Favre-Audry B; Maynadie M; Verhasselt B; Philippe J; Noens L; Garand R; Arnoulet C; Genevieve F; Gardais J; Claisse JF; Petit A; Lespanel C; Daliphard S; Vasselon C; Settegrana C
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18. Freycon F, Trombert-Paviot B, Casagranda L, Bertrand Y, Plantaz D, Marec-Bérard P: Trends in treatment-related deaths (TRDs) in childhood cancer and leukemia over time: a follow-up of patients included in the childhood cancer registry of the Rhône-Alpes region in France (ARCERRA). Pediatr Blood Cancer; 2008 Jun;50(6):1213-20
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  • [Title] Trends in treatment-related deaths (TRDs) in childhood cancer and leukemia over time: a follow-up of patients included in the childhood cancer registry of the Rhône-Alpes region in France (ARCERRA).
  • No difference was observed in treatment- and transplantation-related deaths in patients with acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but OS was better in patients with AML (P = 0.02).
  • Severe graft-versus-host disease was also observed among patients with ALL (P = 0.036).
  • CONCLUSION: Although mortality declined, improved adherence to therapeutic guidelines and more restricted indications of allograft are needed to preclude further treatment- and transplantation-related deaths, particularly among those with leukemia.
  • [MeSH-minor] Central Nervous System Neoplasms / mortality. Central Nervous System Neoplasms / therapy. Child. Cohort Studies. Female. France / epidemiology. Guideline Adherence. Hematopoietic Stem Cell Transplantation / mortality. Humans. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Practice Guidelines as Topic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Registries

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18300318.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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19. Numakura K, Tsuchiya N, Habuchi T, Takahashi N: [Therapy related leukemia with 11q23 abnormality induced by chemotherapy consisted of docetaxel for advanced prostatic carcinoma: case report]. Nihon Hinyokika Gakkai Zasshi; 2009 Jul;100(5):580-5
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  • [Title] [Therapy related leukemia with 11q23 abnormality induced by chemotherapy consisted of docetaxel for advanced prostatic carcinoma: case report].
  • A balanced translocation involving 11q23 (MLL gene) could be observed in therapy related leukemia (TRL) patients generally treated with topoisomerase II inhibitors.
  • Herein, we report a patient who developed acute myelomonocytic leukemia (AMMoL) with t (9;. 11) (p22;.
  • Although, no disease progression of the prostatic carcinoma was observed, AMMoL with t (9;. 11) (p22;.
  • q23) translocation and clinical course.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Carcinoma / therapy. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myelomonocytic, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / genetics. Neoplasms, Second Primary. Prostatic Neoplasms / therapy. Taxoids / adverse effects. Translocation, Genetic

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  • (PMID = 19663246.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Number-of-references] 23
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20. Fujisawa S, Naito K, Matsuoka T, Kobayashi M: Complete remission induced by gemtuzumab ozogamicin in a Jehovah's Witness patient with acute myelogenous leukemia. Int J Hematol; 2007 Jun;85(5):418-20
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  • [Title] Complete remission induced by gemtuzumab ozogamicin in a Jehovah's Witness patient with acute myelogenous leukemia.
  • We report an interesting case of acute myelogenous leukemia (AML) in a Jehovah's Witness patient.
  • The patient's diagnosis was AML (M4).
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Jehovah's Witnesses. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 17562618.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Organic Chemicals; 0 / acrarubicin; 04079A1RDZ / Cytarabine; 93NS566KF7 / gemtuzumab
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21. Pan JL, Xue YQ, Jiang HY, He J, Wang W, Wu YF: [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2005 Aug;22(4):444-6
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  • [Title] [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5].
  • OBJECTIVE: To explore the value of reverse transcription-multiplex nested PCR in detecting MLL rearrangement in lzAML-M4/M5.
  • Five common MLL fusion genes and MLL partial tandem duplication in 40 AML cases, including 12 M4 and 28 M5 were detected by reverse transcription(RT)-multiplex nested PCR.
  • CONCLUSION: RT-multiplex nested PCR is a powerful technique in the detection of MLL rearrangement for tentativelly diagnosed AML-M4/M5.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic

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  • (PMID = 16086288.001).
  • [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] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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22. Woo KS, Kim KE, Kim KH, Kim SH, Park JI, Shaffer LG, Han JY: Deletions of chromosome arms 7p and 7q in adult acute myeloid leukemia: a marker chromosome confirmed by array comparative genomic hybridization. Cancer Genet Cytogenet; 2009 Oct 15;194(2):71-4
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  • [Title] Deletions of chromosome arms 7p and 7q in adult acute myeloid leukemia: a marker chromosome confirmed by array comparative genomic hybridization.
  • Acute myeloid leukemia (AML) cases with monosomy 7 (-7) and del(7q) comprise a heterogeneous subgroup.
  • The association of losses in 7q with myeloid leukemia suggests that this region contains a tumor suppressor gene or genes whose loss of function contributes to leukemic transformation or tumor progression.
  • In the present case, we identified a rare abnormality involving deletion of both arms of chromosome 7 presenting with a marker chromosome-like appearance in an AML patient.
  • Bone marrow aspiration and biopsy revealed acute myelomonocytic leukemia.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosome Deletion. Chromosomes, Human, Pair 7. Leukemia, Myeloid, Acute / genetics


23. Gutierrez JA, Pan YX, Koroniak L, Hiratake J, Kilberg MS, Richards NG: An inhibitor of human asparagine synthetase suppresses proliferation of an L-asparaginase-resistant leukemia cell line. Chem Biol; 2006 Dec;13(12):1339-47
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  • [Title] An inhibitor of human asparagine synthetase suppresses proliferation of an L-asparaginase-resistant leukemia cell line.
  • Drug resistance in lymphoblastic and myeloblastic leukemia cells is poorly understood, with several lines of evidence suggesting that resistance can be correlated with upregulation of human asparagine synthetase (hASNS) expression, although this hypothesis is controversial.
  • These observations represent direct evidence that potent hASNS inhibitors may prove to be effective agents for the clinical treatment of acute lymphoblastic leukemia.

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  • (PMID = 17185229.001).
  • [ISSN] 1074-5521
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052064; United States / NIDDK NIH HHS / DK / R01 DK059315; United States / NIDDK NIH HHS / DK / DK52064; United States / NIDDK NIH HHS / DK / DK59315
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids, Sulfur; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
  • [Other-IDs] NLM/ NIHMS447417; NLM/ PMC3608209
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24. Tarkun P, Hacıhanefioğlu A, Demirbağ E, Turgut T: Development of autoimmune hemolytic anemia during the treatment of a patient with acute myelomonocytic leukemia. Turk J Haematol; 2005 Jun 5;22(2):95-9
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  • [Title] Development of autoimmune hemolytic anemia during the treatment of a patient with acute myelomonocytic leukemia.
  • [Transliterated title] Akut miyelomonositik lösemili bir hastanın tedavisi srasında ortaya çıkan otoimmün hemolitik anemi.

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  • (PMID = 27264668.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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25. Mozziconacci MJ, Carbuccia N, Prebet T, Charbonnier A, Murati A, Vey N, Chaffanet M, Birnbaum D: Common features of myeloproliferative disorders with t(8;9)(p12;q33) and CEP110-FGFR1 fusion: report of a new case and review of the literature. Leuk Res; 2008 Aug;32(8):1304-8
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  • The 8p12 myeloproliferative syndrome is a rare, generally aggressive chronic myeloproliferative disorder (MPD).
  • We report here the tenth case of translocation (8;9)(p12;q33) in an acute myelomonocytic leukemia and provide a review of the literature that points to common syndrome features: the t(8;9)(p11;q33) MPD transforms rapidly, and always in myelomonocytic leukemia, with a possible B- or T-lymphoid involvement, which may include tonsil invasion.
  • [MeSH-major] Chromosomes, Human, Pair 8. Chromosomes, Human, Pair 9. Leukemia, Myelomonocytic, Acute / genetics. Myeloproliferative Disorders / genetics. Oncogene Proteins, Fusion / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism. Translocation, Genetic

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  • (PMID = 18096225.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.- / CEP110-FGFR1 fusion protein, human
  • [Number-of-references] 14
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26. Chevallier P, Mahe B, Garand R, Talmant P, Harousseau JL, Delaunay J: Combination of chemotherapy and gemtuzumab ozogamicin in adult Philadelphia positive acute lymphoblastic leukemia patient harboring CD33 expression. Int J Hematol; 2008 Sep;88(2):209-11
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  • [Title] Combination of chemotherapy and gemtuzumab ozogamicin in adult Philadelphia positive acute lymphoblastic leukemia patient harboring CD33 expression.
  • It was developed at the end of the nineties as 90% of the leukemic blast population of patients with acute myeloid leukaemia (AML) express the CD33 surface antigen (Dinndorf et al. [1] Blood 1986;67:1048-53).
  • GO is currently approved in monotherapy for the treatment of CD33+ AML patients in first relapse, showing a 26% overall response rate and a median disease-free-survival of 5.2 months for responders (Larson et al. [2] Cancer 2005;104:1442-52).
  • CD33 antigen expression is also observed at diagnosis (in 15% of cases) (Pui et al. [3] J Clin Oncol 1998;16:3768-73) or at relapse (Guglielmi et al. [4] Leukemia 1997; 11:1501-7) of acute lymphoblastic leukaemia (ALL), representing a potential cellular target for ALL patients.
  • Case series have already demonstrated the efficacy of GO in children with relapsed CD33+ ALL with documentation of complete remission (CR) (Balduzzi et al. [5] Leukemia 2003;17:2247-8; Cotter et al. [6] Br J Haematol 2003;122:686-91; Zwaan et al. [7] Leukemia 2003;17:468-70).
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Combined Modality Therapy. Fatal Outcome. Hematopoietic Stem Cell Transplantation. Humans. Male. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 18668307.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 93NS566KF7 / gemtuzumab
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27. Merino A, Esteve J: Acute myeloid leukaemia with peculiar blast cell inclusions and pseudo-eosinophilia. Br J Haematol; 2005 Nov;131(3):286
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  • [Title] Acute myeloid leukaemia with peculiar blast cell inclusions and pseudo-eosinophilia.
  • [MeSH-major] Eosinophilia / diagnosis. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 16225647.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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28. Eliashar R, Resnick IB, Goldfarb A, Wohlgelernter J, Gross M: Endoscopic surgery for sinonasal invasive aspergillosis in bone marrow transplantation patients. Laryngoscope; 2007 Jan;117(1):78-81
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  • Demographic data, primary disease, comorbidities, signs and symptoms, blood test results, preparation for surgery, surgical technique, and outcome were recorded.
  • The primary disease was acute myelogenous leukemia in 6, acute lymphoblastic leukemia in 3, chronic myeloblastic leukemia in one, severe combined immunodeficiency disease in 2, and myelodysplastic syndrome in 2 patients.
  • Diagnosis was made by physical examination, biopsy, culture, and computed tomography scan.
  • Six patients died of the primary illness or of comorbidities with no evidence of residual disease.
  • CONCLUSION: Early detection of IA in BMT patients enables aggressive treatment before the disease spreads into the orbit or brain.
  • [MeSH-major] Aspergillosis / surgery. Bone Marrow Transplantation / adverse effects. Endoscopy / methods. Leukemia / complications. Opportunistic Infections / surgery. Paranasal Sinus Diseases / surgery


29. Grövdal M, Karimi M, Khan R, Aggerholm A, Antunovic P, Astermark J, Bernell P, Engström LM, Kjeldsen L, Linder O, Nilsson L, Olsson A, Holm MS, Tangen JM, Wallvik J, Oberg G, Hokland P, Jacobsen SE, Porwit A, Hellström-Lindberg E: Maintenance treatment with azacytidine for patients with high-risk myelodysplastic syndromes (MDS) or acute myeloid leukaemia following MDS in complete remission after induction chemotherapy. Br J Haematol; 2010 Aug;150(3):293-302
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  • [Title] Maintenance treatment with azacytidine for patients with high-risk myelodysplastic syndromes (MDS) or acute myeloid leukaemia following MDS in complete remission after induction chemotherapy.
  • This prospective Phase II study is the first to assess the feasibility and efficacy of maintenance 5-azacytidine for older patients with high-risk myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia and MDS-acute myeloid leukaemia syndromes in complete remission (CR) after induction chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


30. Sino US Leukemia Cooperative Group of Shanghai: [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):444-8
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  • [Title] [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].
  • OBJECTIVE: To evaluate WHO classification of acute leukemia (AL) in Shanghai and compare the difference between WHO and FAB classification.
  • METHODS: Successive and unselected leukemia patients were referred to Sino-US Leukemia Cooperative Group of Shanghai from 2003 to 2006.
  • A total of 572 adult AL cases were diagnosed and classified according to WHO and FAB classification.
  • RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as acute myeloid leukemia (AML), 119 (20.8%) acute lymphoblastic leukemia (ALL).
  • The AML and ALL percentage ratio was 3.66: 1.
  • AML with recurrent cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related AML accounted for 0.9%, and AML not otherwise categorized for 50.7%.
  • The percentage of therapy-related AML in Shanghai was lower than that in the Western.
  • According to FAB classification, AML-M4 was the most (38.5%) common subtype.
  • The percentage of AML-M3 and M4 in Shanghai were higher than that in the Western, but that of AML-M, was lower.
  • The incidence of karyotypic abnormalities in AML was 60.8%.
  • The incidence of AML with t (15;17) was higher than that in the Western.
  • Favorable cytogenetic risk group accounted for 30.6%, intermediate group for 51.5%, unfavorable group for 17.9% of AML.
  • CONCLUSIONS: The percentages of AML with t (15;17) and AML-M4 in Shanghai and the incidence of cytogenetic favorable group were higher than that in the Western.
  • It was different in WHO classification and karyotypic abnormalities of AML between Shanghai and the Western.
  • Comparing to the AL data of Shanghai Leukemia Group between 1984 and 1994, the percentage of AML-M4 was increased, but that of AML-M1 and M5 were decreased.
  • [MeSH-major] Leukemia / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 18072625.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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31. Harani MS, Adil SN, Shaikh MU, Kakepoto GN, Khurshid M: Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):26-9
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  • [Title] Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease.
  • Therefore, various parameters are needed to classify this disease into subtypes, so that specific treatment approaches can be utilized effectively.
  • The commonly used method for diagnosis and classification is based on FAB criteria using morphology and cytochemical stains.
  • The aim of present study is to determine the frequency of various sub types in acute myeloid leukemia using FAB criteria in our population.
  • This will aid in the correct diagnosis of acute leukemia and hence proper management of the patients.
  • The patients were diagnosed on the basis of bone marrow morphology using FAB classification.
  • AML-M4 was the predominant French-American-British (FAB) subtype (36.2%) followed by M2 (30.25%), M3 (10.4%), M1 (8.7%), M0 (7.7%), M5a (3.5%), M5b (2.5%) and M6 (0.8%).
  • CONCLUSIONS: The most common FAB subtype observed in our study was Acute myelomonocytic leukemia (M4) which is in accordance with studies reported from Saudia Arabia and a previous study reported from our institution.
  • However,other national and international studies have reported Myeloblastic Leukemia with maturation (M2) as the predominant subtype of AML.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Female. Hospitals, University. Humans. Infant. Male. Middle Aged. Pakistan

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  • (PMID = 15929522.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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32. Shimizu T, Kuromi A, Takeda K: Synergistic induction of gene expression during the differentiation into mature macrophage in human myeloblastic leukemia cells treated with TPA and KH1060. Leuk Res; 2009 Jun;33(6):803-9
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  • [Title] Synergistic induction of gene expression during the differentiation into mature macrophage in human myeloblastic leukemia cells treated with TPA and KH1060.
  • Treatment of human myeloblastic leukemia ML-1 cells with the phorbol ester TPA in combination with the vitamin D(3) analogue KH1060 will induce a synergistic differentiation to mature macrophage with multinuclei.
  • [MeSH-major] Calcitriol / analogs & derivatives. Cell Differentiation. Gene Expression Regulation / drug effects. Leukemia, Myeloid, Acute / pathology. Macrophages / cytology. Tetradecanoylphorbol Acetate / pharmacology

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  • (PMID = 19144406.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 131875-08-6 / KH 1060; FXC9231JVH / Calcitriol; NI40JAQ945 / Tetradecanoylphorbol Acetate
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33. Blatt J, Greenwood R, Weig S, Rao K, Fedoriw GD, Dent G: Isolated central nervous system relapse in an adolescent with acute myelomonocytic leukemia, Charcot Marie Tooth syndrome, and paraneoplastic autoantibody. J Pediatr Hematol Oncol; 2010 Oct;32(7):571-3
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  • [Title] Isolated central nervous system relapse in an adolescent with acute myelomonocytic leukemia, Charcot Marie Tooth syndrome, and paraneoplastic autoantibody.
  • A 17-year-old boy, with acute myelomonocytic leukemia and inversion 16(p13q22) developed polyneuropathy and isolated central nervous system relapse.
  • Scoliosis and high-arched feet suggested a diagnosis of Charcot Marie Tooth (CMT) syndrome and genetic testing confirmed duplication at the PMP22 locus at chromosome 17p11.12.
  • This case extends the clinical spectrum of cancer with CMT, and of paraneoplastic disorders.
  • [MeSH-major] Autoantibodies / blood. Charcot-Marie-Tooth Disease / immunology. Leukemia, Myelomonocytic, Acute / immunology. Paraneoplastic Syndromes, Nervous System / immunology

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  • (PMID = 20724950.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Myelin Proteins; 0 / PMP22 protein, human
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34. Otsubo K, Kanegane H, Eguchi M, Eguchi-Ishimae M, Tamura K, Nomura K, Abe A, Ishii E, Miyawaki T: ETV6-ARNT fusion in a patient with childhood T lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 Oct 1;202(1):22-6
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  • [Title] ETV6-ARNT fusion in a patient with childhood T lymphoblastic leukemia.
  • Leukemia with t(1;12)(q21;p13) was previously described in a 5-year-old boy with acute myeloblastic leukemia (AML-M2) who exhibited a novel ETV6-aryl hydrocarbon receptor nuclear translocator (ARNT) fusion protein.
  • We herein report the case of a 2-year-old boy with T-cell lymphoblastic leukemia (T-ALL) harboring t(1;12)(q21;p13).
  • The ETV6-ARNT fusion is associated not only with AML but also with T-ALL.
  • [MeSH-major] ARNTL Transcription Factors / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20804916.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARNTL Transcription Factors; 0 / DNA Primers; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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35. Park TS, Lee ST, Song J, Lee KA, Lee JH, Kim J, Lee HJ, Han JH, Kim JK, Cho SR, Choi JR: Detection of a novel CBFB/MYH11 variant fusion transcript (K-type) showing partial insertion of exon 6 of CBFB gene using two commercially available multiplex RT-PCR kits. Cancer Genet Cytogenet; 2009 Mar;189(2):87-92
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  • [Title] Detection of a novel CBFB/MYH11 variant fusion transcript (K-type) showing partial insertion of exon 6 of CBFB gene using two commercially available multiplex RT-PCR kits.
  • We report on a 20-year-old man with acute myeloid leukemia (AML) showing a distinct novel CBFB/MYH11 variant fusion transcript.
  • Initial results of bone marrow, chromosome, and flow cytometric analyses were not in accordance with the diagnosis of acute myelomonocytic leukemia with eosinophilia (AML-M4Eo) or AML with a CBFB/MYH11 rearrangement.
  • Not only does this case show a partial insertion of exon 6 of the CBFB (ENSG00000067955) gene, but it also involves novel breakpoints within both exon 6 of the CBFB gene and exon 28 (previously exon 7) of the MYH11 (ENSG00000133392) gene, which is regarded as a previously non-reported, new type (K-type) of CBFB/MYH11 fusion transcript.
  • Therefore, multiplex RT-PCR and sequence analysis of these atypical products should be performed to diagnose atypical AML with CBFB/MYH11 rearrangement, to predict prognosis of these patients as well as to elucidate the molecular mechanism.
  • [MeSH-major] Core Binding Factor beta Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutagenesis, Insertional. Myosin Heavy Chains / genetics. Reagent Kits, Diagnostic. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19215788.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; 0 / Reagent Kits, Diagnostic; 0 / Recombinant Fusion Proteins; EC 3.6.4.1 / Myosin Heavy Chains
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36. Chou CY, Chien CH, Han YS, Prebanda MT, Hsieh HP, Turk B, Chang GG, Chen X: Thiopurine analogues inhibit papain-like protease of severe acute respiratory syndrome coronavirus. Biochem Pharmacol; 2008 Apr 15;75(8):1601-9
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  • [Title] Thiopurine analogues inhibit papain-like protease of severe acute respiratory syndrome coronavirus.
  • The papain-like protease of severe acute respiratory syndrome coronavirus (PLpro) (EC 3.4.22.46) is essential for the viral life cycle and therefore represents an important antiviral target.
  • Both 6MP and 6TG are still used extensively in clinics, especially for children with acute lymphoblastic or myeloblastic leukemia.

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  • (PMID = 18313035.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protease Inhibitors; 0 / Viral Proteins; E7WED276I5 / 6-Mercaptopurine; EC 3.4.22.- / 3C-like protease, SARS coronavirus; EC 3.4.22.- / Cysteine Endopeptidases; FTK8U1GZNX / Thioguanine
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37. Dăscălescu A, Zlei M, Grigore G, Dănăila C, Jitaru D, Carasevici E: [Prognostic significance of leukemia-associated phenotype in correlation with other biologic markers in acute myeloid leukemia patients]. Rev Med Chir Soc Med Nat Iasi; 2009 Oct-Dec;113(4):1176-81
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  • [Title] [Prognostic significance of leukemia-associated phenotype in correlation with other biologic markers in acute myeloid leukemia patients].
  • Leukemic cells have unique aberrant phenotypes, which permit identification of this cells at diagnose and in evolution of the disease.
  • The main aim of the current study is to identify correlation between recognized prognostic factors in acute myeloid leukemia (AML) patients and other phenotypic markers.
  • MATERIAL AND METHOD: Imunophenotypic analysis (BDFACS CantoII, FACSDiva Software) was performed on peripheral blood/bone marrow aspirate samples of 56 patients diagnosed with AML (9 M0, 3 M1, 10 M2, 4 M3, 28 M4/M5, 1 M6, 1 M7) between 2007-2009 in Hematology Department of "Sf.
  • RESULTS: In our study, IL7R expression on AML blasts was significant correlate with low WBC count at diagnosis (p = 0.04) and with multilinear displasia (p = 0.01), high CXCR4 expression was correlate (p = 0.05) with lack of response at first induction therapy and CD123 (IL3Ra) expression was correlate with M4 FAB phenotype.
  • Survival was negative influenced by presence of IL3R on AML blasts, but flt3 mutations, CXCR4, IL7R expression on leukemic cells, other phenotypic aberrancies did not influenced treatment response and survival in our patients population.
  • CONCLUSION: Complete investigation of leukemic cells phenotype extended with cytokines/chemokines receptors at diagnostic is useful for correct characterization of the disease, for discover new prognostic categories and for better identification of minimal residual disease.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid, Acute / immunology. Receptors, Chemokine / blood. Receptors, Cytokine / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Male. Middle Aged. Phenotype. Predictive Value of Tests. Prognosis. Receptors, CCR5 / blood. Receptors, CXCR4 / blood. Receptors, Interleukin-3 / blood. Receptors, Interleukin-7 / blood. Retrospective Studies. Survival Analysis

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  • (PMID = 20191895.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, CCR5; 0 / Receptors, CXCR4; 0 / Receptors, Chemokine; 0 / Receptors, Cytokine; 0 / Receptors, Interleukin-3; 0 / Receptors, Interleukin-7
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38. Astashkin EI, Suvorov NI, Mikhailova AA, Grachev SV: Change in the Ca2+ response to formyl peptide in HL-60 myeloblastic leukemia cells after the induction of their differentiation by MP-4 myelogenic peptide. Dokl Biol Sci; 2006 May-Jun;408:265-8
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  • [Title] Change in the Ca2+ response to formyl peptide in HL-60 myeloblastic leukemia cells after the induction of their differentiation by MP-4 myelogenic peptide.
  • [MeSH-major] Calcium / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Oligopeptides / therapeutic use

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  • [ISSN] 0012-4966
  • [Journal-full-title] Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections
  • [ISO-abbreviation] Dokl. Biol. Sci.
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39. Pânzaru C, Dan M, Burcoveanu C, Mereuţă A, Buiuc D: Disseminated infection due to Candida guilliermondii in a patient with AML(M4). Case study. Rev Med Chir Soc Med Nat Iasi; 2006 Jul-Sep;110(3):727-30
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  • [Title] Disseminated infection due to Candida guilliermondii in a patient with AML(M4). Case study.
  • A 43-year-old patient admitted with acute myelogenous leukemia, developed bronchopneumonia and sepsis during profound neutropenia.
  • After a few days of therapy with Voriconazol, fever disappeared and the clinical state of patient was improved.
  • [MeSH-major] Candida / isolation & purification. Candidiasis / complications. Fungemia / microbiology. Immunocompromised Host. Leukemia, Myeloid, Acute / complications

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  • (PMID = 17571574.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 7XU7A7DROE / Amphotericin B; 8VZV102JFY / Fluconazole; JFU09I87TR / Voriconazole
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40. Shen M, Yen A: c-Cbl tyrosine kinase-binding domain mutant G306E abolishes the interaction of c-Cbl with CD38 and fails to promote retinoic acid-induced cell differentiation and G0 arrest. J Biol Chem; 2009 Sep 18;284(38):25664-77
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  • Retinoic acid (RA) causes HL-60 human myeloblastic leukemia cell myeloid differentiation that is dependent on MAPK signaling.
  • Unlike wild-type (WT) c-Cbl, the G306E mutant c-Cbl fails to propel RA-induced differentiation, and disrupts the normal association with CD38.

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  • (PMID = 19635790.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / Membrane Glycoproteins; 0 / Multiprotein Complexes; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins c-vav; 0 / SLP-76 signal Transducing adaptor proteins; 5688UTC01R / Tretinoin; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC2757968
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41. Steinherz PG, Shukla N, Kobos R, Steinherz L: Remission re-induction chemotherapy with clofarabine, topotecan, thiotepa, and vinorelbine for patients with relapsed or refractory leukemia. Pediatr Blood Cancer; 2010 May;54(5):687-93
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  • [Title] Remission re-induction chemotherapy with clofarabine, topotecan, thiotepa, and vinorelbine for patients with relapsed or refractory leukemia.
  • BACKGROUND: We determined the maximum tolerated dose (MTD) of clofarabine when administered with topotecan, vinorelbine, thiotepa, and dexamethasone (TVTC) for children with relapsed or refractory acute leukemia, and observed the efficacy and toxicities of this therapy.
  • PROCEDURE: Twelve patients with acute lymphoblastic or myeloblastic leukemia were given a 14-day remission induction therapy.
  • Three patients had progressive disease.
  • One patient died on day 45 with marrow hypoplasia without evidence of leukemia.
  • CONCLUSION: TVTC has significant anti-leukemic activity in both acute lymphoblastic and myeloblastic leukemia.
  • This is the recommended dose for the phase II study in patients with refractory or relapsed leukemia, a population which has limited therapeutic options.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy

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  • (PMID = 20205253.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 5V9KLZ54CY / Vinblastine; 762RDY0Y2H / clofarabine; 7M7YKX2N15 / Topotecan; 905Z5W3GKH / Thiotepa; Q6C979R91Y / vinorelbine
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42. Dalmazzo LF, Jácomo RH, Marinato AF, Figueiredo-Pontes LL, Cunha RL, Garcia AB, Rego EM, Falcão RP: The presence of CD56/CD16 in T-cell acute lymphoblastic leukaemia correlates with the expression of cytotoxic molecules and is associated with worse response to treatment. Br J Haematol; 2009 Jan;144(2):223-9
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  • [Title] The presence of CD56/CD16 in T-cell acute lymphoblastic leukaemia correlates with the expression of cytotoxic molecules and is associated with worse response to treatment.
  • Some cases of T-cell acute lymphoblastic leukaemia (ALL) express markers found in natural-killer (NK) cells, such as CD56 and CD16.
  • Clinical features, laboratory characteristics, survival and expression of cytotoxic molecules were compared in T/NK-ALL and T-ALL patients.
  • The mean overall survival (863 vs. 1869 d, P = 0.02) and disease-free survival (855 vs. 2095 d, P = 0.002) were shorter in patients expressing CD56/CD16.
  • Therefore, the presence of CD56/CD16 was associated with distinct clinical features and expression of cytotoxic molecules in the blasts.
  • [MeSH-major] Antigens, CD56 / analysis. Killer Cells, Natural / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Receptors, IgG / analysis
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antigens, CD / analysis. Antigens, CD3 / analysis. Antigens, CD34 / analysis. Antigens, CD45 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Biomarkers / analysis. Disease-Free Survival. Female. Flow Cytometry. Granzymes / analysis. Humans. Immunophenotyping. Kaplan-Meier Estimate. Male. Perforin / analysis. Platelet Count. Poly(A)-Binding Proteins / analysis. Sialic Acid Binding Ig-like Lectin 3. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 19016721.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, CD56; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers; 0 / CD33 protein, human; 0 / Poly(A)-Binding Proteins; 0 / Receptors, IgG; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / TIA1 protein, human; 126465-35-8 / Perforin; EC 3.1.3.48 / Antigens, CD45; EC 3.4.21.- / Granzymes
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43. Yen A, Varvayanis S, Smith JL, Lamkin TJ: Retinoic acid induces expression of SLP-76: expression with c-FMS enhances ERK activation and retinoic acid-induced differentiation/G0 arrest of HL-60 cells. Eur J Cell Biol; 2006 Feb;85(2):117-32
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  • Retinoic acid (RA) is known to cause MAPK signaling which propels G0 arrest and myeloid differentiation of HL-60 human myeloblastic leukemia cells.
  • A triple Y to F mutant SLP-76 known to be a dominant negative in T-cell receptor signaling failed to enhance RA-induced paxillin expression, but enhanced RA-induced ERK activation, differentiation and G0 arrest essentially as well as wild-type SLP-76.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Blotting, Western. Enzyme Activation. HL-60 Cells. Humans. Immunoprecipitation. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / physiopathology. Mutation. Paxillin / genetics. Paxillin / physiology. Phosphorylation. Receptors, Antigen, T-Cell / physiology. Signal Transduction. Superoxides / metabolism. Transfection. Up-Regulation / drug effects

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  • (PMID = 16439309.001).
  • [ISSN] 0171-9335
  • [Journal-full-title] European journal of cell biology
  • [ISO-abbreviation] Eur. J. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Paxillin; 0 / Phosphoproteins; 0 / Receptors, Antigen, T-Cell; 0 / SLP-76 signal Transducing adaptor proteins; 11062-77-4 / Superoxides; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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44. Gelsi-Boyer V, Trouplin V, Adélaïde J, Bonansea J, Cervera N, Carbuccia N, Lagarde A, Prebet T, Nezri M, Sainty D, Olschwang S, Xerri L, Chaffanet M, Mozziconacci MJ, Vey N, Birnbaum D: Mutations of polycomb-associated gene ASXL1 in myelodysplastic syndromes and chronic myelomonocytic leukaemia. Br J Haematol; 2009 Jun;145(6):788-800
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  • [Title] Mutations of polycomb-associated gene ASXL1 in myelodysplastic syndromes and chronic myelomonocytic leukaemia.
  • The myelodysplastic syndromes (MDSs) are a heterogeneous group of clonal haematological diseases characterized by ineffective haematopoiesis and predisposition to acute myeloid leukaemia (AML).
  • We studied a series of 40 MDS/AML samples by high-density array-comparative genome hybridization (aCGH).
  • To extend these results we searched for mutations of ASXL1 in a series of chronic myelomonocytic leukaemias, a disease classified as MDS/Myeloproliferative disorder, and found mutations in 17 out of 39 patients (43%).
  • These results show that ASXL1 might play the role of a tumour suppressor in myeloid malignancies.
  • [MeSH-major] Leukemia, Myelomonocytic, Chronic / genetics. Mutation. Myelodysplastic Syndromes / genetics. Repressor Proteins / genetics


45. Lamkin TJ, Chin V, Varvayanis S, Smith JL, Sramkoski RM, Jacobberger JW, Yen A: Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels. J Cell Biochem; 2006 Apr 15;97(6):1328-38
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  • [Title] Retinoic acid-induced CD38 expression in HL-60 myeloblastic leukemia cells regulates cell differentiation or viability depending on expression levels.
  • Retinoic acid-induced expression of the CD38 ectoenzyme receptor in HL-60 human myeloblastic leukemia cells is regulated by RARalpha and RXR, and enhanced or prevented cell differentiation depending on the level of expression per cell.
  • Expression of CD38 enhanced retinoic acid-induced myeloid differentiation and G0 cell cycle arrest, but at higher expression levels, induced differentiation was blocked and retinoic acid induced a loss of cell viability instead.
  • In the case of 1,25-dihydroxyvitamin D3, induced monocytic differentiation was also enhanced by CD38 and not enhanced by higher expression levels, but without induced loss of viability.
  • [MeSH-major] Antigens, CD38 / metabolism. Cell Differentiation / drug effects. Cell Survival / drug effects. Leukemia, Myeloid, Acute / metabolism. Tretinoin / pharmacology

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16329108.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / T32 ES007052
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin; EC 3.2.2.5 / Antigens, CD38
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46. Forestier E, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology NOPHO: The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations. J Pediatr Hematol Oncol; 2006 Aug;28(8):486-95
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  • [Title] The incidence peaks of the childhood acute leukemias reflect specific cytogenetic aberrations.
  • The correlation between age and karyotype was studied in 1425, 0 to 14.9 years old children who were diagnosed with acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia.
  • Among B-cell precursor ALL cases, high white blood cell counts correlated with earlier age at diagnosis (rS=-0.23; P<0.001) being most evident for 11q23/MLL-aberrations, translocation t(12;21)(p13;q22), and high-hyperdiploidy.
  • Among acute myeloblastic leukemia patients, frequency peaks were found for those with MLL/11q23 rearrangements (peak: first year), Down syndrome (peak: second to third year), or cytogenetic abnormalities other than translocations t(8;21), t(15;17), and inv(16)/t(16;16) (peak: first to third year).
  • The epidemiology of the cytogenetic subsets of acute leukemias questions whether age as a disease-related prognostic parameter has any relevance in childhood leukemia clinical research beyond being a surrogate marker for more important, truly biologic features such as cytogenetic aberrations and white cell count at diagnosis.
  • Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Age Distribution. Child. Child, Preschool. Cohort Studies. Comorbidity. Cytogenetic Analysis / methods. Down Syndrome / diagnosis. Down Syndrome / epidemiology. Down Syndrome / genetics. Female. Humans. Incidence. Infant. Infant, Newborn. Karyotyping. Male. Ploidies. Recurrence. Registries / statistics & numerical data. Risk Factors. Scandinavian and Nordic Countries / epidemiology

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  • (PMID = 16912588.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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47. Nakamura Y, Ito M, Yamamoto T, Yan XY, Yagasaki H, Kamachi Y, Kudo K, Kojima S: Engraftment of NOD/SCID/gammac(null) mice with multilineage neoplastic cells from patients with juvenile myelomonocytic leukaemia. Br J Haematol; 2005 Jul;130(1):51-7
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  • [Title] Engraftment of NOD/SCID/gammac(null) mice with multilineage neoplastic cells from patients with juvenile myelomonocytic leukaemia.
  • Several lines of evidence indicate the clonal nature of juvenile myelomonocytic leukaemia (JMML), involving myeloid, erythroid, megakaryocyte and B-lymphoid lineages.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myelomonocytic, Acute / pathology. Models, Animal

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  • (PMID = 15982344.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IL2RG protein, human; 0 / Il2rg protein, mouse; 0 / Interleukin Receptor Common gamma Subunit; 0 / Receptors, Interleukin-7
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48. Krivtsov AV, Twomey D, Feng Z, Stubbs MC, Wang Y, Faber J, Levine JE, Wang J, Hahn WC, Gilliland DG, Golub TR, Armstrong SA: Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9. Nature; 2006 Aug 17;442(7104):818-22
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  • [Title] Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9.
  • Here we show that leukaemia stem cells (LSC) can maintain the global identity of the progenitor from which they arose while activating a limited stem-cell- or self-renewal-associated programme.
  • The LSC were capable of transferring leukaemia to secondary recipient mice when only four cells were transferred, and possessed an immunophenotype and global gene expression profile very similar to that of normal granulocyte macrophage progenitors.
  • However, a subset of genes highly expressed in normal haematopoietic stem cells was re-activated in LSC.
  • LSC can thus be generated from committed progenitors without widespread reprogramming of gene expression, and a leukaemia self-renewal-associated signature is activated in the process.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplastic Stem Cells / metabolism. Neoplastic Stem Cells / pathology. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. Cell Line. Cell Lineage. Granulocytes / cytology. Granulocytes / pathology. Humans. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / metabolism. Leukemia, Myelomonocytic, Acute / pathology. Macrophages / cytology. Macrophages / pathology. Mice. Neoplasm Transplantation. Survival Rate


49. Mansoor S, Nasir-Ud-Din, Azam M, Jamshed A: Generalized cutaneous granulocytic sarcoma with joint involvement. J Coll Physicians Surg Pak; 2010 May;20(5):339-40
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  • [Title] Generalized cutaneous granulocytic sarcoma with joint involvement.
  • Granulocytic sarcoma (GS) is a rare extra medullary solid tumour composed of immature myeloid cells.
  • We report a case of generalized cutaneous granulocytic sarcoma with ankle joint involvement who subsequently developed AML-M4.
  • [MeSH-major] Ankle Joint. Leukemia, Myeloid, Acute / pathology. Sarcoma / pathology. Skin Neoplasms / pathology

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  • (PMID = 20642930.001).
  • [ISSN] 1022-386X
  • [Journal-full-title] Journal of the College of Physicians and Surgeons--Pakistan : JCPSP
  • [ISO-abbreviation] J Coll Physicians Surg Pak
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
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50. Koga Y, Matsuzaki A, Suminoe A, Washitoh N, Hara T, Hara T, Tajiri T, Taguchi T: Treatment-related acute myelomonocytic leukemia with t(11;19) in a child following chemotherapy for hepatoblastoma. Pediatr Blood Cancer; 2008 Apr;50(4):943-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment-related acute myelomonocytic leukemia with t(11;19) in a child following chemotherapy for hepatoblastoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hepatoblastoma / drug therapy. Leukemia, Myelomonocytic, Acute / chemically induced. Liver Neoplasms / drug therapy. Neoplasms, Second Primary / chemically induced. Translocation, Genetic


51. Yan Q, Jiang Z, Yang S, Deng W, Han L: A novel homodimeric lectin from Astragalus mongholicus with antifungal activity. Arch Biochem Biophys; 2005 Oct 1;442(1):72-81
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  • A novel lectin (AMML) was isolated from a Chinese herb, i.e., the roots of Astragalus mongholicus, using a combination of ammonium sulfate fraction and ion exchange chromatographies.
  • The molecular mass of intact AMML was determined to be 66,396 Da by MALDI-TOF mass spectrometry and 61.8 kDa by gel filtration, respectively.
  • AMML was a dimeric protein composed of two identical subunits each with a molecular mass of 29.6 kDa.
  • N-terminal amino acid sequence of AMML was determined as ESGINLQGDATLANN.

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  • (PMID = 16140255.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Blood Group Antigens; 0 / Glycoproteins; 0 / Lectins; SU46BAM238 / Ammonium Sulfate; X2RN3Q8DNE / Galactose
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52. Struhal W, Oberndorfer S, Lahrmann H, Lindeck-Pozza E, Hess B, Nussgruber V, Pöhnl R, Dobner T, Grisold W: Myeloid sarcoma in the central nervous system: case report and review of the literature. Acta Clin Croat; 2008 Mar;47(1):19-24
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  • [Title] Myeloid sarcoma in the central nervous system: case report and review of the literature.
  • Myeloid sarcomas are rare manifestations of mainly myeloblastic leukemia.
  • A case is added herewith and a review was performed to investigate clinical characteristics and treatment options of central nervous system myeloid sarcoma.
  • A 61-year-old female with acute myeloblastic leukemia (FAB M5) and progressive left sided hemiparesis showed a right parieto-occipital epidural lesion mimicking meningioma.
  • Partial resection was performed to reveal a myeloid sarcoma.
  • Reviewing the literature we identified 44 cases with sufficient description of the diagnosis, treatment and follow up to one year.
  • [MeSH-major] Brain Neoplasms / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary. Occipital Lobe. Parietal Lobe. Sarcoma, Myeloid / diagnosis

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  • (PMID = 18714643.001).
  • [ISSN] 0353-9466
  • [Journal-full-title] Acta clinica Croatica
  • [ISO-abbreviation] Acta Clin Croat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Croatia
  • [Number-of-references] 20
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53. Kiss F, Simon A, Csáthy L, Hevessy Z, Katona E, Kiss C, Kappelmayer J: A coagulation factor becomes useful in the study of acute leukemias: studies with blood coagulation factor XIII. Cytometry A; 2008 Mar;73(3):194-201
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  • [Title] A coagulation factor becomes useful in the study of acute leukemias: studies with blood coagulation factor XIII.
  • By using 3- and 4-color flow cytometry FXIII expression was investigated in normal peripheral blood and bone marrow samples and in acute myeloblastic (AML) and lymphoblastic (ALL) leukemia cases.
  • In samples derived from patients with AML M4 and M5, FXIII-A sensitively identified blast cells.
  • These data provide evidence that FXIII-A is a sufficiently sensitive marker in differentiating myeloblasts and monoblasts and is suitable for identifying leukemia-associated phenotypes in ALL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Factor XIII / chemistry. Factor XIII / physiology. Leukemia / blood. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Animals. Blood Platelets / chemistry. Blood Platelets / metabolism. Blood Platelets / pathology. Flow Cytometry / methods. Humans. Monocytes / chemistry. Monocytes / metabolism. Monocytes / pathology

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  • [Copyright] Copyright 2007 International Society for Analytical Cytology.
  • (PMID = 18000871.001).
  • [ISSN] 1552-4930
  • [Journal-full-title] Cytometry. Part A : the journal of the International Society for Analytical Cytology
  • [ISO-abbreviation] Cytometry A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 9013-56-3 / Factor XIII
  • [Number-of-references] 56
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54. Monreal MB, Pardo ML, Pavlovsky MA, Fernandez I, Corrado CS, Giere I, Sapia S, Pavlovsky S: Increased immature hematopoietic progenitor cells CD34+/CD38dim in myelodysplasia. Cytometry B Clin Cytom; 2006 Mar;70(2):63-70
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  • METHODS: We analyzed the expression of CD38 and HLA-DR on CD34+ cells by flow cytometry in 36 patients with MDS, as well as in healthy donors (n = 12) and patients with other hematological disorders: non-Hodgkin lymphomas and multiple myeloma, both in complete remission (CR) (n = 32); acute lymphoblastic leukemia in CR (n = 17); de novo acute myeloblastic leukemia (AML) at diagnosis (n = 22) and in CR (n = 37); and AML secondary to MDS at diagnosis (n = 19).
  • RESULTS: Compared to normal BM, the fraction of immature HPC, characterized as CD34+bright, intermediate FSC/SSC, and CD38dim, was significantly increased in high risk MDS and secondary AML, but not in low risk MDS, (P < or = 0.001, P = 0.03, and P = 0.7).
  • De novo AML showed decreased immature HPC.
  • High numbers of immature HPC correlated with higher IPSS risk groups (P = 0.05) and showed significant impact on disease progression (P = 0.03).
  • Increased immature HPC in high risk MDS and secondary AML may reflect blocked differentiation of CD34+ cells in these diseases.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Disease Progression. Female. Flow Cytometry. HLA-DR Antigens / immunology. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / immunology. Male. Middle Aged. Multiple Myeloma / diagnosis. Multiple Myeloma / immunology. Observer Variation. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Reproducibility of Results. Risk Factors

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  • [Copyright] Copyright 2005 International Society for Analytical Cytology.
  • (PMID = 16470534.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; EC 3.2.2.5 / Antigens, CD38
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55. Breccia M, Mengarelli A, Mancini M, Biondo F, Gentilini F, Latagliata R, Mandelli F, Alimena G: Myelodysplastic syndromes in patients under 50 years old: a single institution experience. Leuk Res; 2005 Jul;29(7):749-54
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  • Patients demographics and clinical features at diagnosis were analysed for their prognostic value on survival and on risk of transformation to acute leukaemia.
  • The median age at diagnosis was 43 years (range 21-50).
  • According to FAB criteria there were 30 patients with refractory anaemia (RA), 3 with refractory anaemia with ringed sideroblasts (RARS), 18 with refractory anaemia with excess of blasts (RAEB), 6 with refractory anaemia with excess of blasts in transformation (RAEB-t) and 5 with chronic myelomonocytic leukaemia (CMML).
  • At a median follow-up of 15 months 19 patients (31%) progressed to acute myeloid leukaemia (AML).
  • From univariate analysis we identified some features, which appeared to be predictive of outcome and risk of transformation to AML.
  • Age above 40 years (p = 0.002) and high risk according to IPSS score (p = 0.002) were found to be predictive for a shorter survival; FAB grouping (p = 0.0001), percentage > 5% of blasts in the bone marrow (p = 0.001) and high risk by IPSS score (p = 0.0003) were found to be predictive for a higher risk of transformation to AML.
  • [MeSH-minor] Adult. Anemia / etiology. Anemia, Sideroblastic / etiology. Cell Transformation, Neoplastic. Female. Humans. Leukemia / etiology. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis


56. McGrath P, Suppiah R, Patton MA: Re-entering life: paediatric acute myeloid leukaemia at one year post treatment. Aust J Holist Nurs; 2005 Oct;12(2):23-34
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  • [Title] Re-entering life: paediatric acute myeloid leukaemia at one year post treatment.
  • To date, there is scant psychosocial research on the experience of childhood AML.
  • The findings highlight challenges associated with re-entering life post-treatment with an emphasis on the ongoing sense of uncertainty, the changed sense of normalcy, and the difficulty of returning to the hospital for check-ups.
  • [MeSH-major] Attitude to Health. Holistic Health. Leukemia, Myelomonocytic, Acute / psychology. Parent-Child Relations. Parenting / psychology

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  • (PMID = 19175261.001).
  • [ISSN] 1322-8803
  • [Journal-full-title] The Australian journal of holistic nursing
  • [ISO-abbreviation] Aust J Holist Nurs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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57. Tsavaris N, Kopterides P, Kosmas C, Siakantaris M, Patsouris E, Pangalis G: Spontaneous remission of acute myeloid leukemia associated with GnRH agonist treatment. Leuk Lymphoma; 2006 Mar;47(3):557-60
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  • [Title] Spontaneous remission of acute myeloid leukemia associated with GnRH agonist treatment.
  • Spontaneous remission of acute myeloid leukemia (AML) in adults is a rare but well documented phenomenon.
  • This study reports on a 64-year-old male patient with acute myelogenous leukemia (AML-M4, according to the French-American-British classification) that was developed on a background of chronic myelomonocytic leukemia (CMML) and then underwent remission after treatment with the gonadotropin-releasing hormone agonist (GnRH agonist) triptorelin for presumed prostate cancer.
  • To the author' knowledge, this is the first report of remission in an AML-M4 case associated with hormone manipulation.
  • [MeSH-major] Gonadotropin-Releasing Hormone / agonists. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / pathology. Leukemia, Myelomonocytic, Chronic / drug therapy. Triptorelin Pamoate / therapeutic use

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  • (PMID = 16396781.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone; 57773-63-4 / Triptorelin Pamoate
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58. Takahashi W, Arai Y, Tadokoro J, Takeuchi K, Yamagata T, Mitani K: [Disappearance of a Philadelphia chromosome-positive clone and appearance of a -negative clone following treatment with imatinib mesylate in acute myelomonocytic leukemia]. Rinsho Ketsueki; 2006 Feb;47(2):111-4
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  • [Title] [Disappearance of a Philadelphia chromosome-positive clone and appearance of a -negative clone following treatment with imatinib mesylate in acute myelomonocytic leukemia].
  • A 63-year-old female was diagnosed as having Philadelphia chromosome-positive acute myelomonocytic leukemia in June 2002.
  • The patient received monotherapy with imatinib mesylate or combination therapy with DCM and idarubicin/cytarabine, both of which failed in attaining disease remission.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative. Leukemia, Myelomonocytic, Acute / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 16529013.001).
  • [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 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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59. Ali R, Ozkalemkas F, Ozkocaman V, Ozcelik T, Akalin H, Ozkan A, Altundal Y, Tunali A: Hydatid disease in acute leukemia: effect of anticancer treatment on echinococcosis. Microbes Infect; 2005 Jul;7(9-10):1073-6
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  • [Title] Hydatid disease in acute leukemia: effect of anticancer treatment on echinococcosis.
  • Echinococcosis, also known as hydatid disease or hydatidosis, is a zoonotic illness caused by the larval form of Echinococcus spp.
  • We treated and followed approximately 1200 patients with different hematologic neoplastic diseases between 1985 and 2003, and only one of these individuals had concomitant acute leukemia and liver hydatidosis.
  • This report describes the case of a 19-year-old man who had both primary refractoriness of acute leukemia (AML-M4) and liver hydatidosis.
  • The patient underwent 3 months of treatment with agents that targeted the leukemia (daunorubicin, idarubicin, cytarabine, fludarabine) and its complications (amphotericin B, amphotericin B lipid complex, liposomal amphotericin B).

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  • (PMID = 15996888.001).
  • [ISSN] 1286-4579
  • [Journal-full-title] Microbes and infection
  • [ISO-abbreviation] Microbes Infect.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
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60. Hisasue M, Nishimura T, Neo S, Nagashima N, Ishikawa T, Tsuchiya R, Yamada T: A dog with acute myelomonocytic leukemia. J Vet Med Sci; 2008 Jun;70(6):619-21
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  • [Title] A dog with acute myelomonocytic leukemia.
  • The dog was diagnosed with myelomonocytic leukemia (M4) because the blast cells were demonstrated by cytochemical staining to be both myeloid and monocytic cells.
  • This case is the first report of M4 in Japan.

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  • (PMID = 18628605.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 12001-79-5 / Vitamin K; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 9PHQ9Y1OLM / Prednisolone
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61. Matsuo Y, Drexler HG, Harashima A, Okochi A, Kojima K, Asakura S, Tanimoto M, Orita K: Acute myeloid leukemia cell lines MOLM-17 and MOLM-18 derived from patient with advanced myelodysplastic syndromes. Leuk Res; 2005 Jun;29(6):701-10
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  • [Title] Acute myeloid leukemia cell lines MOLM-17 and MOLM-18 derived from patient with advanced myelodysplastic syndromes.
  • The two acute myelomonocytic leukemia sister cell lines MOLM-17 and MOLM-18 and the Epstein-Barr-virus positive non-malignant B-lymphoblastoid cell lines (B-LCLs) B422 and B423 were established from the bone marrow sample of a 60-year-old Japanese male in the advanced leukemic phase of refractory anemia with excess of blasts, a subtype of myelodysplastic syndromes (MDS).
  • MOLM-17 and B422 were established at eight months after the initial diagnosis, while MOLM-18 and B423 were derived from a sample one month later.
  • Immunophenotyping of the first leukemia sample revealed a mixed lineage leukemia immunophenotype with positivity for terminal deoxynucleotidyl transferase (TdT), CD13 and CD19; the second sample revealed solely myeloid characteristics with positivity for CD13, CD41 and CD61, whereas TdT was negative.
  • MOLM-17/-18 showed immunomarker profiles typical of the myelomonocytic lineage.
  • [MeSH-major] Cell Line, Tumor / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / pathology


62. Naithani R, Mahapatra M: Parotid involvement in acute myelomonocytic leukemia. Indian J Pediatr; 2007 Oct;74(10):965-6
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  • [Title] Parotid involvement in acute myelomonocytic leukemia.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / pathology. Leukemic Infiltration / pathology. Parotid Gland / pathology
  • [MeSH-minor] Biopsy, Needle. Bone Marrow / pathology. Child. Diagnosis, Differential. Facial Paralysis / pathology. Female. Humans

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  • [CommentIn] Indian J Pediatr. 2009 Apr;76(4):438-9 [19412591.001]
  • (PMID = 17978464.001).
  • [ISSN] 0973-7693
  • [Journal-full-title] Indian journal of pediatrics
  • [ISO-abbreviation] Indian J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] India
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63. Mori Y, Yoshimoto G, Kumano T, Miyamoto T, Iino T, Takenaka K, Iwasaki H, Harada N, Kinukawa N, Nagafuji K, Teshima T, Shimoda K, Akashi K, Harada M: Distinctive expression of myelomonocytic markers and down-regulation of CD34 in acute myelogenous leukaemia with FLT3 tandem duplication and nucleophosmin mutation. Eur J Haematol; 2007 Jul;79(1):17-24
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  • [Title] Distinctive expression of myelomonocytic markers and down-regulation of CD34 in acute myelogenous leukaemia with FLT3 tandem duplication and nucleophosmin mutation.
  • OBJECTIVE: Patients with acute myelogenous leukaemia (AML) show co-existing frequently internal tandem duplications of FLT3 (FLT3-ITD) and mutations of nucleophosmin (NPM1-Mt).
  • We investigated the biological and clinical significance of FLT3-ITD and/or NPM1-Mt in this context.
  • METHODS: We analysed 89 AML patients according to whether NPM1 and FLT3-ITD were single mutants, double mutants, or wild type for both.
  • By multivariate analysis, white blood cell count and peripheral blood blast cell count at diagnosis were significantly higher in patients with FLT3-ITD but not in those with only NPM1-Mt.
  • NPM1-Mt was significantly related to female gender, normal karyotype, and M4 or M5 disease according to French-American-British criteria.
  • In addition, leukaemic blast cells with NPM1-Mt, FLT3-ITD, or both expressed CD34 less frequently than wild-type blasts (P < 0.0001 and P = 0.005 respectively), while myelomonocytic markers such as CD11b and CD14 were expressed more frequently in patients with NPM1-Mt.
  • CONCLUSION: FLT3-ITD may increase potential for cell proliferation to produce a leukaemic population; NPM1-Mt may cause cells to develop along the myelomonocytic lineage.
  • [MeSH-major] Antigens, CD34 / immunology. Biomarkers, Tumor / metabolism. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Monocytes / metabolism. Mutation. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17598835.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 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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64. Inukai T, Zhang X, Goto M, Hirose K, Uno K, Akahane K, Nemoto A, Goi K, Sato H, Takahashi K, Honna H, Kagami K, Nakamoto K, Yagita H, Okumura K, Koyama-Okazaki T, Nakazawa S, Sugita K: Resistance of infant leukemia with MLL rearrangement to tumor necrosis factor-related apoptosis-inducing ligand: a possible mechanism for poor sensitivity to antitumor immunity. Leukemia; 2006 Dec;20(12):2119-29
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  • [Title] Resistance of infant leukemia with MLL rearrangement to tumor necrosis factor-related apoptosis-inducing ligand: a possible mechanism for poor sensitivity to antitumor immunity.
  • Immune escape mechanisms also contribute to the failure of graft-versus-leukemia (GVL) effect after allogeneic hematopoietic stem cell transplantation (allo-SCT).
  • Infant leukemias with mixed-lineage leukemia (MLL) rearrangement have a remarkably short latency, and GVL effect after allo-SCT has not been clearly evidenced in these leukemias.
  • We investigated the in vitro sensitivity of MLL-rearranged acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML) cells to TRAIL- and FasL-mediated cytotoxicity.
  • Most of cell lines and primary leukemia cells were highly resistant to TRAIL primarily owing to low cell-surface expression of death receptors in ALL and simultaneous expression of decoy receptors in AML.
  • Nearly half of cell lines and majority of primary leukemia cells showed low sensitivity to FasL.
  • These results suggest that resistance to death-inducing ligands, particularly to TRAIL, could be one of the mechanisms for a rapid clonal expansion and a poor sensitivity to the GVL effect in infant leukemias with MLL rearrangement.
  • [MeSH-major] Gene Rearrangement. Leukemia / immunology. Myeloid-Lymphoid Leukemia Protein / genetics. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tumor Escape
  • [MeSH-minor] Drug Resistance, Neoplasm. Graft vs Leukemia Effect. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / analysis

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  • (PMID = 17066095.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / NF-kappa B; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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65. Karam A, Eveillard JR, Ianoto JC, Quinio D, Le Flohic AM, Le Roy JP, Misery L, Berthou C: [Disseminated cutaneous and visceral fusariosis in an aplastic patient: an unusual digestive entry]. Ann Dermatol Venereol; 2005 Mar;132(3):255-8
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  • We report a case of cutaneous and systemic fusariosis due to Fusarium moniliforme in a patient with acute lymphoblastic leukemia.
  • CASE-REPORT: A 20 year-old male student was suffering from acute type 6 myeloblastic leukemia.
  • Treatment with voriconazole in association with transfusions of leukocytes led to clinical and microbiological cure.
  • DISCUSSION: In our case report, the clinical pattern starting with digestive symptoms suggested dissemination from a digestive site, which is very unusual in Europe.
  • [MeSH-major] Fusarium / pathogenicity. Mycoses / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 15924050.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; 00DPD30SOY / Amsacrine; 04079A1RDZ / Cytarabine; JFU09I87TR / Voriconazole
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66. Elouennass M, Doghmi K, Fagot T, Soler C, Mac Nab C, Foissaud V, De Revel T, Hervé V: [Hepatosplenic and kidneys candidasis complicating an acute myeloblastic leukemia. A case treated with voriconazole and caspofungin]. Ann Biol Clin (Paris); 2005 Jul-Aug;63(4):423-7
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  • [Title] [Hepatosplenic and kidneys candidasis complicating an acute myeloblastic leukemia. A case treated with voriconazole and caspofungin].
  • We report the observation of hepato-splenic and kidneys candidiasis complicating the chemotherapy of a myeloblastic leukemia (LAM5b).
  • [MeSH-major] Antifungal Agents / therapeutic use. Candidiasis / drug therapy. Kidney Diseases / microbiology. Leukemia, Myeloid, Acute / microbiology. Liver Diseases / microbiology. Peptides, Cyclic / therapeutic use. Pyrimidines / therapeutic use. Splenic Diseases / microbiology. Triazoles / therapeutic use


67. Wang C, Chen Z, Li Z, Cen J: The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells. Leuk Res; 2010 Aug;34(8):1083-90
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  • [Title] The essential roles of matrix metalloproteinase-2, membrane type 1 metalloproteinase and tissue inhibitor of metalloproteinase-2 in the invasive capacity of acute monocytic leukemia SHI-1 cells.
  • The frequency of extramedullary infiltration (EMI) in acute myeloblastic leukemia (AML) is reported up to 40% and most prevalent in myelo-monoblastic and monoblastic subtypes of AML (M4 and M5 according to FAB classification).
  • To explore mechanism underlying EMI, we analyzed SHI-1 cells, a highly invasive human acute monocytic leukemia cell line, and found their strong expression of matrix metalloproteinase 2 (MMP-2), membrane type 1 MMP (MT1-MMP) and tissue inhibitor of metalloproteinase 2 (TIMP-2).
  • SHI-1 cells showed higher invasive ability to traverse reconstituted basement membranes (Matrigel) and stronger activation of proMMP-2 than other leukemia cell line such as NB4, K562, U937 and THP-1 cells.
  • Our study indicated that increasing TIMP-2 in AML patients with EMI may potentially cause adverse effects, particularly in patients containing high levels of MMP-2 and MT1-MMP.
  • [MeSH-major] Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Matrix Metalloproteinase 14 / metabolism. Matrix Metalloproteinase 2 / metabolism. Tissue Inhibitor of Metalloproteinase-2 / metabolism

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138666.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Matrix Metalloproteinase Inhibitors; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 119978-18-6 / matrigel; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; 9007-34-5 / Collagen; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.80 / MMP14 protein, human; EC 3.4.24.80 / Matrix Metalloproteinase 14
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68. Jackowska T, Steczowicz M, Pawelec K, Pacholska J: [Congenital leukaemia and transient myeloproliferative disorder: diagnostic difficulties--case reports]. Med Wieku Rozwoj; 2006 Jul-Sep;10(3 Pt 1):595-601
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  • [Title] [Congenital leukaemia and transient myeloproliferative disorder: diagnostic difficulties--case reports].
  • Congenital leukaemia occurs in only 0.8% of all cases of leukaemia in children.
  • Despite great progress in the treatment of childhood leukaemia, prognosis is still poor.
  • This type of leukaemia must be distinguished from leukaemic reactions and transient myeloproliferative disorder.
  • Transient myeloproliferative disorder is a rare condition in the neonatal period, connected with trisomy or other abnormalities of chromosome 21.
  • We present two cases: congenital leukaemia and transient myeloproliferative disorder.
  • The first patient was a boy in whom congenital myelomonoblastic leukaemia (M4 in FAB classification) was diagnosed at age of 6 weeks.
  • He was treated according to BFM-96 for acute myeloblasts leukaemia protocol, but there was no remission and he died of progressive congenital leukaemia after 4 months.
  • These cases confirm the difficulties in differentiation between congenital leukaemia and transient myeloproliferative disorder presented in literature.
  • In spite of the same haematological symptoms the only difference may be detection of nonhematopoietic tissue infiltration (skin and central nervous system) commonly occurring in congenital leukaemia or the presence of trisomy and other abnormalities of chromosome 21 in transient myeloproliferative disorder.
  • [MeSH-major] Leukemia, Lymphoid / congenital. Leukemia, Lymphoid / diagnosis. Leukemia, Myeloid, Acute / congenital. Leukemia, Myeloid, Acute / diagnosis. Myeloproliferative Disorders / congenital. Myeloproliferative Disorders / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Down Syndrome / complications. Down Syndrome / diagnosis. Fatal Outcome. Female. Humans. Infant, Newborn. Male. Treatment Outcome

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  • (PMID = 17317890.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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69. Akimkin VG, Ledin EV, Skvortsov SV, Rukavitsyn OA: [Incidence of hepatitis B virus infection in patients with blood disease]. Ter Arkh; 2007;79(11):28-31
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  • [Title] [Incidence of hepatitis B virus infection in patients with blood disease].
  • AIM: To define incidence of HBV infection in patients with blood diseases caused by blood components transfusion; correlation between infection rate and blood disease nosological entity, intensity of hemoreplacement therapy, time of hepatitis B incubation period in patients with hematological malignancies after the diagnosis and initiation of polychemotherapy (PCT).
  • MATERIAL AND METHODS: In 2000-2007 a prospective clinicoepidemiological trial was made to detect markers of HBV infection among 303 patients 15 to 76 years of age treated in the department of acute leukemia chemotherapy of N.N.
  • Burdenko Military Hospital for acute lymphoid and myeloblastic leukemia, chronic myeloid leukemia in a blastic crisis, myelodysplastic syndrome in blast transformation, lymphoproliferative diseases with bone marrow affection.
  • Among the infected patients there were 16 (53.4%) patients with different variants of acute myeloblastic leukemia, 12 (40.0%) with different immunophenotypes of acute lymphoblastic leukemia, 1 (3.3%) patient with acute biphenotypical leukemia and 1 (3.3%) with lymphoma/leukemia.
  • Most of the patients - 23 (74%) of 30 - were infected with HBV within the first year after hematological diagnosis and PCT induction course.
  • [MeSH-major] Hepatitis B / epidemiology. Leukemia, Myeloid, Acute / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 18219969.001).
  • [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 / Antiviral Agents; 0 / Biomarkers
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70. Wojcik I, Szybka M, Golanska E, Rieske P, Blonski JZ, Robak T, Bartkowiak J: Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias. Neoplasma; 2005;52(4):318-24
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  • [Title] Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias.
  • Abnormalities of the P53 network have been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML).
  • The purpose of this study was to define P53 gene mutations, to detect MDM2 gene amplification and to estimate mRNA expression of P53, MDM2, BCL2 and BAX genes in patients with ALL and AML.
  • Twenty-five patients with ALL and 65 patients with AML, both recently diagnosed, were included into this study.
  • Mutation of the P53 gene was found in one patient of the 25 with ALL and in five patients of the 65 with AML.
  • One mutation in intronic sequence in ALL and four missense mutations and one silent nucleotide substitution in AML were identified.
  • Amplification of MDM2 gene was detected by multiplex-PCR analysis in only one sample from patient with ALL, but was not observed in any case of AML.
  • To gain further insight into the role of P53 network in the evolution of acute leukemias, the P53, MDM2, BCL2 and BAX mRNAexpressions in portion samples from patients with ALL and AML were analyzed using multiplex RT-PCR.
  • A high frequency of BCL2 mRNA overexpression and a relatively low frequency of BAX mRNA overexpression detected in both analyzed leukemias in this study, indicate that altered transcription of these genes may be involved in leukemogenesis.
  • [MeSH-major] Gene Amplification. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16059649.001).
  • [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 / BAX protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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71. Pulte D, Gondos A, Brenner H: Trends in survival after diagnosis with hematologic malignancy in adolescence or young adulthood in the United States, 1981-2005. Cancer; 2009 Nov 1;115(21):4973-9
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  • [Title] Trends in survival after diagnosis with hematologic malignancy in adolescence or young adulthood in the United States, 1981-2005.
  • METHODS: : Period analysis was used to calculate 5- and 10-year relative survival for adolescents and young adults diagnosed with Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL), acute lymphoblastic leukemia (ALL), acute myeloblastic leukemia (AML), and chronic myelocytic leukemia (CML) for 5 5-year periods from 1981-1985 to 2001-2005, using data from the Surveillance, Epidemiology, and End Results database.
  • Increases in 10-year relative survival between 1981-1985 and 2001-2005 were as follows: HL, from 80.4% to 93.4%; NHL, from 55.6% to 76.2%; ALL, from 30.5% to 52.1%; AML, from 15.2% to 45.1%; CML, from 0 to 74.5% (P < .001 in all cases).
  • However, although survival improved steadily throughout the period examined for the lymphomas and CML, survival was stable during the late 1990s and early 21st century for the acute leukemias.
  • However, with the exception of HL, survival rates have not reached the levels observed for children diagnosed with these malignancies, and survival expectations for patients with acute leukemia have stabilized at relatively low levels.
  • [MeSH-minor] Adolescent. Hodgkin Disease / mortality. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myeloid, Acute / mortality. Lymphoma, Non-Hodgkin / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Survival Rate. Time Factors. United States / epidemiology. Young Adult

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  • (PMID = 19705347.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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72. Koh G, Yamane T, Aoyama Y, Sakamoto C, Nakamae H, Hasegawa T, Terada Y, Hino M: [Acute myelomonocytic leukemia complicated with multiple lower intestinal ulcers induced by nonsteroidal anti-inflammatory drugs]. Gan To Kagaku Ryoho; 2005 Jan;32(1):111-3
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  • [Title] [Acute myelomonocytic leukemia complicated with multiple lower intestinal ulcers induced by nonsteroidal anti-inflammatory drugs].
  • We report an 18-year-old woman with acute myelomonocytic leukemia, who developed massive lower intestinal bleeding following induction chemotherapy.
  • Colonoscopy revealed multiple circular ulcers but no infectious colitis or infiltration of leukemia.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Colonic Diseases / chemically induced. Leukemia, Myelomonocytic, Acute / complications. Peptic Ulcer Hemorrhage / chemically induced

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  • (PMID = 15675595.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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73. Reiterer G, Yen A: Platelet-derived growth factor receptor regulates myeloid and monocytic differentiation of HL-60 cells. Cancer Res; 2007 Aug 15;67(16):7765-72
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  • [Title] Platelet-derived growth factor receptor regulates myeloid and monocytic differentiation of HL-60 cells.
  • Here, we show that the platelet-derived growth factor receptor (PDGFR) regulates myeloid and monocytic differentiation of HL-60 myeloblastic leukemia cells in response to retinoic acid (RA) and vitamin D3 (D3), respectively.
  • In addition, we found calcium levels to be decreased by RA and D3 but increased when AG1296 was given in addition to RA or D3, suggesting that calcium levels decrease during myeloid or monocytic differentiation, and elevated calcium levels can disturb the expression of certain differentiation markers.
  • [MeSH-major] Monocytes / pathology. Myeloid Cells / pathology. Receptors, Platelet-Derived Growth Factor / metabolism

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  • (PMID = 17699781.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA33505; United States / NIDDK NIH HHS / DK / DK072105
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD11b; 0 / Antigens, CD14; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / Fc(alpha) receptor; 0 / GPI-Linked Proteins; 0 / ITGAM protein, human; 0 / Membrane Glycoproteins; 0 / Receptors, Fc; 0 / Tyrphostins; 0 / Ubiquitin; 146535-11-7 / 6,7-dimethoxy-3-phenylquinoxaline; 1C6V77QF41 / Cholecalciferol; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; SY7Q814VUP / Calcium
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74. Keating GM: Azacitidine: a review of its use in higher-risk myelodysplastic syndromes/acute myeloid leukaemia. Drugs; 2009;69(17):2501-18
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  • [Title] Azacitidine: a review of its use in higher-risk myelodysplastic syndromes/acute myeloid leukaemia.
  • Subcutaneous azacitidine was recently approved in the EU for the treatment of adults who are not eligible for haematopoietic stem cell transplantation and who have intermediate-2-risk or high-risk myelodysplastic syndromes (MDS) [according to International Prognostic Scoring System (IPSS) criteria], chronic myelomonocytic leukaemia (CMML) with 10-29% marrow blasts without myeloproliferative disorder, or acute myeloid leukaemia (AML) with 20-30% blasts and multilineage dysplasia (according to the WHO classification).
  • Subcutaneous azacitidine is the only drug shown to significantly prolong survival in patients with higher-risk MDS or WHO-defined AML, compared with conventional care (i.e. best supportive care, low-dose cytarabine or intensive chemotherapy).
  • In addition, azacitidine is associated with a lower risk of AML progression and higher rates of complete remission, partial remission, haematological improvement and red blood cell (RBC) transfusion independence.
  • Thus, azacitidine is a valuable option for the first-line treatment of patients with higher-risk MDS/AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Combined Modality Therapy. Leukemia, Myeloid, Acute / drug therapy. Prognosis. Risk Assessment


75. Emerenciano M, Agudelo Arias DP, Coser VM, de Brito GD, Macedo Silva ML, Pombo-de-Oliveira MS, Brazilian Collaborative Study Group of Infant Acute Leukemia: Molecular cytogenetic findings of acute leukemia included in the Brazilian Collaborative Study Group of Infant acute leukemia. Pediatr Blood Cancer; 2006 Oct 15;47(5):549-54
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  • [Title] Molecular cytogenetic findings of acute leukemia included in the Brazilian Collaborative Study Group of Infant acute leukemia.
  • BACKGROUND: Chromosome abnormalities often occur prenatally in childhood leukemia, characterizing an early event in leukemogenesis.
  • We describe the molecular cytogenetic findings of 207 infant acute leukemia (IAL) cases included in the Brazilian Collaborative Study Group of Infant acute leukemia.
  • PROCEDURE: The diagnosis of Acute Lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML) was made according to morphology and immunophenotyping classification, followed by conventional karyotyping.
  • RESULTS: The characteristics of children with IAL were as follows: 115 boys and 92 girls, age range 0-23 months, mean age 12 months, 145 ALL, and 62 AML.
  • [MeSH-major] Cytogenetic Analysis / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16261608.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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76. Park IJ, Park JE, Kim HJ, Jung HJ, Lee WG, Cho SR: Acute myeloid leukemia with t(16;21)(q24;q22) and eosinophilia: case report and review of the literature. Cancer Genet Cytogenet; 2010 Jan 1;196(1):105-8
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  • [Title] Acute myeloid leukemia with t(16;21)(q24;q22) and eosinophilia: case report and review of the literature.
  • The t(16;21)(q24;q22), a rare chromosomal translocation involving chromosome 21 in de novo and therapy-related acute myeloid leukemia (AML), produces a RUNX1-CBFA2T3 fusion gene (previously AML1-MTG16) fusion gene.
  • The translocation has been reported in 20 patients with AML, with eosinophilia present in 3 cases.
  • Here we report a pediatric case of t(16;21)(q24;q22) in de novo AML with eosinophilia and suggest that eosinophilia is a hematologic characteristic of at least a subpopulation of AML with t(16;21)(q24;q22).
  • A 4-year-old Korean girl was admitted with complaints of pale appearance and dizziness, and was diagnosed with acute myelomonocytic leukemia.
  • [MeSH-minor] Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Myeloid, Acute. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19963144.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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77. Sakai R, Fujimaki K, Yamazaki E, Sakamoto H, Kanamori H, Miura I, Ishigatsubo Y: Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22). Int J Hematol; 2006 Dec;84(5):417-20
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  • [Title] Acute myelomonocytic leukemia with dysplastic bone marrow eosinophils showing t(5;17)(q13;q11) and a secondary chromosomal aberration, inv(16)(p13q22).
  • inv(16)(p13q22) is associated with de novo acute myelomonocytic leukemia with dysplastic bone marrow eosinophils (AMML Eo), which has a relatively favorable clinical course with a longer remission duration and better survival prospects.
  • On the other hand, t(5; 17)(q13;q11), although relatively rare, has been reported to be a component of complex chromosomal abnormalities in myelodysplastic syndromes and secondary acute myeloid leukemia (AML).
  • We treated a 29-year-old woman with the first reported case of de novo AMML Eo with inv(16)(p13q22) in addition to t(5; 17)(q13;q11).
  • Although she attained complete remission (CR) immediately after induction therapy, the disease recurred 1 year after the completion of consolidation therapies.
  • In general, certain secondary chromosomal abnormalities are associated with the phenotype of the disease, which retains its essential biologic characteristics established by the primary abnormality.
  • Accordingly, the primary nature of the leukemic cells in this case differs from the findings for core-binding factor AML with inv(16)(p13q22).
  • We believe this report is the first of de novo AMML Eo with t(5; 17)(q13;q11) showing as a secondary chromosomal aberration with inv(16)(p13q22).
  • [MeSH-major] Bone Marrow Cells / pathology. Chromosome Inversion. Chromosomes, Human / genetics. Eosinophils / pathology. Leukemia, Myelomonocytic, Acute. Translocation, Genetic

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  • (PMID = 17189222.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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78. Kuwata T, Nakamura T: BCL11A is a SUMOylated protein and recruits SUMO-conjugation enzymes in its nuclear body. Genes Cells; 2008 Sep;13(9):931-40
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  • Previous studies show that BCL11A is involved in acute myelomonocytic leukemia and chronic lymphoid leukemia in mouse and human, respectively.

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  • (PMID = 18681895.001).
  • [ISSN] 1365-2443
  • [Journal-full-title] Genes to cells : devoted to molecular & cellular mechanisms
  • [ISO-abbreviation] Genes Cells
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL11A protein, human; 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / Recombinant Proteins; 0 / SUMO-1 Protein; 0 / Small Ubiquitin-Related Modifier Proteins; 147336-22-9 / Green Fluorescent Proteins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.- / SENP2 protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes; EC 6.3.2.19 / ubiquitin-conjugating enzyme UBC9; K3Z4F929H6 / Lysine
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79. Tasca S, Furlanello T, Caldin M: High serum and urine lysozyme levels in a dog with acute myeloid leukemia. J Vet Diagn Invest; 2010 Jan;22(1):111-5
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  • [Title] High serum and urine lysozyme levels in a dog with acute myeloid leukemia.
  • A 2-year-old, female German Shepherd Dog with facial nerve paralysis was diagnosed with acute myelomonocytic leukemia based on clinical, cytologic, and immunologic findings.
  • A diagnosis of tubular proteinuria was made, and a chemical evaluation of LZM in serum and urine samples was performed using a turbidimetric assay.
  • [MeSH-major] Dog Diseases / blood. Leukemia, Myeloid, Acute / veterinary. Muramidase / blood

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  • (PMID = 20093697.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.1.17 / Muramidase
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80. Kügler M, Stein C, Kellner C, Mentz K, Saul D, Schwenkert M, Schubert I, Singer H, Oduncu F, Stockmeyer B, Mackensen A, Fey GH: A recombinant trispecific single-chain Fv derivative directed against CD123 and CD33 mediates effective elimination of acute myeloid leukaemia cells by dual targeting. Br J Haematol; 2010 Sep;150(5):574-86
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  • [Title] A recombinant trispecific single-chain Fv derivative directed against CD123 and CD33 mediates effective elimination of acute myeloid leukaemia cells by dual targeting.
  • Two trivalent constructs consisting of single-chain Fv antibody fragments (scFvs) specific for the interleukin-3 receptor alpha chain (CD123), CD33 and the Fcgamma-receptor III (CD16) were designed and characterized for the elimination of acute myeloid leukaemia (AML) cells.
  • Both constructs induced potent antibody-dependent cellular cytotoxicity (ADCC) of two different AML-derived CD33- and CD123 double-positive cell lines in the low picomolar range using isolated mononuclear cells (MNCs) as effector cells.
  • In addition, the sctbs showed a high potency in mediating ADCC of primary leukaemia cells isolated from peripheral blood or bone marrow of seven AML patients.
  • Hence, these novel molecules displayed potent anti-leukaemic effects against AML cells in vitro and represent attractive candidates for further preclinical development.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Interleukin-3 Receptor alpha Subunit / immunology. Leukemia, Myeloid, Acute / immunology. Single-Chain Antibodies / immunology

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  • (PMID = 20636437.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FCGR3B protein, human; 0 / GPI-Linked Proteins; 0 / IL3RA protein, human; 0 / Immunoglobulin Fragments; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Receptors, IgG; 0 / Recombinant Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Single-Chain Antibodies; 0 / immunoglobulin Fv
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81. Patnaik MM, Gangat N, Knudson RA, Keefe JG, Hanson CA, Pardanani A, Ketterling RP, Tefferi A: Chromosome 8p11.2 translocations: prevalence, FISH analysis for FGFR1 and MYST3, and clinicopathologic correlates in a consecutive cohort of 13 cases from a single institution. Am J Hematol; 2010 Apr;85(4):238-42
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  • FISH analysis was performed in 13 patients (12 had myeloid neoplasms) and revealed abnormalities of MYST3 (n = 4) or FGFR1 (n = 4) in eight patients.
  • MYST3 abnormalities were associated with acute myeloid leukemia (AML), M4 in three and M6 in one.
  • Three of the four FGFR1-rearranged cases were associated with myeloproliferative neoplasms but none, including the two with sole 8p11.2, displayed the typical phenotype for stem cell leukemia/lymphoma (SCLL) and only one had eosinophilia; the fourth case had AML-M4.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Hematologic Neoplasms / genetics. Histone Acetyltransferases / genetics. In Situ Hybridization, Fluorescence / methods. Myeloproliferative Disorders / genetics. Oncogene Fusion. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cohort Studies. Eosinophilia / genetics. Female. Genetic Predisposition to Disease. Genetic Testing. Humans. Karyotyping. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Retrospective Studies

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  • (PMID = 20143402.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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82. Karabacak BH, Erbey F, Bayram I, Yilmaz S, Acipayam C, Kilinç Y, Tanyeli A: Fms-like tyrosine kinase 3 mutations in childhood acute leukemias and their association with prognosis. Asian Pac J Cancer Prev; 2010;11(4):923-7
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  • [Title] Fms-like tyrosine kinase 3 mutations in childhood acute leukemias and their association with prognosis.
  • OBJECTIVE: In this study, the presence of FLT3 mutations in childhood acute leukemias patients and their association with prognosis were investigated.
  • MATERIALS AND METHODS: A total of 120 patients, 80 with acute lymphoblastic leukemia (ALL) and 40 with acute myeloblastic leukemia (AML), were included.
  • RESULTS: FLT3/ITD (internal tandem duplication) mutations were found in 6 (7.5%) of the patients with ALL and in 9 (22.5%) of those with AML, whereas no FLT3/TKD (trans kinase domain) mutation was evident in any case.
  • There was no difference between the ALL patients positive and negative for FLT3/ITD with regard to overall survival (OS), event free survival (EFS) and disease free survival (DFS) (p=0.37, p=0.23, p=0.023, respectively).
  • However, in FLT3/ITD positive and negative AML patients, there was a statistically significant difference in OS (p=0.0041), but not EFS and DFS (p=0.09, p=0.095, respectively).
  • CONCLUSION: We found that FLT3/ITD positivity increased with age and that it was associated with decrease in OS in AML patients, providing further evidence that it is an independent factor negatively influencing prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Age Factors. Child. Child, Preschool. Disease-Free Survival. Humans. Infant. Kaplan-Meier Estimate. Male. Prognosis. Recurrence

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  • (PMID = 21133602.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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83. Konuma T, Tomonari A, Takahashi S, Ooi J, Tsukada N, Yamada T, Sato H, Nagayama H, Iseki T, Tojo A, Asano S: Early-onset thyrotoxicosis after unrelated cord blood transplantation for acute myelogenous leukemia. Int J Hematol; 2006 May;83(4):348-50
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  • [Title] Early-onset thyrotoxicosis after unrelated cord blood transplantation for acute myelogenous leukemia.
  • Patient 1 is a 32-year-old woman with acute myelogenous leukemia (AML)-M5a who underwent CBT.
  • Patient 2 is a 42-year-old man with AML-M4 who underwent CBT.
  • [MeSH-major] Autoimmune Diseases / blood. Cord Blood Stem Cell Transplantation. Leukemia, Myeloid, Acute. Thyrotoxicosis / blood

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  • (PMID = 16757437.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Autoantibodies; 06LU7C9H1V / Triiodothyronine; EC 1.11.1.8 / Iodide Peroxidase; Q51BO43MG4 / Thyroxine
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84. Cho WH, Choi YJ, Choi BK, Cha SH: Isolated recurrence of intracranial granulocytic sarcoma mimicking a falx meningioma in acute myeloblastic leukemia. J Korean Neurosurg Soc; 2010 May;47(5):385-8
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  • [Title] Isolated recurrence of intracranial granulocytic sarcoma mimicking a falx meningioma in acute myeloblastic leukemia.
  • Intracranial granulocytic sarcomas are rare tumors, which are composed of immature granulocytic cells.
  • Although it has been well known that these tumors are associated with acute myeloblastic leukemia (AML), they have been almost always related to bone marrow relapse.
  • However, isolated recurrence of granulocytic sarcoma following complete remission from prior AML is extremely rare, especially in the central nervous system.
  • A 44-year-old male presented with isolated recurrence of granulocytic sarcoma mimicking a falx meningioma two years after complete remission by allogenic peripheral blood stem cell transfusion (PBSCT) in the acute myelomonoblastic leukemia (FAB, M4).
  • Pathological findings were compatible with the granulocytic sarcoma.

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  • (PMID = 20539800.001).
  • [ISSN] 1598-7876
  • [Journal-full-title] Journal of Korean Neurosurgical Society
  • [ISO-abbreviation] J Korean Neurosurg Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2883061
  • [Keywords] NOTNLM ; Chloroma / Granulocytic sarcoma / Leukemia
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85. Wonsettler DM, Chang WW, Wenger SL: Extra copy of 20q deletion, acute myelomonocytic leukemia (M4) and Niemann-Pick disease. J Assoc Genet Technol; 2005;31(2):55-8
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  • [Title] Extra copy of 20q deletion, acute myelomonocytic leukemia (M4) and Niemann-Pick disease.
  • A 59-year-old hypertensive white male was diagnosed with acute myelogenous leukemia (AML), M4.
  • The majority of cases with 20q deletion are associated with myeloid disorders; however, an extra copy of the 20q deletion has rarely been reported.
  • Many foamy macrophages with bubbling cytoplasm in the spleen, liver, bone marrow and lymph nodes were suggestive of Niemann-Pick disease, type E.
  • AML has not previously been reported with Niemann-Pick disease.

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  • (PMID = 16027483.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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86. Aoki T, Miyamoto T, Yoshida S, Yamamoto A, Yamauchi T, Yoshimoto G, Mori Y, Kamezaki K, Iwasaki H, Takenaka K, Harada N, Nagafuji K, Teshima T, Akashi K: Additional acquisition of t(1;21)(p32;q22) in a patient relapsing with acute myelogenous leukemia with NUP98-HOXA9. Int J Hematol; 2008 Dec;88(5):571-4
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  • [Title] Additional acquisition of t(1;21)(p32;q22) in a patient relapsing with acute myelogenous leukemia with NUP98-HOXA9.
  • We report a 29-year-old Japanese male with acute myelogenous leukemia (AML)-M4 with a cryptic t(7;11)(p15;p15), in which a chimeric NUP98-HOXA9 fusion was detected by polymerase chain reaction analysis and a chromosomal analysis showed 46,XY.
  • This is the first reported case with AML who had a cryptic t(7;11)(p15;p15), and additionally acquired t(1;21)(p32;q22) at relapse.
  • [MeSH-major] Chromosomes, Human / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 19005624.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Homeodomain Proteins; 0 / NUP98-HOXA9 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion
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87. Golay J, Di Gaetano N, Amico D, Cittera E, Barbui AM, Giavazzi R, Biondi A, Rambaldi A, Introna M: Gemtuzumab ozogamicin (Mylotarg) has therapeutic activity against CD33 acute lymphoblastic leukaemias in vitro and in vivo. Br J Haematol; 2005 Feb;128(3):310-7
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  • [Title] Gemtuzumab ozogamicin (Mylotarg) has therapeutic activity against CD33 acute lymphoblastic leukaemias in vitro and in vivo.
  • Gemtuzumab ozogamicin (GO) is a humanized anti-CD33 antibody conjugated with the cytotoxic drug calicheamicin and approved for the treatment of relapsed acute myeloid leukaemia.
  • As approximately 18% of acute lymphoblastic leukaemias (ALL) are also CD33 positive, we have investigated the cytotoxic activity of GO on CD33+ ALL cells in vitro and in vivo.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Immunotoxins / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15667532.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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88. Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Morice P, Bourquard P, Banzakour S, Le Calvez G, Marion V, Berthou C, De Braekeleer M: Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations. Cancer Genet Cytogenet; 2005 Mar;157(2):169-74
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  • [Title] Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations.
  • We report here 2 male adults in whom a diagnosis of acute myelomonoblastic leukemia (FAB M4) and acute monoblastic leukemia (FAB M5) was made.
  • Fourteen and 24 patients, including ours, with acute myeloblastic leukemia associated with a t(1;11)(p32;q23) and a t(11;17)(q23;q21), respectively have been reported in the literature.
  • Several patients with the latter translocation have also been identified to have acute lymphoblastic leukemia (ALL).
  • Although both translocations are preferentially associated with monocytic differentiation, the t(11;17)(q23;q21) is more common in adults and has been reported in many patients with ALL, compared to the t(1;11)(p32;q23).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

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  • (PMID = 15721641.001).
  • [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 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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89. Kappelmayer J, Simon A, Katona E, Szanto A, Nagy L, Kiss A, Kiss C, Muszbek L: Coagulation factor XIII-A. A flow cytometric intracellular marker in the classification of acute myeloid leukemias. Thromb Haemost; 2005 Aug;94(2):454-9
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  • [Title] Coagulation factor XIII-A. A flow cytometric intracellular marker in the classification of acute myeloid leukemias.
  • This study was designed to study the sensitivity and specificity of factor XIII subunit A (FXIII-A) labelling in cultured myeloblastic and monoblastic cell lines and to investigate the intracytoplasmic expression of FXIII-A in de novo acute myeloid leukemia (AML) samples.
  • Myeloblastic and a monoblastic cell lines were cultured and investigated for lineage specific maturation markers and FXIII-A expression.
  • Furthermore, FXIII-A expression was investigated in 12 normal samples (7 bone marrow and 5 peripheral blood), 86 de novo AML samples and 6 chronic myelomonocytic leukemia (CMML) samples.
  • In the monoblastic MonoMac6 cell line the appearance of FXIII-A preceded that of CD14 while it remained negative in the myeloblastic PLB-985 cell line throughout its maturation period.
  • Among the AML samples the average frequency of FXIII-A positive cells in myeloblastic leukemia samples was below 10%, while in M4 and M5AML samples it was above 50% and was significantly higher than the generally used CD14 marker (p < 0.0001).
  • In the AML M4 and M5 cases, FXIII-A proved sensitive for the identification of monoblasts.
  • FXIII-A can be considered as a reliable intracytoplasmic marker for the monocytic and megakaryocytic series and its presence is highly predictive for mono- and megakaryocytic AML and for CMML.
  • [MeSH-major] Factor XIIIa / metabolism. Factor XIIIa / physiology. Flow Cytometry / methods. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / metabolism. Antigens, CD14 / biosynthesis. Cell Line. Cell Line, Tumor. Cell Lineage. Cells, Cultured. Cytoplasm / metabolism. Granulocytes / cytology. Humans. Leukocytes / metabolism. Megakaryocytes / cytology. Monocytes / cytology. Monocytes / metabolism. Myeloid Cells / cytology. Sensitivity and Specificity

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  • (PMID = 16113839.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD14; EC 2.3.2.13 / Factor XIIIa
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90. Rocquain J, Gelsi-Boyer V, Adélaïde J, Murati A, Carbuccia N, Vey N, Birnbaum D, Mozziconacci MJ, Chaffanet M: Alteration of cohesin genes in myeloid diseases. Am J Hematol; 2010 Sep;85(9):717-9
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  • [Title] Alteration of cohesin genes in myeloid diseases.
  • We have studied by array-comparative genomic hybridization (aCGH) a series of 167 samples including myelodysplastic syndromes, chronic myelomonocytic leukemias, and acute myeloid leukemias.
  • [MeSH-major] Antigens, Nuclear / genetics. Cell Cycle Proteins / genetics. Chromosomal Proteins, Non-Histone / genetics. Gene Deletion. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Phosphoproteins / genetics

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  • (PMID = 20687102.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Antigens, Nuclear; 0 / Cell Cycle Proteins; 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins; 0 / RAD21 protein, human; 0 / Repressor Proteins; 0 / STAG2 protein, human; 0 / TET2 protein, human; 0 / cohesins
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91. Shimizu T, Esaki L, Mizuno H, Takeda K: Granulocyte macrophage colony-stimulating factor enhances retinoic acid-induced gene expression. J Leukoc Biol; 2006 Oct;80(4):889-96
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  • We reported previously that treatment of human myeloblastic leukemia ML-1 cells with all-trans retinoic acid (ATRA) in combination with GM-CSF enhances the granulocytic differentiation, which is induced only slightly by ATRA alone.
  • Further studies of the mechanism underlying this effect may identify better approaches for the treatment of RA-insensitive leukemia.
  • [MeSH-major] Gene Expression / drug effects. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Oligonucleotide Array Sequence Analysis / methods. Tretinoin / pharmacology

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  • (PMID = 16885501.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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92. Sumi M, Ichikawa N, Nasu K, Shimizu I, Ueki T, Ueno M, Kobayashi H: Gemtuzumab ozogamicin-induced long-term remission in a woman with acute myelomonocytic leukemia and bone marrow relapse following allogeneic transplantation. Int J Hematol; 2009 Dec;90(5):643-7
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  • [Title] Gemtuzumab ozogamicin-induced long-term remission in a woman with acute myelomonocytic leukemia and bone marrow relapse following allogeneic transplantation.
  • A 56-year-old woman with acute myelomonocytic leukemia underwent myeloablative allogeneic hematopoietic stem cell transplantation (allo-SCT) from a matched unrelated donor in her first complete remission (CR).
  • Veno-occlusive disease (VOD) prophylaxis consisted of low-dose heparin and ursodeoxycholic acid.
  • Graft-versus-host disease (GVHD) prophylaxis comprised tacrolimus and short-term methotrexate.
  • On day 58, she showed grade II acute GVHD, but this resolved spontaneously.
  • Although the standard treatment for acute myeloid leukemia relapse after allo-SCT still remains to be established, GO may be a promising option.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myelomonocytic, Acute / drug therapy. Salvage Therapy / methods

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  • (PMID = 19904520.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 93NS566KF7 / gemtuzumab
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93. Wittkowski H, Frosch M, Wulffraat N, Goldbach-Mansky R, Kallinich T, Kuemmerle-Deschner J, Frühwald MC, Dassmann S, Pham TH, Roth J, Foell D: S100A12 is a novel molecular marker differentiating systemic-onset juvenile idiopathic arthritis from other causes of fever of unknown origin. Arthritis Rheum; 2008 Dec;58(12):3924-31
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  • The differential diagnosis includes systemic-onset juvenile idiopathic arthritis (JIA), an autoinflammatory syndrome associated with activation of phagocytic cells that, at presentation, is difficult to differentiate from severe systemic infections.
  • METHODS: Serum samples were obtained from 45 healthy control subjects and from 240 patients (60 with systemic-onset JIA, 17 with familial Mediterranean fever [FMF], 18 with neonatal-onset multisystem inflammatory disease [NOMID], 17 with Muckle-Wells syndrome [MWS], 40 with acute lymphoblastic leukemia [ALL], 5 with acute myeloblastic leukemia [AML], and 83 with systemic infections).
  • RESULTS: The mean +/- 95% confidence interval serum levels of S100A12 were as follows: in patients with JIA, 7,190 +/- 2,690 ng/ml; in patients with FMF, 6,720 +/- 4,960 ng/ml; in patients with NOMID, 720 +/- 450 ng/ml; in patients with MWS, 150 +/- 60 ng/ml; in patients with infections, 470 +/- 160 ng/ml; in patients with ALL, 130 +/- 80 ng/ml; in patients with AML, 45 +/- 60 ng/ml; in healthy control subjects, 50 +/- 10 ng/ml.
  • [MeSH-major] Arthritis, Juvenile / blood. Arthritis, Juvenile / diagnosis. Biomarkers / blood. Fever of Unknown Origin / blood. Fever of Unknown Origin / diagnosis. S100 Proteins / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Diagnosis, Differential. Enzyme-Linked Immunosorbent Assay. Familial Mediterranean Fever / blood. Familial Mediterranean Fever / diagnosis. Familial Mediterranean Fever / immunology. Female. Granulocytes / immunology. Humans. Infant. Infection / blood. Infection / diagnosis. Infection / immunology. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. S100A12 Protein. Sensitivity and Specificity. Young Adult

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  • (PMID = 19035478.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AR041138-05
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / S100 Proteins; 0 / S100A12 Protein; 0 / S100A12 protein, human
  • [Other-IDs] NLM/ NIHMS58669; NLM/ PMC2680303
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94. Cruse JM, Lewis RE, Pierce S, Lam J, Tadros Y: Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias. Exp Mol Pathol; 2005 Aug;79(1):39-41
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  • [Title] Aberrant expression of CD7, CD56, and CD79a antigens in acute myeloid leukemias.
  • CD7 and CD56 expression at diagnosis has been associated with low remission rates and biological aggressiveness in a significant proportion of acute leukemias.
  • Among 46 patients with acute myeloid leukemia, we found CD7 expression in 15 cases (32.6%) and CD56 positivity in 10 patients (21.7%).
  • Six of these myeloid leukemia cases (13%) showed expression of both CD7 and CD56.
  • Among the 10 that were acute myeloblastic leukemia, 8 expressed CD7, 4 expressed CD56, and 4 were positive for CD79a.
  • Thus, these markers were expressed early in hemopoietic ontogeny in the lesser-differentiated acute myeloid leukemia subtypes, including FAB M0, M1, and M2.
  • Whereas CD7 and CD56 were each positive in 4 cases of acute myelomonocytic leukemia (FAB M4 subtype), there was no CD79a expression in the M4 cases.
  • CD7 is expressed by mature T cells, NK cells, and an immature myeloid cell subset.
  • By contrast, CD79a is a B cell marker that is assigned a high score of 2.0 in the differentiation of acute leukemias of ambiguous lineage in the WHO classification.
  • The aberrant expression of CD7, CD56, and CD79a, representing the capacity of these leukemias for trilineal expression of leukocyte differentiation antigens, portends a poor prognosis.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, CD56 / biosynthesis. Antigens, CD7 / biosynthesis. Biomarkers, Tumor / analysis. Leukemia, Myeloid, Acute / metabolism. Receptors, Antigen, B-Cell / biosynthesis

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  • (PMID = 16005710.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD56; 0 / Antigens, CD7; 0 / Antigens, CD79; 0 / Biomarkers, Tumor; 0 / CD79A protein, human; 0 / Receptors, Antigen, B-Cell
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95. Mylonakis ME, Petanides TA, Valli VE, Vernau W, Koytinas AF, Michael RS: Acute myelomonocytic leukaemia with short-term spontaneous remission in a cat. Aust Vet J; 2008 Jun;86(6):224-8
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  • [Title] Acute myelomonocytic leukaemia with short-term spontaneous remission in a cat.
  • A complete blood count (CBC) and a biochemistry profile showed leukocytosis, numerous blast cells in the peripheral blood, thrombocytopenia, hyperglobulinaemia and a positive test for feline leukaemia virus antigen.
  • A diagnosis of acute myelomonocytic leukaemia was made on the basis of the results of bone marrow cytology, histopathology, and immunochemistry (CD3, CD79a, lysozyme, and myeloperoxidase) tests.
  • Following an unexpected 1-month period of clinical and clinicopathological remission without chemotherapy, the cat relapsed and died 1 week later.
  • [MeSH-major] Cat Diseases / diagnosis. Leukemia, Myelomonocytic, Acute / veterinary. Neoplasm Regression, Spontaneous

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  • (PMID = 18498558.001).
  • [ISSN] 0005-0423
  • [Journal-full-title] Australian veterinary journal
  • [ISO-abbreviation] Aust. Vet. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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96. Faraci M, Micalizzi C, Lanino E, Scuderi F, Morreale G, Dini G, Cappelli B, Dallorso S: Three consecutive related bone marrow transplants for juvenile myelomonocytic leukaemia. Pediatr Transplant; 2005 Dec;9(6):797-800
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  • [Title] Three consecutive related bone marrow transplants for juvenile myelomonocytic leukaemia.
  • Allogeneic haematopoietic stem cell transplantation (allo-HSCT) is the only cure for juvenile myelomonocytic leukaemia (JMML), but relapse remains the major cause of failure.
  • A second transplant may be considered a way to induce the graft vs. leukaemia effect in patients who relapse after their first HSCT.
  • [MeSH-major] Bone Marrow Transplantation / physiology. Leukemia, Myelomonocytic, Acute / therapy. Living Donors

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  • (PMID = 16269054.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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97. Pinto AC, Silva LF, Cavalcanti BC, Melo MR, Chaves FC, Lotufo LV, de Moraes MO, de Andrade-Neto VF, Tadei WP, Pessoa CO, Vieira PP, Pohlit AM: New antimalarial and cytotoxic 4-nerolidylcatechol derivatives. Eur J Med Chem; 2009 Jun;44(6):2731-5
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  • Mono-O-methyl ethers 6 and 7 inhibited the in vitro growth of human tumor cell lines HCT-8 (colon carcinoma), SF-295 (central nervous system), LH-60 (human myeloblastic leukemia) and MDA/MB-435 (melanoma).

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  • (PMID = 19084293.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 4-nerolidylcatechol; 0 / Antimalarials; 0 / Antineoplastic Agents, Phytogenic; 0 / Catechols; 0 / Plant Extracts
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98. Tosić N, Stojiljković M, Colović N, Colović M, Pavlović S: Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review. Cancer Genet Cytogenet; 2009 Sep;193(2):98-103
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  • [Title] Acute myeloid leukemia with NUP98-HOXC13 fusion and FLT3 internal tandem duplication mutation: case report and literature review.
  • We report a case of de novo AML M4 subtype, with a t(11;12)(p15;q13) translocation, generating a NUP98-HOXC13 chimeric transcript.
  • The patient was also positive for FLT3 internal tandem duplication (ITD), another molecular marker for the disease.
  • Comparative study of data on the fusion of HOXC cluster and NUP98 gene revealed that it is a rare event, found exclusively in AML patients.
  • To our knowledge, this is the first case of t(11;12)(p15;q13) in de novo AML-M4 in association with FLT3 ITD mutation.
  • [MeSH-major] Gene Duplication. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Pore Complex Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19665070.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HOXC13 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 32
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99. Turhan N, Yürür-Kutlay N, Topcuoglu P, Sayki M, Yüksel M, Gürman G, Tükün A: Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4. Leuk Res; 2006 Jul;30(7):903-5
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  • [Title] Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4.
  • We report a case of AML-M4 in which G-band karyotyping revealed a previously unreported t(13;17)(q14;q25) in metaphase preparations.
  • This report of AML-M4 harboring t(13;17)(q14;q25) as a unique cytogenetic abnormality provides more data on the leukomogenesis with rearrangements related with 13q14 and 17q25.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myelomonocytic, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 16469377.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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100. Zhang L, Alsabeh R, Mecucci C, La Starza R, Gorello P, Lee S, Lill M, Schreck R: Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature. Cancer Genet Cytogenet; 2007 Oct 1;178(1):42-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare t(1;11)(q23;p15) in therapy-related myelodysplastic syndrome evolving into acute myelomonocytic leukemia: a case report and review of the literature.
  • Balanced chromosome rearrangements are the hallmark of therapy-related leukemia that develops in patients treated with topoisomerase II inhibitors.
  • With time, the patient's disorder progressed to acute myelomonocytic leukemia with cytogenetic evidence of clonal evolution.
  • To our knowledge, this is the first report of a patient presenting with a myelodysplastic syndrome with isolated t(1;11) (q23;p15), which evolved into therapy-related acute myeloid leukemia (t-AML).
  • This patient is the third reported with this cytogenetic rearrangement and t-AML, and is compared with the other two reports of t(1;11)(q23;p15).
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Leukemia, Myelomonocytic, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Myelodysplastic Syndromes / therapy. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Neutrophils / metabolism






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