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1. Larson RA, Sievers EL, Stadtmauer EA, Löwenberg B, Estey EH, Dombret H, Theobald M, Voliotis D, Bennett JM, Richie M, Leopold LH, Berger MS, Sherman ML, Loken MR, van Dongen JJ, Bernstein ID, Appelbaum FR: Final report of the efficacy and safety of gemtuzumab ozogamicin (Mylotarg) in patients with CD33-positive acute myeloid leukemia in first recurrence. Cancer; 2005 Oct 1;104(7):1442-52
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  • [Title] Final report of the efficacy and safety of gemtuzumab ozogamicin (Mylotarg) in patients with CD33-positive acute myeloid leukemia in first recurrence.
  • BACKGROUND: In this study, the authors analyzed the efficacy and safety of gemtuzumab ozogamicin (GO) (Mylotarg), an antibody-targeted chemotherapy for CD33-positive acute myeloid leukemia (AML).
  • METHODS: Patients with CD33-positive AML in first recurrence were entered in 3 open-label, single-arm, Phase II studies.
  • Grade 3 or 4 hyperbilirubinemia and hepatic aspartate aminotransferase and alanine aminotransferase elevations were reported in 29%, 18%, and 9% of patients, respectively; 0.9% of patients who did not undergo prior or subsequent hematopoietic stem cell transplantation developed hepatic venoocclusive disease after GO treatment.
  • CONCLUSIONS: When it was administered to patients with CD33-positive AML in first recurrence, single-agent GO induced a 26% remission rate with a generally acceptable safety profile.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Clinical Trials, Phase II as Topic. Dose-Response Relationship, Drug. Drug Administration Schedule. Evaluation Studies as Topic. Female. Follow-Up Studies. Humans. Male. Maximum Tolerated Dose. Middle Aged. Recurrence. Risk Assessment. Severity of Illness Index. Sialic Acid Binding Ig-like Lectin 3. Single-Blind Method. Survival Rate. Treatment Outcome

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  • (PMID = 16116598.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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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. Hartwig M, Ocheni S, Asenova S, Wiedemann B, Zabelina T, Ayuk F, Kabisch H, Erttmann R, Kröger N, Zander AR, Bacher U: Second allogeneic stem cell transplantation in myeloid malignancies. Acta Haematol; 2009;122(4):185-92
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  • [Title] Second allogeneic stem cell transplantation in myeloid malignancies.
  • For patients with myeloid malignancies who relapse after allogeneic stem cell transplantation (allo-SCT), one salvage option is a second SCT.
  • We retrospectively analyzed outcomes of the second allo-SCT in 25 patients who received at least 2 allografts from related/unrelated donors due to relapse of acute myeloid leukemia, myelodysplastic syndrome or myelofibrosis after the first SCT.
  • A minority of the acute myeloid leukemia/myelodysplastic syndrome patients had reached complete hematological remission before the second SCT (6/25, 24%).
  • In conclusion, a second SCT offers the chance of stable remission for some patients relapsing with a myeloid malignancy after a first allo-SCT, although high treatment-related mortality and relapse rates remain a problem.
  • [MeSH-major] Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / surgery. Peripheral Blood Stem Cell Transplantation. Primary Myelofibrosis / surgery
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Transplantation. Child, Preschool. Female. Graft Survival. Graft vs Host Disease / etiology. Humans. Leukemia, Myelomonocytic, Juvenile / surgery. Male. Middle Aged. Polycythemia / complications. Recurrence. Reoperation. Retrospective Studies. Salvage Therapy. Transplantation Conditioning. Transplantation, Homologous. Young Adult


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4. Raepple D, von Lintig F, Zemojtel T, Duchniewicz M, Jung A, Lübbert M, Boss GR, Scheele JS: Determination of Ras-GTP and Ras-GDP in patients with acute myelogenous leukemia (AML), myeloproliferative syndrome (MPS), juvenile myelomonocytic leukemia (JMML), acute lymphocytic leukemia (ALL), and malignant lymphoma: assessment of mutational and indirect activation. Ann Hematol; 2009 Apr;88(4):319-24
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  • [Title] Determination of Ras-GTP and Ras-GDP in patients with acute myelogenous leukemia (AML), myeloproliferative syndrome (MPS), juvenile myelomonocytic leukemia (JMML), acute lymphocytic leukemia (ALL), and malignant lymphoma: assessment of mutational and indirect activation.
  • The 24 patient samples comprised of seven acute myelogenous leukemia (AML) samples, five acute lymphocytic leukemia (ALL) samples, four myeloproliferative disease (MPD) samples, four lymphoma samples, four juvenile myelomonocytic leukemia (JMML) samples, and WBC from a healthy donor.
  • Mutation analysis revealed ras mutations in two of the seven AML samples, one in codon 12 and one in codon 61; ras mutations were also found in two of the four JMML samples, and in one of the four lymphoma samples (codon 12).
  • [MeSH-minor] DNA Mutational Analysis. Guanosine Diphosphate / analysis. Guanosine Triphosphate / analysis. Humans. Leukemia, Myeloid, Acute. Leukemia, Myelomonocytic, Juvenile. Lymphoma. Mutation. Myeloproliferative Disorders. Oncogenes. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Signal Transduction / genetics. Tumor Cells, Cultured


5. 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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6. 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


7. Jacobs SA, Foon KA: Monoclonal antibody therapy of leukaemias and lymphomas. Expert Opin Biol Ther; 2005 Sep;5(9):1225-43
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  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / immunology. Antigens, CD20 / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoma, Follicular / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Randomized Controlled Trials as Topic. Rituximab. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16120052.001).
  • [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 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 170
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8. Lagrou K, Massonet C, Theunissen K, Meersseman W, Lontie M, Verbeken E, Van Eldere J, Maertens J: Fatal pulmonary infection in a leukaemic patient caused by Hormographiella aspergillata. J Med Microbiol; 2005 Jul;54(Pt 7):685-8
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  • A case of autopsy-proven fungal pneumonia in a relapsed leukaemia patient is reported.
  • [MeSH-major] Agaricales / classification. Aspergillosis / complications. Leukemia, Myelomonocytic, Acute / complications. Lung Diseases, Fungal / microbiology

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  • (PMID = 15947435.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Intergenic; 0 / Mannans; 11078-30-1 / galactomannan
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9. Tefferi A, Gilliland G: Classification of chronic myeloid disorders: from Dameshek towards a semi-molecular system. Best Pract Res Clin Haematol; 2006;19(3):365-85
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  • [Title] Classification of chronic myeloid disorders: from Dameshek towards a semi-molecular system.
  • Hematological malignancies are phenotypically organized into lymphoid and myeloid disorders, although such a distinction might not be precise from the standpoint of lineage clonality.
  • In turn, myeloid malignancies are broadly categorized into either acute myeloid leukemia (AML) or chronic myeloid disorder (CMD), depending on the presence or absence, respectively, of AML-defining cytomorphologic and cytogenetic features.
  • The CMD are traditionally classified by their morphologic appearances into discrete clinicopathologic entities based primarily on subjective technologies.
  • It has now become evident that most CMD represent clonal stem cell processes where the primary oncogenic event has been characterized in certain instances; Bcr/Abl in chronic myeloid leukemia, FIP1L1-PDGFRA or c-kit(D816V) in systemic mastocytosis, rearrangements of PDGFRB in chronic eosinophilic leukemia, and rearrangements of FGFR1 in stem cell leukemia/lymphoma syndrome.
  • In addition, Bcr/Abl-negative classic myeloproliferative disorders are characterized by recurrent JAK2(V617F) mutations, whereas other mutations affecting the RAS signaling pathway molecules have been associated with juvenile myelomonocytic leukemia.
  • [MeSH-minor] Fusion Proteins, bcr-abl / genetics. Genes, abl. Humans. Janus Kinase 2. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / classification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myelodysplastic Syndromes / classification. Myelodysplastic Syndromes / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics

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  • (PMID = 16781478.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Number-of-references] 232
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10. Batty GN, Kantarjian H, Issa JP, Jabbour E, Santos FP, McCue D, Garcia-Manero G, Pierce S, O'Brien S, Cortés JE, Ravandi F: Feasibility of therapy with hypomethylating agents in patients with renal insufficiency. Clin Lymphoma Myeloma Leuk; 2010 Jun;10(3):205-10
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  • PATIENTS AND METHODS: We reviewed 41 patients with a diagnosis of acute myeloid leukemia (n = 17), myelodysplastic syndromes (n = 15), and chronic myelomonocytic leukemia (n = 9) who had RI and were receiving therapy with azacitidine or decitabine.
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / complications. Leukemia, Myelomonocytic, Chronic / drug therapy. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy

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  • [Cites] Blood. 2007 Jan 1;109(1):52-7 [16882708.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3271-9 [16882711.001]
  • [Cites] Blood. 2006 Jul 15;108(2):419-25 [16609072.001]
  • [Cites] Cancer. 2006 Apr 15;106(8):1794-803 [16532500.001]
  • [Cites] J Clin Pharmacol. 2005 May;45(5):597-602 [15831784.001]
  • [Cites] Cancer Treat Rep. 1984 Dec;68(12):1483-7 [6210142.001]
  • [Cites] Blood. 1981 Jan;57(1):182-5 [6160887.001]
  • [Cites] Biochem Pharmacol. 1979 Apr 15;28(8):1443-4 [87202.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1133-7 [17315156.001]
  • [Cites] Am J Health Syst Pharm. 2009 Apr 1;66(7):642-8 [19299371.001]
  • [Cites] Nature. 2002 Apr 4;416(6880):552-6 [11932749.001]
  • [Cites] Curr Opin Investig Drugs. 2003 Dec;4(12):1442-50 [14763130.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120.001]
  • (PMID = 20511166.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS493668; NLM/ PMC3726276
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11. Gözdaşoğlu S, Ertem M, Uysal Z, Babacan E, Yüksel M, Bökesoy I, Sunguroğlu A, Arcasoy A, Çavdar A: Acute myeloid leukemia in Turkish children with Fanconi anemia. One center experience in the period between 1964-1995. Turk J Haematol; 2009 Sep 5;26(3):118-22
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  • [Title] Acute myeloid leukemia in Turkish children with Fanconi anemia. One center experience in the period between 1964-1995.
  • [Transliterated title] Fanconi anemili Türk çocuklarında akut miyeloid lösemi. 1964-1995 döneminde bir merkezin deneyimleri.
  • OBJECTIVE: Fanconi's anemia(FA) is an autosomal recessive disorder characterized by a progressive pancytopenia,variable congenital abnormalities and an increased risk for the development of acute myeloid leukemia (AML).
  • The objective of this study is to evaluate AML in the patients with FA diagnosed and followed-up in the Department of Pediatric Hematology at Ankara University School of Medicine in the period between 1964-1995.
  • METHODS: A total of 39 patients within the age range 2-14 years( mean 8.2±3.16),28 male and 11 female were diagnosed as FA on the basis of congenital abnormalities,pancytopenia, bone marrow hypoplasia and diepoxybutane induced chromosomal abnormalities that observed in all patients The hereditary and familial basis of FA was apparent in this series.Common abnormalities were growth retardation,cefe'- au- laitspots,hyperpigmentation,microcephaly, finger and thumb deformities,mental retardation and hypogenitalismus RESULTS: Four AML (10.2%) were observed in our series.Cytogenetic analysis of these cases revealed 46/ XX,dup(3)(q22;q26) t(7;17) (p11;p11) in one where it was unsuccessful in three.Two cases could not achieve remission and died.The other two achieved complete remission and remained in remission for2 and 6 months.
  • CONCLUSION: Acute myelomonocytic type in three cases and acute monocytic type in one patient were diagnosed in our series.
  • The patients with FA should be followed with regard to AML and solid tumors.
  • AML and solid tomors should be taken into the consideration as the first manifestation of FA.

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  • (PMID = 27265494.001).
  • [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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12. Farhat M, Venugopal P: Long-term remission of extramedullary relapse from acute promyelocytic leukemia after treatment with arsenic trioxide, intrathecal chemotherapy, and brain irradiation. Clin Adv Hematol Oncol; 2007 Apr;5(4):320-3; discussion 323-4
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  • [Title] Long-term remission of extramedullary relapse from acute promyelocytic leukemia after treatment with arsenic trioxide, intrathecal chemotherapy, and brain irradiation.
  • [MeSH-major] Arsenicals / administration & dosage. Cranial Irradiation. Ear Neoplasms / therapy. Leukemia, Myelomonocytic, Acute. Oxides / administration & dosage. Sarcoma, Myeloid / therapy

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  • (PMID = 17607291.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide; ZS7284E0ZP / Daunorubicin
  • [Number-of-references] 48
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13. Schwemmlein M, Peipp M, Barbin K, Saul D, Stockmeyer B, Repp R, Birkmann J, Oduncu F, Emmerich B, Fey GH: A CD33-specific single-chain immunotoxin mediates potent apoptosis of cultured human myeloid leukaemia cells. Br J Haematol; 2006 Apr;133(2):141-51
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  • [Title] A CD33-specific single-chain immunotoxin mediates potent apoptosis of cultured human myeloid leukaemia cells.
  • The purified recombinant fusion protein induced potent apoptosis of the human myeloid cell lines U937, HL-60 and THP-1.
  • The CD33-ETA toxin also mediated apoptosis of fresh patient-derived acute myeloid leukaemia cells from bone marrow and peripheral blood.
  • [MeSH-major] ADP Ribose Transferases / pharmacology. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antineoplastic Agents / pharmacology. Bacterial Toxins / pharmacology. Exotoxins / pharmacology. Immunotoxins / pharmacology. Leukemia, Myeloid / pathology. Virulence Factors / pharmacology

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  • (PMID = 16611304.001).
  • [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 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Bacterial Toxins; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Epitopes; 0 / Exotoxins; 0 / Immunoglobulin Fragments; 0 / Immunoglobulin Variable Region; 0 / Immunotoxins; 0 / Recombinant Fusion Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Virulence Factors; 0 / immunoglobulin Fv; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
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14. Malbora B, Senel E, Avci Z, Ozbek N: Purpuric nodules and macules on the scalp of an 18-month-old boy. Skinmed; 2010 Sep-Oct;8(5):305-6
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  • Bone marrow aspirate results showed 68.4% blast cells and a biopsy specimen confirmed the diagnosis of acute myeloid leukemia, with flow cytometry findings positive for acute monoblastic leukemia (AML) French-American-British (FAB)-M5 phenotype.
  • We initiated induction chemotherapy for AML (AML-M5) according to the AML Berlin-Frankfurt-Munster 2004 protocol.
  • ' Complete resolution of the leukemia cutis lesions was attained with chemotherapy at the end of the first month of treatment.
  • [MeSH-major] Leukemia, Monocytic, Acute / pathology. Scalp Dermatoses / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Antigens, CD / metabolism. Antigens, CD45 / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Antineoplastic Agents / therapeutic use. Blood Cell Count. Flow Cytometry. Humans. Infant. Male. Treatment Outcome

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  • [ErratumIn] Skinmed. 2011 Jan-Feb;9(1):66
  • (PMID = 21137646.001).
  • [ISSN] 1540-9740
  • [Journal-full-title] Skinmed
  • [ISO-abbreviation] Skinmed
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD68 antigen, human; EC 3.1.3.48 / Antigens, CD45
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15. Di Rocco A, Finolezzi E, Anaclerico B, Calabrese E, Levi A, Trasarti S, Tafuri A: [Therapeutic advances in neoplastic hematology: target therapy anti-CD33]. Clin Ter; 2005 Jul-Aug;156(4):183-6
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  • The CD33 antigen is present on 90% of acute myeloid leukemia blasts and is shared on normal hemopoietic cells only on the non stem dillerentiating fraction.
  • Gemtuzumab Ozogamicin (GO) is an engineered humanized antibody anti-CD33 conjugated with a potent intercalating agent, named calicheamicin, which is release only at intracellular level (lower pH), following a selective binding to CD33-positive cells, thus representing a promising approach for target anti-leukemia therapy.
  • GO was approved conditionally by the Federal Drug Administration in May 2000 as a single therapy for first recurrence of Acute Myeloid Leukemia (AML) in a subset of older patients.
  • Phase II trials have confirmed the activity and the efficacy of GO as single agent in the treatment of relapsed AML.
  • More recently, clinical trials on induction and post-remission treatment of adult AML have shown efficacy of GO in combination chemotherapy.
  • The strong and homogeneous CD33 expression in Acute Promyelocytic Leukemia (APL), have resulted in an effective treatment of this disease with GO used as salvage treatment, as well as innovative approach for molecular relapsed patients.
  • However, the incidence of veno-occlusive disease, better defined as sinusoidal occlusive syndrome (SOS), must be taken into account as potential complication associated with the GO administration, especially in patients treated with ablative regimens.
  • In conclusion, the extension of the approval in Italy to AML CD33+ in relapsed, regardless age limitation, along with the ongoing evaluation by the European EMEA, represent the basis for a large clinical application of GO in myeloid malignancies potentially extended to paediatric patients with AML and to ALL CD33+.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Clinical Trials as Topic. Clinical Trials, Phase II as Topic. Enediynes. Humans. Middle Aged. Pilot Projects. Recurrence. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16342520.001).
  • [ISSN] 0009-9074
  • [Journal-full-title] La Clinica terapeutica
  • [ISO-abbreviation] Clin Ter
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Enediynes; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 108212-75-5 / calicheamicin gamma(1)I
  • [Number-of-references] 27
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16. 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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  • [Cites] J Pediatr Hematol Oncol. 2000 Sep-Oct;22(5):412-6 [11037851.001]
  • [Cites] Leuk Res. 2006 Jul;30(7):841-8 [16423392.001]
  • [Cites] J Immunol. 2001 Nov 15;167(10):6021-30 [11698483.001]
  • [Cites] Blood. 2002 Jul 15;100(2):701-3 [12091369.001]
  • [Cites] Immunol Lett. 2002 Oct 1;83(3):163-9 [12095706.001]
  • [Cites] Pediatr Res. 2003 Jul;54(1):105-12 [12672905.001]
  • [Cites] J Altern Complement Med. 2003 Aug;9(4):491-7 [14499024.001]
  • [Cites] Oncol Rep. 2004 Sep;12(3):659-62 [15289852.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Oct 8;323(1):133-41 [15351712.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1983 Spring;5(1):65-71 [6859456.001]
  • [Cites] Anticancer Res. 1992 Jul-Aug;12(4):1211-5 [1503411.001]
  • [Cites] Crit Rev Immunol. 1999;19(1):65-96 [9987601.001]
  • [Cites] Acta Pharmacol Sin. 2004 Nov;25(11):1387-95 [15525457.001]
  • [Cites] J Immunol. 2004 Nov 15;173(10):5989-99 [15528333.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Aug 5;333(3):896-907 [15963458.001]
  • [Cites] J Leukoc Biol. 2005 Aug;78(2):533-43 [15894585.001]
  • [Cites] Br J Haematol. 2005 Sep;130(5):777-80 [16115136.001]
  • [Cites] J Altern Complement Med. 2005 Dec;11(6):1047-57 [16398597.001]
  • [Cites] Exp Mol Med. 2006 Feb 28;38(1):72-84 [16520555.001]
  • [Cites] J Altern Complement Med. 2001 Jun;7(3):281-7 [11439851.001]
  • (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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17. Vyas HK, Pal R, Vishwakarma R, Lohiya NK, Talwar GP: Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit. Oncology; 2009;76(2):101-11
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  • [Title] Selective killing of leukemia and lymphoma cells ectopically expressing hCGbeta by a conjugate of curcumin with an antibody against hCGbeta subunit.
  • EXPERIMENTAL DESIGN: The study was carried out on MOLT-4 and U-937 cells expressing hCGbeta and on peripheral blood leukocytes of acute myeloid leukemia (AML) patients.
  • The immunoconjugate killed tumor cells bearing the CD33 marker of an AML patient expressing hCGbeta but did not have a similar action on cells of another AML patient with the CD13 marker but who was negative for hCGbeta.
  • [MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / metabolism. Curcumin / metabolism. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Aged. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Cell Separation. Drug Design. Female. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Sialic Acid Binding Ig-like Lectin 3. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. U937 Cells

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  • (PMID = 19127081.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; IT942ZTH98 / Curcumin
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18. Huang CT, Kuo PH, Yao M, Tsai YJ, Yang PC: Pleural effusion heralds acute leukemic transformation of chronic myelomonocytic leukemia. South Med J; 2008 Dec;101(12):1279-80
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  • [Title] Pleural effusion heralds acute leukemic transformation of chronic myelomonocytic leukemia.
  • [MeSH-major] Blast Crisis / pathology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myelomonocytic, Chronic / pathology. Pleural Effusion, Malignant / etiology
  • [MeSH-minor] Bone Marrow / pathology. Disease Progression. Fatal Outcome. Female. Humans. Hydroxyurea / therapeutic use. Leukocyte Count. Middle Aged


19. Tang R, Cohen S, Perrot JY, Faussat AM, Zuany-Amorim C, Marjanovic Z, Morjani H, Fava F, Corre E, Legrand O, Marie JP: P-gp activity is a critical resistance factor against AVE9633 and DM4 cytotoxicity in leukaemia cell lines, but not a major mechanism of chemoresistance in cells from acute myeloid leukaemia patients. BMC Cancer; 2009 Jun 23;9:199
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  • [Title] P-gp activity is a critical resistance factor against AVE9633 and DM4 cytotoxicity in leukaemia cell lines, but not a major mechanism of chemoresistance in cells from acute myeloid leukaemia patients.
  • It is undergoing a phase I clinical trial.
  • The aim of the present study was to investigate the potential roles of P-gp, MRP1 and BCRP in cytotoxicity in AVE9633-induced acute myeloid leukaemia (AML).
  • METHODS: This study used AML cell lines expressing different levels of P-gp, MRP1 or BCRP proteins and twenty-five samples from AML patients.
  • RESULTS: P-gp activity, but not MRP1 and BCRP, attenuated AVE9633 and DM4 cytotoxicity in myeloid cell lines.
  • However, the data from AML patients show that 10/25 samples of AML cells (40%) were resistant to AVE9633 or DM4 (IC(50) > 500 nM), and this was not related to P-gp activity (p-Value: 0.7).
  • Zosuquidar also failed to re-establish drug sensitivity.
  • For patients whose resistance to conventional anthracycline AML regimens is related to ABC protein expression, a combination with AVE9633 could be beneficial.
  • [MeSH-major] ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Immunoconjugates / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Maytansine / analogs & derivatives
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / metabolism. Antibodies, Monoclonal / pharmacology. Antigens, CD / biosynthesis. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / biosynthesis. Antigens, Differentiation, Myelomonocytic / immunology. Dibenzocycloheptenes / pharmacology. Drug Resistance, Neoplasm. HL-60 Cells. Humans. K562 Cells. Multidrug Resistance-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Quinolines / pharmacology. Sialic Acid Binding Ig-like Lectin 3

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  • [Cites] Blood. 2001 Jan 15;97(2):502-8 [11154229.001]
  • [Cites] BMC Cancer. 2008;8:51 [18271955.001]
  • [Cites] Blood. 2001 Aug 15;98(4):988-94 [11493443.001]
  • [Cites] Oncogene. 2003 Jun 5;22(23):3548-53 [12789263.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1466-73 [12689934.001]
  • [Cites] Clin Cancer Res. 2003 Aug 1;9(8):2992-7 [12912947.001]
  • [Cites] Mol Cancer Ther. 2004 Sep;3(9):1119-25 [15367706.001]
  • [Cites] Science. 1975 Sep 19;189(4207):1002-5 [1241159.001]
  • [Cites] J Natl Cancer Inst. 1978 Jan;60(1):93-6 [628025.001]
  • [Cites] Cancer Treat Rep. 1978 Mar;62(3):425-8 [348310.001]
  • [Cites] Cancer Treat Rep. 1978 Mar;62(3):429-33 [348311.001]
  • [Cites] Cancer Treat Rep. 1978 Mar;62(3):435-8 [348312.001]
  • [Cites] Cancer Treat Rev. 1978 Dec;5(4):199-207 [367597.001]
  • [Cites] Blood. 1986 Apr;67(4):1048-53 [2937468.001]
  • [Cites] Br J Haematol. 1993 May;84(1):24-30 [7687858.001]
  • [Cites] Int J Cancer. 1996 Jan 26;65(3):365-71 [8575859.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Adv Exp Med Biol. 1999;457:1-9 [10500774.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):298-305 [15671559.001]
  • [Cites] Bull Cancer. 2005 Feb;92(2):E25-30 [15749640.001]
  • [Cites] Clin Cancer Res. 2005 Nov 1;11(21):7764-72 [16278398.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:143-50 [16304372.001]
  • [Cites] Clin Cancer Res. 2006 May 1;12(9):2774-9 [16675570.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:185-91 [17124059.001]
  • [Cites] Clin Cancer Res. 2007 Feb 1;13(3):994-9 [17289895.001]
  • [Cites] Int J Cancer. 2007 May 15;120(10):2078-85 [17285590.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9356-63 [17909044.001]
  • [Cites] J Pharmacol Exp Ther. 2008 Feb;324(2):434-42 [17986648.001]
  • [Cites] Clin Cancer Res. 2001 Jun;7(6):1490-6 [11410481.001]
  • (PMID = 19549303.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Dibenzocycloheptenes; 0 / Immunoconjugates; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Quinolines; 0 / Sialic Acid Binding Ig-like Lectin 3; 14083FR882 / Maytansine; 813AGY3126 / zosuquidar trihydrochloride; Y49M64GZ4Q / multidrug resistance-associated protein 1
  • [Other-IDs] NLM/ PMC2708190
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20. Glasow A, Prodromou N, Xu K, von Lindern M, Zelent A: Retinoids and myelomonocytic growth factors cooperatively activate RARA and induce human myeloid leukemia cell differentiation via MAP kinase pathways. Blood; 2005 Jan 1;105(1):341-9
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  • [Title] Retinoids and myelomonocytic growth factors cooperatively activate RARA and induce human myeloid leukemia cell differentiation via MAP kinase pathways.
  • Use of all-trans-retinoic acid (ATRA) in combinatorial differentiation therapy of acute promyelocytic leukemia (APL) results in exceptional cure rates.
  • However, potent cell differentiation effects of ATRA are so far largely restricted to this disease and long-term survival rates in non-APL acute myelogeneous leukemia (AML) remain unacceptably poor, requiring development of novel therapeutic strategies.
  • We demonstrate here that myelomonocytic growth factors (granulocyte colony-stimulating factor [G-CSF] and/or granulocyte macrophage colony-stimulating factor [GM-CSF]) potentiate differentiation effects of ATRA in different AML cell lines and primary cells from patients with myeloid leukemia.
  • Our data demonstrate that acting, at least in part, via the MAP kinase pathways, myelomonocytic growth factors enhance ATRA-dependent activation of the RARalpha isoforms and maturation of myeloid leukemia cells.
  • These results suggest that combinatorial use of these agents may be effective in differentiation therapy of AML.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / pharmacology. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. MAP Kinase Signaling System / drug effects. Receptors, Retinoic Acid / metabolism. Tretinoin / pharmacology

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  • (PMID = 15339853.001).
  • [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 / Protein Isoforms; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5688UTC01R / Tretinoin; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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21. Ghoshal K, Bai S: DNA methyltransferases as targets for cancer therapy. Drugs Today (Barc); 2007 Jun;43(6):395-422
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  • Food and Drug Administration (FDA) for chemotherapy against myelodysplastic syndrome (MDS), a heterogeneous bone marrow disorder.
  • Interest in clinical trials of these drugs as anticancer agents has been renewed only recently because of reversal of methylation-mediated silencing of critical genes in cancer.
  • Clinical trials have shown that both drugs have therapeutic potential against leukemia such as MDS, acute myeloid leukemia, chronic myelogenous leukemia and chronic myelomonocytic leukemia.
  • In this monograph we review historical perspective and recent advances on the molecular mechanisms of action and clinical applications of these DNA hypomethylating agents.
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Azacitidine / therapeutic use. Epigenesis, Genetic. Female. Gene Expression Regulation. Gene Silencing. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / metabolism. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / metabolism. Transcriptional Activation

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  • (PMID = 17612710.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA086978; United States / NCI NIH HHS / CA / CA86978
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; M801H13NRU / Azacitidine
  • [Number-of-references] 252
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22. Harms PW, Bandarchi B, Ma L: CD163 expression in leukemia cutis. J Cutan Pathol; 2010 Sep;37(9):953-7
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  • [Title] CD163 expression in leukemia cutis.
  • BACKGROUND: Proper diagnosis of myeloid leukemia cutis (LC) is of great clinical importance but can be difficult because no single immunohistochemical marker is adequately sensitive or specific for definitive diagnosis.
  • In this study, we examined the value of CD163 in the diagnosis of acute myeloid LC.
  • METHODS: A total of 34 cases, including 18 cases of myelomonocytic or monocytic LC, 10 cases of myeloid LC without monocytic component and 6 cases of acute lymphoblastic leukemia/lymphoma (ALL), were stained with CD163.
  • RESULTS: CD163 was expressed in 8 of 18 (44%) of myelomonocytic or monocytic LC and 1 of 10 (10%) of other myeloid LC, but in none of the ALL cases (0/6).
  • CD163 was highly specific (90%) for myeloid LC with a monocytic component, but showed low sensitivity in the diagnosis of both myeloid LC in general (24%) and myeloid LC with a monocytic component (44%).
  • CONCLUSIONS: Our results suggest that CD163 has utility as a specific marker for myeloid LC in conjunction with currently used immunohistochemical stains, but should not be used alone for diagnosis.
  • [MeSH-major] Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Leukemia, Myeloid, Acute / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Cell Surface / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 20175823.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD163 antigen; 0 / Receptors, Cell Surface
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23. Jurcic JG: Immunotherapy for acute myeloid leukemia. Curr Oncol Rep; 2005 Sep;7(5):339-46
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  • [Title] Immunotherapy for acute myeloid leukemia.
  • Although the humanized anti-CD33 antibody HuM195 has only modest activity against overt acute myeloid leukemia (AML), it can eliminate minimal residual disease in acute promyelocytic leukemia.
  • Targeted chemotherapy with the anti-CD33- calicheamicin construct gemtuzumab ozogamicin has produced remissions in relapsed AML and appears promising when used in combination with standard chemotherapy for newly diagnosed AML.
  • T-cell recognition of peptide antigens presented on the cell surface in combination with major histocompatibility complex antigen provides another potentially promising approach for the treatment of AML.
  • [MeSH-major] Immunotherapy / methods. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD / chemistry. Antigens, CD45 / chemistry. Antigens, Differentiation, Myelomonocytic / chemistry. Bismuth / chemistry. Cell Adhesion Molecules / chemistry. Humans. Immunotoxins / chemistry. Radioimmunotherapy. Radioisotopes / chemistry. Recurrence. Remission Induction. Sialic Acid Binding Ig-like Lectin 3. T-Lymphocytes / metabolism

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  • [Cites] Leukemia. 1996 Feb;10(2):321-6 [8637241.001]
  • [Cites] Int J Hematol. 2003 Jul;78(1):56-61 [12894852.001]
  • [Cites] Cancer Res. 1983 Jan;43(1):265-72 [6571707.001]
  • [Cites] Blood. 1998 Jul 15;92(2):589-95 [9657759.001]
  • [Cites] Bone Marrow Transplant. 2003 Sep;32(6):549-56 [12953125.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):478-90 [1999719.001]
  • [Cites] Cancer Res. 1994 Aug 15;54(16):4362-70 [8044783.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1802-7 [10677537.001]
  • [Cites] Leuk Res. 2003 Oct;27(10 ):887-91 [12860007.001]
  • [Cites] Leuk Lymphoma. 2002 Nov;43(11):2125-31 [12533037.001]
  • [Cites] Blood. 1996 Oct 1;88(7):2450-7 [8839835.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4222-4 [12010830.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):294-303 [8426207.001]
  • [Cites] Cancer. 2001 Jul 15;92(2):406-13 [11466696.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3678-84 [10339474.001]
  • [Cites] Leukemia. 2003 Feb;17(2):314-8 [12592328.001]
  • [Cites] Bone Marrow Transplant. 2002 May;29(10):807-16 [12058230.001]
  • [Cites] Blood. 2003 Jun 15;101(12 ):5068-75 [12609833.001]
  • [Cites] Biol Blood Marrow Transplant. 2003 Jun;9(6):364-72 [12813444.001]
  • [Cites] Clin Cancer Res. 2000 Feb;6(2):372-80 [10690513.001]
  • [Cites] Blood. 1986 Nov;68(5):1030-5 [3768529.001]
  • [Cites] Blood. 2002 Aug 15;100(4):1233-9 [12149203.001]
  • [Cites] Blood. 1994 Apr 1;83(7):1760-8 [8142644.001]
  • [Cites] Haematologica. 2004 Aug;89(8):950-6 [15339678.001]
  • [Cites] Cancer Res. 1992 Dec 15;52(24):6761-7 [1458463.001]
  • [Cites] Science. 2001 Nov 16;294(5546):1537-40 [11711678.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2310-4 [11895761.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • [Cites] Transplantation. 1992 Nov;54(5):829-33 [1440849.001]
  • [Cites] Clin Cancer Res. 1995 Oct;1(10):1179-87 [9815910.001]
  • [Cites] J Cancer Res Clin Oncol. 2005 Jan;131(1):1-13 [15565456.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1891-5 [12569172.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4277-83 [12933575.001]
  • [Cites] Clin Cancer Res. 2002 May;8(5):1004-13 [12006512.001]
  • [Cites] Clin Cancer Res. 1998 Jun;4(6):1421-8 [9626458.001]
  • [Cites] Blood. 1999 Aug 15;94(4):1237-47 [10438711.001]
  • [Cites] Blood. 2002 Jul 1;100(1):318-26 [12070043.001]
  • [Cites] Blood. 2002 Jul 1;100(1):208-16 [12070029.001]
  • (PMID = 16091194.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD66 antigens; 0 / Cell Adhesion Molecules; 0 / Immunotoxins; 0 / Radioisotopes; 0 / Sialic Acid Binding Ig-like Lectin 3; 93NS566KF7 / gemtuzumab; EC 3.1.3.48 / Antigens, CD45; U015TT5I8H / Bismuth
  • [Number-of-references] 51
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24. Chen P, Levis M, Brown P, Kim KT, Allebach J, Small D: FLT3/ITD mutation signaling includes suppression of SHP-1. J Biol Chem; 2005 Feb 18;280(7):5361-9
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  • Mutations in the FLT3 gene are the most common genetic alteration found in AML patients.
  • Loss-of-function or deficiency of SHP-1 activity results in a hyperproliferative response of myelomonocytic cell populations to growth factor stimulation.
  • SHP-1 protein levels also increased in naturally occurring FLT3/ITD expressing AML cell lines and in primary FLT3/ITD AML samples after CEP-701 treatment.
  • [MeSH-minor] Acute Disease. Carbazoles / pharmacology. Cell Line, Tumor. Cell Proliferation. Cell Survival. Down-Regulation. Humans. Hydrolysis. Indoles / pharmacology. Intracellular Signaling Peptides and Proteins. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Phosphorylation / drug effects. Phosphotyrosine / metabolism. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Protein Tyrosine Phosphatase, Non-Receptor Type 6. RNA Interference. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Vanadates / pharmacology. fms-Like Tyrosine Kinase 3

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  • (PMID = 15574429.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 90668; United States / NCI NIH HHS / CA / CA 91177
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbazoles; 0 / Indoles; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / pervanadate; 21820-51-9 / Phosphotyrosine; 3WHH0066W5 / Vanadates; DO989GC5D1 / lestaurtinib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / PTPN6 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 6; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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25. Zhao W, Claxton DF, Medeiros LJ, Lu D, Vadhan-Raj S, Kantarjian HM, Nguyen MH, Bueso-Ramos CE: Immunohistochemical analysis of CBFbeta-SMMHC protein reveals a unique nuclear localization in acute myeloid leukemia with inv(16)(p13q22). Am J Surg Pathol; 2006 Nov;30(11):1436-44
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  • [Title] Immunohistochemical analysis of CBFbeta-SMMHC protein reveals a unique nuclear localization in acute myeloid leukemia with inv(16)(p13q22).
  • The inv(16)(p13q22) or, less commonly the t(16;16)(p13;q22), is characteristic of acute myeloid leukemia (AML) with abnormal bone marrow eosinophils, also known as AML-M4Eo.
  • This abnormality creates a fusion gene, 5' core binding factor beta (CBF-beta) gene and the 3' MYH11 gene, the latter encoding smooth muscle myosin heavy chain gene (SMMHC).
  • Detection of this abnormality is important for diagnosis and is most commonly done by cytogenetics or molecular methods.
  • In this study, we determined the utility of immunohistochemical and immunofluorescence methods using a rabbit polyclonal antibody (AH107) against the C-terminus of the CBFbeta-SMMHC chimeric protein for diagnosis of AML-M4Eo.
  • Thirty-nine AML-M4Eo cases and 55 cases of other types of AML were evaluated.
  • Immunohistochemical analysis of routinely processed paraffin-embedded bone marrow sections showed that CBFbeta-SMMHC staining is predominantly nuclear in all cases of AML-M4Eo and is not nuclear in other AML types.
  • Four cases of AML-M4Eo double-stained for CBFbeta-SMMHC and CD34 showed the fusion protein in CD34-positive blasts.
  • Indirect immunofluorescence analysis of fresh bone marrow aspirate smears showed that AML-M4Eo blasts have a distinct nuclear microgranular or fine-speckled pattern of staining, with or without faint cytoplasmic staining.
  • By contrast, other types of AML and normal bone marrow specimens were either negative or had a nonspecific pattern of staining.
  • In summary, immunostaining for CBFbeta-SMMHC using either immunohistochemical or immunofluorescense analysis as described here reveals a distinctive pattern of staining for AML-M4Eo.
  • This approach is a specific, reliable, and convenient alternative to cytogenetic and molecular methods for the diagnosis of AML-M4Eo and may be particularly helpful in cases with indeterminate histologic features or in cases in which cytogenetic and molecular studies are either uninformative or not available.
  • [MeSH-major] Cell Nucleus / metabolism. Chromosome Inversion. Immunohistochemistry. Leukemia, Myelomonocytic, Acute / diagnosis. Oncogene Proteins, Fusion / metabolism

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  • (PMID = 17063086.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 3.6.4.1 / Myosin Heavy Chains
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26. Oliver JW, Farnsworth B, Tonk VS: Juvenile myelomonocytic leukemia in a child with Crohn disease. Cancer Genet Cytogenet; 2006 May;167(1):70-3
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  • [Title] Juvenile myelomonocytic leukemia in a child with Crohn disease.
  • Intestinal adenocarcinoma is a well-known complication of inflammatory bowel disease.
  • Hematologic malignancies, most commonly lymphoma or acute myeloid leukemia, represent a much less well-recognized complication of these disorders; these typically occur in adults with ulcerative colitis.
  • We report a fatal case of juvenile myelomonocytic leukemia associated with monosomy 7 in a young child with a clinical history of Crohn disease.
  • Neither the leukemia nor the cytogenetic aberration has been previously reported in a patient with inflammatory bowel disease.
  • The aggressive disease course emphasizes the need for proper recognition and further study of this unusual complication.
  • [MeSH-major] Crohn Disease / complications. Crohn Disease / diagnosis. Leukemia, Myelomonocytic, Chronic / complications. Leukemia, Myelomonocytic, Chronic / diagnosis


27. Follo MY, Mongiorgi S, Bosi C, Cappellini A, Finelli C, Chiarini F, Papa V, Libra M, Martinelli G, Cocco L, Martelli AM: The Akt/mammalian target of rapamycin signal transduction pathway is activated in high-risk myelodysplastic syndromes and influences cell survival and proliferation. Cancer Res; 2007 May 1;67(9):4287-94
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  • Myelodysplastic syndromes (MDS) are a group of heterogeneous hematopoietic stem cell disorders characterized by ineffective hematopoiesis and by a high risk of evolution into acute myelogenous leukemia (AML).
  • The pathogenesis of the MDS evolution into AML is still unclear, although some recent studies indicate that aberrant activation of survival signaling pathways could be involved.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Aged. Antibodies / chemistry. Antibodies / immunology. Antibody Specificity. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Apoptosis / drug effects. Apoptosis / physiology. Cell Growth Processes / physiology. Cell Lineage. Cell Survival / physiology. Female. HL-60 Cells. Humans. Immunohistochemistry. Leukocytes, Mononuclear / enzymology. Leukocytes, Mononuclear / pathology. Male. Middle Aged. Phosphoproteins / metabolism. Phosphorylation. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Risk Factors. Sialic Acid Binding Ig-like Lectin 3. Signal Transduction. Sirolimus / pharmacology. TOR Serine-Threonine Kinases


28. Ball L, Bredius R, Lankester A, Schweizer J, van den Heuvel-Eibrink M, Escher H, Fibbe W, Egeler M: Third party mesenchymal stromal cell infusions fail to induce tissue repair despite successful control of severe grade IV acute graft-versus-host disease in a child with juvenile myelo-monocytic leukemia. Leukemia; 2008 Jun;22(6):1256-7
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  • [Title] Third party mesenchymal stromal cell infusions fail to induce tissue repair despite successful control of severe grade IV acute graft-versus-host disease in a child with juvenile myelo-monocytic leukemia.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Gastrointestinal Tract / pathology. Graft vs Host Disease / therapy. Leukemia, Myelomonocytic, Acute / therapy. Mesenchymal Stromal Cells. Wound Healing
  • [MeSH-minor] Acute Disease. Female. Humans. Infant. Stromal Cells / physiology

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  • [CommentOn] Leukemia. 2007 Nov;21(11):2271-6 [17611560.001]
  • (PMID = 17972946.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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29. 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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30. Malliah RB, Chang VT, Choe JK: Infection-associated haemophagocytic syndrome associated with recurrent acute myeloid leukaemia/myelodysplastic syndrome: an autopsy case. J Clin Pathol; 2007 Apr;60(4):431-3
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  • [Title] Infection-associated haemophagocytic syndrome associated with recurrent acute myeloid leukaemia/myelodysplastic syndrome: an autopsy case.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / etiology. Lymphohistiocytosis, Hemophagocytic / complications

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  • [Cites] Cancer Genet Cytogenet. 2000 Oct 1;122(1):26-9 [11104028.001]
  • [Cites] Leuk Lymphoma. 2001 Nov-Dec;42(6):1401-4 [11911425.001]
  • [Cites] Arch Pediatr. 2002 Feb;9(2):125-9 [11915492.001]
  • [Cites] Int J Hematol. 1998 Oct;68(3):333-6 [9846019.001]
  • [Cites] J Clin Pathol. 1991 Apr;44(4):297-9 [2030147.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1583-6 [9193356.001]
  • [Cites] Leuk Res. 1998 Oct;22(10):893-8 [9766749.001]
  • [Cites] Int J Hematol. 2002 Feb;75(2):174-7 [11939264.001]
  • (PMID = 17405980.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2001111
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31. Narimatsu H, Murata M, Terakura S, Sugimoto K, Naoe T: Potential role of a mismatched HLA-specific CTL clone developed pre-transplant in graft rejection following cord blood transplantation. Biol Blood Marrow Transplant; 2008 Apr;14(4):397-402
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  • [MeSH-major] Cord Blood Stem Cell Transplantation / adverse effects. Graft Rejection / immunology. HLA Antigens / immunology. Leukemia, Myelomonocytic, Acute / therapy. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18342781.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / HLA-DR Antigens; 0 / HLA-DRB1 Chains; 0 / Receptors, Antigen, T-Cell; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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32. ten Cate B, Bremer E, de Bruyn M, Bijma T, Samplonius D, Schwemmlein M, Huls G, Fey G, Helfrich W: A novel AML-selective TRAIL fusion protein that is superior to Gemtuzumab Ozogamicin in terms of in vitro selectivity, activity and stability. Leukemia; 2009 Aug;23(8):1389-97
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  • [Title] A novel AML-selective TRAIL fusion protein that is superior to Gemtuzumab Ozogamicin in terms of in vitro selectivity, activity and stability.
  • GO has improved the treatment outcome for a subgroup of acute myeloid leukemia (AML) patients, but its use is associated with severe myelosuppression and hepatotoxicity.
  • Here, we report on a novel anti-leukemia agent, designated scFvCD33:sTRAIL, in which an anti-CD33 single chain fragment of variable regions (scFv) antibody fragment is genetically linked to soluble tumor necrosis factor-related apoptosis-inducing ligand (sTRAIL).
  • The activity of scFvCD33:sTRAIL towards AML cells was up to 30-fold higher than GO.
  • The CD33-restricted anti-leukemia activity of scFvCD33:sTRAIL remained stable during prolonged storage at 37 degrees C, whereas GO showed a rapid increase in CD33-independent cytotoxicity.
  • Moreover, scFvCD33:sTRAIL showed potent anti-leukemia activity towards CD33+ CML cells when treatment was combined with the Bcr-Abl tyrosine kinase inhibitor, Gleevec.
  • Importantly, ex vivo treatment of patient-derived CD33+ AML tumor cells with scFvCD33:sTRAIL resulted in potent apoptosis induction that was enhanced by valproic acid, mitoxantrone and 17-(Allylamino)-17-demethoxygeldanamycin (17-AAG).
  • Taken together, scFvCD33:sTRAIL is superior to GO in terms of tumor selectivity, activity and stability, warranting its further development for the treatment of CD33-positive leukemias.
  • [MeSH-minor] Acute Disease. Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Apoptosis / drug effects. Bystander Effect. Cells, Cultured / drug effects. Drug Delivery Systems. Drug Screening Assays, Antitumor. Drug Stability. Enzyme Activation / drug effects. Humans. Leukemia, Myeloid / pathology. Leukocytes, Mononuclear / drug effects. Neoplasm Proteins / metabolism. Sialic Acid Binding Ig-like Lectin 3. Single-Chain Antibodies. Tumor Cells, Cultured / drug effects

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  • (PMID = 19262596.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Neoplasm Proteins; 0 / Recombinant Fusion Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / Single-Chain Antibodies; 0 / gemtuzumab; 0 / scFvCD33-sTRAIL protein
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33. Walter RB, Raden BW, Kamikura DM, Cooper JA, Bernstein ID: Influence of CD33 expression levels and ITIM-dependent internalization on gemtuzumab ozogamicin-induced cytotoxicity. Blood; 2005 Feb 1;105(3):1295-302
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  • Gemtuzumab ozogamicin (GO; Mylotarg), a novel immunoconjugate used for treatment of acute myeloid leukemia (AML), contains the humanized anti-CD33 antibody (hP67.6) as a carrier to facilitate cellular uptake of the toxic calicheamicin-gamma(1) derivative.
  • By use of lentivirus-mediated gene transfer to manipulate CD33 expression in myeloid cell lines that normally lack CD33 (murine 32D cells) or have very low levels of CD33 (human OCI-AML3 and KG-1a cells), we here show a quantitative relationship between CD33 expression and GO-induced cytotoxicity.
  • Together, our data imply a pivotal role of both the number of CD33 molecules expressed on the cell surface and the amount of internalization of CD33 following antibody binding for GO-induced cytotoxicity and suggest novel therapeutic approaches for improvement of clinical outcome of patients treated with GO.
  • [MeSH-major] Aminoglycosides / toxicity. Antibodies, Monoclonal / toxicity. Antigens, CD / genetics. Antigens, Differentiation, Myelomonocytic / genetics
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Binding Sites. Blast Crisis. Cell Line, Tumor. Cell Survival / drug effects. Flow Cytometry. Humans. Leukemia, Myeloid, Acute / pathology. Protein Transport. Sialic Acid Binding Ig-like Lectin 3. Tyrosine

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  • (PMID = 15454492.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA92316; United States / NIDDK NIH HHS / DK / DK56465; United States / NIGMS NIH HHS / GM / GM066257
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 42HK56048U / Tyrosine
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34. Delluc S, Hachem P, Rusakiewicz S, Gaston A, Marchiol-Fournigault C, Tourneur L, Babchia N, Fradelizi D, Regnault A, Sang KH, Chiocchia G, Buzyn A: Dramatic efficacy improvement of a DC-based vaccine against AML by CD25 T cell depletion allowing the induction of a long-lasting T cell response. Cancer Immunol Immunother; 2009 Oct;58(10):1669-77
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  • [Title] Dramatic efficacy improvement of a DC-based vaccine against AML by CD25 T cell depletion allowing the induction of a long-lasting T cell response.
  • Dendritic cell (DC)-based vaccination is a promising approach to enhance anti-tumor immunity that could be considered for acute myeloid leukemia (AML) patients with high-risk of relapse.
  • Our purpose was to study the efficiency and to optimize the immunogenicity of a DC-based vaccine in a preclinical AML murine model.
  • In this report, C57BL6 mice were vaccinated with DC pulsed with peptides eluted (EP) from the syngeneic C1498 myelomonocytic leukemic cell line in a prophylactic setting.
  • Treatment with anti-CD25 antibody to deplete CD4(+) CD25(+) regulatory T cells before DC-vaccination dramatically improved the antileukemic immune response induced by immunization, and allowed the development of long-lasting immune responses that were tumor protective after a re-challenge with leukemic cells.
  • Our results suggest that this approach could be successful against weakly immunogenic tumors such as AML, and could be translated in human.
  • [MeSH-major] Cancer Vaccines / immunology. Dendritic Cells / immunology. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. T-Lymphocytes / immunology

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  • (PMID = 19225777.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines; 0 / Interleukin-2 Receptor alpha Subunit
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35. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • The clinical evidence was derived from an open-label randomised controlled trial referred to as study AZA-001.
  • It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.
  • The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


36. Daskalakis M, Mauritzson N, Johansson B, Bouabdallah K, Onida F, Kunzmann R, Müller-Berndorff H, Schmitt-Gräff A, Lübbert M: Trisomy 19 as the sole chromosomal abnormality in proliferative chronic myelomonocytic leukemia. Leuk Res; 2006 Aug;30(8):1043-7
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  • [Title] Trisomy 19 as the sole chromosomal abnormality in proliferative chronic myelomonocytic leukemia.
  • Distinct morphologic and clinical features associated with specific chromosomal abnormalities have been described in subgroups of myelodysplastic syndromes (MDS), which often are losses or gains and only rarely translocations.
  • Among 103 consecutive MDS patients diagnosed and karyotyped at the Albert-Ludwigs University of Freiburg (ALU) between 1993 and 1999, two chronic myelomonocytic leukemias (CMMoL) displayed trisomy 19 (+19) as the sole chromosomal abnormality.
  • Three further CMMoL cases with +19 as the single abnormality, two of which previously reported, were collected from other centers.
  • Transformation to acute myeloid leukemias (AML) occurred in three/five patients (cases 1, 2, and 4) 26, 12, and 22 months after diagnosis of CMMoL, respectively.
  • We conclude that +19 as the sole anomaly is a rare but recurrent change in CMMoL, in particular of the proliferative type.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 19 / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Myelodysplastic Syndromes / genetics


37. Wirk B, Wingard JR: Strongyloides stercoralis hyperinfection in hematopoietic stem cell transplantation. Transpl Infect Dis; 2009 Apr;11(2):143-8
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  • The diagnosis of strongyloidiasis can be difficult because of intermittent larval output in stool and nonspecific symptoms with mild peripheral eosinophilia.
  • In this case report, a patient with acute myelogenous leukemia underwent peripheral blood hematopoietic stem cell transplantation (HSCT) and was subsequently diagnosed with strongyloidiasis.
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Immunocompromised Host. Strongyloides stercoralis. Strongyloidiasis / diagnosis. Superinfection / diagnosis
  • [MeSH-minor] Adult. Animals. Bronchoalveolar Lavage Fluid / parasitology. Eosinophilia / diagnosis. Eosinophilia / immunology. Fatal Outcome. Female. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Ivermectin / therapeutic use. Leukemia, Myelomonocytic, Acute / surgery

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  • (PMID = 19144095.001).
  • [ISSN] 1399-3062
  • [Journal-full-title] Transplant infectious disease : an official journal of the Transplantation Society
  • [ISO-abbreviation] Transpl Infect Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Immunosuppressive Agents; 70288-86-7 / Ivermectin
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38. 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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39. 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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40. Chung HJ, Park CJ, Jang S, Chi HS, Seo EJ, Seo JJ: A case of lineage switch from acute lymphoblastic leukemia to acute myeloid leukemia. Korean J Lab Med; 2007 Apr;27(2):102-5
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  • [Title] A case of lineage switch from acute lymphoblastic leukemia to acute myeloid leukemia.
  • Lineage switch from acute lymphoblastic leukemia (ALL) to acute myeloid leukemia (AML) is very rare.
  • We report a case of a 9 yr-old ALL patient relapsed as acute myelomonocytic leukemia.
  • At the initial diagnosis, the blast cell morphology and immunophenotype were consistent with the diagnosis of typical ALL (L1 subtype according to FAB classification).
  • Nine months, which is a very short time compared with other cases in the literatures, after the diagnosis of ALL, she relapsed with completely different blasts (typical AML, M4 according to FAB classification) in morphology, cytochemistry, and immunophenotyping.
  • The karyotype has changed from 56,XY,+X,+Y,+Y,+4,+8,+10, +14,+17,-20,+21,+21,+21[6]/57,idem,+Y[19] to 46,XY,t(8;16)(p11.2;p13.1)[19]/46,XY[1], showing unrelated chromosomal abnormality to the karyotype at the initial diagnosis.
  • Moreover, both findings were quite specific for each common cell ALL and acute myelomonocytic leukemia.
  • The treatment with AML 2000 protocol chemotherapy failed, and he underwent the chemotherapy with the combination of high dose cytarabine and mitoxantrone and has been in CR state for 21 months, until now.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


41. Chevallier P, Touzeau C, Ayari S, Guillaume T, Harousseau JL, Delaunay J: Re-administration of a combination of chemotherapy + Gemtuzumab at relapse in CD33+ AML patient allows to second remission and is feasible without extra toxicity. Leuk Res; 2008 Aug;32(8):1321-2
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  • [Title] Re-administration of a combination of chemotherapy + Gemtuzumab at relapse in CD33+ AML patient allows to second remission and is feasible without extra toxicity.
  • As combination of chemotherapy and Gemtuzumab may become a common induction regimen for CD33+ AML patients, there is no report assessing the safety and toxicity of a re-treatment at relapse with such combination in a same patient.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antigens, CD / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 18029013.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 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; 0 / gemtuzumab
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42. Stam RW, Hubeek I, den Boer ML, Buijs-Gladdines JG, Creutzig U, Kaspers GJ, Pieters R: MLL gene rearrangements have no direct impact on Ara-C sensitivity in infant acute lymphoblastic leukemia and childhood M4/M5 acute myeloid leukemia. Leukemia; 2006 Jan;20(1):179-82
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  • [Title] MLL gene rearrangements have no direct impact on Ara-C sensitivity in infant acute lymphoblastic leukemia and childhood M4/M5 acute myeloid leukemia.
  • [MeSH-major] Cytarabine / therapeutic use. Drug Resistance, Neoplasm / genetics. Gene Rearrangement. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Acute / drug therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


43. Mallo M, Espinet B, Salido M, Ferrer A, Pedro C, Besses C, Pérez-Vila E, Serrano S, Florensa L, Solé F: Gain of multiple copies of the CBFB gene: a new genetic aberration in a case of granulocytic sarcoma. Cancer Genet Cytogenet; 2007 Nov;179(1):62-5
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  • [Title] Gain of multiple copies of the CBFB gene: a new genetic aberration in a case of granulocytic sarcoma.
  • Granulocytic sarcomas (GS) are tumor masses of immature myeloid cells presenting at an extramedullary site, mainly the skin, bone, and lymph node.
  • They are often associated with acute myeloid leukemia (AML) with monoblastic or myelomonocytic differentiation, including either AML M2 with t(8;21)(q22;q22) or AML M4Eo with inv(16)(p13q22).
  • We present a case diagnosed with GS associated with AML M4 that presented a normal karyotype with conventional cytogenetic analysis.
  • [MeSH-major] Core Binding Factor beta Subunit / genetics. Gene Dosage. Gene Duplication. Sarcoma, Myeloid / diagnosis. Sarcoma, Myeloid / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 16. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Middle Aged

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  • (PMID = 17981216.001).
  • [ISSN] 0165-4608
  • [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 / CBFB protein, human; 0 / Core Binding Factor beta Subunit
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44. Gerritsen A, Lam K, Marion Schneider E, van den Heuvel-Eibrink MM: An exclusive case of juvenile myelomonocytic leukemia in association with Kikuchi's disease and hemophagocytic lymphohistiocytosis and a review of the literature. Leuk Res; 2006 Oct;30(10):1299-303
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  • [Title] An exclusive case of juvenile myelomonocytic leukemia in association with Kikuchi's disease and hemophagocytic lymphohistiocytosis and a review of the literature.
  • We present a case of juvenile myelomonocytic leukemia (JMML) accompanied by immune-mediated hemophagocytic lymphohistiocytosis (HLH) and Kikuchi's disease, both as a paraneoplastic phenomenon.
  • Our patient was treated with prednisolone according to the few described cases of HLH and Kikuchi's disease in non-JMML patients, resulting in disappearance of the clinical symptoms.
  • [MeSH-major] Histiocytic Necrotizing Lymphadenitis / complications. Leukemia, Myelomonocytic, Acute / complications. Lymphohistiocytosis, Hemophagocytic / complications. Lymphohistiocytosis, Hemophagocytic / drug therapy. Prednisolone / therapeutic use


45. Xiang Z, Kreisel F, Cain J, Colson A, Tomasson MH: Neoplasia driven by mutant c-KIT is mediated by intracellular, not plasma membrane, receptor signaling. Mol Cell Biol; 2007 Jan;27(1):267-82
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  • Activating mutations in c-KIT are associated with gastrointestinal stromal tumors, mastocytosis, and acute myeloid leukemia.
  • In attempting to establish a murine model of human KIT(D816V) (hKIT(D816V))-mediated leukemia, we uncovered an unexpected relationship between cellular transformation and intracellular trafficking.
  • When expressed in murine bone marrow, endoplasmic reticulum-localized hKIT(D816V) failed to induce disease in mice, while expression of either Golgi-localized HyKIT(D816V) or cytosol-localized, ectodomain-deleted KIT(D816V) uniformly caused fatal myeloproliferative diseases.
  • Taken together, these data demonstrate that intracellular, non-plasma membrane receptor signaling is sufficient to drive neoplasia caused by mutant c-KIT and provide the first animal model of myelomonocytic neoplasia initiated by human KIT(D816V).

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  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):916-21 [12538861.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8118-21 [11719439.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3754-7 [15304388.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9 [15650049.001]
  • [Cites] Mol Cell Biol. 2005 May;25(9):3690-703 [15831474.001]
  • [Cites] Biochem Soc Trans. 2005 Aug;33(Pt 4):657-61 [16042567.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2452-61 [15972450.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Nov 11;337(1):289-96 [16188233.001]
  • [Cites] Cancer Cell. 2005 Dec;8(6):467-78 [16338660.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9506-11 [12881486.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] Nature. 1986 Apr 3-9;320(6061):415-21 [3007997.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2317-21 [3031678.001]
  • [Cites] Science. 1988 Feb 19;239(4842):914-6 [2829358.001]
  • [Cites] EMBO J. 1988 Apr;7(4):1003-11 [2456920.001]
  • [Cites] Cell. 1988 Oct 7;55(1):185-92 [2458842.001]
  • [Cites] Mol Cell Biol. 1988 Nov;8(11):4896-903 [2463468.001]
  • [Cites] Cell. 1989 Mar 10;56(5):801-13 [2647301.001]
  • [Cites] Science. 1989 Sep 29;245(4925):1496-9 [2551043.001]
  • [Cites] Nature. 1989 Sep 28;341(6240):345-8 [2797153.001]
  • [Cites] Biochim Biophys Acta. 1990 May 7;1031(2):225-46 [2160275.001]
  • [Cites] J Biol Chem. 1992 Aug 5;267(22):15970-7 [1379243.001]
  • [Cites] Mol Cell Biol. 1993 Apr;13(4):2224-34 [7681144.001]
  • [Cites] J Clin Invest. 1993 Oct;92(4):1736-44 [7691885.001]
  • [Cites] Leukemia. 1994 Apr;8 Suppl 1:S18-22 [7512180.001]
  • [Cites] Blood. 1994 May 1;83(9):2619-26 [7513208.001]
  • [Cites] J Cell Biol. 1994 Dec;127(6 Pt 2):1843-57 [7806564.001]
  • [Cites] Blood. 1995 Feb 1;85(3):790-8 [7530509.001]
  • [Cites] Int Arch Allergy Immunol. 1995 Apr;106(4):377-85 [7536501.001]
  • [Cites] Nature. 1995 Sep 21;377(6546):242-6 [7545788.001]
  • [Cites] Nat Genet. 1996 Mar;12(3):312-4 [8589724.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3347-50 [8631931.001]
  • [Cites] Blood. 1996 Aug 1;88(3):995-1004 [8704259.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1345-64 [9269751.001]
  • [Cites] Blood. 1997 Dec 1;90(11):4539-52 [9373265.001]
  • [Cites] Blood. 1998 Jul 15;92(2):701-2 [9657776.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Oct;31(10):1053-74 [10582339.001]
  • [Cites] J Mol Biol. 1999 Dec 17;294(5):1351-62 [10600390.001]
  • [Cites] Blood. 2000 Jan 15;95(2):726-7 [10660321.001]
  • [Cites] J Clin Invest. 2000 Feb;105(4):423-32 [10683371.001]
  • [Cites] Br J Haematol. 2002 Mar;116(4):744-57 [11886377.001]
  • (PMID = 17060458.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / P01 CA 101937-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  • [Other-IDs] NLM/ PMC1800644
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46. 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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47. Langebrake C, Creutzig U, Reinhardt D: Immunophenotype of Down syndrome acute myeloid leukemia and transient myeloproliferative disease differs significantly from other diseases with morphologically identical or similar blasts. Klin Padiatr; 2005 May-Jun;217(3):126-34
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  • [Title] Immunophenotype of Down syndrome acute myeloid leukemia and transient myeloproliferative disease differs significantly from other diseases with morphologically identical or similar blasts.
  • BACKGROUND AND OBJECTIVES: Children with Down Syndrome (DS) have a 20-40 fold increased risk of developing acute myeloid leukemia (AML), mainly of the megakaryoblastic subtype (AMKL).
  • Approximately 10 % of newborns with DS show transient myeloproliferative disease (TMD) which normally resolves spontaneously.
  • Non-DS children with morphologically related diseases, i. e. myelodysplastic syndrome (MDS), juvenile myelomonocytic leukemia (JMML), or AML-M6 and AML-M7, did not show this expression profile.
  • The higher amount of CD34 co-expression in TMD may be interpreted to indicate that TMD is a slightly more immature disease than DS-AMKL.
  • [MeSH-major] Down Syndrome / complications. Immunophenotyping. Leukemia, Myeloid / immunology. Myeloproliferative Disorders / immunology
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Data Interpretation, Statistical. Diagnosis, Differential. Flow Cytometry / methods. Humans. Infant. Infant, Newborn. Leukemia, Megakaryoblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / immunology. Microscopy, Fluorescence / methods. Sensitivity and Specificity. Time Factors


48. 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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49. Simard P, Leroux JC: In vivo evaluation of pH-sensitive polymer-based immunoliposomes targeting the CD33 antigen. Mol Pharm; 2010 Aug 2;7(4):1098-107
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  • The purpose of this study was to evaluate in vivo a targeted pH-sensitive liposomal formulation tailored to promote the efficient intracellular delivery of 1-beta-d-arabinofuranosylcytosine (ara-C) to human myeloid leukemia cells.
  • Specifically, pH-sensitive immunoliposomes were obtained by anchoring a copolymer of dioctadecyl, N-isopropylacrylamide and methacrylic acid in bilayers of PEGylated liposomes (LP) and by coupling the whole anti-CD33 monoclonal antibody (mAb) or its Fab' fragments.
  • In naive mice, nontargeted and pH-sensitive Fab'-LP had longer circulation times than LP with whole mAb.
  • In SCID/HL60 (CD33(+)) mice, the pharmacokinetic and biodistribution profiles of LP and encapsulated ara-C were comparable between nontargeted and pH-sensitive Fab'-LP.
  • In leukemic mice, only pH-insensitive, ara-C-loaded Fab' induced prolonged survival times.
  • The apparent absence of pH-sensitive Fab'-LP effect could be related to lower exposure to ara-C in SCID mice.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Liposomes / chemistry. Polymers / chemistry
  • [MeSH-minor] Acrylamides / chemistry. Animals. Antibodies, Monoclonal / chemistry. Antibodies, Monoclonal / immunology. Chromatography, High Pressure Liquid. Female. HL-60 Cells. Humans. Hydrogen-Ion Concentration. Leukemia, Myeloid, Acute / therapy. Mice. Mice, Inbred BALB C. Mice, SCID. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 20476756.001).
  • [ISSN] 1543-8392
  • [Journal-full-title] Molecular pharmaceutics
  • [ISO-abbreviation] Mol. Pharm.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylamides; 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Liposomes; 0 / Polymers; 0 / Sialic Acid Binding Ig-like Lectin 3; B7GFF17L9U / N-isopropylacrylamide
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50. Korthof ET, Snijder PP, de Graaff AA, Lankester AC, Bredius RG, Ball LM, Lie JL, Vossen JM, Egeler RM: Allogeneic bone marrow transplantation for juvenile myelomonocytic leukemia: a single center experience of 23 patients. Bone Marrow Transplant; 2005 Mar;35(5):455-61
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  • [Title] Allogeneic bone marrow transplantation for juvenile myelomonocytic leukemia: a single center experience of 23 patients.
  • Juvenile myelomonocytic leukemia (JMML) is a childhood leukemia for which allogeneic BMT is the only curative therapy.
  • Relapse or persistent disease was observed in eight and two patients, respectively.
  • Nine of these patients died, one achieved a second remission following acute nonlymphatic leukemia chemotherapy (duration to date 5.3 years).
  • Together with a trend towards less relapse in patients with graft-versus-host-disease and in patients transplanted with matched unrelated donors, this suggests a graft-versus-leukemia effect of allogeneic BMT in JMML.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myelomonocytic, Chronic / therapy
  • [MeSH-minor] Child. Child, Preschool. Female. Graft vs Host Disease. Graft vs Leukemia Effect. Histocompatibility. Humans. Infant. Lymphocyte Depletion. Male. Multivariate Analysis. Recurrence. Retrospective Studies. Risk Factors. Survival Analysis. Transplantation Conditioning / methods. Transplantation Conditioning / mortality. Transplantation, Homologous. Treatment Outcome


51. Ruiz-Argüelles GJ, Garcés-Eisele J, Reyes-Núñez V, Ruiz-Delgado GJ, Navarro-Vázquez M, González-Carrillo ML: The Janus Kinase 2 (JAK2) V617F mutation in hematological malignancies in México. Rev Invest Clin; 2006 Sep-Oct;58(5):458-61
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  • A new mutation (V617F) affecting the JAK2 gene has been recently described as acquired in patients with myeloproliferative disorders and other myeloid malignancies.
  • Using an amplification refractory mutation system, we investigated this mutation in 70 Mexican mestizo patients with hematological malignancies: 28 cases of acute lymphoblastic leukemia, 17 cases of Ph1-positive chronic myelogenous leukemia, 8 patients with acute myelogenous leukemia, 6 patients with chronic lymphocytic leukemia, 6 patients with polycythemia vera (PV), two patients with essential thrombocythemia (ET), one patient with hypereosinophilic syndrome one patient with primary myelofibrosis (MF) and one patient with chronic myelomonocytic leukemia.
  • Our data add to the observation that the JAK2 V617F mutation seems to be rather uncommon in myeloid malignancies other than the classic BCR/ABL negative MPD.

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  • (PMID = 17408106.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
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52. Balaian L, Ball ED: Cytotoxic activity of gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukemia correlates with the expression of protein kinase Syk. Leukemia; 2006 Dec;20(12):2093-101
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  • [Title] Cytotoxic activity of gemtuzumab ozogamicin (Mylotarg) in acute myeloid leukemia correlates with the expression of protein kinase Syk.
  • Acute myeloid leukemia (AML) cells express the cell surface antigen CD33 that, upon ligation with a monoclonal antibody (mAb), is a downregulator of cell growth in a Syk-dependent manner.
  • An anti-CD33 mAb coupled to a toxin, gemtuzumab ozogamicin (GO), is used for the treatment of AML (Mylotarg).
  • Therefore, we investigated whether the response of AML cells to GO treatment also depends on Syk expression.
  • Forty primary AML samples (25 Syk-positive and 15 Syk-negative) were tested for their response to the anti-proliferative effects of GO and unmodified anti-CD33 mAb.
  • A correlation between Syk expression and the response of leukemia cells to GO and anti-CD33 mAb was found.
  • 'Blocking' of Syk by small interfering RNA resulted in unresponsiveness of AML cells to both GO and anti-CD33 mAb-mediated cytotoxicity.
  • Syk upregulation by the de-methylating agent 5-azacytidine (5-aza) induced re-expression of Syk in some cases, resulting in enhanced GO and anti-CD33-mediated inhibition of leukemia cell growth.
  • Thus, the cytotoxicity of both GO and anti-CD33 in primary AML samples was associated with Syk expression.
  • These data have clinical significance for predicting response to GO and designing clinical trials.
  • [MeSH-major] Aminoglycosides / pharmacology. Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Immunotoxins / pharmacology. Intracellular Signaling Peptides and Proteins / analysis. Leukemia, Myeloid, Acute / drug therapy. Protein-Tyrosine Kinases / analysis
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Azacitidine / pharmacology. Cell Line, Tumor. Humans. RNA, Small Interfering. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17051243.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; M801H13NRU / Azacitidine
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53. 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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  • [Cites] Br J Haematol. 2000 Dec;111(4):1103-5 [11167746.001]
  • [Cites] Am J Hematol. 1996 Mar;51(3):251-2 [8619417.001]
  • [Cites] Br J Haematol. 1998 Mar;100(4):664-8 [9531331.001]
  • [Cites] Leukemia. 2005 Feb;19(2):176-82 [15592433.001]
  • [Cites] J Intern Med. 2000 May;247(5):521-34 [10809991.001]
  • [Cites] Cancer. 2003 Nov 15;98 (10 ):2095-104 [14601078.001]
  • [Cites] Ann Hematol. 1998 Jan;76(1):43-4 [9486924.001]
  • [Cites] Leuk Lymphoma. 2005 Aug;46(8):1115-20 [16085551.001]
  • [Cites] Int J Hematol. 1997 Jun;65(4):415-6 [9195782.001]
  • [Cites] Transfus Med. 2005 Oct;15(5):445-8 [16202062.001]
  • [Cites] Eur J Haematol. 2004 Apr;72(4):264-7 [15089764.001]
  • [Cites] Int J Hematol. 2000 Dec;72(4):418-24 [11197207.001]
  • (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
  •  go-up   go-down


54. Pollard JA, Alonzo TA, Gerbing RB, Woods WG, Lange BJ, Sweetser DA, Radich JP, Bernstein ID, Meshinchi S: FLT3 internal tandem duplication in CD34+/CD33- precursors predicts poor outcome in acute myeloid leukemia. Blood; 2006 Oct 15;108(8):2764-9
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  • [Title] FLT3 internal tandem duplication in CD34+/CD33- precursors predicts poor outcome in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a clonal disease characterized by heterogeneous involvement of hematopoietic stem cell/progenitor cell populations.
  • Using FLT3 internal tandem duplication (FLT3/ITD) as a molecular marker, we tested the hypothesis that clinical outcome in AML correlates with disease involvement of CD34(+)/CD33(-) precursors.
  • Diagnostic specimens from 24 children with FLT3/ITD-positive AML were sorted by fluorescence-activated cell sorting (FACS), and resultant CD34(+)/CD33(-) and CD34(+)/CD33(+) progenitors were analyzed directly and after colony-forming cell (CFC) assay for the presence of FLT3/ITD.
  • Those patients in whom CD34(+)/CD33(-) precursors harbored the FLT3/ITD had worse clinical outcome; actuarial event-free survival (EFS) at 4 years from study entry for those patients with and without FLT3/ITD detection in CD34(+)/CD33(-) progenitors was 11% +/- 14% versus 100% +/- 0%, respectively (P = .002).
  • This study suggests that FLT3/ITD involvement in CD34(+)/CD33(-) precursors is heterogeneous and that detection of the mutation in the less-mature progenitor population may be associated with disease resistance.

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  • [Cites] Blood. 2004 Oct 1;104(7):1995-9 [15187030.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] J Exp Med. 1989 May 1;169(5):1721-31 [2469766.001]
  • [Cites] Blood. 1992 Apr 1;79(7):1811-6 [1373089.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):5847-51 [1631067.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] Genome Res. 1999 May;9(5):482-91 [10330128.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1345-9 [15959528.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2054-62 [16136168.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3654-61 [16912228.001]
  • [Cites] Leukemia. 2000 Apr;14(4):675-83 [10764154.001]
  • [Cites] Blood. 2001 Jan 1;97(1):56-62 [11133742.001]
  • [Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3292-8 [12115363.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2002;3:179-98 [12194988.001]
  • [Cites] Blood. 2003 May 1;101(9):3398-406 [12506020.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2387-94 [12816873.001]
  • [Cites] Br J Haematol. 2003 Nov;123(3):431-5 [14617001.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):150-6 [14701777.001]
  • [Cites] Arch Med Res. 2003 Nov-Dec;34(6):507-14 [14734090.001]
  • [Cites] Br J Cancer. 1993 Mar;67(3):413-23 [8439493.001]
  • [Cites] PCR Methods Appl. 1994 Jun;3(6):317-9 [7522723.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2154-61 [7536493.001]
  • [Cites] Blood. 1995 May 15;85(10):2643-53 [7742522.001]
  • [Cites] N Engl J Med. 1987 Aug 20;317(8):468-73 [3614291.001]
  • (PMID = 16809615.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 114563; United States / NCI NIH HHS / CA / 5T32 CA 009351-27; United States / NCI NIH HHS / CA / U10 CA 98543; United States / NCI NIH HHS / CA / R21 CA 102624; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / R01 CA 092316; United States / NCI NIH HHS / CA / U24 CA 114766
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1895585
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55. Pardanani AD, Levine RL, Lasho T, Pikman Y, Mesa RA, Wadleigh M, Steensma DP, Elliott MA, Wolanskyj AP, Hogan WJ, McClure RF, Litzow MR, Gilliland DG, Tefferi A: MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients. Blood; 2006 Nov 15;108(10):3472-6
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  • [Title] MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients.
  • Recently, a gain-of-function MPL mutation, MPLW515L, was described in patients with JAK2V617F-negative myelofibrosis with myeloid metaplasia (MMM).
  • To gain more information on mutational frequency, disease specificity, and clinical correlates, genomic DNA from 1182 patients with myeloproliferative and other myeloid disorders and 64 healthy controls was screened for MPL515 mutations, regardless of JAK2V617F mutational status: 290 with MMM, 242 with polycythemia vera, 318 with essential thrombocythemia (ET), 88 with myelodysplastic syndrome, 118 with chronic myelomonocytic leukemia, and 126 with acute myeloid leukemia (AML).
  • The diagnosis of patients with mutant MPL alleles at the time of molecular testing was de novo MMM in 12 patients, ET in 4, post-ET MMM in 1, and MMM in blast crisis in 3.
  • We conclude that MPLW515L or MPLW515K mutations are present in patients with MMM or ET at a frequency of approximately 5% and 1%, respectively, but are not observed in patients with polycythemia vera (PV) or other myeloid disorders.
  • Furthermore, MPL mutations may occur concurrently with the JAK2V617F mutation, suggesting that these alleles may have functional complementation in myeloproliferative disease.

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  • (PMID = 16868251.001).
  • [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 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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56. Wex H, Ahrens D, Hohmann B, Redlich A, Mittler U, Vorwerk P: Insulin-like growth factor-binding protein 4 in children with acute lymphoblastic leukemia. Int J Hematol; 2005 Aug;82(2):137-42
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  • [Title] Insulin-like growth factor-binding protein 4 in children with acute lymphoblastic leukemia.
  • To investigate the functional relevance of IGFBP-4 in leukemia, we measured plasma IGFBP-4 levels and messenger RNA expression in leukemic cell clones of patients with acute lymphoblastic leukemia (ALL) and in control subjects.
  • The IGFBP-4 levels of ALL patients at diagnosis were significantly lower than the levels of healthy control subjects.
  • We evaluated the patients at diagnosis and after 33 days of chemotherapy and found plasma IGFBP-4 levels at day 33 to be significantly lower than the levels at diagnosis.
  • Gene expression analysis of the leukemic blast population at diagnosis revealed that the leukemic clones did not significantly contribute to systemic IGFBP-4 levels.
  • IGFBP-4 was exclusively expressed in cell lines derived either from B-cells or from myelomonocytic cells, whereas IGFBP-4 was not expressed in T-cell lines.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Insulin-Like Growth Factor Binding Protein 4 / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood

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  • [Cites] Growth Horm IGF Res. 2004 Apr;14(2):71-84 [15123166.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Oct 5;263(3):786-9 [10512758.001]
  • [Cites] Endocrinology. 1995 Jun;136(6):2470-6 [7538463.001]
  • [Cites] Biol Reprod. 2000 Aug;63(2):390-400 [10906042.001]
  • [Cites] Endocrinology. 1999 Dec;140(12):5719-28 [10579337.001]
  • [Cites] Endocrinology. 1998 May;139(5):2605-14 [9564877.001]
  • [Cites] Eur J Pediatr. 1996 Feb;155(2):81-6 [8775218.001]
  • [Cites] Endocrinology. 1998 Aug;139(8):3456-64 [9681496.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8338-42 [2479022.001]
  • [Cites] Hum Exp Toxicol. 1999 Mar;18(3):154-61 [10215105.001]
  • [Cites] J Cell Biochem. 1999 Dec 15;75(4):652-64 [10572248.001]
  • [Cites] Circ Res. 2000 Feb 4;86(2):125-30 [10666406.001]
  • [Cites] Mol Genet Metab. 1999 Oct;68(2):161-81 [10527667.001]
  • [Cites] Br J Cancer. 1998 Aug;78(4):515-20 [9716037.001]
  • [Cites] Endocrinology. 1998 Apr;139(4):1556-63 [9528934.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Apr;81(4):1389-96 [8636339.001]
  • [Cites] Endocrinology. 1994 Jan;134(1):126-32 [7506203.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 May;54(5):655-64 [11380497.001]
  • [Cites] Endocrinol Metab Clin North Am. 1996 Sep;25(3):591-614 [8879988.001]
  • [Cites] Leukemia. 1996 May;10(5):877-95 [8656686.001]
  • [Cites] Mol Endocrinol. 1990 Oct;4(10):1451-8 [1704481.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 16;96(6):3149-53 [10077652.001]
  • [Cites] Cancer Res. 1994 Dec 15;54(24):6563-70 [7527300.001]
  • [Cites] Biochemistry. 2000 May 2;39(17):5082-8 [10819974.001]
  • [Cites] J Biol Chem. 1992 Jun 25;267(18):12692-9 [1377672.001]
  • [Cites] J Endocrinol. 2003 Aug;178(2):177-93 [12904166.001]
  • [Cites] Acta Endocrinol (Copenh). 1991 Jun;124(6):707-14 [1712529.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21285-90 [11923290.001]
  • [Cites] Endocrinology. 2001 Jun;142(6):2641-8 [11356715.001]
  • [Cites] Int J Biochem Cell Biol. 1996 Jun;28(6):619-37 [8673727.001]
  • [Cites] Endocr Rev. 1992 Nov;13(4):641-69 [1281087.001]
  • [Cites] Mol Pathol. 2002 Feb;55(1):40-5 [11836446.001]
  • [Cites] Endocrinology. 2001 Jan;142(1):241-8 [11145587.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2000 Jun;278(6):E967-76 [10826997.001]
  • [Cites] Mol Pathol. 2001 Aug;54(4):227-9 [11477136.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Feb;80(2):443-9 [7531712.001]
  • (PMID = 16146846.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Insulin-Like Growth Factor Binding Protein 4; 0 / RNA, Messenger; 67763-96-6 / Insulin-Like Growth Factor I
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57. Tessema M, Länger F, Bock O, Seltsam A, Metzig K, Hasemeier B, Kreipe H, Lehmann U: Down-regulation of the IGF-2/H19 locus during normal and malignant hematopoiesis is independent of the imprinting pattern. Int J Oncol; 2005 Feb;26(2):499-507
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  • In order to elucidate the contribution of H19 and IGF-2 to leukemogenesis, the mRNA expression level of both genes were quantitated in bone marrow biopsies and peripheral blood samples from normal (n=98), chronic myelomonocytic leukemia (CMML, n=43), chronic myelogenous leukemia (CML, n=40) and, acute myelogenous leukemia (AML, n=32) cases.
  • No correlations between imprinting status (mono- versus biallelic expression), quantitative mRNA expression levels and course of disease were found for the IGF-2 gene.
  • The data suggest a disturbed regulation of the IGF-2/H19 locus in myeloid leukemias which is not caused by loss of imprinting.
  • [MeSH-minor] Alleles. Biopsy. Bone Marrow Cells / metabolism. DNA Methylation. DNA, Complementary / metabolism. Genotype. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Models, Genetic. RNA, Long Noncoding. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15645136.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / H19 long non-coding RNA; 0 / RNA, Long Noncoding; 0 / RNA, Messenger; 0 / RNA, Untranslated; 67763-97-7 / Insulin-Like Growth Factor II
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58. Erikci AA, Ozturk A, Tekgunduz E, Sayan O: Acute myeloid leukemia complicating multiple myeloma: a case successfully treated with etoposide, thioguanine, and cytarabine. Clin Lymphoma Myeloma; 2009 Aug;9(4):E14-5
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  • [Title] Acute myeloid leukemia complicating multiple myeloma: a case successfully treated with etoposide, thioguanine, and cytarabine.
  • BACKGROUND: The association of acute leukemia and multiple myeloma (MM) has been usually described not only as a complication of chemotherapy but also in the absence of chemotherapy or together at the time of diagnosis.
  • Such leukemias are typically acute myeloid leukemia (AML).
  • The myelomonocytic subtype is particularly found.
  • CASE REPORT: We report a case of a 68-year-old female who developed AML 2 years after the diagnosis of light chain (kappa) myeloma.
  • This therapy might be a safe alternative in secondary leukemia especially for elderly patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Etoposide / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Multiple Myeloma / drug therapy. Thioguanine / therapeutic use


59. Fischer C, Drexler HG, Reinhardt J, Zaborski M, Quentmeier H: Epigenetic regulation of brain expressed X-linked-2, a marker for acute myeloid leukemia with mixed lineage leukemia rearrangements. Leukemia; 2007 Feb;21(2):374-7
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  • [Title] Epigenetic regulation of brain expressed X-linked-2, a marker for acute myeloid leukemia with mixed lineage leukemia rearrangements.
  • [MeSH-major] Brain / physiopathology. Gene Expression Regulation, Neoplastic. Gene Rearrangement. Leukemia, Myelomonocytic, Acute / genetics. Nerve Tissue Proteins / genetics

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  • (PMID = 17251904.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BEX1 protein, human; 0 / Nerve Tissue Proteins
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60. Goasguen JE, Bennett JM, Bain BJ, Vallespi T, Brunning R, Mufti GJ, International Working Group on Morphology of Myelodysplastic Syndrome: Morphological evaluation of monocytes and their precursors. Haematologica; 2009 Jul;94(7):994-7
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  • [MeSH-major] Leukemia, Myelomonocytic, Acute / diagnosis. Leukemia, Myelomonocytic, Chronic / diagnosis. Microscopy / methods. Monocytes / cytology

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  • [Cites] J Leukoc Biol. 2001 Jan;69(1):11-20 [11200054.001]
  • [Cites] Clin Immunol. 2001 Sep;100(3):325-38 [11513546.001]
  • [Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]
  • [Cites] Am J Clin Pathol. 1989 Sep;92(3):280-5 [2476027.001]
  • [Cites] Blood. 1993 Nov 15;82(10):3170-6 [7693040.001]
  • [Cites] J Leukoc Biol. 2007 Mar;81(3):584-92 [17135573.001]
  • [Cites] Keio J Med. 2007 Jun;56(2):41-7 [17609587.001]
  • [Cites] J Leukoc Biol. 2007 Aug;82(2):244-52 [17475785.001]
  • [Cites] Immunol Cell Biol. 2008 Jul;86(5):398-408 [18392044.001]
  • [Cites] Haematologica. 2008 Nov;93(11):1712-7 [18838480.001]
  • [CommentIn] Haematologica. 2009 Nov;94(11):1623-4 [19880784.001]
  • (PMID = 19535346.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2704310
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61. Chevallier P, Roland V, Mahé B, Juge-Morineau N, Dubruille V, Guillaume T, Vigouroux S, Moreau P, Milpied N, Garand R, Avet-Loiseau H, Harousseau JL: Administration of mylotarg 4 days after beginning of a chemotherapy including intermediate-dose aracytin and mitoxantrone (MIDAM regimen) produces a high rate of complete hematologic remission in patients with CD33+ primary resistant or relapsed acute myeloid leukemia. Leuk Res; 2005 Sep;29(9):1003-7
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  • [Title] Administration of mylotarg 4 days after beginning of a chemotherapy including intermediate-dose aracytin and mitoxantrone (MIDAM regimen) produces a high rate of complete hematologic remission in patients with CD33+ primary resistant or relapsed acute myeloid leukemia.
  • We have used the dose of 9 mg/m(2) of mylotarg 4 days after the beginning of a chemotherapy including intermediate-dose aracytin and mitoxantrone (MIDAM) in 17 patients with refractory (n=4) or relapsed (n=13) AML.
  • The MIDAM protocol appears to be highly effective especially in patients with poor risk cytogenetic and/or refractory disease.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Cytarabine / administration & dosage. Humans. Mitoxantrone / administration & dosage. Recurrence. Remission Induction. Salvage Therapy. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16038726.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [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 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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62. Wang J, Wang T, Li S, Lin L, Gang Y: [Flt-3/ITD mutation in pediatric leukemia and its clinical significance]. Ai Zheng; 2007 Jan;26(1):58-63
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  • [Title] [Flt-3/ITD mutation in pediatric leukemia and its clinical significance].
  • BACKGROUND & OBJECTIVE: Flt-3 internal tandem duplication (Flt-3/ITD) in transmembrane region is the most frequently identified mutation in Flt-3 gene, which is the most frequently happened in acute myeloid leukemia (AML) and correlated to prognosis.
  • This study was to explore the correlation of Flt-3/ITD mutation to the occurrence of pediatric leukemia, and analyze its clinical significance.
  • METHODS: Flt-3/ITD mutation status in bone marrow samples from 302 children with leukemia, including 122 cases of AML, 124 cases of acute lymphoblastic leukemia (ALL), 17 cases of juvenile chronic myelogenous leukemia (JCML), and 39 cases of myelodysplastic syndromes (MDS), were examined by polymerase chain reaction (PCR) and sequencing.
  • RESULTS: Of the 122 AML patients, 98 (80.32%) had Flt-3 gene products in bone marrow.
  • Flt-3/ITD mutation was detected in 21 (17.21%) of the 122 patients; the mutation rates were 42.86% (3/7) in M0, 22.22% (2/9) in M1, 12.90% (4/31) in M2, 44.44% (8/18) in M4, and 15.38% (4/26) in M5.
  • Of the 19 AML patients with Flt3/ITD mutation, the median survival time was 13.5 months (0-47 months), which was significantly shorter than that of the patients without Flt-3/ITD mutation (P<0.05).
  • Chromosome karyotype analysis showed chromosome abnormity, including t(11; 12)(p15; q13), inv16(q21; q23), and t(6; 9)(p23; q23), in 3 AML patients with Flt-3/ITD.
  • CONCLUSIONS: Flt-3/ITD mutations are usually detected in AML, seldom in ALL, not in MDS and JCML.
  • Flt-3/ITD mutation is correlated to AML onset and progress.
  • Flt-3/ITD is a significant marker to analyze AML prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Base Sequence. Child. Child, Preschool. Chromosome Aberrations. DNA, Neoplasm / genetics. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Infant. Leukemia, Myelomonocytic, Juvenile / genetics. Leukemia, Myelomonocytic, Juvenile / metabolism. Male. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Prognosis

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  • (PMID = 17222369.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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63. Hasle H: Malignant diseases in Noonan syndrome and related disorders. Horm Res; 2009 Dec;72 Suppl 2:8-14
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  • Juvenile myelomonocytic leukemia (JMML) is a rare aggressive leukemia in young children.
  • A JMML-like myeloproliferative disorder has been described in about 30 neonates with NS and the PTPN11 mutation.
  • The disorder often regresses spontaneously, but fatal complications may occur.
  • A review of the literature indicates an increased risk of acute lymphoblastic leukemia and acute myeloid leukemia in NS.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Costello Syndrome / complications. Costello Syndrome / genetics. Female. Genetic Predisposition to Disease. Genotype. Humans. Infant. Infant, Newborn. LEOPARD Syndrome / complications. LEOPARD Syndrome / genetics. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Juvenile / epidemiology. Leukemia, Myelomonocytic, Juvenile / genetics. Male. Neuroblastoma / epidemiology. Neuroblastoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Rhabdomyosarcoma / epidemiology. Rhabdomyosarcoma / genetics. Risk Factors. Urinary Bladder Neoplasms / epidemiology. Urinary Bladder Neoplasms / genetics


64. Hegedus CM, Gunn L, Skibola CF, Zhang L, Shiao R, Fu S, Dalmasso EA, Metayer C, Dahl GV, Buffler PA, Smith MT: Proteomic analysis of childhood leukemia. Leukemia; 2005 Oct;19(10):1713-8
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  • [Title] Proteomic analysis of childhood leukemia.
  • Childhood acute lymphoblastic and myeloid leukemias are stratified into molecular and cytogenetic subgroups important for prognosis and therapy.
  • Studies have shown that gene expression profiles can discriminate between leukemia subtypes.
  • Thus, proteome analysis similarly holds the potential for characterizing different subtypes of childhood leukemia.
  • We used surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to analyze cell lysates from childhood leukemia cell lines as well as pretreatment leukemic bone marrow derived from childhood leukemia cases.
  • Comparison of the acute myeloid leukemia (AML) cell line, Kasumi, and the biphenotypic myelomonocytic cell line, MV4;11, with the acute lymphoblastic leukemia (ALL) cell lines, 697 and REH, revealed many differentially expressed proteins.
  • Analysis of childhood leukemia bone marrow showed differentially expressed proteins between AML and ALL, including a similar peak at 8.3 kDa, as well as several proteins that differentiate between the ALL t(12;21) and hyperdiploid subtypes.
  • These results demonstrate the potential for proteome analysis to distinguish between various forms of childhood leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Myeloid / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proteomics
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Humans. Peptide Mapping. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 16136170.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P30 ES01896; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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65. 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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  • [Cites] Biochemistry. 1999 Dec 7;38(49):16146-57 [10587437.001]
  • [Cites] Annu Rev Biochem. 2006;75:629-54 [16756505.001]
  • [Cites] Adv Drug Deliv Rev. 2001 Mar 1;46(1-3):3-26 [11259830.001]
  • [Cites] Biochemistry. 2001 May 15;40(19):5655-64 [11341830.001]
  • [Cites] Biochem J. 2001 Jul 1;357(Pt 1):321-8 [11415466.001]
  • [Cites] Nat Struct Biol. 2001 Aug;8(8):689-94 [11473259.001]
  • [Cites] Biochem J. 2001 Aug 15;358(Pt 1):59-67 [11485552.001]
  • [Cites] Biochemistry. 2001 Sep 18;40(37):11168-75 [11551215.001]
  • [Cites] Annu Rev Biochem. 2001;70:149-80 [11395405.001]
  • [Cites] Methods Enzymol. 2002;354:260-71 [12418233.001]
  • [Cites] Arch Biochem Biophys. 2003 May 1;413(1):23-31 [12706338.001]
  • [Cites] Org Lett. 2003 Jun 12;5(12):2033-6 [12790521.001]
  • [Cites] Adv Drug Deliv Rev. 2003 Sep 26;55(10):1293-302 [14499708.001]
  • [Cites] Biochemistry. 1969 Jun;8(6):2681-5 [5799144.001]
  • [Cites] J Biol Chem. 1969 Aug 10;244(15):4112-21 [4895361.001]
  • [Cites] Annu Rev Pharmacol. 1970;10:421-40 [4911021.001]
  • [Cites] Biochem Pharmacol. 1969 Oct;18(10):2578-80 [4935103.001]
  • [Cites] Cancer. 1971 Oct;28(4):819-24 [5286444.001]
  • [Cites] J Biol Chem. 1972 Oct 25;247(20):6708-19 [5076775.001]
  • [Cites] Biochem Biophys Res Commun. 1973 Apr 2;51(3):529-35 [4512981.001]
  • [Cites] J Biol Chem. 1973 Jun 10;248(11):3997-4002 [4145324.001]
  • [Cites] Biochem Pharmacol. 1975 Dec 1;24(23):2177-85 [1212266.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] Anal Biochem. 1976 Dec;76(2):423-30 [11707.001]
  • [Cites] Cancer Treat Rep. 1976 Oct;60(10):1493-557 [14784.001]
  • [Cites] Cancer Treat Rep. 1979 Jun;63(6):1095-108 [38003.001]
  • [Cites] Cancer Res. 1979 Oct;39(10):3893-6 [383278.001]
  • [Cites] Methods Enzymol. 1979;63:103-38 [502857.001]
  • [Cites] Ann Occup Hyg. 1980;23(1):27-33 [6445702.001]
  • [Cites] Arch Biochem Biophys. 1985 Mar;237(2):335-46 [2858178.001]
  • [Cites] Anal Biochem. 1987 Mar;161(2):438-41 [3495203.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1988;61:201-301 [3281418.001]
  • [Cites] Anal Biochem. 1988 Apr;170(1):220-7 [3389513.001]
  • [Cites] Leukemia. 1989 Apr;3(4):294-7 [2564453.001]
  • [Cites] Biochemistry. 1990 Jan 16;29(2):366-72 [1967948.001]
  • [Cites] J Comput Aided Mol Des. 1990 Mar;4(1):1-105 [2197373.001]
  • [Cites] Biochemistry. 1991 Jun 25;30(25):6135-41 [1676298.001]
  • [Cites] J Comput Aided Mol Des. 1991 Feb;5(1):55-80 [2072126.001]
  • [Cites] Anal Biochem. 1991 May 1;194(2):268-77 [1677799.001]
  • [Cites] Am J Pediatr Hematol Oncol. 1992 May;14(2):136-9 [1530118.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1993;66:203-309 [8430515.001]
  • [Cites] Biochemistry. 1994 Jan 25;33(3):675-81 [7904828.001]
  • [Cites] J Biol Chem. 1994 Mar 11;269(10):7450-7 [7907328.001]
  • [Cites] J Biol Chem. 1994 Oct 28;269(43):26789-95 [7929415.001]
  • [Cites] Biol Pharm Bull. 1996 Nov;19(11):1518-20 [8951178.001]
  • [Cites] Am J Physiol. 1997 May;272(5 Pt 1):C1691-9 [9176161.001]
  • [Cites] Nat Struct Biol. 1998 Jan;5(1):15-9 [9437423.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1998;72:87-144 [9559052.001]
  • [Cites] Adv Enzymol Relat Areas Mol Biol. 1998;72:145-98 [9559053.001]
  • [Cites] Biochemistry. 1998 Sep 22;37(38):13230-8 [9748330.001]
  • [Cites] Bioorg Med Chem. 1998 Oct;6(10):1935-53 [9839023.001]
  • [Cites] Biochemistry. 1999 Mar 23;38(12):3677-82 [10090755.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):291-9 [15665306.001]
  • [Cites] Curr Opin Chem Biol. 2005 Feb;9(1):25-30 [15701449.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4223-5 [15718422.001]
  • [Cites] Arch Biochem Biophys. 2005 Aug 1;440(1):18-27 [16023613.001]
  • [Cites] Annu Rev Genomics Hum Genet. 2005;6:261-86 [16124862.001]
  • [Cites] Br J Haematol. 2006 Mar;132(6):740-2 [16487174.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4244-9 [16497975.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7975-9 [10713115.001]
  • (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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66. Lamkin TJ, Chin V, Yen A: All-trans retinoic acid induces p62DOK1 and p56DOK2 expression which enhances induced differentiation and G0 arrest of HL-60 leukemia cells. Am J Hematol; 2006 Aug;81(8):603-15
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  • [Title] All-trans retinoic acid induces p62DOK1 and p56DOK2 expression which enhances induced differentiation and G0 arrest of HL-60 leukemia cells.
  • Originally identified in chronic myelogenous leukemia cells as a highly phosphorylated substrate for the chimeric p210(bcr-abl) protein, DOK1 was suspected to play a role in leukemogenesis.
  • The data in this report show that both the DOK1 and the DOK2 adaptor proteins are constitutively expressed in the myelomonoblastic leukemia cell line, HL-60, and that expression of both proteins is induced by the chemotherapeutic differentiation causing agents, all-trans retinoic acid (atRA) and 1,25-dihydroxyvitamin D3 (VD3).
  • [MeSH-major] Adaptor Proteins, Signal Transducing / drug effects. DNA-Binding Proteins / drug effects. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Leukemia, Myelomonocytic, Acute / drug therapy. Phosphoproteins / drug effects. RNA-Binding Proteins / drug effects. Tretinoin / pharmacology

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  • (PMID = 16823827.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB009298/ NT022184/ NT023666
  • [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 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / DOK1 protein, human; 0 / DOK2 protein, human; 0 / Phosphoproteins; 0 / RNA-Binding Proteins; 5688UTC01R / Tretinoin; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; FXC9231JVH / Calcitriol
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67. Al-Sweedan SA, Neglia JP, Steiner ME, Bostrom BC, Casey T, Hirsch BA: Characteristics of patients with TEL-AML1-positive acute lymphoblastic leukemia with single or multiple fusions. Pediatr Blood Cancer; 2007 May;48(5):510-4
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  • [Title] Characteristics of patients with TEL-AML1-positive acute lymphoblastic leukemia with single or multiple fusions.
  • Some TEL-AML1+ ALL patients present at diagnosis with extra copies of the fusion, enumerated by FISH.
  • The aim of the study was to determine whether additional copies of TEL-AML1 have clinical significance.
  • Patients with double TEL-AML1+ had a higher frequency of myeloid markers CD13 (P = 0.04) or CD33 (P = 0.003) than single TEL-AML1+ patients.
  • Single TEL-AML1+ patients had higher WBC (P = 0.04) than double TEL-AML1+ patients.
  • A larger and longer-term follow-up study will be required to verify the possible clinical significance of the presence of multiple TEL-AML1 fusions.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics
  • [MeSH-minor] Antigens, CD / analysis. Antigens, CD13 / analysis. Antigens, Differentiation, Myelomonocytic / analysis. Child. Child, Preschool. Chromosomes, Human, 21-22 and Y. Chromosomes, Human, 6-12 and X. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Leukocyte Count. Male. Prognosis. Retrospective Studies. Sialic Acid Binding Ig-like Lectin 3. Translocation, Genetic

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  • (PMID = 16763978.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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68. Takeshita A: [Antibody therapy for acute leukemia]. Nihon Rinsho; 2007 Jan 28;65 Suppl 1:408-15
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  • [Title] [Antibody therapy for acute leukemia].
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Aminoglycosides / administration & dosage. Aminoglycosides / therapeutic use. Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Humans. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17474439.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 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; 0 / gemtuzumab
  • [Number-of-references] 19
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69. 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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70. Taksin AL, Legrand O, Raffoux E, de Revel T, Thomas X, Contentin N, Bouabdallah R, Pautas C, Turlure P, Reman O, Gardin C, Varet B, de Botton S, Pousset F, Farhat H, Chevret S, Dombret H, Castaigne S: High efficacy and safety profile of fractionated doses of Mylotarg as induction therapy in patients with relapsed acute myeloblastic leukemia: a prospective study of the alfa group. Leukemia; 2007 Jan;21(1):66-71
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  • [Title] High efficacy and safety profile of fractionated doses of Mylotarg as induction therapy in patients with relapsed acute myeloblastic leukemia: a prospective study of the alfa group.
  • Pivotal phase II studies in acute myeloblastic leukemia (AML) patients in first relapse have used gemtuzumab ozogamicin (GO) (Mylotarg) at a dose of 9 mg/m(2) on days 1 and 14.
  • Based on in vitro studies showing a re-expression of CD33 antigenic sites on the cell surface of blasts cells after exposure to GO, we hypothesized that fractionated doses of GO may be efficient and better tolerated.
  • Fifty-seven patients with AML in first relapse received GO at a dose of 3 mg/m(2) on days 1, 4 and 7 for one course.
  • No veno-occlusive disease occurred after GO or after hematopoietic stem cell transplantation given after GO in seven patients.
  • [MeSH-major] Aminoglycosides / administration & dosage. Antibodies, Monoclonal / administration & dosage. Antineoplastic Agents / administration & dosage. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Antigens, CD / blood. Antigens, Differentiation, Myelomonocytic / blood. Disease-Free Survival. Drug Administration Schedule. Humans. Middle Aged. Multidrug Resistance-Associated Proteins / blood. P-Glycoprotein / blood. Recurrence. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17051246.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [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 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 0 / multidrug resistance-associated protein 1
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71. Cloos J, Goemans BF, Hess CJ, van Oostveen JW, Waisfisz Q, Corthals S, de Lange D, Boeckx N, Hählen K, Reinhardt D, Creutzig U, Schuurhuis GJ, Zwaan ChM, Kaspers GJ: Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples. Leukemia; 2006 Jul;20(7):1217-20
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  • [Title] Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples.
  • In acute myeloid leukemia (AML), activating mutations in the fms-like tyrosine kinase 3 (FLT3) gene predict poor prognosis.
  • We determined FLT3 internal tandem duplications (FLT3/ITD) and D835 point mutations in paired initial and relapse samples from 80 pediatric and adult AML patients.
  • One D835 point mutation was found in an initial pediatric AML sample.
  • However, FLT3/ITD status changed between diagnosis and relapse in 14 cases.
  • Studying FLT3/ITD kinetics in minimal residual disease setting may provide some answers for the changes we observed.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Point Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Female. Genetic Markers. Genetic Predisposition to Disease / epidemiology. Humans. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Neoplasm, Residual / epidemiology. Neoplasm, Residual / genetics. Prognosis. Recurrence. Risk Factors. Tandem Repeat Sequences

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  • (PMID = 16642044.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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72. Tefferi A: Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1. Leukemia; 2010 Jun;24(6):1128-38
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  • [Title] Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1.
  • Beginning in early 2005, a number of novel mutations involving Janus kinase 2 (JAK2), Myeloproliferative Leukemia Virus (MPL), TET oncogene family member 2 (TET2), Additional Sex Combs-Like 1 (ASXL1), Casitas B-lineage lymphoma proto-oncogene (CBL), Isocitrate dehydrogenase (IDH) and IKAROS family zinc finger 1 (IKZF1) have been described in BCR-ABL1-negative MPNs.
  • The incidence of TET2, ASXL1, CBL, IDH or IKZF1 mutations in these disorders ranges from 0 to 17%; these latter mutations are more common in chronic (TET2, ASXL1, CBL) or juvenile (CBL) myelomonocytic leukemias, mastocytosis (TET2), myelodysplastic syndromes (TET2, ASXL1) and secondary acute myeloid leukemia, including blast-phase MPN (IDH, ASXL1, IKZF1).
  • However, it is not clear as to whether and how these abnormalities contribute to disease initiation, clonal evolution or blastic transformation.

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  • [Cites] Haematologica. 2007 Dec;92(12):1717-8 [18056003.001]
  • [Cites] Haematologica. 2008 Jan;93(1):34-40 [18166783.001]
  • [Cites] Leukemia. 2008 Jan;22(1):216 [17851549.001]
  • [Cites] N Engl J Med. 1976 Oct 21;295(17):913-6 [967201.001]
  • [Cites] Blood. 1981 Nov;58(5):916-9 [7296002.001]
  • [Cites] Lancet. 2005 Mar 19-25;365(9464):1054-61 [15781101.001]
  • [Cites] Nature. 2005 Apr 28;434(7037):1144-8 [15793561.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1411-5 [15920487.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1207-9 [15860661.001]
  • [Cites] N Engl J Med. 2005 Sep 29;353(13):1416-7; author reply 1416-7 [16192494.001]
  • [Cites] Br J Haematol. 2005 Oct;131(2):166-71 [16197445.001]
  • [Cites] Br J Haematol. 2005 Nov;131(3):320-8 [16225651.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3377-9 [16081687.001]
  • [Cites] Lancet. 2005 Dec 3;366(9501):1945-53 [16325696.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):18962-7 [16365288.001]
  • [Cites] Cancer. 2006 Feb 1;106(3):631-5 [16369984.001]
  • [Cites] Blood. 2006 Mar 1;107(5):2098-100 [16293597.001]
  • [Cites] Leukemia. 2006 Jan;20(1):157-8 [16331280.001]
  • [Cites] Leukemia. 2006 Jun;20(6):971-8 [16598306.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2031-8 [16762626.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1377-80 [16675710.001]
  • [Cites] J Cell Physiol. 2006 Oct;209(1):21-43 [16741904.001]
  • [Cites] Leukemia. 2006 Nov;20(11):2067-70 [16990759.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3472-6 [16868251.001]
  • [Cites] PLoS Med. 2006 Jul;3(7):e270 [16834459.001]
  • [Cites] Br J Haematol. 2006 Dec;135(5):683-7 [17107350.001]
  • [Cites] N Engl J Med. 2007 Feb 1;356(5):459-68 [17267906.001]
  • [Cites] Br J Haematol. 2007 Feb;136(4):678-9 [17223913.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2623-9 [17312100.001]
  • [Cites] Br J Haematol. 2007 May;137(3):244-7 [17408465.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2279-84 [17440984.001]
  • [Cites] Blood. 2007 Jul 1;110(1):375-9 [17363731.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1658-68 [17541402.001]
  • [Cites] Blood. 2007 Aug 1;110(3):840-6 [17379742.001]
  • [Cites] Blood. 2007 Aug 1;110(3):1004-12 [17446348.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1092-7 [17488875.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2074-5 [17476276.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1960-3 [17597810.001]
  • [Cites] Leukemia. 2007 Sep;21(9):1952-9 [17625606.001]
  • [Cites] Stem Cells. 2007 Sep;25(9):2358-62 [17540852.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2206-7 [17507998.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3735-43 [17709604.001]
  • [Cites] Blood. 2007 Dec 1;110(12):4030-6 [17712047.001]
  • [Cites] Leukemia. 2008 Jan;22(1):14-22 [17882280.001]
  • [Cites] Leukemia. 2008 Jan;22(1):23-30 [17882282.001]
  • [Cites] Leukemia. 2008 Jan;22(1):3-13 [17882283.001]
  • [Cites] Leukemia. 2008 Jan;22(1):87-95 [18033315.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1686-9 [17984312.001]
  • [Cites] Leukemia. 2008 Feb;22(2):450-1 [17851561.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2785-9 [18006699.001]
  • [Cites] Blood. 2008 Apr 15;111(8):3931-40 [18160670.001]
  • [Cites] Leukemia. 2008 Apr;22(4):870-3 [17914411.001]
  • [Cites] Leukemia. 2008 Sep;22(9):1790-2 [18354492.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1595-7 [18698078.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1813-7 [18754026.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1841-8 [18754034.001]
  • [Cites] Leukemia. 2008 Oct;22(10):1828-40 [18769448.001]
  • [Cites] Trends Cell Biol. 2008 Nov;18(11):545-51 [18848449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17050-4 [18957548.001]
  • [Cites] Acta Neuropathol. 2008 Dec;116(6):597-602 [18985363.001]
  • [Cites] Leukemia. 2009 Jan;23(1):144-52 [18843287.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] Leuk Lymphoma. 2009 Feb;50(2):247-53 [19235016.001]
  • [Cites] Blood. 2009 Feb 26;113(9):2022-7 [19047681.001]
  • [Cites] Br J Haematol. 2009 Mar;144(6):904-8 [19170680.001]
  • [Cites] Leukemia. 2009 Mar;23(3):610-4 [18818701.001]
  • [Cites] J Cell Mol Med. 2009 Feb;13(2):215-37 [19175693.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):273-87 [19290934.001]
  • [Cites] Blood. 2009 Mar 26;113(13):2895-901 [18988864.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):446-9 [19287382.001]
  • [Cites] Nat Genet. 2009 Apr;41(4):450-4 [19287385.001]
  • [Cites] Blood. 1978 Feb;51(2):189-94 [620081.001]
  • [Cites] Clin Cancer Res. 2009 Apr 1;15(7):2238-47 [19276253.001]
  • [Cites] Science. 2009 Apr 10;324(5924):261-5 [19359588.001]
  • [Cites] Eur J Haematol. 2009 May;82(5):329-38 [19141119.001]
  • [Cites] Leukemia. 2009 May;23(5):1008-9 [19151782.001]
  • [Cites] Leukemia. 2009 May;23(5):852-5 [19194467.001]
  • [Cites] Leukemia. 2009 May;23(5):900-4 [19262599.001]
  • [Cites] Leukemia. 2009 May;23(5):905-11 [19262601.001]
  • [Cites] Leukemia. 2009 May;23(5):834-44 [19295544.001]
  • [Cites] Science. 2009 May 15;324(5929):930-5 [19372391.001]
  • [Cites] N Engl J Med. 2009 May 28;360(22):2289-301 [19474426.001]
  • [Cites] Int J Cancer. 2009 Jul 15;125(2):353-5 [19378339.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6182-92 [19387008.001]
  • [Cites] Blood. 2009 Jun 18;113(25):6403-10 [19372255.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):838-42 [19483684.001]
  • [Cites] Blood. 2009 Jul 2;114(1):144-7 [19420352.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1343-5 [19295549.001]
  • [Cites] Br J Haematol. 2009 Jun;145(6):788-800 [19388938.001]
  • [Cites] Blood. 2009 Jul 30;114(5):937-51 [19357394.001]
  • [Cites] Leukemia. 2009 Aug;23(8):1441-5 [19295546.001]
  • [Cites] Nature. 2009 Aug 13;460(7257):904-8 [19620960.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):4002-6 [19528370.001]
  • [Cites] Blood. 2009 Aug 20;114(8):1477-83 [19549988.001]
  • [Cites] Blood. 2009 Aug 27;114(9):1859-63 [19571318.001]
  • [Cites] J Clin Oncol. 2009 Sep 1;27(25):4150-4 [19636000.001]
  • [Cites] Acta Neuropathol. 2009 Oct;118(4):469-74 [19554337.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1117; author reply 1117-8 [19741235.001]
  • [Cites] Leukemia. 2003 Mar;17(3):637-41 [12646957.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):214-9 [12696071.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 3;101(31):11444-7 [15269348.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):387-97 [15837627.001]
  • [Cites] N Engl J Med. 2005 Apr 28;352(17):1779-90 [15858187.001]
  • [Cites] J Clin Oncol. 2009 Dec 20;27(36):6109-16 [19901108.001]
  • [Cites] Am J Hematol. 2010 Jan;85(1):81-3 [19957346.001]
  • [Cites] J Biol Chem. 2010 Jan 1;285(1):18-29 [19880879.001]
  • [Cites] Blood. 2010 Jan 7;115(1):38-46 [19861679.001]
  • [Cites] Haematologica. 2010 Jan;95(1):65-70 [19713221.001]
  • [Cites] Leukemia. 2010 Jan;24(1):201-3 [19710701.001]
  • [Cites] Leukemia. 2010 Jan;24(1):110-4 [19847198.001]
  • [Cites] Leukemia. 2010 Jan;24(1):105-9 [19847199.001]
  • [Cites] Cancer Res. 2010 Jan 15;70(2):447-52 [20068184.001]
  • [Cites] N Engl J Med. 2010 Jan 28;362(4):369-70 [20107228.001]
  • [Cites] Blood. 2010 Jan 28;115(4):778-82 [19965680.001]
  • [Cites] Blood. 2010 Feb 4;115(5):1037-48 [19996410.001]
  • [Cites] Leukemia. 2010 Feb;24(2):469-73 [19865112.001]
  • [Cites] Blood. 2010 Feb 11;115(6):1254-63 [19880496.001]
  • [Cites] J Biol Chem. 2010 Feb 19;285(8):5296-307 [20028972.001]
  • [Cites] J Exp Med. 2010 Feb 15;207(2):339-44 [20142433.001]
  • [Cites] Hum Mutat. 2010 Mar;31(3):E1186-99 [20077503.001]
  • [Cites] J Clin Endocrinol Metab. 2010 Mar;95(3):1274-8 [19915015.001]
  • [Cites] Haematologica. 2010 Mar;95(3):518-9 [19903679.001]
  • [Cites] Blood. 2010 Mar 11;115(10):1969-75 [20008299.001]
  • [Cites] Blood. 2010 Mar 11;115(10):2003-7 [20061559.001]
  • [Cites] Cancer Cell. 2010 Mar 16;17(3):225-34 [20171147.001]
  • [Cites] Acta Neuropathol. 2010 Apr;119(4):487-94 [20127344.001]
  • [Cites] Hum Mol Genet. 2010 Apr 15;19(8):1507-14 [20093295.001]
  • [Cites] Blood. 2010 Apr 8;115(14):2891-900 [20008300.001]
  • [Cites] Leukemia. 2010 Apr;24(4):859-60 [20111067.001]
  • [Cites] Blood. 2010 Apr 29;115(17):3589-97 [20197548.001]
  • [Cites] Leukemia. 2010 May;24(5):1069-73 [20182460.001]
  • [Cites] Leukemia. 2010 Jun;24(6):1146-51 [20410924.001]
  • [Cites] Leukemia. 2008 Apr;22(4):740-7 [18079739.001]
  • [Cites] Leukemia. 2008 Apr;22(4):756-61 [18216871.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Leuk Lymphoma. 2008 May;49(5):847-9 [18464105.001]
  • [Cites] Leukemia. 2008 May;22(5):1059-62 [17972958.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1295-8 [18059483.001]
  • [Cites] Leukemia. 2008 Jun;22(6):1289 [18079740.001]
  • [Cites] Blood. 2008 Jul 1;112(1):141-9 [18451306.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1472-4 [18239619.001]
  • [Cites] Leukemia. 2008 Jul;22(7):1299-307 [18496562.001]
  • [Cites] Blood. 2008 Aug 1;112(3):844-7 [18519816.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1402-12 [18515659.001]
  • [Cites] Leukemia. 2008 Aug;22(8):1557-66 [18528423.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2199-204 [18451307.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2429-38 [18612101.001]
  • [Cites] Int J Cancer. 2009 Nov 15;125(10):2485-6 [19530255.001]
  • [Cites] Blood. 2009 Oct 1;114(14):3018-23 [19541820.001]
  • [Cites] Clin Cancer Res. 2009 Oct 1;15(19):6002-7 [19755387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16616-21 [19805346.001]
  • [Cites] Nature. 2009 Oct 8;461(7265):819-22 [19783980.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3285-91 [19666869.001]
  • [Cites] Leukemia. 2009 Oct;23(10):1924-6 [19440215.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2009 Nov;297(5):H1545-56 [19717737.001]
  • [Cites] N Engl J Med. 2009 Nov 5;361(19):1872-85 [19890130.001]
  • [Cites] Blood. 2009 Nov 5;114(19):4197-208 [19734451.001]
  • [Cites] Leukemia. 2009 Nov;23(11):2183-6 [19609284.001]
  • [Cites] J Clin Oncol. 2009 Dec 1;27(34):5743-50 [19805672.001]
  • [Cites] Haematologica. 2009 Dec;94(12):1676-81 [19797729.001]
  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):5874-80 [19901110.001]
  • [Cites] Nature. 2009 Dec 10;462(7274):739-44 [19935646.001]
  • (PMID = 20428194.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Thrombopoietin; 0 / Repressor Proteins; 0 / TET2 protein, human; 143641-95-6 / MPL protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Number-of-references] 171
  • [Other-IDs] NLM/ PMC3035972
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73. Flotho C, Kratz C, Niemeyer CM: Targeting RAS signaling pathways in juvenile myelomonocytic leukemia. Curr Drug Targets; 2007 Jun;8(6):715-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting RAS signaling pathways in juvenile myelomonocytic leukemia.
  • Juvenile myelomonocytic leukemia (JMML) is a rapidly fatal myeloproliferative disorder of early childhood for which no effective treatment other than hematopoietic stem cell transplantation is currently available.
  • Hence, targeting RAS or its interactors on a molecular level is a promising strategy in the development of novel rational therapies for this menacing disease.
  • Preclinical and clinical data of these pharmaceuticals in JMML and other myeloid malignancies is discussed.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia, Myelomonocytic, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Child. Disease Models, Animal. Humans. Mice. ras Proteins / drug effects. ras Proteins / metabolism

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  • (PMID = 17584027.001).
  • [ISSN] 1873-5592
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.6.5.2 / ras Proteins
  • [Number-of-references] 97
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74. Somervaille TC, Cleary ML: PU.1 and Junb: suppressing the formation of acute myeloid leukemia stem cells. Cancer Cell; 2006 Dec;10(6):456-7
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  • [Title] PU.1 and Junb: suppressing the formation of acute myeloid leukemia stem cells.
  • PU.1 is a transcription factor that is required for normal myelomonocytic differentiation in hematopoiesis, and reduced PU.1 activity has been associated with myeloid leukemogenesis in man and in mouse models.
  • A recent study by Steidl et al. demonstrates that Junb and Jun, two AP-1 transcription factors, are critical downstream effectors of the tumor suppressor activity of PU.1, and that reduced expression of Junb, in particular, may be a common feature of acute myeloid leukemogenesis.
  • [MeSH-major] Leukemia, Myeloid, Acute / prevention & control. Neoplastic Stem Cells / physiology. Proto-Oncogene Proteins / physiology. Proto-Oncogene Proteins c-jun / physiology. Trans-Activators / physiology. Tumor Suppressor Proteins / physiology


75. Goddard SL, Chesney AE, Reis MD, Ghorab Z, Brzozowski M, Wright FC, Wells RA: Pathological splenic rupture: a rare complication of chronic myelomonocytic leukemia. Am J Hematol; 2007 May;82(5):405-8
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  • [Title] Pathological splenic rupture: a rare complication of chronic myelomonocytic leukemia.
  • Chronic myelomonocytic leukemia (CMML) is an uncommon disorder characterized by monocytosis of the peripheral blood, absence of the Philadelphia chromosome, fewer than 20% blasts, and one or more lineages showing dysplastic features.
  • This report should alert physicians to consider this diagnosis in patients with CMML and acute abdominal pain.
  • [MeSH-major] Abdomen, Acute / etiology. Leukemia, Myelomonocytic, Chronic / complications. Splenic Rupture / etiology

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17133422.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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76. Monma F, Nishii K, Ezuki S, Miyazaki T, Yamamori S, Usui E, Sugimoto Y, Lorenzo V F, Katayama N, Shiku H: Molecular and phenotypic analysis of Philadelphia chromosome-positive bilineage leukemia: possibility of a lineage switch from T-lymphoid leukemic progenitor to myeloid cells. Cancer Genet Cytogenet; 2006 Jan 15;164(2):118-21
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  • [Title] Molecular and phenotypic analysis of Philadelphia chromosome-positive bilineage leukemia: possibility of a lineage switch from T-lymphoid leukemic progenitor to myeloid cells.
  • The occurrence of acute bilineage leukemia is thought to be the malignant transformation of a myeloid or lymphoid leukemic progenitor with the potential to differentiate into the other lineages; however, the mechanisms of this lineage switch are not well understood.
  • Here, we report on the extremely rare case of adult Philadelphia chromosome-positive acute bilineage leukemia, which is characterized by T-cell acute lymphoblastic leukemia and acute myelomonocytic leukemia.
  • These results suggest that leukemic progenitor cells in the T-lineage with the del(7) and t(9;22) have the potential to differentiate into myeloid lineage, and that enforced PU.1 expression may contribute in part of this phenomenon.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Philadelphia Chromosome
  • [MeSH-minor] Cell Lineage. Fusion Proteins, bcr-abl / genetics. Gene Rearrangement. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Lymphocyte Subsets. Male. Middle Aged. Myeloid Progenitor Cells / pathology. Receptors, Antigen, T-Cell, gamma-delta / genetics. Translocation, Genetic. Treatment Failure

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  • (PMID = 16434313.001).
  • [ISSN] 0165-4608
  • [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 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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77. 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


78. Braham-Jmili N, Sendi-Senana H, Labiadh S, Ben Abdelali R, Ben Abdelaziz A, Khelif A, Saad A, Kortas M: [Haematological characteristics, FAB and WHO classification of 153 cases of myeloid acute leukaemia in Tunisia]. Ann Biol Clin (Paris); 2006 Sep-Oct;64(5):457-65
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  • [Title] [Haematological characteristics, FAB and WHO classification of 153 cases of myeloid acute leukaemia in Tunisia].
  • [Transliterated title] Caractéristiques hématologiques et classification FAB et OMS de 153 cas de leucémies aiguës myéloïdes en Tunisie.
  • A complete blood analysis with a careful morphologic examination of peripheral blood and bone morrow smears completed by cytochemical reaction will help to classify the most acute myeloid leukaemia (AML).
  • Actually, the study of other cytogenetis and immunophenotypic markers are now necessary to confirm diagnosis.
  • The purpose of this study is a bio-clinical review according to the WHO recommendations in 153 cases of LAM diagnosed between January 1998 and December 2003.
  • The morphologic conclusion was difficult in 12% cases.
  • 3 cases of LAM were noted at patients treated for breast cancer with chirurgic chemotherapy and radiotherapy 3, 4 et 5 years after treatment (LAM3 with t(15;17), LAM4 with genetic abnormalities of chromosomes 3, 5, 7, 8, 9, 14 et 16 et LAM 6 with genetic abnormalities of chromosomes 4, 7, 12, 14, 19 et 21).
  • In WHO classification, cytology is essential in diagnosis of LAM even if the karytype have an important prognostic value.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Child. Child, Preschool. Chromosome Aberrations. Diagnosis, Differential. Female. Humans. Infant. Karyotyping. Leukemia, Erythroblastic, Acute / blood. Leukemia, Erythroblastic, Acute / diagnosis. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Myelomonocytic, Acute / blood. Leukemia, Myelomonocytic, Acute / diagnosis. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / blood. Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. Retrospective Studies. Tunisia. World Health Organization

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  • (PMID = 17040877.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] France
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79. Bodzioch M, Dembinska-Kiec A, Hartwich J, Lapicka-Bodzioch K, Banas A, Polus A, Grzybowska J, Wybranska I, Dulinska J, Gil D, Laidler P, Placha W, Zawada M, Balana-Nowak A, Sacha T, Kiec-Wilk B, Skotnicki A, Moehle C, Langmann T, Schmitz G: The microarray expression analysis identifies BAX as a mediator of beta-carotene effects on apoptosis. Nutr Cancer; 2005;51(2):226-35
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  • We performed a microarray expression analysis in normal [human umbilical vein endothelial cells (HUVECs)] and neoplastic (melanoma A375 and myelomonocytic leukemia U937) actively proliferating cells and found evidence that beta-carotene stimulated vital cellular functions in the former and suppressed them in the latter.
  • [MeSH-major] Antioxidants / pharmacology. Apoptosis / drug effects. Leukemia, Myelomonocytic, Acute / metabolism. Melanoma / metabolism. Protein Array Analysis. Proto-Oncogene Proteins c-bcl-2 / genetics. beta Carotene / pharmacology

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  • (PMID = 15860445.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / BAX protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 01YAE03M7J / beta Carotene
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80. Ondrousková E, Povolná K, Vána P, Benes P, Konecná H, Zdráhal Z, Smarda J: A proteomic analysis of protein variations during differentiation of v-myb-transformed monoblasts. Leuk Res; 2007 Feb;31(2):221-9
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  • v-myb oncogene of avian myeloblastosis virus (AMV) transforms myelomonocytic cells in vitro and induces acute monoblastic leukemia in vivo.
  • The transforming effect of the v-myb can be suppressed using phorbol ester (TPA) or histone deacetylase inhibitor trichostatin A (TSA), the inducers of cell differentiation that are in clinical trials.

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  • (PMID = 16930693.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hydroxamic Acids; 0 / Oncogene Proteins v-myb; 0 / Phorbol Esters; 0 / Proteins; 3X2S926L3Z / trichostatin A
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81. Roche-Gamón E, Febrer-Bosch I, Verdeguer A, Alegre de Miquel V: [Cutaneous chloromas as the presenting feature of acute myeloid leukemia in a child]. Actas Dermosifiliogr; 2007 May;98(4):293-4
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  • [Title] [Cutaneous chloromas as the presenting feature of acute myeloid leukemia in a child].
  • [Transliterated title] Cloromas cutáneos como primera manifestación de leucemia mielode aguda en un niño.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / diagnosis. Leukemic Infiltration / diagnosis. Sarcoma, Myeloid / etiology. Skin / pathology

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  • (PMID = 17506966.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens, CD
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82. Yang G, Khalaf W, van de Locht L, Jansen JH, Gao M, Thompson MA, van der Reijden BA, Gutmann DH, Delwel R, Clapp DW, Hiebert SW: Transcriptional repression of the Neurofibromatosis-1 tumor suppressor by the t(8;21) fusion protein. Mol Cell Biol; 2005 Jul;25(14):5869-79
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  • Von Recklinghausen's disease is a relatively common familial genetic disorder characterized by inactivating mutations of the Neurofibromatosis-1 (NF1) gene that predisposes these patients to malignancies, including an increased risk for juvenile myelomonocytic leukemia.
  • However, NF1 mutations are not common in acute myeloid leukemia (AML).
  • Given that the RUNX1 transcription factor is the most common target for chromosomal translocations in acute leukemia, we asked if NF1 might be regulated by RUNX1.
  • In addition, similar to loss of NF1, R/M expression enhanced the sensitivity of primary myeloid progenitor cells to granulocyte-macrophage colony-stimulating factor.
  • Our results indicate that the NF1 tumor suppressor gene is a direct transcriptional target of RUNX1 and the t(8;21) fusion protein, suggesting that suppression of NF1 expression contributes to the molecular pathogenesis of AML.

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  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6470-83 [11533236.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):709-15 [11544276.001]
  • [Cites] Nat Med. 2002 Jul;8(7):743-50 [12091906.001]
  • [Cites] Nature. 2004 Aug 12;430(7001):743-7 [15269782.001]
  • [Cites] Haematologica. 2004 Aug;89(8):920-5 [15339674.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3319-21 [15618474.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12822-7 [10536006.001]
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2658-69 [10541552.001]
  • [Cites] Science. 1990 Jul 13;249(4965):181-6 [2134734.001]
  • [Cites] EMBO J. 1990 Oct;9(10):3137-44 [2209540.001]
  • [Cites] Blood. 1991 Mar 1;77(5):925-9 [1704804.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9658-62 [1946382.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):9914-8 [1946460.001]
  • [Cites] Cell. 1992 Apr 17;69(2):265-73 [1568246.001]
  • [Cites] Mol Cell Biol. 1992 Dec;12(12):5355-62 [1448070.001]
  • [Cites] Dev Dyn. 1992 Nov;195(3):216-26 [1301085.001]
  • [Cites] Leukemia. 1993 Jul;7(7):1058-60 [8321021.001]
  • [Cites] Leukemia. 1993 Jul;7(7):1071 [8321023.001]
  • [Cites] Science. 1993 Aug 20;261(5124):1041-4 [8351518.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6336-45 [8413232.001]
  • [Cites] Mol Cell Biol. 1994 Jan;14(1):373-81 [8264604.001]
  • [Cites] N Engl J Med. 1994 Mar 3;330(9):597-601 [8302341.001]
  • [Cites] Leukemia. 1994 May;8(5):878-80 [8182944.001]
  • [Cites] Nat Genet. 1994 Jul;7(3):353-61 [7920653.001]
  • [Cites] Genes Dev. 1994 May 1;8(9):1019-29 [7926784.001]
  • [Cites] Genomics. 1994 Jun;21(3):649-52 [7959746.001]
  • [Cites] Int J Hematol. 1995 Apr;61(3):113-6 [7599322.001]
  • [Cites] Mol Cell Biol. 1995 Oct;15(10):5830-45 [7565736.001]
  • [Cites] Oncogene. 1995 Nov 2;11(9):1761-9 [7478604.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):137-43 [8563750.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):144-8 [8563751.001]
  • [Cites] Mol Cell Biol. 1996 Mar;16(3):1231-40 [8622667.001]
  • [Cites] J Virol. 1996 May;70(5):3280-5 [8627811.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11895-900 [8876234.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):322-33 [9418879.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3604-11 [9584201.001]
  • [Cites] Mol Cell Biol. 1998 Jul;18(7):3915-25 [9632776.001]
  • [Cites] Mol Cell Biol. 1998 Jul;18(7):4252-61 [9632809.001]
  • [Cites] Blood. 1998 Jul 1;92(1):267-72 [9639526.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11590-5 [9751710.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7432-43 [9819429.001]
  • [Cites] EMBO J. 1999 Mar 15;18(6):1609-20 [10075931.001]
  • [Cites] Nat Struct Biol. 1999 Jul;6(7):624-7 [10404216.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1104-9 [15650049.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]
  • [Cites] Am J Pathol. 1999 Dec;155(6):1879-84 [10595918.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):651-6 [10617663.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):181-8 [10620616.001]
  • [Cites] Gene. 2000 Mar 21;245(2):223-35 [10717473.001]
  • [Cites] Genes Dev. 2000 Sep 15;14(18):2358-65 [10995391.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):723-33 [11179217.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] Oncogene. 2002 Jul 25;21(32):4978-82 [12118376.001]
  • [Cites] Blood. 2002 Aug 1;100(3):998-1007 [12130514.001]
  • [Cites] Nat Genet. 2002 Oct;32(2):261-6 [12219088.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3656-62 [12393709.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):607-19 [12509458.001]
  • [Cites] Cancer. 2003 Jan 15;97(2):441-9 [12518368.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1299-307 [12393504.001]
  • [Cites] Nat Genet. 2003 Mar;33(3):422-5 [12567189.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4243-50 [14982883.001]
  • [Cites] Glia. 2001 Mar 15;33(4):314-23 [11246230.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9889-95 [11150306.001]
  • [Cites] Nat Med. 2001 Apr;7(4):444-51 [11283671.001]
  • [Cites] J Biol Chem. 2001 Mar 9;276(10):7240-5 [11080503.001]
  • [Cites] J Exp Med. 2001 Jul 2;194(1):57-69 [11435472.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • (PMID = 15988004.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077274; United States / NCI NIH HHS / CA / R29 CA074177; United States / NCI NIH HHS / CA / R01 CA087549; United States / NCI NIH HHS / CA / R01-CA77274; United States / NCI NIH HHS / CA / R01-CA74177; United States / NCI NIH HHS / CA / R01-CA87549; United States / NCI NIH HHS / CA / P30 CA068485; United States / NCI NIH HHS / CA / R01 CA074177; United States / NCI NIH HHS / CA / R01-CA64140; United States / NCI NIH HHS / CA / R01 CA064140
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Neurofibromin 1; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Repressor Proteins; 0 / Runx1 protein, mouse; 0 / Transcription Factors; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC1168824
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83. Sheng LX, Xie XB, Qiu GQ, Gu WY, Wang ZL, Wu HQ: [In vitro stimulation of specific antileukemia T-cell response by dendritic cells derived from CD14+ acute monocytic leukemia cells]. Ai Zheng; 2005 Nov;24(11):1338-44
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  • [Title] [In vitro stimulation of specific antileukemia T-cell response by dendritic cells derived from CD14+ acute monocytic leukemia cells].
  • BACKGROUND & OBJECTIVE: Dendritic cells (DCs) or DC-like cells had been successfully induced in vitro from leukemia cells, which may provide a promising immunotherapeutic protocol for leukemia.
  • This study was designed to investigate the efficiency of in vitro generation of dendritic cells from CD14+ acute myelomonocytic (M4) or monocytic (M5) leukemia cells and their ability of stimulating specific antileukemia T-cell response.
  • METHODS: Bone marrow mononuclear cells (BMMNCs) were isolated from 5 M4/M5 leukemia patients with high CD14 expression, and then divided into 3 groups: adherent leukemia cells, nonadherent blasts, and total unfractioned blasts.
  • When cultured with or without granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-4 (IL-4) and tumor necrosis factor alpha (TNF-alpha) for 7-10 days, monocytic leukemia cell-derived dendritic cells (Mo-LDCs) were identified through morphologic observation and immunophenotype analysis using FCM.
  • The leukemic origin of Mo-LDCs was confirmed by chromosomal karyotype analysis combined with the aberrant expression of myeloid antigens.
  • RESULTS: The amount of CD14+ cells, which could differentiate into CD83+ mature DCs under induction of the cytokine combination, was higher in adherent leukemia cells than in nonadherent blasts and total unfractioned blasts.
  • Mo-LDCs exhibited typical morphology and phenotype as mature DCs, induced potent proliferation of homogeneous T cells in Allo-MLR, stimulated the expansion of leukemia-specific CTLs, and continued to possess the cytogenetic abnormalities of the original leukemia, as well as the aberrant expression of myeloid antigens.
  • CONCLUSIONS: In M4/M5 subtype of AML, CD14+ cells could differentiate into immune-competent Mo-LDCs under the induction of the cytokine combination.
  • CD14 expression level may predict the DCs differentiation ability of monocytic leukemia.
  • Mo-LDCs, which possess the classical phenotype and function of DCs, as well as the abnormal leukemic antigens, may be useful for the immunotherapy of M4/M5 AML.
  • [MeSH-major] Antigens, CD14 / analysis. Dendritic Cells / immunology. Leukemia, Monocytic, Acute / pathology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 16552959.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / CD83 antigen; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
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84. 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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  • [Cites] Exp Cell Res. 1987 Jan;168(1):247-54 [3023118.001]
  • [Cites] Blood. 1983 Oct;62(4):709-21 [6192859.001]
  • [Cites] Diabetologia. 1989 May;32(5):316-21 [2526769.001]
  • [Cites] Science. 1990 Sep 21;249(4975):1429-31 [2402637.001]
  • [Cites] Science. 1993 Nov 12;262(5136):1056-9 [8235624.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Nov 15;196(3):1459-65 [8250903.001]
  • [Cites] Prog Clin Biol Res. 1995;392:369-73 [8524944.001]
  • [Cites] Blood. 1996 Jan 1;87(1):227-37 [8547646.001]
  • [Cites] Immunogenetics. 1996;45(1):35-43 [8881035.001]
  • [Cites] FEBS Lett. 1997 Aug 11;413(1):99-103 [9287124.001]
  • [Cites] Cancer Res. 1998 Jul 15;58(14):3163-72 [9679985.001]
  • [Cites] Biosci Biotechnol Biochem. 1998 Dec;62(12):2351-6 [9972261.001]
  • [Cites] Immunogenetics. 1999 Jul;49(7-8):597-604 [10369916.001]
  • [Cites] Mol Cell. 2005 Apr 1;18(1):83-96 [15808511.001]
  • [Cites] J Cell Physiol. 2005 Sep;204(3):964-74 [15799027.001]
  • [Cites] Horm Metab Res. 2006 Jan;38(1):12-5 [16477534.001]
  • [Cites] J Cell Biochem. 2006 Apr 15;97(6):1328-38 [16329108.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982.001]
  • [Cites] Autoimmunity. 2006 Jun;39(4):333-40 [16891222.001]
  • [Cites] Biochem Pharmacol. 2007 Mar 15;73(6):831-42 [17188249.001]
  • [Cites] Ann N Y Acad Sci. 2006 Dec;1091:356-67 [17341628.001]
  • [Cites] Mol Med. 2006 Nov-Dec;12(11-12):334-41 [17380201.001]
  • [Cites] Eur Respir J. 2007 Aug;30(2):199-204 [17504797.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8624-32 [17875702.001]
  • [Cites] J Biol Chem. 2008 Feb 15;283(7):4375-86 [18006504.001]
  • [Cites] Diabetologia. 2000 Nov;43(11):1337-45 [11126400.001]
  • [Cites] J Virol. 2001 Jun;75(11):5302-14 [11333911.001]
  • [Cites] J Biol Chem. 2002 Jan 4;277(1):13-22 [11689561.001]
  • [Cites] Exp Biol Med (Maywood). 2002 Oct;227(9):753-62 [12324654.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49453-8 [12386160.001]
  • [Cites] Clin Exp Immunol. 2003 Jan;131(1):48-52 [12519385.001]
  • [Cites] Curr Med Chem. 2003 Feb;10(4):321-40 [12570705.001]
  • [Cites] Biosci Biotechnol Biochem. 2003 May;67(5):1132-5 [12834294.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2146-55 [12763926.001]
  • [Cites] Transplant Proc. 2003 Aug;35(5):2021-3 [12962883.001]
  • [Cites] Proc Soc Exp Biol Med. 1969 Mar;130(3):992-4 [4304354.001]
  • [Cites] Leuk Res. 1987;11(2):191-6 [3469486.001]
  • (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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85. Mulford D: Antibody therapy for acute myeloid leukemia. Semin Hematol; 2008 Apr;45(2):104-9
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  • [Title] Antibody therapy for acute myeloid leukemia.
  • Due to the high rate of relapse in younger patients and the overall poor outcome in older patients, novel therapies are needed for the treatment of acute myeloid leukemia (AML).
  • Gemtuzumab ozogamicin (GO), an anti-CD33 immunoconjugate, was approved by the US Food and Drug Administration (FDA) for the treatment of elderly patients with relapsed AML who are not candidates for standard chemotherapy.
  • Single-agent GO and combinations with standard chemotherapeutics have been explored extensively in this disease.
  • In patients with acute promyelocytic leukemia (APL), the addition of GO can produce molecular remissions and is well tolerated.
  • Targeted immunotherapy with GO for treatment of AML has produced remissions.
  • In order to reduce toxicity and improve efficacy, its optimal dose and schedule and pairing with other standard chemotherapeutic agents need to be defined better in large clinical trials.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Humanized. Antigens, CD / immunology. Antigens, CD45 / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Cell Adhesion Molecules / immunology. Clinical Trials as Topic. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / immunology. Leukemia, Promyelocytic, Acute / physiopathology. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 18381105.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD66 antigens; 0 / Cell Adhesion Molecules; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 0 / lintuzumab; EC 3.1.3.48 / Antigens, CD45
  • [Number-of-references] 43
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86. Loh ML: Childhood myelodysplastic syndrome: focus on the approach to diagnosis and treatment of juvenile myelomonocytic leukemia. Hematology Am Soc Hematol Educ Program; 2010;2010:357-62
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  • [Title] Childhood myelodysplastic syndrome: focus on the approach to diagnosis and treatment of juvenile myelomonocytic leukemia.
  • Expansion of myeloid blasts with suppression of normal hematopoiesis is a hallmark of acute myeloid leukemia (AML).
  • Juvenile myelomonocytic leukemia (JMML) is an aggressive MPN of childhood that is clinically characterized by the overproduction of monocytic cells that can infiltrate organs, including the spleen, liver, gastrointestinal tract, and lung.
  • The spectrum of mutations described thus far in JMML occur in genes that encode proteins that signal through the Ras/mitogen-activated protein kinase (MAPK) pathways, thus providing potential new opportunities for both diagnosis and therapy.
  • Rarely, spontaneous resolution of this disorder can occur but is unpredictable.
  • This review is focused on the genetic abnormalities that occur in JMML, with particular attention to germ-line predisposition syndromes associated with the disorder.


87. Pantanowitz L, Steingart R, Miller KB, Kruskal JB, Pihan G: Leukemic ascites. Arch Pathol Lab Med; 2005 Feb;129(2):262-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Ascites / diagnosis. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 15679438.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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88. 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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89. Kalina T, Vaskova M, Mejstrikova E, Madzo J, Trka J, Stary J, Hrusak O: Myeloid antigens in childhood lymphoblastic leukemia: clinical data point to regulation of CD66c distinct from other myeloid antigens. BMC Cancer; 2005;5:38
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  • [Title] Myeloid antigens in childhood lymphoblastic leukemia: clinical data point to regulation of CD66c distinct from other myeloid antigens.
  • BACKGROUND: Aberrant expression of myeloid antigens (MyAgs) on acute lymphoblastic leukemia (ALL) cells is a well-documented phenomenon, although its regulating mechanisms are unclear.
  • Granulocytic marker CD66c -- Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is aberrantly expressed on ALL with strong correlation to genotype (negative in TEL/AML1 and MLL/AF4, positive in BCR/ABL and hyperdiploid cases).
  • The most frequent MyAg (CD66c) is studied further regarding its stability from diagnosis to relapse, prognostic significance and regulation of surface expression.
  • Our data show that different myeloid antigens often differ in biological importance, which may be obscured by combining them into "MyAg positive ALL".
  • CONCLUSION: In contrast to general notion we show that different MyAgs in lymphoblastic leukemia represent different biological circumstances.
  • We chose the most frequent and tightly genotype-associated MyAg CD66c to show its stabile expression in patients from diagnosis to relapse, which differs from what is known on the other MyAgs.
  • [MeSH-major] Antigens, CD / biosynthesis. Cell Adhesion Molecules / biosynthesis. Gene Expression Regulation, Neoplastic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Antigens, CD13 / biosynthesis. Antigens, CD15 / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Blotting, Western. Cell Membrane / metabolism. Child. Child, Preschool. Cohort Studies. Cytoplasm / metabolism. Czech Republic. Disease-Free Survival. Flow Cytometry. GPI-Linked Proteins. Genotype. Glycosylation. Humans. Immunophenotyping. Infant. Prognosis. RNA / metabolism. Recurrence. Reverse Transcriptase Polymerase Chain Reaction. Sialic Acid Binding Ig-like Lectin 3. Time Factors. Transcription, Genetic

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  • [Cites] Crit Rev Oncol Hematol. 1999 Dec;32(3):175-85 [10633847.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1092-4 [15830012.001]
  • [Cites] Cancer Res. 2000 Jul 1;60(13):3419-24 [10910050.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):794-9 [11564065.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1952-8 [11877265.001]
  • [Cites] Best Pract Res Clin Haematol. 2002 Mar;15(1):1-19 [11987913.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1233-58 [12094248.001]
  • [Cites] Cancer. 2003 Jan 1;97(1):105-13 [12491511.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3638-46 [14512395.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):465-73 [14724575.001]
  • [Cites] Biochem Biophys Res Commun. 2004 May 7;317(3):837-43 [15081416.001]
  • [Cites] Oncogene. 2004 Jul 29;23(34):5834-42 [15208677.001]
  • [Cites] Cancer Res. 1968 Sep;28(9):1908-14 [5676741.001]
  • [Cites] Science. 1986 Nov 7;234(4777):697-704 [3535067.001]
  • [Cites] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3305-14 [8205554.001]
  • [Cites] Leukemia. 1994 Dec;8(12):2127-33 [7808000.001]
  • [Cites] Leukemia. 1995 Jul;9(7):1233-9 [7543176.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]
  • [Cites] J Leukoc Biol. 1996 Jul;60(1):106-17 [8699114.001]
  • [Cites] Infect Immun. 1996 Nov;64(11):4574-9 [8890209.001]
  • [Cites] Leukemia. 1998 Jul;12(7):1064-70 [9665191.001]
  • [Cites] Blood. 1998 Aug 1;92(3):795-801 [9680347.001]
  • [Cites] Tissue Antigens. 1998 Jul;52(1):1-8 [9714468.001]
  • [Cites] Leukemia. 1999 May;13(5):779-85 [10374883.001]
  • [Cites] Cytometry. 1999 Aug 15;38(4):139-52 [10440852.001]
  • [Cites] Am J Pathol. 2000 Feb;156(2):595-605 [10666389.001]
  • (PMID = 15826304.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD65s antigen, human; 0 / CEACAM6 protein, human; 0 / Cell Adhesion Molecules; 0 / GPI-Linked Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 63231-63-0 / RNA; EC 3.4.11.2 / Antigens, CD13
  • [Other-IDs] NLM/ PMC1112585
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90. 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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91. 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


92. Chen J, Li CF: [Effect of FK506 and CSA on the cell survival of engrafted HSC and the level of IL-2 and IL-4 in leukemia mice]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2009 May;40(3):478-80
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  • [Title] [Effect of FK506 and CSA on the cell survival of engrafted HSC and the level of IL-2 and IL-4 in leukemia mice].
  • METHODS: The WEHI23 cells were injected into vein from tail of mice to set up the leukemia model.
  • The Hematopoietic stem cells (HSCs) were harvested from GFP mice and cultured in vitro, then injected into the vein of leukemia mice.
  • FK506 and CSA, as two immunosuppress agents, were applied in leukemia mice and intact mice, and leukemia mice were as control.
  • RESULTS: Some HSCs could survive in the host treated with FK506 and CSA at least 2 weeks, while HSCs survived only 1 week in intact or leukemia control mice.
  • Simultaneously, the level of IL-2 and IL-4 in leukemia mice treated with FK506 and CSA decreased significantly than those of intact or leukemia control mice.
  • [MeSH-major] Cyclosporine / therapeutic use. Graft Survival / drug effects. Hematopoietic Stem Cell Transplantation. Leukemia, Myelomonocytic, Acute / therapy. Tacrolimus / therapeutic use

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  • (PMID = 19627009.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Interleukin-2; 207137-56-2 / Interleukin-4; 83HN0GTJ6D / Cyclosporine; WM0HAQ4WNM / Tacrolimus
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93. 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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94. Schirrmann T, Pecher G: Specific targeting of CD33(+) leukemia cells by a natural killer cell line modified with a chimeric receptor. Leuk Res; 2005 Mar;29(3):301-6
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  • [Title] Specific targeting of CD33(+) leukemia cells by a natural killer cell line modified with a chimeric receptor.
  • We directed the human natural killer (NK) cell line YT by gene transfer of a humanized chimeric immunoglobulin T cell receptor to CD33, a marker on myeloid leukemias.
  • YT cells transfected by electroporation with the chimeric receptor gene specifically lysed the acute myeloid leukemia (AML) cell line KG1.
  • [MeSH-major] Gene Transfer Techniques. Killer Cells, Natural / immunology. Leukemia / drug therapy. Receptors, Immunologic / immunology
  • [MeSH-minor] Antibodies, Monoclonal / genetics. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal, Humanized. Antigens, CD / genetics. Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / genetics. Antigens, Differentiation, Myelomonocytic / immunology. Cell Line. Cytotoxicity Tests, Immunologic. Electroporation. Flow Cytometry. Humans. Immunoglobulin Fc Fragments / genetics. Immunoglobulin Fc Fragments / immunology. Immunoglobulin G / genetics. Immunoglobulin G / immunology. Recombinant Fusion Proteins. Sialic Acid Binding Ig-like Lectin 3. Transfection

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  • (PMID = 15661266.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Immunoglobulin Fc Fragments; 0 / Immunoglobulin G; 0 / Receptors, Immunologic; 0 / Recombinant Fusion Proteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / lintuzumab
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95. 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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96. 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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97. Mori T, Aisa Y, Watanabe R, Yamazaki R, Kato J, Shimizu T, Shigematsu N, Kubo A, Yajima T, Hibi T, Ikeda Y, Okamoto S: Long-term follow-up of allogeneic hematopoietic stem cell transplantation for de novo acute myelogenous leukemia with a conditioning regimen of total body irradiation and granulocyte colony-stimulating factor-combined high-dose cytarabine. Biol Blood Marrow Transplant; 2008 Jun;14(6):651-7
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  • [Title] Long-term follow-up of allogeneic hematopoietic stem cell transplantation for de novo acute myelogenous leukemia with a conditioning regimen of total body irradiation and granulocyte colony-stimulating factor-combined high-dose cytarabine.
  • We retrospectively evaluated the efficacy and safety of total body irradiation (TBI) and granulocyte colony-stimulating factor (G-CSF)-combined high-dose cytarabine as a conditioning regimen for allogeneic hematopoietic stem cell transplantation (HSCT) in patients with de novo acute myelogenous leukemia (AML).
  • The 5-year estimated overall survival (OS) and disease-free survival (DFS) rates were 85.5% (95% confidence interval [CI], 73.7%-97.3%) and 82.1% (95% CI, 69.0%-95.2%) in patients with AML in the first or second CR, 46.7% (95% CI, 21.4%-72.0%), and 40.0% (95% CI, 15.3%-64.7%) in patients with AML in other stages.
  • The only factors affecting the OS and DFS were disease status at transplant and cytogenetics by multivariate analysis.
  • These results suggest that G-CSF-combined high-dose cytarabine could be a promising component of the conditioning regimen for allogeneic HSCT for AML, providing a high DFS and low TRM.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Bone Marrow Transplantation / adverse effects. Bone Marrow Transplantation / mortality. Cytarabine / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Infusions, Intravenous. Kaplan-Meier Estimate. Leukemia, Myelomonocytic, Acute / mortality. Leukemia, Myelomonocytic, Acute / surgery. Male. Middle Aged. Recombinant Proteins / administration & dosage. Remission Induction. Retrospective Studies. Survival Analysis. Transplantation, Homologous. Treatment Outcome. Whole-Body Irradiation

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  • (PMID = 18489990.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6WS4C399GB / lenograstim
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98. Kantarjian HM, O'Brien S, Huang X, Garcia-Manero G, Ravandi F, Cortes J, Shan J, Davisson J, Bueso-Ramos CE, Issa JP: Survival advantage with decitabine versus intensive chemotherapy in patients with higher risk myelodysplastic syndrome: comparison with historical experience. Cancer; 2007 Mar 15;109(6):1133-7
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  • BACKGROUND: Decitabine, a hypomethylating agent, is active and has been approved for the treatment of myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia.
  • METHODS: The authors compared lower intensity decitabine therapy (n = 115 patients) with intensive chemotherapy (as it is used in acute myeloid leukemia [AML]) in patients with higher risk MDS.
  • RESULTS: The complete remission (CR) rate according to AML criteria was 43% with decitabine, 46% with intensive chemotherapy in Group A, and 52% with intensive chemotherapy in Group B.


99. Walter RB, Gooley TA, van der Velden VH, Loken MR, van Dongen JJ, Flowers DA, Bernstein ID, Appelbaum FR: CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy. Blood; 2007 May 15;109(10):4168-70
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  • [Title] CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy.
  • While recent in vitro data demonstrated a quantitative relationship between CD33 expression and GO cytotoxicity, previous correlative studies failed to identify a significant association between CD33 expression and clinical outcome.
  • Studying patients undergoing GO monotherapy for relapsed acute myeloid leukemia (AML), we now find that AML blasts of responders have a significantly higher mean CD33 level and lower P-glycoprotein (Pgp) activity compared with nonresponders.

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  • [Cites] Leukemia. 1999 Dec;13(12):1943-53 [10602414.001]
  • [Cites] Exp Hematol. 2006 Jan;34(1):54-65 [16413391.001]
  • [Cites] Blood. 2001 May 15;97(10):3197-204 [11342449.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • [Cites] Blood. 2001 Aug 15;98(4):988-94 [11493443.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1544-53 [11587212.001]
  • [Cites] Leukemia. 2002 May;16(5):813-9 [11986941.001]
  • [Cites] Am J Clin Pathol. 2002 Oct;118(4):560-6 [12375643.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1466-73 [12689934.001]
  • [Cites] Cancer. 2003 Nov 15;98(10):2095-104 [14601078.001]
  • [Cites] Leukemia. 2004 Feb;18(2):316-25 [14614514.001]
  • [Cites] Cancer. 2004 Feb 1;100(3):441-54 [14745859.001]
  • [Cites] Haematologica. 2004 May;89(5):634-6 [15136240.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4276-84 [14962898.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1086-99 [10419902.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 6):2-8 [10530710.001]
  • [Cites] Haematologica. 2005 Jan;90(1):54-9 [15642669.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1295-302 [15454492.001]
  • [Cites] Leukemia. 2005 Feb;19(2):176-82 [15592433.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]
  • [Cites] Glycobiology. 2006 Jan;16(1):1R-27R [16014749.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1436-43 [10942240.001]
  • (PMID = 17227830.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA091 316
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [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 / P-Glycoprotein; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  • [Other-IDs] NLM/ PMC1885511
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100. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. MERCAPTOPURINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
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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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