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6. Shimoni A, Kröger N, Zabelina T, Ayuk F, Hardan I, Yeshurun M, Shem-Tov N, Avigdor A, Ben-Bassat I, Zander AR, Nagler A: Hematopoietic stem-cell transplantation from unrelated donors in elderly patients (age >55 years) with hematologic malignancies: older age is no longer a contraindication when using reduced intensity conditioning. Leukemia; 2005 Jan;19(1):7-12
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  • [Title] Hematopoietic stem-cell transplantation from unrelated donors in elderly patients (age >55 years) with hematologic malignancies: older age is no longer a contraindication when using reduced intensity conditioning.
  • Allogeneic stem cell transplantation (SCT) is a potentially curative approach for patients with hematological malignancies.
  • The probabilities of overall survival, disease-free survival, and nonrelapse mortality at 1 year after SCT were 52, 43, and 39%, respectively.
  • Acute graft-versus-host disease (GVHD) grade II-IV and chronic GVHD occurred in 31 and 45%, respectively.
  • Multivariable analysis determined that survival rates were higher in patients with chemosensitive disease (HR 4.5), and patients conditioned with intravenous busulfan or treosulfan (HR 3.9).
  • Favorable outcome was observed in patients with myeloid malignancies, and those transplanted in remission and early in the course of disease.
  • Age alone should not be considered a contraindication to unrelated donor SCT.
  • [MeSH-major] Hematologic Neoplasms / surgery. Hematopoietic Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Graft vs Host Disease. Humans. Middle Aged. Retrospective Studies. Survival Analysis

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  • [CommentIn] Leukemia. 2005 Jan;19(1):31-3 [15526015.001]
  • (PMID = 15526016.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab
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7. Figueroa ME, Wouters BJ, Skrabanek L, Glass J, Li Y, Erpelinck-Verschueren CA, Langerak AW, Löwenberg B, Fazzari M, Greally JM, Valk PJ, Melnick A, Delwel R: Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features. Blood; 2009 Mar 19;113(12):2795-804
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  • [Title] Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features.
  • Acute myeloid leukemia is a heterogeneous disease from the molecular and biologic standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity.
  • We studied the epigenetic profiles of a cohort of patients who shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, whereas the rest presented with silencing of this gene and coexpression of certain T-cell markers.
  • Furthermore, CEBPA silencing was associated with the presence of an aberrant DNA hypermethylation signature, which was not present in the CEBPA mutant group.
  • CEBPA-silenced leukemias also displayed marked hypermethylation compared with normal CD34(+) hematopoietic cells, whereas CEBPA mutant cases showed only mild changes in DNA methylation compared with these normal progenitors.
  • Biologically, CEBPA-silenced leukemias presented with a decreased response to myeloid growth factors in vitro.

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  • (PMID = 19168792.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE14417
  • [Grant] United States / NIGMS NIH HHS / GM / GM007288; United States / NCI NIH HHS / CA / R01 CA118316; United States / NCI NIH HHS / CA / CA118316; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / R01 CA104348
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / DNA, Neoplasm; 0 / Interleukin-3; 0 / Neoplasm Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2945920
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8. Arana-Yi C, Block AW, Sait SN, Ford LA, Barcos M, Baer MR: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine. Leuk Res; 2008 Jul;32(7):1043-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) have been reported only rarely following treatment of AML.
  • We report five patients treated for de novo AML who developed t-MDS/t-AML, all with chromosome 7 abnormalities, including -7, del(7)(q22q36) and del(7)(p11.22p22).
  • These cases further document t-MDS/t-AML as a complication of therapy for AML.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytarabine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / drug therapy


9. Konieczna I, Horvath E, Wang H, Lindsey S, Saberwal G, Bei L, Huang W, Platanias L, Eklund EA: Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia. J Clin Invest; 2008 Mar;118(3):853-67
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  • [Title] Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia.
  • Development of a block in myeloid differentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor prognosis.
  • Interferon consensus sequence binding protein (ICSBP, also known as IRF8) is an interferon-regulatory transcription factor that functions as a leukemia tumor suppressor.
  • In mice, ICSBP deficiency induces an MPD that progresses to AML over time, suggesting that ICSBP deficiency is sufficient for myeloproliferation, but additional genetic lesions are necessary for AML.
  • Since activity of ICSBP is influenced by tyrosine phosphorylation state, we hypothesized that mutations in molecular pathways that regulate this process might synergize with ICSBP deficiency for progression to AML.
  • Consistent with this, we found that constitutive activation of SHP2 protein tyrosine phosphatase synergized with ICSBP haploinsufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid progression to AML in a murine bone marrow transplantation model.
  • Constitutive SHP2 activation cooperated with ICSBP deficiency to increase the number of progenitors in the bone marrow and myeloid blasts in circulation, indicating a block in differentiation.
  • Since SHP2 activation and ICSBP deficiency may coexist in human myeloid malignancies, our studies have identified a molecular mechanism potentially involved in disease progression in such diseases.

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  • (PMID = 18246201.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095266; United States / NCI NIH HHS / CA / R01-CA095266
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-8; 42HK56048U / Tyrosine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2214847
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10. Soupir CP, Vergilio JA, Dal Cin P, Muzikansky A, Kantarjian H, Jones D, Hasserjian RP: Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis. Am J Clin Pathol; 2007 Apr;127(4):642-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis.
  • We performed a multi-institutional retrospective analysis of the morphologic features, immunophenotype, cytogenetics, and BCR-ABL transcript characterization of cases of Philadelphia chromosome-positive acute myeloid leukemia (Ph+ AML).
  • We compared these cases with cases of documented chronic myelogenous leukemia in myeloid blast crisis (CML-MBC).
  • Patients with Ph+ AML were less likely to have splenomegaly or peripheral basophilia and had lower bone marrow cellularity and myeloid/erythroid ratios than patients with CML-MBC.
  • Additional specific cytogenetic abnormalities that typically occur in CML-MBC were less common in Ph+ AML.
  • Of 7 patients with Ph+ AML treated with imatinib mesylate, 6 showed at least a partial hematologic response, but the responses were of a short duration (median, 2.5 months).
  • The median survival of patients with Ph+ AML was 9 months, similar to that of patients with CML-MBC (7 months).
  • Ph+ AML is a rare aggressive acute leukemia with some features distinct from CML-MBC.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antigens, CD / metabolism. Female. Fusion Proteins, bcr-abl / metabolism. Humans. Immunophenotyping. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis


11. Cencic R, Carrier M, Trnkus A, Porco JA Jr, Minden M, Pelletier J: Synergistic effect of inhibiting translation initiation in combination with cytotoxic agents in acute myelogenous leukemia cells. Leuk Res; 2010 Apr;34(4):535-41
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  • [Title] Synergistic effect of inhibiting translation initiation in combination with cytotoxic agents in acute myelogenous leukemia cells.
  • We have previously shown that inhibition of translation initiation, using the small molecule inhibitor silvestrol, induces apoptosis in a pre-clinical murine lymphoma model when combined with daunorubicin.
  • Here we investigate the sensitivity of acute myelogenous leukemia (AML) cell lines to protein synthesis inhibition in combination with the standard cytotoxic agents daunorubicin, etoposide, and cytarabine.
  • Silvestrol shows synergy with standard-of-care agents in AML cell lines and synergizes with ABT-737, a small molecule inhibitor of Bcl-X(L) and Bcl-2.
  • The in vitro synergy between silvestrol and the cytotoxic drugs used in AML therapy provides a basis for in vivo evaluation of these combinations.

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
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  • (PMID = 19726085.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM073855; Canada / Canadian Institutes of Health Research / / MOP-79385
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABT-737; 0 / Biphenyl Compounds; 0 / Cytotoxins; 0 / Nitrophenols; 0 / Peptide Initiation Factors; 0 / Piperazines; 0 / Protein Synthesis Inhibitors; 0 / Sulfonamides; 0 / Triterpenes; 0 / silvestrol; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS616104; NLM/ PMC4117193
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12. Raffoux E, Cras A, Recher C, Boëlle PY, de Labarthe A, Turlure P, Marolleau JP, Reman O, Gardin C, Victor M, Maury S, Rousselot P, Malfuson JV, Maarek O, Daniel MT, Fenaux P, Degos L, Chomienne C, Chevret S, Dombret H: Phase 2 clinical trial of 5-azacitidine, valproic acid, and all-trans retinoic acid in patients with high-risk acute myeloid leukemia or myelodysplastic syndrome. Oncotarget; 2010 May;1(1):34-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase 2 clinical trial of 5-azacitidine, valproic acid, and all-trans retinoic acid in patients with high-risk acute myeloid leukemia or myelodysplastic syndrome.
  • In this Phase 2 study, we evaluated the efficacy of combination of 5-azacitidine (AZA), valproic acid (VPA), and all-trans retinoic acid (ATRA) in patients with high-risk acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • Sixty-five patients were enrolled (median age, 72 years; 55 AML including 13 relapsed/refractory patients, 10 MDS; 30 unfavorable karyotypes).
  • Best responses included 14 CR and 3 PR (26%), 75% of the responders and 36% of the non-responders achieving an erythroid response.
  • In patients who fulfilled the 6 planned cycles, OS did not appear to depend on CR/PR achievement, suggesting that stable disease while on-treatment would be a surrogate for survival with this approach.
  • Epigenetic modulation deserves prospective comparisons to conventional care in patients with high-risk AML, at least in those presenting previously untreated disease and low blast count.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Valproic Acid / therapeutic use


13. Stevens JM, Macdougall F, Jenner M, Oakervee H, Cavenagh J, Lister AT: Patterns of recruitment into acute myeloid leukaemia (AML) 15 and outcome for young patients with AML at a single referral centre. Br J Haematol; 2009 Apr;145(1):40-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of recruitment into acute myeloid leukaemia (AML) 15 and outcome for young patients with AML at a single referral centre.
  • This study assessed the recruitment to an acute myeloid leukaemia (AML) trial (AML15) in a single centre, evaluated whether outcome was influenced by trial entry and whether the trial population could be considered representative of all AML patients by retrospective comparison of patient characteristics, trial entry and outcome for 81 consecutive patients (<60 years).
  • All patients were considered for trial entry, however the trial was not offered to 12 (15%) patients.
  • Thus the overall survival estimates generated from large phase III trials may indicate that the outcome for patients with AML is better than the outcome experienced in the 'real' world.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase III as Topic. Leukemia, Myeloid, Acute / drug therapy. Patient Selection. Randomized Controlled Trials as Topic

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  • (PMID = 19210510.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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4. Estey EH: "3+7" therapy for the treatment of acute myeloid leukemia. CON. Clin Adv Hematol Oncol; 2005 Feb;3(2):129-132, 141
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] "3+7" therapy for the treatment of acute myeloid leukemia. CON.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Drug Therapy, Combination. Humans. Middle Aged. Remission Induction. Risk Factors. Survival Analysis. Treatment Outcome

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  • [CommentIn] Clin Adv Hematol Oncol. 2005 Feb;3(2):127-9 [16166981.001]
  • (PMID = 16173152.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Phillips CL, Gerbing R, Alonzo T, Perentesis JP, Harley IT, Meshinchi S, Bhatla D, Radloff G, Davies SM: MDM2 polymorphism increases susceptibility to childhood acute myeloid leukemia: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2010 Aug;55(2):248-53
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  • [Title] MDM2 polymorphism increases susceptibility to childhood acute myeloid leukemia: a report from the Children's Oncology Group.
  • PROCEDURE: We genotyped children (n = 575) with de novo acute myeloid leukemia (AML) treated on three Children's Oncology Group protocols (CCG 2941/2961/AAML 03P1) for the presence of SNP309.
  • RESULTS: The variant G/G genotype was associated with an increased susceptibility to AML (OR 1.5; P = 0.049).
  • However, the presence of the variant allele at SNP309 did not modify disease response or toxicity in children treated on CCG protocols 2941/2961.
  • CONCLUSIONS: The variant SNP 309 influences susceptibility to pediatric AML, but does not impact overall response to therapy.

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
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  • (PMID = 20582981.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM063483-08S2; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA093552-01; United States / NINR NIH HHS / NR / R21 NR010262-01; United States / NCI NIH HHS / CA / CA 98543; United States / NCI NIH HHS / CA / CA098543-05; United States / NIGMS NIH HHS / GM / T32 GM063483; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / U10 CA098543-05; United States / NINR NIH HHS / NR / R21 NR010262; United States / NIGMS NIH HHS / GM / T32 GM063483-08S2; United States / NCI NIH HHS / CA / R01 CA093552; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA093552-01; United States / NCI NIH HHS / CA / R01 CA93552-01; United States / NINR NIH HHS / NR / NR010262-01; United States / NCI NIH HHS / CA / CA114563-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ NIHMS217002; NLM/ PMC2915901
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16. Haltrich I, Kost-Alimova M, Kovács G, Kriván G, Dobos M, Imreh S, Fekete G: [Identification of 3q21q26 syndrome by "multipoint" interphase FISH analyses in childhood myeloid leukemia]. Magy Onkol; 2005;49(2):141-7
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  • [Title] [Identification of 3q21q26 syndrome by "multipoint" interphase FISH analyses in childhood myeloid leukemia].
  • [Transliterated title] A "3q21q26-szindróma" azonosítása sokpontos interfázis-FISH vizsgálattal gyermekkori myeloid leukaemiában.
  • Cytogenetic syndrome involving bands 3q21 and 3q26, known as "3q21q26 syndrome" has been observed in adult patients with acute myelogenous leukemia (0.5-2%), chronic myelogenous leukemia in blast crisis (20%), myelodysplastic syndromes and myeloproliferative disorders.
  • In the present study bone marrow samples from two boys (12 and 16 years), diagnosed with CML and AML respectively, were investigated using conventional cytogenetic methods, interphase "multipoint" fluorescence in situ hybridization (FISH), dual color-FISH and multiplex FISH.
  • The "multipoint" FISH analysis identified in de novo childhood AML case an inv(3)(q21q26) and a complex 3q rearrangement including inversion and duplication in the CML case.
  • This syndrome is very rare in de novo childhood AML, and simultaneous presence of 3q inversion and duplication, to our knowledge, has not yet been identified in hematological malignancies.
  • The results of our study emphasize the importance of classical and modern cytogenetic analysis in the diagnosis of hematologic malignancies, because in the majority of cases they can provide additional diagnostic information for the clinicians in deciding the best therapeutic approach, precise classification and prognosis of the disease.
  • [MeSH-major] Chromosomes, Human, Pair 3. Gene Rearrangement. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16249810.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
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17. Xie C, Edwards H, Xu X, Zhou H, Buck SA, Stout ML, Yu Q, Rubnitz JE, Matherly LH, Taub JW, Ge Y: Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia. Clin Cancer Res; 2010 Nov 15;16(22):5499-510
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  • [Title] Mechanisms of synergistic antileukemic interactions between valproic acid and cytarabine in pediatric acute myeloid leukemia.
  • PURPOSE: To determine the possibility of synergistic antileukemic activity and the underlying molecular mechanisms associated with cytarabine combined with valproic acid (VPA; a histone deacetylase inhibitor and a Food and Drug Administration-licensed drug for treating both children and adults with epilepsy) in pediatric acute myeloid leukemia (AML).
  • EXPERIMENTAL DESIGN: The type and extent of antileukemic interactions between cytarabine and VPA in clinically relevant pediatric AML cell lines and diagnostic blasts from children with AML were determined by MTT assays and standard isobologram analyses.
  • The effects of cytarabine and VPA on apoptosis and cell cycle distributions were determined by flow cytometry analysis and caspase enzymatic assays.
  • RESULTS: We showed synergistic antileukemic activities between cytarabine and VPA in four pediatric AML cell lines and nine diagnostic AML blast samples. t(8;21) AML blasts were significantly more sensitive to VPA and showed far greater sensitivities to combined cytarabine and VPA than non-t(8;21) AML cases.
  • CONCLUSIONS: Our results establish global synergistic antileukemic activity of combined VPA and cytarabine in pediatric AML and provide compelling evidence to support the use of VPA in the treatment of children with this deadly disease.

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  • [Copyright] ©2010 AACR.
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  • (PMID = 20889917.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120772-01A2; United States / NCI NIH HHS / CA / R01 CA120772; United States / NCI NIH HHS / CA / CA120772; United States / NCI NIH HHS / CA / R01 CA120772-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 614OI1Z5WI / Valproic Acid; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
  • [Other-IDs] NLM/ NIHMS238223; NLM/ PMC3018695
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18. Lee SJ, Kukreja M, Wang T, Giralt SA, Szer J, Arora M, Woolfrey AE, Cervantes F, Champlin RE, Gale RP, Halter J, Keating A, Marks DI, McCarthy PL, Olavarria E, Stadtmauer EA, Abecasis M, Gupta V, Khoury HJ, George B, Hale GA, Liesveld JL, Rizzieri DA, Antin JH, Bolwell BJ, Carabasi MH, Copelan E, Ilhan O, Litzow MR, Schouten HC, Zander AR, Horowitz MM, Maziarz RT: Impact of prior imatinib mesylate on the outcome of hematopoietic cell transplantation for chronic myeloid leukemia. Blood; 2008 Oct 15;112(8):3500-7
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  • [Title] Impact of prior imatinib mesylate on the outcome of hematopoietic cell transplantation for chronic myeloid leukemia.
  • Imatinib mesylate (IM, Gleevec) has largely supplanted allogeneic hematopoietic cell transplantation (HCT) as first line therapy for chronic myeloid leukemia (CML).
  • Data from the Center for International Blood and Marrow Transplant Research on 409 subjects treated with IM before HCT (IM(+)) and 900 subjects who did not receive IM before HCT (IM(-)) were analyzed.
  • Among patients in first chronic phase, IM therapy before HCT was associated with better survival but no statistically significant differences in treatment-related mortality, relapse, and leukemia-free survival.
  • Better HLA-matched donors, use of bone marrow, and transplantation within one year of diagnosis were also associated with better survival.
  • Among patients transplanted with advanced CML, use of IM before HCT was not associated with treatment-related mortality, relapse, leukemia-free survival, or survival.
  • Acute graft-versus-host disease rates were similar between IM(+) and IM(-) groups regardless of leukemia phase.


19. Neumann F, Gattermann N, Barthelmes HU, Haas R, Germing U: Levels of beta 2 microglobulin have a prognostic relevance for patients with myelodysplastic syndrome with regard to survival and the risk of transformation into acute myelogenous leukemia. Leuk Res; 2009 Feb;33(2):232-6
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  • [Title] Levels of beta 2 microglobulin have a prognostic relevance for patients with myelodysplastic syndrome with regard to survival and the risk of transformation into acute myelogenous leukemia.
  • The risk of AML evolution was higher in patients with B2M> or =2mg/dl.
  • Using multivariate analysis we found the B2M level at the time of diagnosis to be an independent prognostic parameter for survival and for the risk of developing AML in high-risk MDS patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / diagnosis. beta 2-Microglobulin / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis. Survival Rate. Young Adult


20. 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.
  • This down-regulation was not accompanied by changes in methylation of the differentially methylated region (DMR).
  • 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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26. Fuh B, Lurito J, Grossi M, Daeschner C, Russo S: Bilateral internal carotid artery occlusions in a pediatric patient with refractory acute myeloid leukemia. Pediatr Blood Cancer; 2010 May;54(5):770-2
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  • [Title] Bilateral internal carotid artery occlusions in a pediatric patient with refractory acute myeloid leukemia.
  • Thromboembolism is a well-known complication of cancer including acute myeloid leukemia (AML) especially in patients with high myeloblast counts.
  • We report the case of a 3-year-old male with refractory AML who developed spontaneous bilateral internal carotid artery occlusion with diffuse cerebral infarcts.
  • [MeSH-major] Carotid Artery, Internal. Carotid Stenosis / etiology. Cerebral Infarction / etiology. Leukemia, Myeloid, Acute / complications

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  • (PMID = 20052773.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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27. Cripe LD, Rader K, Tallman MS, Gordon MS, Paietta E, Bennett J, Neuberg D, Litzow MR, O'brien TE, Rowe JM: Phase II trial of subcutaneous recombinant human interleukin 11 with subcutaneous recombinant human granulocyte-macrophage colony stimulating factor in patients with acute myeloid leukemia (AML) receiving high-dose cytarabine during induction: ECOG 3997. Leuk Res; 2006 Jul;30(7):823-7
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  • [Title] Phase II trial of subcutaneous recombinant human interleukin 11 with subcutaneous recombinant human granulocyte-macrophage colony stimulating factor in patients with acute myeloid leukemia (AML) receiving high-dose cytarabine during induction: ECOG 3997.
  • Randomized trials of substituting high-dose cytarabine (HiDAC) for standard dose cytarabine (SDAC) during induction therapy for newly diagnosed AML have not demonstrated an improvement in the complete remission (CR) rate.
  • Therefore, 34 patients were treated, with newly diagnosed AML less than 56 years of age, with daunorubicin 45 mg/m2 on days 1-3, cytarabine 100mg/m2 days 1-7 and cytarabine 2g/m2 for 12 h on days 8-10 (7+3+3).
  • The trial does not confirm the high CR rate observed in phase II trials, despite optimal supportive care.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Interleukin-11 / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Injections, Subcutaneous. Male. Middle Aged. Recombinant Proteins / administration & dosage. Remission Induction. Survival Rate. Treatment Outcome

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  • (PMID = 16413056.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA11083; United States / NCI NIH HHS / CA / CA13650; United States / NCI NIH HHS / CA / CA14548; United States / NCI NIH HHS / CA / CA17145; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / CA23318; United States / NCI NIH HHS / CA / CA49883; United States / NCI NIH HHS / CA / CA66636
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IL11 protein, human; 0 / Interleukin-11; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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28. Kawaguchi-Ihara N, Murohashi I, Nara N, Tohda S: Promotion of the self-renewal capacity of human acute leukemia cells by Wnt3A. Anticancer Res; 2008 Sep-Oct;28(5A):2701-4
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  • [Title] Promotion of the self-renewal capacity of human acute leukemia cells by Wnt3A.
  • MATERIALS AND METHODS: The effects of recombinant Wnt3A protein on the in vitro growth of four acute myeloid leukemia (AML) and four acute T-lymphoblastic leukemia (T-ALL) cell lines was examined.
  • RESULTS: Wnt3A stimulation either had no effect on, or slightly suppressed, the short-term growth of these cell lines.
  • In three cell lines, Wnt3A promoted clonogenic cell recovery after suspension culture, suggesting the promotion of the self-renewal capacity of leukemic stem or progenitor cells.
  • CONCLUSION: Wnt3A stimulation did not promote the growth of whole cell populations, but did promote the self-renewal of leukemic stem/progenitor cells in some AML and T-ALL cell lines.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Wnt Proteins / pharmacology
  • [MeSH-minor] Acute Disease. Antigens, CD34 / biosynthesis. Antigens, CD38 / biosynthesis. Calcium-Binding Proteins / biosynthesis. Calcium-Binding Proteins / genetics. Cell Growth Processes / drug effects. Cell Line, Tumor. Gene Expression / drug effects. Humans. Intercellular Signaling Peptides and Proteins / biosynthesis. Intercellular Signaling Peptides and Proteins / genetics. Membrane Proteins / biosynthesis. Membrane Proteins / genetics. Neoplastic Stem Cells / drug effects. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptor, Notch1 / biosynthesis. Receptor, Notch1 / genetics. Recombinant Proteins / pharmacology. Wnt3 Protein. Wnt3A Protein

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  • (PMID = 19035298.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Calcium-Binding Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / NOTCH1 protein, human; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Recombinant Proteins; 0 / WNT3A protein, human; 0 / Wnt Proteins; 0 / Wnt3 Protein; 0 / Wnt3A Protein; 134324-36-0 / Serrate proteins; EC 3.2.2.5 / Antigens, CD38
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29. Rulina AV, Spirin PV, Prassolov VS: Activated leukemic oncogenes AML1-ETO and c-kit: role in development of acute myeloid leukemia and current approaches for their inhibition. Biochemistry (Mosc); 2010 Dec;75(13):1650-66
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  • [Title] Activated leukemic oncogenes AML1-ETO and c-kit: role in development of acute myeloid leukemia and current approaches for their inhibition.
  • Acute myeloid leukemia (AML) is a malignant blood disease caused by different mutations that enhance the proliferative activity and survival of blood cells and affect their differentiation and apoptosis.
  • The most frequent disorders in AML are translocations between chromosomes 21 and 8 leading to production of a chimeric oncogene, AML1-ETO, and hyperexpression of the receptor tyrosine kinase KIT.
  • The current approaches for treatment of oncologic diseases (bone marrow transplantation, radiotherapy, and chemotherapy) have significant shortcomings, and thus many laboratories are intensively developing new approaches against leukemias.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / antagonists & inhibitors. Core Binding Factor Alpha 2 Subunit / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / therapy. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / metabolism. Proto-Oncogene Proteins c-kit / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / metabolism

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  • (PMID = 21417999.001).
  • [ISSN] 1608-3040
  • [Journal-full-title] Biochemistry. Biokhimii︠a︡
  • [ISO-abbreviation] Biochemistry Mosc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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30. Vigil CE, Martin-Santos T, Garcia-Manero G: Safety and efficacy of azacitidine in myelodysplastic syndromes. Drug Des Devel Ther; 2010;4:221-9
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  • SUMMARY: Azacitidine is the first drug FDA-approved for the treatment of myelodysplastic syndromes that has demonstrated improvements in overall survival and delaying time to progression to acute myelogenous leukemia.
  • [MeSH-minor] Disease Progression. Drug Administration Schedule. Humans. Leukemia, Myeloid, Acute / prevention & control. Survival

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  • (PMID = 20957213.001).
  • [ISSN] 1177-8881
  • [Journal-full-title] Drug design, development and therapy
  • [ISO-abbreviation] Drug Des Devel Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2948932
  • [Keywords] NOTNLM ; Azacitidine / MDS / hypomethylating agents
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31. Wang X, Schmitt A, Chen B, Xu X, Mani J, Linnebacher M, Freund M, Schmitt M: Streptamer-based selection of WT1-specific CD8+ T cells for specific donor lymphocyte infusions. Exp Hematol; 2010 Nov;38(11):1066-73
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  • [Title] Streptamer-based selection of WT1-specific CD8+ T cells for specific donor lymphocyte infusions.
  • OBJECTIVE: Donor lymphocyte infusions may generate a desirable graft-versus-leukemia effect, but also elicit a noxious graft-versus-host disease.
  • A positive selection of leukemia (antigen)-specific T cells would be highly desirable.
  • In this study, we focused on the immunogenic leukemia antigen Wilms' Tumor gene 1 (WT1).
  • Then, specific cells were labeled with streptamers and selected by magnetic cell separation.
  • RESULTS: Twenty-one of 40 healthy donors had naïve WT1-specific CD8(+) T-cell frequencies of >0.5%, and 8 of 40 even >1.0% of all CD8(+) T cells.
  • In 7 of 10 acute myeloid leukemia patients, the frequencies were 0.5% to 3.65%.
  • After positive selection by magnetic cell separation, a 60-fold increase with a purity of up to 17.79% in the lymphocyte gate and 86.18% in the CD8(+) T-cell gate could be achieved for CD8(+)WT1 streptamer(+)CD28(+/-)CD45RA(+)CCR7(-) effector T cells.
  • This is a prerequisite for clinical applications targeting tumor-specific antigens, such as adoptive T-cell transfer.
  • [MeSH-minor] Acute Disease. Adoptive Transfer / methods. Antigens, CD28 / immunology. Antigens, CD28 / metabolism. Antigens, CD45 / immunology. Antigens, CD45 / metabolism. Cell Separation / methods. Flow Cytometry. Humans. Immunophenotyping. Leukemia, Myeloid / blood. Magnetics. Receptors, CCR7 / immunology. Receptors, CCR7 / metabolism

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  • [Copyright] Copyright © 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20637829.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD28; 0 / CCR7 protein, human; 0 / HLA-A2 Antigen; 0 / Receptors, CCR7; 0 / WT1 Proteins; EC 3.1.3.48 / Antigens, CD45
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32. Montesinos JJ, Sánchez-Valle E, Flores-Figueroa E, Martínez-Jaramillo G, Flores-Guzmán P, Miranda-Peralta E, Gutiérrez-Romero M, Mayani H: Deficient proliferation and expansion in vitro of two bone marrow cell populations from patients with acute myeloid leukemia in response to hematopoietic cytokines. Leuk Lymphoma; 2006 Jul;47(7):1379-86
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  • [Title] Deficient proliferation and expansion in vitro of two bone marrow cell populations from patients with acute myeloid leukemia in response to hematopoietic cytokines.
  • One has previously characterized two different hematopoietic cell populations (obtained by negative-selection) from normal bone marrow.
  • One has also characterized the chronic myeloid leukemia (CML) counterparts of these two populations and demonstrated functional deficiencies in terms of their growth in culture.
  • In keeping with this line of research, the goal of the present study was to obtain the same two populations (Populations I and II) from acute myeloid leukemia (AML) bone marrow and to characterize their biological behavior under the same culture conditions.
  • The results demonstrated that AML-derived Populations I and II were unable to proliferate in culture conditions that allowed significant proliferation of Populations I and II from normal marrow.
  • Population I from AML also showed a deficient expansion capacity; in contrast, Population II cells were able to expand to a similar extent to the one observed for Population II from normal marrow.
  • Both normal and AML populations were highly sensitive to the inhibitory effects of TNF-alpha; interestingly, whereas in normal fractions TNF-alpha showed a more pronounced inhibitory effect on more mature cells (Population I), this cytokine inhibited proliferation and expansion of AML Populations I and II in a similar degree.
  • It is noteworthy that the functional deficiencies observed in AML cells were even more pronounced than those previously reported for cultures of CML cells.
  • [MeSH-major] Bone Marrow / metabolism. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Cytokines / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adolescent. Adult. Antigens, CD34 / biosynthesis. Antigens, CD38 / biosynthesis. Cell Culture Techniques / methods. Cell Proliferation. Culture Media, Serum-Free. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Male. Middle Aged. Stem Cells / metabolism

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  • (PMID = 16923572.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Culture Media, Serum-Free; 0 / Cytokines; EC 3.2.2.5 / Antigens, CD38
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33. Ruan GR, Li JL, Qin YZ, Li LD, Xie M, Chang Y, Zhang Y, Liu YR, Jiang B, Chen SS, Huang XJ: Nucleophosmin mutations in Chinese adults with acute myelogenous leukemia. Ann Hematol; 2009 Feb;88(2):159-66
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  • [Title] Nucleophosmin mutations in Chinese adults with acute myelogenous leukemia.
  • Recently, mutations in the nucleophosmin (NPM1) gene were detected in 50-60% of adult acute myelogenous leukemia (AML) patients, mainly with a normal karyotype.
  • In this study, we detected typical NPM1 mutations (types A, B, D) in untreated Chinese AML patients using real-time quantitative polymerase chain reaction (RQ-PCR) followed by sequence analysis.
  • The detection rate of NPM1 mutations in 220 AML patients was 16.4%, including 107 (14.2%) with the French-American-British (FAB) subtype M2, 43 (2.3%) with M3, and 52 (30.8%) with M4/M5.
  • Only one case each with an NPM1 mutation was detected in four M0, seven M1, five M6, and two M7 cases.
  • Further, 38.9% (14/36) patients with NPM1 mutations simultaneously exhibited internal tandem duplications in the FLT3 gene, and 66.7% (22/33) patients did not express CD34.
  • The results demonstrated that RQ-PCR was a reliable and sensitive method for detecting NPM1 mutations, for screening AML, and for the quantitative analysis of minimal residual diseases.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics


34. Venizelos ID, Klonizakis I, Vlahaki E, Haralambidou S, Tatsiou Z, Ioannidou E: Skin relapse of acute myeloid leukemia associated with trisomy 8. Acta Dermatovenerol Alp Pannonica Adriat; 2007 Jun;16(2):77-80
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  • [Title] Skin relapse of acute myeloid leukemia associated with trisomy 8.
  • Acute myeloid leukemia (AML) is a morphologically diverse group of hematopoietic malignancies characterized by proliferation of immature cells that arise in the myeloid progenitor cells of the bone marrow.
  • It shows cutaneous lesions relatively rarely.
  • An association of AML with skin involvement and trisomy 8 has rarely been reported.
  • We present the case of a 74-year-old woman that presented with fatigue, nausea, dyspnea, and night sweats.
  • Accordingly, a diagnosis of AML involving the skin was made.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / pathology. Skin Neoplasms / pathology. Trisomy

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  • (PMID = 17992463.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
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35. Buccisano F, Maurillo L, Gattei V, Del Poeta G, Del Principe MI, Cox MC, Panetta P, Consalvo MI, Mazzone C, Neri B, Ottaviani L, Fraboni D, Tamburini A, Lo-Coco F, Amadori S, Venditti A: The kinetics of reduction of minimal residual disease impacts on duration of response and survival of patients with acute myeloid leukemia. Leukemia; 2006 Oct;20(10):1783-9
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  • [Title] The kinetics of reduction of minimal residual disease impacts on duration of response and survival of patients with acute myeloid leukemia.
  • We assessed by multiparametric flow cytometry the levels of minimal residual disease (MRD) in 100 adult patients with acute myelogenous leukemia (AML) achieving complete remission after intensive chemotherapy.
  • By applying the maximally selected log-rank statistics, the threshold discriminating MRD- from MRD+ cases was set at 3.5 x 10(-4) residual leukemic cells, a level that allowed the identification of distinct subgroups of patients, both at post-Ind and post-Cons time points.
  • (1) the threshold of 3.5 x 10(-4) is valid in discriminating risk categories in adult AML and (2) post-Cons MRD assessment is critical to predict disease outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / pathology. Neoplasm, Residual / mortality. Neoplasm, Residual / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Disease-Free Survival. Female. Flow Cytometry. Humans. Immunophenotyping. Kinetics. Male. Middle Aged. Multivariate Analysis. Predictive Value of Tests. Prognosis. Remission Induction. Survival Analysis

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  • (PMID = 16838027.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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36. Aref S, El-Sherbiny M, Azmy E, Goda T, Selim T, El-Refaie M, Emaad T: Elevated serum endostatin levels is associated with favorable outcome in acute myeloid leukemia. Indian J Hematol Blood Transfus; 2008 Mar;24(1):1-6
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  • [Title] Elevated serum endostatin levels is associated with favorable outcome in acute myeloid leukemia.
  • The levels and the prognostic relevance of serum endostatin in AML patient is not fully clear.
  • AIM: To evaluate serum levels of endostatin in acute myeloid leukemia patients before chemotherapy and after achieving complete remission and to correlate endostatin levels with patients outcome.
  • MATERIALS AND METHODS: Serum samples from 30 adult patients (22 males and 8 females, median age 37, range 19-66 years) with AML had been taken before chemotherapy was administered.
  • RESULTS: Endostatin serum levels were not significantly different in the pretreatment AML patients as compared to that in normal controls (P>0.05).
  • In AML patients the baseline endostatin levels were significantly lower than at CR (P=0.001).
  • No significant correlation were detected between pretreatment serum endostatin levels and age, peripheral blood white cell counts, platelet counts, bone marrow blast cell counts, blast cell distribution ratio.
  • The prognostic value of sE was also evaluated by dividing AML patients into high and low sE groups using the 75 percentile sE levels of the patients group as cutoff.
  • CONCLUSIONS: Elevated endostatin levels at AML diagnosis is a good prognostic marker for patients' outcome.

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  • (PMID = 23100932.001).
  • [ISSN] 0971-4502
  • [Journal-full-title] Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
  • [ISO-abbreviation] Indian J Hematol Blood Transfus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3453162
  • [Keywords] NOTNLM ; AML / Angiogenesis / Endostatin / Prognosis
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37. LaFiura KM, Edwards H, Taub JW, Matherly LH, Fontana JA, Mohamed AN, Ravindranath Y, Ge Y, Children's Oncology Group: Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children's Oncology Group. Oncogene; 2008 Aug 21;27(36):4933-42
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  • [Title] Identification and characterization of novel AML1-ETO fusion transcripts in pediatric t(8;21) acute myeloid leukemia: a report from the Children's Oncology Group.
  • t(8;21)(q22;q22) results in the AML1-ETO (A1E) fusion gene and is a common cytogenetic abnormality in acute myeloid leukemia (AML).
  • By RT-PCR amplifications and DNA sequencing, numerous in-frame and out-of-frame AML1b-ETO and AML1c-ETO transcripts were identified in 13 pediatric t(8;21) AMLs, likely resulting from alternate splicing, internal deletions and/or breakpoint region insertions involving both the AML1 (RUNX1) and ETO regions.
  • These structure alterations were found in AML1c-ETO but not AML1b-ETO transcripts in two adult t(8;21) AMLs.
  • When transfected into HeLa cells, only AML1b, and not the in-frame A1E forms, transactivated the GM-CSF promoter.

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  • (PMID = 18469864.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA092308; United States / NCI NIH HHS / CA / CA30969; United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / R01 CA076641; United States / NCI NIH HHS / CA / CA76641; United States / NCI NIH HHS / CA / P30 CA022453; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / CA92308
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS505499; NLM/ PMC3763903
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38. Perkins JL, Kunin-Batson AS, Youngren NM, Ness KK, Ulrich KJ, Hansen MJ, Petryk A, Steinberger J, Anderson FS, Baker KS: Long-term follow-up of children who underwent hematopoeitic cell transplant (HCT) for AML or ALL at less than 3 years of age. Pediatr Blood Cancer; 2007 Dec;49(7):958-63
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  • [Title] Long-term follow-up of children who underwent hematopoeitic cell transplant (HCT) for AML or ALL at less than 3 years of age.
  • BACKGROUND: Hematopoeitic cell transplantation (HCT) in childhood has been associated with late complications including endocrine, neurocognitive, and cardiopulmonary abnormalities.
  • PROCEDURE: Eligible subjects underwent HCT for acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML) at less than 3 years of age.
  • Eleven patients had AML, 11 were female.
  • Dyslipidemias affect more than half of patients and may be associated with metabolic syndrome, placing patients at increased risk for early cardiovascular disease.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation Conditioning
  • [MeSH-minor] Child, Preschool. Dyslipidemias / pathology. Female. Follow-Up Studies. Humans. Infant. Male. Metabolic Syndrome X / diagnosis. Quality of Life. Risk Factors. Survival Rate. Time. Transplantation, Homologous. Treatment Outcome. Whole-Body Irradiation


39. Bereshchenko O, Mancini E, Moore S, Bilbao D, Månsson R, Luc S, Grover A, Jacobsen SE, Bryder D, Nerlov C: Hematopoietic stem cell expansion precedes the generation of committed myeloid leukemia-initiating cells in C/EBPalpha mutant AML. Cancer Cell; 2009 Nov 06;16(5):390-400
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  • [Title] Hematopoietic stem cell expansion precedes the generation of committed myeloid leukemia-initiating cells in C/EBPalpha mutant AML.
  • We here use knockin mutagenesis in the mouse to model the spectrum of acquired CEBPA mutations in human acute myeloid leukemia.
  • We find that C-terminal C/EBPalpha mutations increase the proliferation of long-term hematopoietic stem cells (LT-HSCs) in a cell-intrinsic manner and override normal HSC homeostasis, leading to expansion of premalignant HSCs.
  • However, such mutations impair myeloid programming of HSCs and block myeloid lineage commitment when homozygous.
  • In contrast, N-terminal C/EBPalpha mutations are silent with regards to HSC expansion, but allow the formation of committed myeloid progenitors, the templates for leukemia-initiating cells.
  • The combination of N- and C-terminal C/EBPalpha mutations incorporates both features, accelerating disease development and explaining the clinical prevalence of this configuration of CEBPA mutations.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Cell Transformation, Neoplastic / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Animals. Cell Cycle / physiology. Cell Growth Processes / physiology. Cell Line. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cell Transplantation. Humans. Mice. Mice, Knockout


40. Fujita A, Fujisawa S, Hyo R, Kuwabara H, Yamazaki E, Tomita N, Ishigatsubo Y: [Discrepant results of ABO type of red cells and serum in a patient with acute myelogenous leukemia]. Rinsho Ketsueki; 2008 Jan;49(1):51-4
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  • [Title] [Discrepant results of ABO type of red cells and serum in a patient with acute myelogenous leukemia].
  • A 42-year-old woman was admitted to our hospital with acute myelogenous leukemia.
  • We should be aware that blood group antigens are not entirely independent of the environment and are occasionally modified by disease.
  • [MeSH-major] ABO Blood-Group System / immunology. Blood Grouping and Crossmatching. Leukemia, Myeloid, Acute / blood

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  • (PMID = 18277597.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ABO Blood-Group System; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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41. Dick JE: Acute myeloid leukemia stem cells. Ann N Y Acad Sci; 2005 Jun;1044:1-5
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  • [Title] Acute myeloid leukemia stem cells.
  • The concept that only a subpopulation of rare cancer stem cells (CSCs) is responsible for maintenance of the neoplasm emerged nearly 50 years ago; however, conclusive proof for the existence of a CSC was obtained only relatively recently.
  • The evidence for the existence of CSCs was first derived from the study of human acute myeloid leukemia (AML), largely because of the availability of quantitative stem cell assays for the leukemic stem cell (LSC).
  • These studies showed that only rare cells within the leukemic clone had the capacity to initiate AML growth after transplant into NOD/SCID mice, establishing the hierarchical organization of AML.
  • These findings have important implications for our understanding of the leukemogenic process as well as the design of more effective therapies to eliminate AML based on eradication of the LSCs.
  • [MeSH-major] Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Animals. Humans. Neoplastic Stem Cells / classification. Neoplastic Stem Cells / pathology. Neoplastic Stem Cells / transplantation


42. Lahaye T, Riehm B, Berger U, Paschka P, Müller MC, Kreil S, Merx K, Schwindel U, Schoch C, Hehlmann R, Hochhaus A: Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up. Cancer; 2005 Apr 15;103(8):1659-69
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  • [Title] Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up.
  • BACKGROUND: The advent of imatinib has considerably changed the treatment of chronic myeloid leukemia (CML).
  • Early studies demonstrated high rates of hematologic and cytogenetic responses in all phases of the disease after limited observation periods.
  • METHODS: The authors evaluated long-term outcome, rates of response, and resistance in 300 patients with BCR-ABL-positive leukemias (CML in chronic phase after failure to respond to interferon-alpha [CP], n = 139; accelerated phase [AP], n = 80; myeloid blast crisis [BC], n = 76; lymphoid BC and Philadelphia chromosome-positive acute lymphoblastic leukemia, n = 5) who entered clinical trials with imatinib in a single center after an observation time of 4.5 years.
  • In myeloid BC, the median survival period after the start of imatinib and after diagnosis of BC was 6 and 9 months, respectively.
  • Hematologic resistance occurred in 25%, 41%, and 92% of patients in CP, AP, and myeloid BC, respectively, and was associated with BCR-ABL mutations in 45% of patients and with clonal evolution in 58% of patients.
  • CONCLUSIONS: The data emphasized the need for a prolonged follow-up of patients treated with imatinib to define the clinical potential of the drug and to establish methods to optimize therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Blast Crisis. Cytogenetic Analysis. Female. Humans. Imatinib Mesylate. Interferon-alpha / adverse effects. Male. Middle Aged. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Salvage Therapy. Survival Rate. Treatment Outcome

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 15747376.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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43. Braess J, Spiekermann K, Staib P, Grüneisen A, Wörmann B, Ludwig WD, Serve H, Reichle A, Peceny R, Oruzio D, Schmid C, Schiel X, Hentrich M, Sauerland C, Unterhalt M, Fiegl M, Kern W, Buske C, Bohlander S, Heinecke A, Baurmann H, Beelen DW, Berdel WE, Büchner T, Hiddemann W: Dose-dense induction with sequential high-dose cytarabine and mitoxantone (S-HAM) and pegfilgrastim results in a high efficacy and a short duration of critical neutropenia in de novo acute myeloid leukemia: a pilot study of the AMLCG. Blood; 2009 Apr 23;113(17):3903-10
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  • [Title] Dose-dense induction with sequential high-dose cytarabine and mitoxantone (S-HAM) and pegfilgrastim results in a high efficacy and a short duration of critical neutropenia in de novo acute myeloid leukemia: a pilot study of the AMLCG.
  • Dose density during early induction has been demonstrated to be one of the prime determinants for treatment efficacy in acute myeloid leukemia (AML).
  • The German AML Cooperative Group has therefore piloted a dose-dense induction regimen sequential high-dose AraC and mitoxantrone followed by pegfilgrastim (S-HAM) in which 2 induction cycles are applied over 11 to 12 days instead of 25 to 29 days as used in conventional double induction, thereby increasing dose density 2-fold.
  • Of 172 de novo AML patients (excluding acute promyelocytic leukemia), 61% reached a complete remission, 22% a complete remission with incomplete peripheral recovery, 7% had persistent leukemia, 10% died (early death) resulting in an overall response rate of 83%.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Mitoxantrone / therapeutic use. Neutropenia / chemically induced

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  • (PMID = 19131552.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3A58010674 / pegfilgrastim; BZ114NVM5P / Mitoxantrone; PVI5M0M1GW / Filgrastim
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44. Wykrzykowska JJ, Carrozza J, Laham RJ: Aortocoronary dissection with acute left main artery occlusion: successful treatment with emergent stenting. J Invasive Cardiol; 2006 Aug;18(8):E217-20
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  • [Title] Aortocoronary dissection with acute left main artery occlusion: successful treatment with emergent stenting.
  • Of the type-A dissections in the International Registry of Aortic Dissections (IRAD), 27% were caused by coronary interventions.
  • [MeSH-major] Aneurysm, Dissecting / therapy. Aortic Aneurysm / therapy. Coronary Aneurysm / therapy. Coronary Disease / therapy. Stents

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  • (PMID = 16877790.001).
  • [ISSN] 1557-2501
  • [Journal-full-title] The Journal of invasive cardiology
  • [ISO-abbreviation] J Invasive Cardiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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45. Markovic A, MacKenzie KL, Lock RB: FLT-3: a new focus in the understanding of acute leukemia. Int J Biochem Cell Biol; 2005 Jun;37(6):1168-72
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  • [Title] FLT-3: a new focus in the understanding of acute leukemia.
  • FLT-3 is also expressed in the majority of acute leukemias, in which the presence of FLT-3 activating mutations is associated with poor prognosis.
  • Consequently, there has been a recent surge in the development of FLT-3 inhibitors for the molecular targeting of leukemia, and many of these are now in clinical trials.
  • An improved understanding of how FLT-3 interacts with its ligand, as well as how FLT-3 activating mutations are able to trigger downstream intracellular signaling pathways, will provide greater insight to how small molecule inhibitors may best be utilized and combined with established chemotherapeutic drugs for the management of patients with high-risk acute leukemia.
  • [MeSH-major] Leukemia, Myeloid / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Proto-Oncogene Proteins / physiology. Receptor Protein-Tyrosine Kinases / physiology
  • [MeSH-minor] Acute Disease. Clinical Trials as Topic. Hematopoiesis. Humans. Signal Transduction / physiology. fms-Like Tyrosine Kinase 3

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  • (PMID = 15778081.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 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
  • [Number-of-references] 21
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46. Evrard AS, Hémon D, Billon S, Laurier D, Jougla E, Tirmarche M, Clavel J: Ecological association between indoor radon concentration and childhood leukaemia incidence in France, 1990-1998. Eur J Cancer Prev; 2005 Apr;14(2):147-57
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  • [Title] Ecological association between indoor radon concentration and childhood leukaemia incidence in France, 1990-1998.
  • The objective of this study was to evaluate the ecological association between indoor radon concentration and acute leukaemia incidence among children under 15 years of age in the 348 geographical units (zones d'emploi, ZE) of France between 1990 and 1998.
  • During that period, 4015 cases were registered by the French National Registry of Childhood Leukaemia and Lymphoma.
  • A positive ecological association, on the borderline of statistical significance (P=0.053), was observed between indoor radon concentration and childhood leukaemia incidence.
  • The association was highly significant for acute myeloid leukaemia (AML) (P=0.004) but not for acute lymphocytic leukaemia (ALL) (P=0.49).
  • The standardized incidence ratio (SIR) increased by 7, 3 and 24% for all acute leukaemia, ALL and AML, respectively, when radon concentration increased by 100 Bq/m.
  • In conclusion, the present ecological study supports the hypothesis of a moderate association between indoor radon concentration and childhood acute myeloid leukaemia.
  • Since the association is moderate, this result does not appear inconsistent with the five published case-control studies, most of which found no significant association.
  • [MeSH-major] Air Pollution, Indoor / adverse effects. Environmental Exposure. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Radon / adverse effects. Registries / statistics & numerical data

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  • (PMID = 15785319.001).
  • [ISSN] 0959-8278
  • [Journal-full-title] European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP)
  • [ISO-abbreviation] Eur. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] Q74S4N8N1G / Radon
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47. Tsurumi H, Kanemura N, Hara T, Kasahara S, Yamada T, Sawada M, Oyama M, Moriwaki H: Therapeutic strategy of untreated de novo acute myeloid leukemia in the elderly: the efficacy of continuous drip infusion with low dose cytarabine and etoposide. J Cancer Res Clin Oncol; 2007 Aug;133(8):547-53
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  • [Title] Therapeutic strategy of untreated de novo acute myeloid leukemia in the elderly: the efficacy of continuous drip infusion with low dose cytarabine and etoposide.
  • PURPOSE: To evaluate the efficacy and safety of a novel low dose chemotherapy as a remission induction regimen for elderly de novo AML patients ineligible for intensive chemotherapy.
  • METHOD: Fifty consecutive patients, aged 60 to 85, with untreated de novo AML were enrolled.
  • Patients with poor PS or defined non-hematological complications were given continuous drip infusion of low dose cytarabine (Ara-C), 20 mg/body and etoposide (VP-16), 50 mg/body for 10 days (AV group).
  • CONCLUSION: Therapeutic strategy consisting of remission induction using AV regimen and consolidation using intensive regimen after improving PS is beneficial in the management of elderly AML patients who have difficulty in tolerating for intensive induction chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Drug Administration Schedule. Etoposide / administration & dosage. Female. Humans. Infusions, Intravenous. Kaplan-Meier Estimate. Male. Middle Aged. Remission Induction. Treatment Outcome

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  • (PMID = 17453240.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
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  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide
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48. Hatfield K, Øyan AM, Ersvaer E, Kalland KH, Lassalle P, Gjertsen BT, Bruserud Ø: Primary human acute myeloid leukaemia cells increase the proliferation of microvascular endothelial cells through the release of soluble mediators. Br J Haematol; 2009 Jan;144(1):53-68
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  • [Title] Primary human acute myeloid leukaemia cells increase the proliferation of microvascular endothelial cells through the release of soluble mediators.
  • Bone marrow angiogenesis is suggested to play a role in the pathogenesis of acute myeloid leukaemia (AML) and endothelial cells may mediate chemosensitivity.
  • This study investigated in vitro endothelial effects of coculture of microvascular endothelial cells (MVEC) with AML cells derived from 33 consecutive AML patients.
  • A proliferation assay showed that (i) AML cells from the majority of patients examined increased endothelial cell proliferation, while cytokine neutralizing experiments had divergent effects on proliferation and (ii) the angiopoietin/Tie2 system was important for growth of AML cells, and angiopoietin-1 induced phosphorylation of signal transducers and activators of transcription (STAT) proteins in AML cells.
  • Finally, gene expression profiling of MVEC cocultured with AML cells was conducted in non-contact cultures.
  • Microarray analysis revealed that the majority of significantly expressed genes could be categorized into gene ontology terms involved in transcription, cellular organization and intracellular signalling.
  • Our study indicates a role for the leukaemic-endothelium crosstalk in leukaemogenesis with enhancement of endothelial cell growth and increased AML cell proliferation possibly mediated by angiopoietin-1 and the STAT signalling pathway.
  • [MeSH-major] Angiopoietin-1 / metabolism. Endothelial Cells / pathology. Leukemia, Myeloid, Acute / pathology. STAT Transcription Factors / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Cell Proliferation. Chemokine CXCL10 / genetics. Chemokine CXCL11 / genetics. Chemokine CXCL9 / genetics. Coculture Techniques. Female. Gene Expression Profiling. Humans. Interleukin-8 / genetics. Lung / blood supply. Male. Microcirculation. Middle Aged. Molecular Sequence Data. Neovascularization, Pathologic. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Up-Regulation

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  • (PMID = 19016730.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiopoietin-1; 0 / Chemokine CXCL10; 0 / Chemokine CXCL11; 0 / Chemokine CXCL9; 0 / Interleukin-8; 0 / STAT Transcription Factors
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49. Ciurea SO, Andersson BS: Busulfan in hematopoietic stem cell transplantation. Biol Blood Marrow Transplant; 2009 May;15(5):523-36
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  • [Title] Busulfan in hematopoietic stem cell transplantation.
  • The development of intravenous busulfan (Bu) and its incorporation in the preparative regimens for allogeneic stem cell transplantation has changed transplantation for myelogenous malignancies.
  • Bypassing the oral route to achieve 100% bioavailability translated into improved control over drug administration, with increased safety and reliability of generating therapeutic Bu levels, maximizing antileukemic efficacy.
  • Bu-nucleoside analog-based conditioning chemotherapy, thus far represented by fludarabine (Flu), is becoming the conditioning chemotherapy regimen of choice for patients with acute myelogenous leukemia (AML) at many transplant centers.
  • The use of busulfan Bu-based conditioning is extending rapidly also to hematopoietic stem cell transplantation (HSCT) for lymphoid malignancies, genetic diseases, and umbilical cord blood transplantation.

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  • (PMID = 19361744.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; G1LN9045DK / Busulfan
  • [Number-of-references] 115
  • [Other-IDs] NLM/ NIHMS111769; NLM/ PMC4261695
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50. Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR: Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia. Blood; 2005 Jan 15;105(2):584-91
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  • [Title] Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia.
  • Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections.
  • In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
  • Here, we report a novel mutation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN without AML who was refractory to G-CSF treatment.
  • Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.

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  • (PMID = 15353486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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51. Sacchi S, Marcheselli L, Bari A, Marcheselli R, Pozzi S, Luminari S, Lombardo M, Buda G, Lazzaro A, Gobbi PG, Stelitano C, Morabito F, Quarta G, Brugiatelli M: Secondary malignancies after treatment for indolent non-Hodgkin's lymphoma: a 16-year follow-up study. Haematologica; 2008 Mar;93(3):398-404
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  • [Title] Secondary malignancies after treatment for indolent non-Hodgkin's lymphoma: a 16-year follow-up study.
  • BACKGROUND: Relatively little information is available on the incidence of secondary cancer in non-Hodgkin's lymphoma.
  • The aim of this long-term follow-up study was to determine the incidence, the time free of second tumors, and risk factors for developing secondary cancer in a homogeneous group of patients with non-Hodgkin's lymphoma.
  • DESIGN AND METHODS: We evaluated a total of 563 patients with indolent non-Hodgkin's lymphoma enrolled in Gruppo Italiano Studio Linfomi trials from 1988 to 2003.
  • RESULTS: After a median follow-up of 62 months, 39 patients (6.9%) developed secondary cancer: 12 myelodysplastic syndromes/acute myeloid leukemia, and 27 solid tumors.
  • The overall standardized incidence ratio of secondary malignancy in patients with non-Hodgkin's lymphoma was higher than the risk of malignancy in the general population.
  • Univariate and multivariate Cox regression analyses showed that older age at the time of diagnosis, male sex, and fludarabine-containing therapy had significant negative impacts on the time free of second tumors.
  • CONCLUSIONS: We have identified subgroups of non-Hodgkin's lymphoma patients with increased standardized incidence ratios of secondary malignancy and variables that have a negative impact on the time free of second tumors.
  • [MeSH-major] Lymphoma, Non-Hodgkin / therapy. Neoplasms, Second Primary / epidemiology
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms / epidemiology. Breast Neoplasms / etiology. Female. Follow-Up Studies. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Incidence. Italy / epidemiology. Leukemia, Myeloid / epidemiology. Leukemia, Myeloid / etiology. Male. Middle Aged. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / etiology. Neoplasms, Radiation-Induced / epidemiology. Neoplasms, Radiation-Induced / etiology. Radioimmunotherapy / adverse effects. Radiotherapy / adverse effects. Transplantation, Autologous / adverse effects. Vidarabine / administration & dosage. Vidarabine / adverse effects. Vidarabine / analogs & derivatives

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  • [CommentIn] Haematologica. 2008 Jul;93(7):e57; author reply e58 [18591617.001]
  • [CommentIn] Haematologica. 2008 Mar;93(3):336-8 [18310538.001]
  • (PMID = 18268277.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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52. Kojima K, Konopleva M, Samudio IJ, Ruvolo V, Andreeff M: Mitogen-activated protein kinase kinase inhibition enhances nuclear proapoptotic function of p53 in acute myelogenous leukemia cells. Cancer Res; 2007 Apr 1;67(7):3210-9
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  • [Title] Mitogen-activated protein kinase kinase inhibition enhances nuclear proapoptotic function of p53 in acute myelogenous leukemia cells.
  • Activation of the Raf/MEK/ERK pathway and inactivation of wild-type p53 by Mdm2 overexpression are frequent molecular events in acute myelogenous leukemia (AML).
  • We investigated the interaction of Raf/MEK/ERK and p53 pathways after their simultaneous blockades using a selective small-molecule antagonist of Mdm2, Nutlin-3a, and a pharmacologic MEK-specific inhibitor, PD98059.
  • We found that PD98059, which itself has minimal apoptogenic activity, acts synergistically with Nutlin-3a to induce apoptosis in wild-type p53 AML cell lines OCI-AML-3 and MOLM-13.
  • In accordance with the activation of transcription-dependent apoptosis, PD98059 treatment promoted the translocation of p53 from the cytoplasm to the nucleus in OCI-AML-3 cells, in which p53 primarily initiates transcription-independent apoptosis when cells are treated with Nutlin-3a alone.
  • [MeSH-major] Apoptosis / physiology. Leukemia, Myeloid, Acute / enzymology. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / enzymology. Cell Nucleus / physiology. Drug Synergism. Fatty Acids, Unsaturated / pharmacology. Flavonoids / pharmacology. Humans. Imidazoles. Piperazines. Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors. Transcription, Genetic. raf Kinases / metabolism

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  • (PMID = 17409429.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / CA89346; United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Fatty Acids, Unsaturated; 0 / Flavonoids; 0 / Imidazoles; 0 / Piperazines; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; 87081-35-4 / leptomycin B; EC 2.7.11.1 / raf Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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53. Mann G, Attarbaschi A, Schrappe M, De Lorenzo P, Peters C, Hann I, De Rossi G, Felice M, Lausen B, Leblanc T, Szczepanski T, Ferster A, Janka-Schaub G, Rubnitz J, Silverman LB, Stary J, Campbell M, Li CK, Suppiah R, Biondi A, Vora A, Valsecchi MG, Pieters R, Interfant-99 Study Group: Improved outcome with hematopoietic stem cell transplantation in a poor prognostic subgroup of infants with mixed-lineage-leukemia (MLL)-rearranged acute lymphoblastic leukemia: results from the Interfant-99 Study. Blood; 2010 Oct 14;116(15):2644-50
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  • [Title] Improved outcome with hematopoietic stem cell transplantation in a poor prognostic subgroup of infants with mixed-lineage-leukemia (MLL)-rearranged acute lymphoblastic leukemia: results from the Interfant-99 Study.
  • To define a role for hematopoietic stem cell transplantation (HSCT) in infants with acute lymphoblastic leukemia and rearrangements of the mixed-lineage-leukemia gene (MLL(+)), we compared the outcome of MLL(+) patients from trial Interfant-99 who either received chemotherapy only or HSCT.
  • Among the 277 of 297 MLL(+) patients (93%) in first remission (CR), there appeared to be a significant difference in disease-free survival (adjusted by waiting time to HSCT) between the 37 (13%) who received HSCT and the 240 (87%) who received chemotherapy only (P = .03).
  • In summary, HSCT seems to be a valuable option for a subgroup of infant MLL(+) acute lymphoblastic leukemia carrying further poor prognostic factors.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Age Factors. Disease-Free Survival. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Leukocyte Count. Prognosis. Risk Factors. Survival Analysis. Treatment Outcome


54. Crispino JD: GATA1 mutations in Down syndrome: implications for biology and diagnosis of children with transient myeloproliferative disorder and acute megakaryoblastic leukemia. Pediatr Blood Cancer; 2005 Jan;44(1):40-4
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  • [Title] GATA1 mutations in Down syndrome: implications for biology and diagnosis of children with transient myeloproliferative disorder and acute megakaryoblastic leukemia.
  • Although physicians have known for many decades that children with Down syndrome are predisposed to developing transient myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL), many questions regarding these disorders remain unresolved.
  • Finally, what factors lead to the increased predisposition to these myeloid disorders?
  • In addition, I will discuss whether assaying for the presence of a GATA1 mutation can aid in the diagnosis of these and related megakaryoblastic leukemias.
  • Future research aimed at defining the activity of mutant GATA-1 protein and identifying interacting factors encoded by chromosome 21 will likely lead to an even greater understanding of this intriguing leukemia.

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15390312.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101774-03; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-03
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Transcription Factors
  • [Number-of-references] 30
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55. Adachi S, Manabe A, Imaizumi M, Taga T, Tawa A, Tsurusawa M, Kikuchi A, Masunaga A, Tsuchida M, Nakahata T, MDS Committee of the Japanese Society of Pediatric Hematology: Acute myeloid leukemia with multilineage dysplasia in children. Int J Hematol; 2007 Nov;86(4):358-63
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  • [Title] Acute myeloid leukemia with multilineage dysplasia in children.
  • We retrospectively surveyed pediatric acute myeloid leukemia (AML) patients with multilineage dysplasia treated with the AML 99 and the Children's Cancer and Leukemia Study Group (CCLSG) AML 9805 protocols.
  • We found only 9 AML patients (2.6%) with multilineage dysplasia among the 341 patients with newly diagnosed de novo AML.
  • Eight of the 9 patients obtained complete remission (CR) following the intensive AML-oriented treatments.
  • Three of 7 patients who underwent stem cell transplantation were alive in CR for more than 4 years, and the 2 patients treated only with chemotherapy were alive in CR for more than 30 months.
  • We did not identify any particular chromosomal abnormalities or differentiation according to the French-American-British classification in these 9 patients.
  • No reports have described AML with multilineage dysplasia in children, and the incidence of the disease is expected to be very low.
  • We plan to conduct a prospective pathologic review to select cases with this disease entity in the next Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) AML-05 protocol.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 18055345.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
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56. Vicente D, Lamparelli T, Gualandi F, Occhini D, Raiola AM, Ibatici A, Van Lint MT, Gobbi M, Miglino M, Clavio M, Risso M, Frassoni F, Bacigalupo A: Improved outcome in young adults with de novo acute myeloid leukemia in first remission, undergoing an allogeneic bone marrow transplant. Bone Marrow Transplant; 2007 Aug;40(4):349-54
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  • [Title] Improved outcome in young adults with de novo acute myeloid leukemia in first remission, undergoing an allogeneic bone marrow transplant.
  • We assessed the outcome of 170 patients with AML in first complete remission, aged 1-47 years (median 29), who had undergone an allogeneic BMT before or after 1990 (n=80 and n=90, respectively); all patients were prepared with cyclophosphamide and TBI; the median follow-up for surviving patients was 13 years.
  • Patients transplanted after 1990 were older, had a shorter interval diagnosis-BMT, had less FAB-M3 cases, received a higher dose of TBI, a higher marrow cell dose and combined (cyclosporine+methotrexate) GVHD prophylaxis.
  • In conclusion, the overall survival of first remission AML undergoing an allogeneic BMT has almost doubled in the past two decades, despite older age and fewer M3 cases.
  • Improvement has come not only from changes in transplant procedures, but also from effective rescue of patients relapsing after transplant.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cohort Studies. Female. Graft vs Host Disease / prevention & control. Graft vs Host Disease / therapy. Humans. Infant. Italy / epidemiology. Male. Neoplasm Recurrence, Local / therapy. Remission Induction / methods. Risk. Survival Analysis. Transplantation, Homologous


57. Drexler HG, Dirks WG, Macleod RA: Many are called MDS cell lines: one is chosen. Leuk Res; 2009 Aug;33(8):1011-6
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  • [Title] Many are called MDS cell lines: one is chosen.
  • Myelodysplastic syndromes (MDS) comprise a heterogenous group of clonal disorders of hematopoietic progenitors, showing genetic instability and in many cases progression to acute myeloid leukemia (AML).
  • When MDS progress towards AML (AML/MDS), additional genetic lesions cause a block in differentiation and an accumulation of blast cells.
  • Hence, both pathophysiologically and clinically the MDS and AML/MDS phases are distinguishable.
  • Leukemia cell lines are key resources for modelling hematological malignancies.
  • Characterization of these cell lines has provided a rich vein of insights into the mechanisms underlying malignant transformation.
  • Some 31 cell lines have been described in the literature purportedly established from patients with MDS.
  • However, a significant minority of these has proved false after DNA profiling which revealed their cross-contamination with older established leukemia cell lines.
  • Most remaining ("authentic") MDS cell lines were established during the leukemic phase of the disease progression rather than during the MDS phase.
  • Based on these data we have assigned the 31 candidate MDS cell lines to one of the three categories:.
  • (1) false (cross-contaminated) cell lines and non-malignant cell lines;.
  • (2) malignant cell lines established in the AML/MDS leukemic phase; and (3) apparently legitimate MDS cell lines established during the MDS phase.
  • While MDS and AML/MDS cell lines both provide singular resources for modelling pathology, mining oncogenically modified macromolecules, and testing druggability, we contend these groups should be considered separately.
  • [MeSH-major] Cell Line, Tumor. Hematopoietic Stem Cells. Myelodysplastic Syndromes
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Genomic Instability. Humans. Leukemia, Myeloid, Acute. Models, Biological


58. Wang YZ, Liu YR, Zhu HH, Wu HH, Cao H, Chan Y, Hao L, Jiang B, Huang XJ: [Prognostic significance of minimal residual disease detected by multiparameter flow cytometry in acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):551-6
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  • [Title] [Prognostic significance of minimal residual disease detected by multiparameter flow cytometry in acute myeloid leukemia].
  • This study was aimed to explore prognostic significance of minimal residual disease (MRD) detection in patients with acute myeloid leukemia (AML) by multiparameter flow cytometry (MCF).
  • Leukemia-associated immunophenotype (LAIP) of newly diagnosed AML patients were determined by 4-color 5 antibody panels and patients with sensitive LAIP were chosen for MRD detection.
  • Patients with MRD positive had a median relapse-free survival time of 11 months, 11.5 months and 11 months at 1 - 2, 3 - 4 and 5 - 6 months respectively, while all patients with MRD negative were not observed to reach median release-free survival time (p < 0.05).
  • It is concluded that MRD detection by multi-parameter flow cytometry can predict outcome of AML patients, which should be continuously monitored after treatment.

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  • (PMID = 19549362.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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59. Stone RM, DeAngelo DJ, Janosova A, Galinsky I, Canning C, Ritz J, Soiffer RJ: Low dose interleukin-2 following intensification therapy with high dose cytarabine for acute myelogenous leukemia in first complete remission. Am J Hematol; 2008 Oct;83(10):771-7
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  • [Title] Low dose interleukin-2 following intensification therapy with high dose cytarabine for acute myelogenous leukemia in first complete remission.
  • The most important problem in the therapy of patients with acute myeloid leukemia (AML) is relapse after intensive therapy.
  • We sought to determine if interleukin-2 (low-dose with intermittent boluses) administration could be feasibly administered after standard therapy to potentiate anti-tumor immunity in a fashion analogous to the post-allogeneic stem cell transplant "graft-vs-leukemic" effect.
  • Adults with de novo AML received daunorubicin and cytosine arabinoside induction therapy.
  • Mononuclear cells from patients receiving rIL-2 exhibited enhanced cytolytic activity in vitro against cryopreserved autologous leukemia cells.
  • This study supports further investigation of immunotherapy in the post-intensive chemotherapy setting in the management of patients with AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Clinical Trials as Topic. Cytarabine / administration & dosage. Cytarabine / adverse effects. Dose-Response Relationship, Drug. Fatigue / chemically induced. Feasibility Studies. Female. Fever / chemically induced. Follow-Up Studies. Humans. Interleukin-2 / administration & dosage. Interleukin-2 / genetics. Killer Cells, Natural / drug effects. Male. Middle Aged. Recombinant Proteins / administration & dosage. Recombinant Proteins / adverse effects. Remission Induction. Survival Analysis. T-Lymphocytes / drug effects. Thrombocytopenia / chemically induced. Time Factors. Treatment Outcome

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18756547.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA66996
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-2; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine
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60. Pearce DJ, Taussig D, Zibara K, Smith LL, Ridler CM, Preudhomme C, Young BD, Rohatiner AZ, Lister TA, Bonnet D: AML engraftment in the NOD/SCID assay reflects the outcome of AML: implications for our understanding of the heterogeneity of AML. Blood; 2006 Feb 01;107(3):1166-73
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  • [Title] AML engraftment in the NOD/SCID assay reflects the outcome of AML: implications for our understanding of the heterogeneity of AML.
  • We explored why 51% of 59 acute myeloid leukemia (AML) patients were unable to initiate leukemia in NOD/SCID mice.
  • Increasing the cell dose, using more permissive recipients, and alternative tissue sources did not cause AML engraftment in most previously nonengrafting AML samples.
  • Homing of AML cells to the marrow was the same between engrafters and nonengrafters.
  • The only variable that was related to engraftment ability was the karyotypically defined risk stratification of individual AML cases.
  • Of interest, follow-up of younger patients with intermediate-risk AML revealed a significant difference in overall survival between NOD/SCID engrafting and nonengrafting AMLs.
  • Hence, the ability of AML to engraft in the NOD/SCID assay seems to be an inherent property of AML cells, independent of homing, conditioning, or cell frequency/source, which is directly related to prognosis.
  • Our results suggest an important difference between leukemic initiating cells between engrafting and nonengrafting AML cases that correlates with treatment response.
  • [MeSH-major] Biological Assay. Graft Survival. Leukemia, Myeloid, Acute. Neoplastic Stem Cells. Stem Cell Transplantation

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  • (PMID = 16234360.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United States / NHLBI NIH HHS / HL / HL-64856
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC1895911
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61. Calvo KL, Ojeda MJ, Ammatuna E, Lavorgna S, Ottone T, Targovnik HM, Lo-Coco F, Noguera NI: Detection of the nucleophosmin gene mutations in acute myelogenous leukemia through RT-PCR and polyacrylamide gel electrophoresis. Eur J Haematol; 2009 Jan;82(1):69-72
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  • [Title] Detection of the nucleophosmin gene mutations in acute myelogenous leukemia through RT-PCR and polyacrylamide gel electrophoresis.
  • OBJECTIVES: Mutations in the C-terminal region of the nucleophosmin (NPM1) gene occur in approximately 60% of acute myeloid leukemia (AML) cases with normal karyotype and represent the most common genetic lesion presently known in this disease.
  • Because of their frequency and favorable impact on prognostic outcome, screening for this aberration is currently recommended in routine diagnostic characterization of AML.
  • A hemi-nested method was designed to increase sensitivity for the study of minimal residual disease (MRD).
  • The results were independently validated in 24 AML cases by sequencing analysis.
  • CONCLUSIONS: This simple and low-cost assay may integrate diagnostic work-up of AML and could be used for assessment of response to therapy in patients with NPM1 mutations.
  • [MeSH-major] Electrophoresis, Polyacrylamide Gel / methods. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / analysis. Nuclear Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Base Sequence. Exons / genetics. Female. Humans. Male. Middle Aged. Mutation / genetics. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics

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  • (PMID = 18801061.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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62. Bhayat F, Das-Gupta E, Hubbard R: Bone marrow transplantation in AML, and socioeconomic class: a UK population-based cohort study. BMC Cancer; 2010;10:514
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  • [Title] Bone marrow transplantation in AML, and socioeconomic class: a UK population-based cohort study.
  • BACKGROUND: We have previously shown that in the UK mortality in people with Acute Myeloid Leukaemia (AML) was nearly 50% greater among the most socio-economically deprived.
  • The aim of this study was to determine whether AML patients from lower socioeconomic classes had a lower chance of receiving a bone marrow transplant.
  • METHODS: Using Hospital Episode Statistics (HES) data, we identified all incident cases of AML admitted to UK hospitals between 1998 and 2007.
  • We calculated the number of bone marrow transplantations undertaken in AML patients, stratifying our results by gender, age at diagnosis, year of diagnosis, degree of socioeconomic deprivation and co-morbidity.
  • We used logistic regression to calculate odds ratios for bone marrow transplantation, adjusting for gender, age at diagnosis, year of diagnosis, degree of socioeconomic deprivation and co-morbidity score.
  • RESULTS: We identified a total of 23 910 incident cases of AML over this 10-year time period, of whom 1 140 (4.8%) underwent BMT.
  • Bone marrow transplantation declined with increasing socioeconomic deprivation (p for trend < 0.001) such that people in the most deprived socioeconomic quintile were 40% less likely to have a transplant than those in the most advantaged group (Odds Ratio 0.60, 95% confidence interval 0.49, 0.73), even after adjusting for gender, age at diagnosis, year of diagnosis and co-morbidity.
  • CONCLUSION: This large cohort study demonstrates that AML patients from lower socioeconomic classes are less likely to undergo bone marrow transplantation than their better off counter-parts.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy


63. Maurillo L, Buccisano F, Spagnoli A, Del Poeta G, Panetta P, Neri B, Del Principe MI, Mazzone C, Consalvo MI, Tamburini A, Ottaviani L, Fraboni D, Sarlo C, De Fabritiis P, Amadori S, Venditti A: Monitoring of minimal residual disease in adult acute myeloid leukemia using peripheral blood as an alternative source to bone marrow. Haematologica; 2007 May;92(5):605-11
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  • [Title] Monitoring of minimal residual disease in adult acute myeloid leukemia using peripheral blood as an alternative source to bone marrow.
  • BACKGROUND AND OBJECTIVES: To date, bone marrow (BM) is the most common source of cells to use in order to assess minimal residual disease (MRD) in acute myeloid leukemia (AML).
  • In the present study, we investigated whether peripheral blood (PB) could be an alternative source of cells for monitoring MRD in AML.
  • DESIGN AND METHODS: Fifty patients with AML were monitored for MRD after the achievement of complete remission.
  • Thirty-three of 43 (77%) patients with >1.5x10 (-4)residual leukemic cells in PB after induction had a relapse, whereas the seven patients with lower levels did not (p=0.0002).
  • INTERPRETATION AND CONCLUSIONS: These preliminary results indicate that: (i) PB evaluation can integrate BM assessment for MRD detection in patients with AML;.
  • [MeSH-major] Blood Cells / chemistry. Bone Marrow Examination. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Idarubicin / administration & dosage. Kaplan-Meier Estimate. Male. Middle Aged. Mitoxantrone / administration & dosage. Neoplasm, Residual. Organ Specificity. Randomized Controlled Trials as Topic / statistics & numerical data. Remission Induction. Survival Analysis. Treatment Outcome

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  • (PMID = 17488683.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin; EORTC GIMEMA AML-10 protocol; EORTC GIMEMA AML-13 protocol
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64. Choi WT, Folsom MR, Azim MF, Meyer C, Kowarz E, Marschalek R, Timchenko NA, Naeem RC, Lee DA: C/EBPbeta suppression by interruption of CUGBP1 resulting from a complex rearrangement of MLL. Cancer Genet Cytogenet; 2007 Sep;177(2):108-14
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  • Translocations involving the mixed-lineage leukemia gene (MLL) confer a poor prognosis in acute leukemias.
  • We then showed that these cells have reduced expression of CUGBP1 and C/EBPbeta when compared to other AML blasts.

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  • (PMID = 17854664.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA90433; United States / NCI NIH HHS / CA / R01 CA100070-03; United States / NCI NIH HHS / CA / R21 CA114251-01; United States / NCI NIH HHS / CA / R01 CA100070; United States / NCI NIH HHS / CA / R01 CA 100070; United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / K12 CA090433-04; United States / NCI NIH HHS / CA / R21 CA114251
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / CELF1 Protein; 0 / CELF1 protein, human; 0 / MLL protein, human; 0 / RNA, Messenger; 0 / RNA-Binding Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ NIHMS358652; NLM/ PMC3311538
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65. Carneiro BA, Kaminer L, Eldibany M, Sreekantaiah C, Kaul K, Locker GY: Oxaliplatin-related acute myelogenous leukemia. Oncologist; 2006 Mar;11(3):261-2
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  • [Title] Oxaliplatin-related acute myelogenous leukemia.
  • Bone marrow biopsy was consistent with therapy-related acute myelogenous leukemia.
  • It is likely that the leukemia was related to the oxaliplatin administration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 16549810.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Organoplatinum Compounds; 2S9ZZM9Q9V / Bevacizumab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; Folfox protocol
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66. Smith AE, Mohamedali AM, Kulasekararaj A, Lim Z, Gäken J, Lea NC, Przychodzen B, Mian SA, Nasser EE, Shooter C, Westwood NB, Strupp C, Gattermann N, Maciejewski JP, Germing U, Mufti GJ: Next-generation sequencing of the TET2 gene in 355 MDS and CMML patients reveals low-abundance mutant clones with early origins, but indicates no definite prognostic value. Blood; 2010 Nov 11;116(19):3923-32
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  • Mutations in the TET2 gene are frequent in myeloid disease, although their biologic and prognostic significance remains unclear.
  • Seventy-one TET2 mutations, with a relative mutation abundance (RMA) ≥ 10%, were identified in 39 of 320 (12%) myelodysplastic syndrome and 16 of 35 (46%) chronic myelomonocytic leukemia patients (P < .001).
  • There was no significant prognostic association between TET2 mutations and World Health Organization subtypes, International Prognostic Scoring System score, cytogenetic status, or transformation to acute myeloid leukemia.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Mutation. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Base Sequence. Cell Differentiation / genetics. DNA Mutational Analysis. Female. Gene Expression. Humans. Janus Kinase 2 / genetics. Karyotyping. Loss of Heterozygosity. Male. Middle Aged. Molecular Sequence Data. Polymorphism, Single Nucleotide. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Survival Analysis. T-Lymphocytes / metabolism. Young Adult

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  • (PMID = 20693430.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TET2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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67. Bradstock KF, Hertzberg MS, Kerridge IH, Svennilson J, McGurgan M, Huang G, Antonenas V, Gottlieb DJ: Unrelated umbilical cord blood transplantation for adults with haematological malignancies: results from a single Australian centre. Intern Med J; 2006 Jun;36(6):355-61
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  • BACKGROUND: A number of haematological malignancies can be cured by allogeneic stem cell transplantation but only approximately 30% of Australians have a suitable histocompatible related donor.
  • Matched donors can be found on international registries of unrelated volunteers for a proportion of the remaining patients.
  • AIMS: The aim of this study was to define the feasibility of allogeneic stem cell transplantation using single unrelated cord blood units in a cohort of adults with poor prognosis leukaemia or lymphoma.
  • METHODS: Nine patients with haematological malignancies (five with acute myeloid leukaemia, one with acute lymphoblastic leukaemia, one with Hodgkin lymphoma and two with non-Hodgkin lymphomas) received transplants of cryopreserved cord blood after conditioning therapy with high-dose cyclophosphamide, total body irradiation and antithymocyte globulin.
  • Acute graft versus host disease (GVHD) grades II-IV was seen in four of seven evaluable patients and limited chronic GVHD was seen in four of five.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Leukemia / therapy. Lymphoma / therapy
  • [MeSH-minor] Adult. Antiviral Agents / therapeutic use. Cyclosporine / therapeutic use. Disease-Free Survival. Feasibility Studies. Female. Graft vs Host Disease / etiology. Graft vs Host Disease / prevention & control. Humans. Immunosuppressive Agents / therapeutic use. Male. Middle Aged. Pancytopenia / etiology. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16732860.001).
  • [ISSN] 1445-5994
  • [Journal-full-title] Internal medicine journal
  • [ISO-abbreviation] Intern Med J
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine
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68. Cybulla M, Schaefer E, Wendt S, Ling H, Kröber SM, Hövelborn U, Schandelmaier S, Rohrbach R, Neumann HP: Chronic renal failure and proteinuria in adulthood: Fabry disease predominantly affecting the kidneys. Am J Kidney Dis; 2005 May;45(5):e82-9
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  • [Title] Chronic renal failure and proteinuria in adulthood: Fabry disease predominantly affecting the kidneys.
  • The prognosis of Fabry disease has changed since enzyme-replacement treatment was introduced.
  • Therefore, early diagnosis is instrumental.
  • We describe a family presenting with chronic renal failure and proteinuria in which classic skin and neurological features were absent and the diagnosis of Fabry disease was difficult and not established until a second family member developed renal abnormalities.
  • Because 1 brother, who died years ago at the age of 32 years of acute myeloid leukemia, also had chronic renal failure and proteinuria, the diagnosis of Fabry disease was entertained.
  • In the index patient, acroparesthesia, hypohidrosis, pain, angiokeratomas of the skin, and cornea verticillata suggesting Fabry disease were absent.
  • In the brother who died, Fabry disease, missed at autopsy because of cancer-related findings, could be confirmed after repeated review of histological slides.
  • We conclude that familial chronic renal failure combined with proteinuria is suggestive of Fabry disease, and such specific mutations as E66K predominantly may affect the kidneys.
  • [MeSH-major] Fabry Disease / complications. Kidney Failure, Chronic / etiology. Proteinuria / etiology
  • [MeSH-minor] Adult. Amino Acid Substitution. Child. Creatinine / blood. Diagnosis, Differential. Female. Humans. Hypertension / complications. Kidney / chemistry. Kidney / pathology. Male. Middle Aged. Mutation, Missense. Obesity / complications. Pedigree. Point Mutation. Trihexosylceramides / analysis

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  • (PMID = 15861341.001).
  • [ISSN] 1523-6838
  • [Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation
  • [ISO-abbreviation] Am. J. Kidney Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Trihexosylceramides; 71965-57-6 / globotriaosylceramide; AYI8EX34EU / Creatinine
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69. Rea D, Legros L, Raffoux E, Thomas X, Turlure P, Maury S, Dupriez B, Pigneux A, Choufi B, Reman O, Stéphane D, Royer B, Vigier M, Ojeda-Uribe M, Recher C, Dombret H, Huguet F, Rousselot P, Intergroupe Français des Leucémies Myéloïdes Chronique, Group for Research in Adult Acute Lymphoblastic Leukemia: High-dose imatinib mesylate combined with vincristine and dexamethasone (DIV regimen) as induction therapy in patients with resistant Philadelphia-positive acute lymphoblastic leukemia and lymphoid blast crisis of chronic myeloid leukemia. Leukemia; 2006 Mar;20(3):400-3
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  • [Title] High-dose imatinib mesylate combined with vincristine and dexamethasone (DIV regimen) as induction therapy in patients with resistant Philadelphia-positive acute lymphoblastic leukemia and lymphoid blast crisis of chronic myeloid leukemia.
  • Imatinib combined with high-dose chemotherapy is now becoming the gold standard for treatment of Philadelphia chromosome-positive acute leukemias.
  • Thirty-one patients (18 relapsing or refractory Ph+ acute lymphoblastic leukemias and 13 lymphoid blast crisis chronic myelogenous leukemias) were enrolled.
  • Nine out of 19 patients under 55 years received allogenic stem cell transplantation after a median time of 78 days post-CR.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Benzamides. Dexamethasone / administration & dosage. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Pilot Projects. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Vincristine / administration & dosage


70. Kamineni P, Baptiste A, Hassan M, Dawkins FW, Zaidi S, Tefferi A, Lindsey M, Taddesse-Heath L: Case of chronic eosinophilic leukemia with deletion of chromosome 16 and hepatitis C. J Natl Med Assoc; 2006 Aug;98(8):1356-60
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  • [Title] Case of chronic eosinophilic leukemia with deletion of chromosome 16 and hepatitis C.
  • Chronic eosinophilic leukemia is a rare entity, characterized by eosinophilia of >1.5 x 10(9)/L, persisting for >6 months after exclusion of other reactive and neoplastic causes of eosinophilia, and occurring in association with a clonal cytogenetic abnormality.
  • Various chromosomal abnormalities have been associated with chronic eosinophilic leukemia.
  • Partial deletion of the long arm of chromosome 16 is a cytogenetic abnormality first reported 20 years ago in patients with acute myeloid leukemia associated with bone marrow eosinophilia (AML-M4Eo).
  • We report a case of a 45-year-old African-American male with hepatitis C and sustained peripheral blood eosinophilia who presented with gross hematuria, dyspnea on exertion, chills, decreased appetite and weight loss of 40 pounds associated with hepatosplenomegaly and lymphadenopathy.
  • Bone marrow biopsy showed clonal cytogenetic abnormality consisting of deletion of the long arm of chromosome 16 (16q22).
  • To our knowledge, this is the first case report of isolated del (16) (q22), a cytogenetic abnormality associated with AML-M4Eo, occurring in chronic eosinophilic leukemia.
  • Whether this cytogenetic abnormality might represent a prodromal phase of AML-M4Eo is not known.
  • [MeSH-minor] Biopsy. Bone Marrow / pathology. Chronic Disease. Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 16916138.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2569582
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71. Di Cataldo A, La Spina M, Bertuna G, Lo Nigro L, Branciforte F, Castagnola E: Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia. Pediatr Blood Cancer; 2006 Feb;46(2):266
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  • [Title] Spleen and lung involvement by Acinetobacter calcoaceticus bacteremia mimicking deep fungal infection in a child with acute non-lymphoblastic leukemia.
  • [MeSH-major] Acinetobacter Infections / drug therapy. Acinetobacter calcoaceticus. Anti-Infective Agents / administration & dosage. Ciprofloxacin / administration & dosage. Leukemia, Myeloid, Acute / complications


72. Farah C, Bulai Livideanu C, Jegu J, Paul C, Viraben R, Lamant L, Delavigne K, Adoue D, Laurent G, Beyne Rauzy O: Prevalence and prognostic value of cutaneous manifestations in patients with myelodysplastic syndrome. J Eur Acad Dermatol Venereol; 2010 Oct;24(10):1171-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Skin manifestations associated with myelodysplastic syndrome (MDS) may reveal bone marrow transformation into acute myeloid leukaemia.
  • In addition, we evaluated the risk of acute myeloid leukaemia transformation associated with skin manifestations.
  • METHODS: We studied a cohort of 157 patients with primary MDS followed up prospectively for a median of 44 months.
  • Skin lesions were prospectively assessed as part of medical examination every 6 months by a board certified dermatologist.
  • Survival analyses were performed to assess the association between the presence of skin lesions and the risk of acute myeloid leukaemia.
  • RESULTS: Fifteen patients (9.55%) experienced skin lesions previously reported as associated with MDS.
  • These were neutrophilic dermatosis (7, 4.46%), specific lesions (5, 3.18%), cutaneous vasculitis (2, 1.27%) and Behçet disease (1, 0.63%).
  • Survival analysis showed that the risk of transformation into acute myeloid leukaemia was slightly but not significantly increased in patients with skin lesions as compared with patients without skin lesions with a relative risk of 2.08 (95% CI 0.92-4.67).
  • CONCLUSION: The prevalence of skin lesions, mostly neutrophilic dermatosis and specific lesions, is relatively high in patients with MDS.
  • There is a trend for a higher risk of transformation into acute myeloid leukaemia in patients with skin lesions.
  • [MeSH-major] Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / diagnosis. Skin Diseases / epidemiology. Skin Diseases / etiology
  • [MeSH-minor] Adult. Aged. Cohort Studies. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Leukemia, Myeloid, Acute / epidemiology. Male. Middle Aged. Prevalence. Prognosis. Prospective Studies. Retrospective Studies. Risk Factors


73. Liu Y, Ke XY, Ma J, Shen ZX, Zhang XH, Du X, Zhao YM, Lv JQ, Zhan ZM, Zeng XY, Xu XH, Lu ZS: [Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia]. Zhonghua Zhong Liu Za Zhi; 2006 Sep;28(9):706-8
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  • [Title] [Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia].
  • OBJECTIVE: To evaluate the safety of domestically produced idarubicin in the treatment of acute leukemia by a multicenter randomized control trial.
  • METHODS: This trial was carried out in the hemotologica department of five hospitals throughout China, with hospitalized patients who suffered from acute myelogenous leukemia ( AML except M3 type) , acute lymphocytic leukemia ( ALL) , chronic myelogenous leukemia-blast (CML-blast) , totally 155 patients.
  • In this study, 155 leukemia patients were randomly grouped into: 1. test group treated using domestic idarubicin, 2. control group using imported idarubicin.
  • The acute myelogenous leukemia regimen included idarubicin 8 mg/m(2), dl -3 plus cytosine arabinoside 100 mg/m(2), dl - 7 for 1-2 cycles.
  • The regimen for acute lymphocytic leukemia was idarubicin 8 mg/m2, dl - 3; vincristine 2 mg/mr, dl; cyclophosphamide 750 mg/m2, dl ; plus prednisone 60 mg/m(2),dl - 14 for 1-2 cycles.
  • The incidence of non-hematological toxicities in domestic idarubicin group and imported idarubicin group was 84.
  • Discontinuation of treatment due to non-hematological toxicity was not neccessary.
  • CONCLUSION: Domestic idarubicin is comparable to imported counterpart in efficiency and safety for the treatment of acute leukemia.
  • The most severe side effects of domestic idarubicin is hematological toxicity, which should be closely observed and treated in time, while its non-hematological toxicity is tolerable.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17274381.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; ZRP63D75JW / Idarubicin
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74. Tang JM, Meng FY, Chen AW: [Gene expression profile of refractory acute myeloid leukemia (M2a)]. Ai Zheng; 2005 Jun;24(6):676-9
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  • [Title] [Gene expression profile of refractory acute myeloid leukemia (M2a)].
  • BACKGROUND & OBJECTIVE: Recurrence is the major cause of treatment failure of acute myeloid leukemia (AML).
  • Drug resistance, the main cause of refractoriness of AML, is related to abnormal genes expression.
  • This study was to detect differential expression of genes in naive and recurrent/refractory AML, and explore potential mechanisms of recurrent/refractory AML.
  • METHODS: Differential gene expressions of bone marrow mononuclear cells between naive and recurrent/refractory diseases in 5 self-paired patients with AML-M(2a) were detected by DNA microarray.
  • RESULTS: In 925 tested genes, 14 were differentially expressed between naive and recurrent/refractory diseases in the 5 self-paired patients.
  • Of the 14 genes, 12 (involved in signal transduction, DNA replication, regulation of transcription, RNA processing, and regulation of cell cycle) were obviously up-regulated in recurrent diseases, and up-regulation of RRM1 (involved in DNA replication) was the most obvious.
  • CONCLUSIONS: Development of recurrent/refractory AML-M(2a) is concerned with various genes.
  • Up-regulation of these genes suggests that proliferation of recurrent/refractory AML-M(2a) blasts may be higher than that of naive AML-M(2a) blasts.
  • [MeSH-major] Gene Expression Profiling. Immunophenotyping. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / metabolism. Cell Proliferation. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Recurrence. Tumor Suppressor Proteins / metabolism. Up-Regulation

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  • (PMID = 15946477.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins
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75. Huang MJ, Cheng YC, Liu CR, Lin S, Liu HE: A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemia. Exp Hematol; 2006 Nov;34(11):1480-9
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  • [Title] A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemia.
  • OBJECTIVE: The protooncogene c-Myc plays an important role in the control of cell proliferation, apoptosis, and differentiation, and its aberrant expression is frequently seen in multiple human cancers, including acute myeloid leukemia (AML).
  • Inhibition of the c-Myc/Max heterodimerization by the recently identified small-molecule compound, 10058-F4, might be a novel antileukemic strategy.
  • MATERIALS AND METHODS: HL-60, U937, and NB4 cells and primary AML cells were used to examine the effects of 10058-F4 on apoptosis and myeloid differentiation.
  • RESULTS: We showed that 10058-F4 arrested AML cells at G0/G1 phase, downregulated c-Myc expression and upregulated CDK inhibitors, p21 and p27.
  • Furthermore, 10058-F4 also induced myeloid differentiation, possibly through activation of multiple transcription factors.
  • Similarly, 10058-F4-induced apoptosis and differentiation could also be observed in primary AML cells.
  • CONCLUSION: Our study has shown that inhibition of c-Myc/Max dimerization with small-molecule inhibitors affects multiple cellular activities in AML cells and represents a potential antileukemic approach.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Differentiation / drug effects. Leukemia, Myeloid / metabolism. Proto-Oncogene Proteins c-myc / antagonists & inhibitors. Thiazoles / pharmacology
  • [MeSH-minor] Acute Disease. Basic-Leucine Zipper Transcription Factors / antagonists & inhibitors. Basic-Leucine Zipper Transcription Factors / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / drug effects. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Dimerization. Down-Regulation / drug effects. Drug Screening Assays, Antitumor. G0 Phase / drug effects. G1 Phase / drug effects. HL-60 Cells. Humans. Myeloid Cells / drug effects. Structure-Activity Relationship. U937 Cells. Up-Regulation / drug effects

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  • (PMID = 17046567.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 5-(4-ethylbenzylidene)-2-thioxothiazolidin-4-one; 0 / Antineoplastic Agents; 0 / Basic-Leucine Zipper Transcription Factors; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Myc associated factor X; 0 / Proto-Oncogene Proteins c-myc; 0 / Thiazoles; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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76. Park SH, Chi HS, Park SJ, Jang S, Park CJ: [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes]. Korean J Lab Med; 2010 Jun;30(3):231-8
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  • [Title] [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes].
  • BACKGROUND: AML with myelodysplasia related changes (AML MRC) is known to show a poor prognosis compared with de novo AML, but controversies exist about the prognostic impact of multilineage dysplasia (MLD) among MRC.
  • We investigated the prognostic impact of MLD in AML MRC.
  • METHODS: A total of 357 patients newly diagnosed as AML at Asan Medical Center from January 2001 to December 2005 were analyzed.
  • They were diagnosed and classified as AML with recurrent genetic abnormalities, AML MRC, and AML not otherwise specified (AML NOS).
  • RESULTS: AML MRC patients showed a lower complete remission (CR) rate (44.7% vs. 64.9%, P=0.002) and shorter OS (297 vs. 561 days, P=0.004) and EFS (229 vs. 374 days, P=0.004) than AML NOS patients.
  • Patients with MLD among AML MRC also showed a lower CR rate (37.7%, P=0.001) and shorter OS (351 days, P=0.036) and EFS (242 days, P=0.076) than AML NOS patients.
  • However, among AML MRC patients, there were no differences in OS, EFS and CR between patients with and without MLD.
  • CONCLUSIONS: AML MRC patients showed a lower CR rate and shorter OS and EFS than AML NOS patients.
  • AML MRC patients with MLD showed similar results and their prognosis was not different from those without MLD.
  • MLD findings among AML MRC could be an independent poor prognostic factor in de novo AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Data Interpretation, Statistical. Disease-Free Survival. Female. Humans. Infant. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis


77. Ustun C: Laparoscopic appendectomy in a patient with acute myelogenous leukemia with neutropenia. J Laparoendosc Adv Surg Tech A; 2007 Apr;17(2):213-5
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  • [Title] Laparoscopic appendectomy in a patient with acute myelogenous leukemia with neutropenia.
  • The management of acute myelogenous leukemia is often complicated by infections due to neutropenia, but the appendix is not a common site of infection in adult patients with acute myelogenous leukemia.
  • The diagnosis of acute appendicitis may be delayed or even missed because of the lack of characteristic signs and symptoms associated with acute appendicitis in neutropenic patients.
  • The case presented here is of a 33-year-old Hispanic man with acute myelogenous leukemia who developed severe diffuse acute abdominal pain with positive signs of rebound tenderness, fever, and hypotension ten days after receiving reinduction chemotherapy.
  • The patient was at his nadir, with a white blood cell count of 0.2 x 10(9)/L, platelet count of 20 x 10(9)/L, and hemoglobin of 7 g/dL.
  • A computed tomography scan of the abdomen was suspicious for acute appendicitis.
  • [MeSH-major] Appendicitis / surgery. Leukemia, Myeloid, Acute / complications

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  • (PMID = 17484650.001).
  • [ISSN] 1092-6429
  • [Journal-full-title] Journal of laparoendoscopic & advanced surgical techniques. Part A
  • [ISO-abbreviation] J Laparoendosc Adv Surg Tech A
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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78. Krauze E, Brzezińska-Wcisło L, Kamińska-Winciorek G, Wygledowska-Kania M, Sygula E: Pyoderma gangrenosum coexisting with acute myelogenous leukaemia. J Eur Acad Dermatol Venereol; 2005 Sep;19(5):589-92
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  • [Title] Pyoderma gangrenosum coexisting with acute myelogenous leukaemia.
  • The frequency of occurrence of malignant neoplasms in the cases of pyoderma gangrenosum is not exactly determined, but it can be assessed to be at 7%.
  • The aim of the study was to report a 26-year-old male patient with pyoderma gangrenosum coexisting with acute myelogenous leukaemia.
  • The first skin lesions on both tibia occurred in June 2001.
  • Prior to the proper diagnosis of pyoderma gangrenosum, the patient was treated surgically.
  • Because of the dramatic dermatological and general condition in November 2001, the patient was admitted to the Dermatological Department of the Silesian Medical Academy in Katowice where the diagnosis of pyoderma gangrenosum was established.
  • On the clinical and biochemical picture, the diagnosis of pyoderma gangrenosum within acute myelogenous leukaemia was made.
  • Although chemotherapy leukaemia was performed, the patient died after 4 months of the confirmation of the acute myelogenous leukaemia diagnosis.
  • [MeSH-major] Leg Ulcer / etiology. Leg Ulcer / therapy. Leukemia, Myeloid, Acute / complications. Pyoderma Gangrenosum / etiology. Pyoderma Gangrenosum / therapy
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Agents / therapeutic use. Blood Transfusion. Combined Modality Therapy. Disease Progression. Fatal Outcome. Humans. Male. Risk Assessment. Severity of Illness Index

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  • (PMID = 16164714.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents
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79. SDyshlevaia ZM, Skorobogatova EV, Maschan MA, Shipitsyna IP, Skvortsova IuV, Trakhtman PE, Balashov DN, Pashko IuV, Kurnikova EE, Suntsova EV, Goronkova OV, Solopova GG, Baĭdil'dina DD, Kalinina II, Khachatrian LA, Shneĭder MM, Maschan AA: [Results of hematopoietic cell transplantation in the first complete remission in children with acute myeloid leukemia from an intermediate risk group]. Ter Arkh; 2010;82(7):34-40
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  • [Title] [Results of hematopoietic cell transplantation in the first complete remission in children with acute myeloid leukemia from an intermediate risk group].
  • AIM: To analyze the results of allogeneic and autologous hemopoietic cell transplantations (allo- and auto-HCT) in children with acute myeloid leukemia (AML) from an intermediate risk group, most of which were performed using lower-intensity conditioning modes.
  • Acute and chronic graft-versus-host reactions developed in 57.1 and 23.1%, respectively.
  • CONCLUSION: Transplantation of allogeneic hemopoietic cells from a compatible related donor in the intermediate risk group children with AML, by using melphalan-based conditioning regimen, demonstrates a high survival rate with the minimum toxicity.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / surgery. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Graft Survival. Graft vs Host Reaction. Humans. Infant. Male. Recurrence. Remission Induction. Risk. Transplantation, Autologous. Transplantation, Homologous


80. Miron I, Mihăilă D, Aprodu G, Miron L, Plămădeală P, Moisă SM: Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy. Rom J Morphol Embryol; 2009;50(4):733-8
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  • [Title] Immunoproliferative small intestinal disease versus colonic monoblastic sarcoma in a 2-year-old boy.
  • The authors present a case of colonic monoblastic sarcoma, previously treated for other digestive abnormalities (malabsorbtion, Hirschprung's disease).
  • Important similitudes with immunoproliferative small intestinal disease (IPSID) lymphoma were demonstrated for this patient (male, 2-year-old).
  • Some particularities of this case are the young age and the extremely rapid development of the malignant disease in a patient with no previous signs of acute non-lymphoblastic leukemia.
  • The initial diagnosis was of malabsorbtion syndrome, based on the clinical exam at presentation, and then the patient was thought to have a form of Hirschprung's disease, due to a functional intestinal disorder (slow transit).
  • After the necropsy, pathologists diagnosed an immunoproliferative small intestinal disease, and four years later, they performed a more appropriate pathological exam, which explained better clinical symptoms associated to this complex case.
  • [MeSH-major] Colonic Neoplasms / diagnosis. Immunoproliferative Small Intestinal Disease / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Child, Preschool. Diagnosis, Differential. Hirschsprung Disease / diagnosis. Humans. Malabsorption Syndromes / diagnosis. Male

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  • (PMID = 19942975.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
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81. Praga C, Bergh J, Bliss J, Bonneterre J, Cesana B, Coombes RC, Fargeot P, Folin A, Fumoleau P, Giuliani R, Kerbrat P, Hery M, Nilsson J, Onida F, Piccart M, Shepherd L, Therasse P, Wils J, Rogers D: Risk of acute myeloid leukemia and myelodysplastic syndrome in trials of adjuvant epirubicin for early breast cancer: correlation with doses of epirubicin and cyclophosphamide. J Clin Oncol; 2005 Jun 20;23(18):4179-91
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  • [Title] Risk of acute myeloid leukemia and myelodysplastic syndrome in trials of adjuvant epirubicin for early breast cancer: correlation with doses of epirubicin and cyclophosphamide.
  • PURPOSE: We reviewed follow-up of patients treated in 19 randomized trials of adjuvant epirubicin in early breast cancer to determine incidence, risk, and risk factors for subsequent acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Cases of AML or MDS (AML/MDS) were reported, with disease characteristics.
  • RESULTS: In 7,110 patients treated with epirubicin-containing regimens (92% of whom also received cyclophosphamide), 8-year cumulative probability of AML/MDS was 0.55% (95% CI, 0.33% to 0.78%).
  • The risk of developing AML/MDS increased in relation to planned epirubicin dose per cycle, planned epirubicin dose-intensity, and administered cumulative doses of epirubicin and cyclophosphamide.
  • Patients with administered cumulative doses of both epirubicin and cyclophosphamide not exceeding those used in standard regimens (</= 720 mg/m(2) and </= 6,300 mg/m(2), respectively) had an 8-year cumulative probability of developing AML/MDS of 0.37% (95% CI, 0.13% to 0.61%) compared with 4.97% (95% CI, 2.06% to 7.87%) for patients administered higher cumulative doses of both epirubicin and cyclophosphamide.
  • CONCLUSION: Patients treated with standard cumulative doses of adjuvant epirubicin (</= 720 mg/m(2)) and cyclophosphamide (</= 6,300 mg/m(2)) for early breast cancer have a lower probability of secondary leukemia than patients treated with higher cumulative doses.
  • Increased risk of secondary leukemia must be considered when assessing the potential benefit to risk ratio of higher than standard doses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cyclophosphamide / adverse effects. Epirubicin / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced


82. Bae SY, Kim JS, Ryeu BJ, Lee KN, Lee CK, Kim YK, Lim CS, Cho Y, Choi CW, Ryu SW, Yoon SY: Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases. Cancer Genet Cytogenet; 2010 May;199(1):31-7
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  • [Title] Acute myeloid leukemia (AML-M2) associated with variant t(8;21): report of three cases.
  • Variants of the t(8;21)(q22;q22) involving chromosome 8, 21, and other chromosomes account for approximately 3% of all t(8;21)(q22;q22) found in patients with acute myeloid leukemia (AML).
  • The clinicopathologic features of AML with the variant t(8;21) have not been well established.
  • We report three cases of AML with variants of t(8;21) characterized, respectively, by derivative 8 with the interstitial inverted insertion of 21q and concurrent monosomy 21, t(8;18;21)(p22;q11.3;q22), and t(2;21;8)(q11.2;q22;q22).
  • Among these cases, three-way breakpoints 18p11.3 and 2q11.2 have not been previously reported.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic


83. Paupert J, Mansat-De Mas V, Demur C, Salles B, Muller C: Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features. Cell Cycle; 2008 Apr 15;7(8):1047-53
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  • [Title] Cell-surface MMP-9 regulates the invasive capacity of leukemia blast cells with monocytic features.
  • The metalloprotease 9 (MMP-9), a known mediator of tumour invasion, is secreted as a 92 kDa pro-form but a non-secreted variant of 85 Kda has been described.
  • We previously showed that the DNA repair protein Ku interacts at the cell surface of leukaemia cell lines with the 85 Kda pro-form of MMP-9 and these Ku/MMP-9 complexes regulates cell invasion, highlighting their importance in haematological malignancies.
  • We demonstrate here that all samples of acute myeloid leukaemia (AML) blasts purified from bone marrow of 16 affected patients express the 85 Kda form of MMP-9.
  • However, only AML that display monocytic lineage markers (AML4/5) express this form at the cell surface with co-expression of the membrane associated form of Ku.
  • Blocking antibodies directed against Ku or MMP-9 specifically inhibited cell invasion of those expressing Ku/MMP-9 on the cell surface.
  • The membrane form of Ku might represent an important factor in the exposition to the cell surface of this specific MMP-9 pro-form in AML with monocytic features.
  • These results might have important functional significance in the occurrence of extra-medullar infiltrates of leukaemia cells that occurs frequently during the onset of monocyte-related AML sub-types.
  • [MeSH-major] DNA Helicases / metabolism. Leukemia, Myeloid, Acute / metabolism. Matrix Metalloproteinase 9 / metabolism. Membrane Proteins / metabolism. Monocytes / metabolism. Neoplasm Invasiveness / physiopathology
  • [MeSH-minor] Adult. Aged. Blotting, Western. Cell Line, Tumor. Female. Humans. Male. Middle Aged

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  • (PMID = 18414048.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Membrane Proteins; 0 / XRCC5 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.6.4.- / DNA Helicases
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84. Valent P, Wieser R: Update on genetic and molecular markers associated with myelodysplastic syndromes. Leuk Lymphoma; 2009 Mar;50(3):341-8
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  • Myelodysplastic syndromes (MDS) are a heterogeneous group of myeloid neoplasms defined by morphologic dysplasia, peripheral cytopenia and clonal instability with enhanced risk of transformation into acute myeloid leukemia.
  • The prognosis and clinical picture in MDS vary depending on patient-related factors (age, gender, comorbidity), the disease variant, cell types affected and genes involved in the malignant process.
  • Although certain molecular defects are indicative of distinct cytogenetic abnormalities, others represent point mutations in critical target genes (RUNX1, N-RAS, JAK2, KIT, others) and sometimes are associated with a particular type of MDS, an overlap disease, a co-existing hematopoietic neoplasm or disease progression.
  • Some of these mutations may influence the natural course of disease, iron accumulation or disease progression.


85. Saito Y, Uchida N, Tanaka S, Suzuki N, Tomizawa-Murasawa M, Sone A, Najima Y, Takagi S, Aoki Y, Wake A, Taniguchi S, Shultz LD, Ishikawa F: Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML. Nat Biotechnol; 2010 Mar;28(3):275-80
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  • [Title] Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML.
  • Cancer stem cells have been proposed to be important for initiation, maintenance and recurrence of various malignancies, including acute myeloid leukemia (AML).
  • We have previously reported that CD34+CD38- human primary AML stem cells residing in the endosteal region of the bone marrow are relatively chemotherapy resistant.
  • Using a NOD/SCID/IL2rgamma(null) mouse model of human AML, we now show that the AML stem cells in the endosteal region are cell cycle quiescent and that these stem cells can be induced to enter the cell cycle by treatment with granulocyte colony-stimulating factor (G-CSF).
  • In combination with cell cycle-dependent chemotherapy, G-CSF treatment significantly enhances induction of apoptosis and elimination of human primary AML stem cells in vivo.
  • The combination therapy leads to significantly increased survival of secondary recipients after transplantation of leukemia cells compared with chemotherapy alone.

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  • (PMID = 20160717.001).
  • [ISSN] 1546-1696
  • [Journal-full-title] Nature biotechnology
  • [ISO-abbreviation] Nat. Biotechnol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA020408; United States / NCI NIH HHS / CA / CA20408
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS519081; NLM/ PMC3857633
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86. Zhang Y, He Q, Huang XJ, Jiang H, Yang SM, Lu J, Qing YZ, Shi Y, Dang H, Qiu JY, Lu DP: [Cytogenetic study on eosinophilia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):454-7
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  • The aim of study was to investigate the importance of chromosome aberration in differential diagnosis of eosinophilia and the chromosomal aberrations involved in patients with clonal eosinophilia.
  • Combining clinical, hematological and cytogenetical data, the 5 patients were diagnosed as acute myeloid leukemia with eosinophilia, chronic eosinophilic leukemia, 8p11 myeloproliferative syndrome, chronic myeloid leukemia in acute phase and acute myeloid leukemia-M(4Eo) respectively.
  • In conclusion, cytogenetical detection is very important in differential diagnosis of clonal eosinophilic disorders and chronic eosinophilic leukemia, which is suggested to be done routinely in clinic.

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  • (PMID = 17605843.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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87. Coppage M, Belanger T, Zauderer M, Sahasrabudhe D: In vitro generation of tumor specific T cells that recognize a shared antigen of AML: molecular characterization of TCR genes. Leuk Res; 2007 Feb;31(2):195-202
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  • [Title] In vitro generation of tumor specific T cells that recognize a shared antigen of AML: molecular characterization of TCR genes.
  • We present data demonstrating in vitro induction of autologous acute myelogenous leukemia (AML)-specific CTL.
  • The specific T cell receptor has been identified and cloned.
  • The CTL demonstrated specific lysis to autologous tumor blasts, but not to autologous BLCL or the NK-sensitive target K562.
  • The clone secreted GM-CSF, TNFa, and IFNg when stimulated with AML blasts from 3 of 11 patients or cell lines tested, but not with K562 or autologous B-LCL.
  • These three AML samples share a single HLA Class I antigen, HLA-A24.
  • The T cell receptor genes identified by molecular methods are Vbeta7.9-J2.3-Cbeta2 and Valpha17-J49-Calpha.
  • [MeSH-major] Antigens, Neoplasm / immunology. HLA Antigens / immunology. Leukemia, Myeloid / immunology. Receptors, Antigen, T-Cell / genetics. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Acute Disease. Amino Acid Sequence. CD8-Positive T-Lymphocytes / immunology. Cell Line, Tumor. Humans. Molecular Sequence Data

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  • [CommentIn] Leuk Res. 2007 Feb;31(2):127-8 [17137625.001]
  • (PMID = 16750565.001).
  • [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 / Antigens, Neoplasm; 0 / HLA Antigens; 0 / Receptors, Antigen, T-Cell
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88. 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 conditioning regimen consisted of 12 Gy of TBI followed by high-dose cytarabine (3 g/m(2)) every 12 hours for 4 days in combination with the continuous administration of G-CSF.
  • Stem cell sources included bone marrow or peripheral blood stem cells (PBSC) from human leukocyte antigen (HLA)-identical siblings (n = 24), or bone marrow from HLA serologically matched unrelated donors (n = 26).
  • At HSCT, 35 patients were in the first or second complete remission (CR1/2), and 15 patients were not in remission (n = 14) or in the third CR (n = 1).
  • 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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89. Kang LC, Dunphy CH: Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes. Arch Pathol Lab Med; 2006 Feb;130(2):153-7
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  • [Title] Immunoreactivity of MIC2 (CD99) and terminal deoxynucleotidyl transferase in bone marrow clot and core specimens of acute myeloid leukemias and myelodysplastic syndromes.
  • CONTEXT: MIC2 ("thymus leukemia") antigen has been shown to be expressed by T cells and monocytes, as well as B cells and granulocyte-lineage cells.
  • It is most intensely expressed by the most immature thymus T-lineage cells and is more intensely expressed by CD34-positive/CD33-positive myeloid cells (compared to more mature myeloid cells) and the earliest CD34-positive/CD10-positive B-cell precursor cells (compared to cells of later B-cell precursor stages).
  • CD99 (MIC2) is characteristically expressed in precursor B- and T-cell lymphoblastic lymphomas/leukemias, as well as in Ewing sarcoma/primitive neuroectodermal tumors (ES/PNET).
  • It has also been shown to be expressed in a few terminal deoxynucleotidyl transferase (TdT)-positive myeloid processes, but has been uniformly negative in TdT-negative myeloid processes.
  • A more recent study showed that 43% of acute myeloid leukemias (AMLs) and 55% of chloromas express CD99, concluding that CD99 is commonly expressed in AML and rarely seen in myeloproliferative disorders, myelodysplastic syndromes, or normal bone marrow.
  • Although this study speculated that MIC2 expression was probably not limited to TdT-positive AML, there was no comparison with TdT reactivity in this study.
  • OBJECTIVE: Since AML and high-grade myelodysplastic syndrome may occasionally be difficult to distinguish morphologically from acute lymphoblastic leukemia and ES/ PNET, we undertook a study to analyze MIC2 expression in conjunction with TdT reactivity in distinguishing AML or high-grade myelodysplastic syndrome from acute lymphoblastic leukemia and ES/PNET.
  • DESIGN: We studied bone marrow core and clot paraffin specimens from AML (classified according to criteria of the World Health Organization; n = 49), myelodysplastic syndromes (n = 4), precursor B-cell acute lymphoblastic leukemia (n = 4), ES/PNET (n = 1), and normal bone marrow (n = 3) with MIC2 (CD99) and TdT immunohistochemistry.
  • RESULTS: Overall, CD99 was expressed in 24 (49%) of 49 AML cases, including all (11/11) TdT-positive cases.
  • CD99 was expressed in all subtypes of AML except M5.
  • Expression of TdT was limited to a subset of AML-M0, -M1, -M2, and -M4, and AML with multilineage dysplasia.
  • CONCLUSIONS: In contrast to a previous study, CD99 expression was not restricted to TdT-positive hematologic proliferations.
  • In particular, the CD99-positive M3 and M7 AMLs were TdT negative.
  • An M5 AML may likely be excluded based on a uniform TdT-negative/CD99-negative immunophenotype.
  • [MeSH-major] Antigens, CD / metabolism. Bone Marrow / metabolism. Cell Adhesion Molecules / metabolism. DNA Nucleotidylexotransferase / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism
  • [MeSH-minor] Diagnosis, Differential. Flow Cytometry. Humans. Immunohistochemistry. Neuroectodermal Tumors, Primitive / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retrospective Studies. Sarcoma, Ewing / diagnosis

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  • (PMID = 16454553.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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90. Schalk E, Franke A, Koenigsmann M: [Acute myeloid leukemia with pulmonary manifestation]. Pneumologie; 2005 Sep;59(9):588-91
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  • [Title] [Acute myeloid leukemia with pulmonary manifestation].
  • [Transliterated title] Akute myeloische Leukämie mit pulmonaler Manifestation.
  • BACKGROUND: Extramedullary manifestations of leukemias are often misinterpreted.
  • The prognosis of pulmonary manifested leukemias is poor.
  • CASE REPORT: A 57-year-old female patient was admitted to our hospital because of refractory pneumonia and the suspicion of acute leukemia.
  • The diagnosis of acute myeloid leukemia (AML, FAB M5a) was derived from bone marrow aspiration.
  • The cytologic aspect of a bronchoalveolar lavage was dominated by leukemic blasts, therefore AML with pulmonary manifestation was diagnosed.
  • CONCLUSIONS: The pulmonary manifestation of AML can be diagnosed by bronchoscopy.
  • In contrast to the literature the initial course of the disease in this case was favourable possibly due to the addition of prednisolone to the cytotoxic treatment.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Lung Diseases / etiology
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Female. Humans. Middle Aged

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  • [ErratumIn] Pneumologie. 2005 Nov;59(11):782
  • (PMID = 16170731.001).
  • [ISSN] 0934-8387
  • [Journal-full-title] Pneumologie (Stuttgart, Germany)
  • [ISO-abbreviation] Pneumologie
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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91. Yoneda K, Morii T, Nieda M, Tsukaguchi N, Amano I, Tanaka H, Yagi H, Narita N, Kimura H: The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy. Leuk Res; 2005 Feb;29(2):147-52
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  • [Title] The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy.
  • In this study, we assessed the Valpha24+ NKT cell numbers in peripheral blood (PB) from 30 healthy donors and 70 patients with haematopoietic malignancy including chronic myelogenous leukemia (CML), malignant lymphoma (ML), acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).
  • Here, we demonstrated that PB Valpha24+ NKT cell numbers were significantly decreased in all the patients with haematopoietic malignancy in comparison with that in healthy donors (P < 0.005).
  • In particular CD4- CD8- Valpha24+ NKT cell numbers were more significantly decreased in the patients with haematopoietic malignancy (P < 0.0001).
  • [MeSH-major] Hematologic Neoplasms / blood. Killer Cells, Natural / cytology. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Antigens, CD8 / biosynthesis. Flow Cytometry. Humans. Lymphocyte Count. Lymphocytes / cytology. Lymphocytes / immunology. Survival Analysis

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  • (PMID = 15607362.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Receptors, Antigen, T-Cell, alpha-beta
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92. Santos FP, Rodrigues M, Mac-Donald Bley do Nascimento C, Kerbauy FR, Ribeiro AA, Mauro Kutner J, Hamerschlak N: Philadelphia-negative acute lymphoblastic leukemia in a chronic myeloid leukemia patient receiving dasatinib. Cytotherapy; 2010;12(1):113-5
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  • [Title] Philadelphia-negative acute lymphoblastic leukemia in a chronic myeloid leukemia patient receiving dasatinib.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Protein Kinase Inhibitors / adverse effects. Pyrimidines / adverse effects. Thiazoles / adverse effects
  • [MeSH-minor] Aged. Benzamides. Blast Crisis / chemically induced. Blast Crisis / immunology. Blast Crisis / physiopathology. Dasatinib. Hematopoietic Stem Cell Transplantation. Humans. Iatrogenic Disease / prevention & control. Imatinib Mesylate. Immunosuppressive Agents / therapeutic use. Male. Middle Aged. Piperazines / pharmacology. Piperazines / therapeutic use. Prednisone / therapeutic use. Remission Induction / methods. Treatment Outcome


93. Campana D: Status of minimal residual disease testing in childhood haematological malignancies. Br J Haematol; 2008 Nov;143(4):481-9
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  • [Title] Status of minimal residual disease testing in childhood haematological malignancies.
  • In children with acute leukaemia, measurements of minimal residual disease (MRD) provide unique information on treatment response and have become a crucial component of contemporary treatment protocols.
  • In acute lymphoblastic leukaemia (ALL), the most useful MRD assays are based on polymerase chain reaction (PCR) amplification of antigen-receptor genes, and on flow cytometric detection of abnormal immunophenotypes.
  • The latter is the only MRD assay available for most patients with acute myeloid leukaemia (AML).
  • PCR amplification of chromosomal breakpoints and fusion transcripts can also be used to track MRD in a minority of patients with ALL or AML.
  • Treatment de-intensification for patients with early MRD clearance is also being tested.
  • The identification of new markers of leukaemia and the use of increasingly sophisticated technologies for detection of rare cells should further facilitate routine monitoring of MRD and elucidate the features of drug-resistant leukaemic cells.

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  • (PMID = 18710378.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115422-04; United States / NCI NIH HHS / CA / CA115422; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / U01 CA060419-04; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA060419-04; United States / NCI NIH HHS / CA / R01 CA115422-04; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Number-of-references] 72
  • [Other-IDs] NLM/ NIHMS154353; NLM/ PMC2784675
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94. Gianfaldoni G, Mannelli F, Baccini M, Antonioli E, Leoni F, Bosi A: Clearance of leukaemic blasts from peripheral blood during standard induction treatment predicts the bone marrow response in acute myeloid leukaemia: a pilot study. Br J Haematol; 2006 Jul;134(1):54-7
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  • [Title] Clearance of leukaemic blasts from peripheral blood during standard induction treatment predicts the bone marrow response in acute myeloid leukaemia: a pilot study.
  • Although several parameters are useful for risk stratification of patients with acute myeloid leukaemia (AML), there are no firm criteria for predicting response to induction treatment of individual patients.
  • Daily flow cytometry (FC) analysis, carried out during induction treatment in 30 AML patients, showed that the clearance of blasts from peripheral blood (PBC) correlated closely with response, as assessed by bone marrow FC on day 14, and by morphologic analysis at haematopoietic recovery.
  • Therefore, a major treatment outcome can be predicted very early in AML patients, thus providing an opportunity for tailoring treatment modalities from the outset.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow / immunology. Cytarabine / administration & dosage. Female. Flow Cytometry. Humans. Idarubicin / administration & dosage. Leukocyte Count. Male. Middle Aged. Pilot Projects. Prognosis. Remission Induction

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  • (PMID = 16803567.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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95. Ahmad EI, Gawish HH, Al-Azizi NM, El-Hefni AM: The Prognostic Impact of K-RAS Mutations in Adult Acute Myeloid Leukemia Patients Treated with High Dose Cytarabine. J Egypt Natl Canc Inst; 2009 Dec;21(4):343-50
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  • [Title] The Prognostic Impact of K-RAS Mutations in Adult Acute Myeloid Leukemia Patients Treated with High Dose Cytarabine.
  • It represents one of the most common genetic alterations in acute myeloid leukemia (AML).
  • However there is still controversy about its clinical relevance on the treatment outcome of this leukemia.
  • OBJECTIVE: This study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in post induction consolidation chemotherapy in adult AML patients.
  • PATIENTS AND METHODS: The study comprised 71de novo AML patients with a male: Female ratio of 1.4: 1; their ages ranged from 21-59 years with a median of 37 years.
  • Blast cell percentage was significantly lower in mutRAS compared to wtRAS patients (p≤0.001).
  • The M4 subtype of AML and cases with Inv 16 showed significantly higher frequencies in mutRAS compared to wtRAS patients, (p=0.015, 0.003, respectively).
  • The patients were followed up for a median of 43 months (range 11-57 months).
  • This was not the case in the wtRAS group (p=0.285).
  • There was no significant difference in disease free survival (DFS) between mutRAS and wtRAS groups (p=0.923).
  • CONCLUSION: Adult AML patients carrying mutations in the K-RAS gene benefit from higher cytarabine doses more than wtRAS patients, so pretreatment mutation detection could be an important predictor for treatment strategy and survival of adult AML patients.
  • KEY WORDS: K-RAS mutations - Acute myeloid leukemia - Cytarabine.

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  • (PMID = 21415871.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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96. Löwenberg B: Acute myeloid leukemia: the challenge of capturing disease variety. Hematology Am Soc Hematol Educ Program; 2008;:1-11
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  • [Title] Acute myeloid leukemia: the challenge of capturing disease variety.
  • The difference between success and failure of treatment of acute myeloid leukemia (AML) is largely determined by genotypic leukemia-specific differences among patients.
  • The diversity of AML genotypes result from somatic genetic alterations settling down in succession in an individual's leukemia clone during the development of the disease.
  • Gene mutations, gene expression abnormalities and other molecular alterations (e.g., microRNA variations) affect critical functions in AML cells, and may exert profound effects on the therapeutic response and outcome of the disease.
  • Prototypes of common clinically significant gene aberrations involve transcription factors, signaling molecules and growth factor receptors.
  • The expanding knowledge in this area allowing for risk stratified therapy decisions and the development of targeted drug therapy, is becoming an increasingly important part of the modern individualized clinical management of AML.

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  • (PMID = 19074046.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / MECOM protein, human; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Transcription Factors
  • [Number-of-references] 80
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97. Leroy H, Roumier C, Huyghe P, Biggio V, Fenaux P, Preudhomme C: CEBPA point mutations in hematological malignancies. Leukemia; 2005 Mar;19(3):329-34
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  • The CCAAT/enhancer-binding protein-alpha (CEBPA) is a transcription factor strongly implicated in myelopoiesis through control of proliferation and differentiation of myeloid progenitors.
  • In this work, we analyzed characteristics of mutations and their correlation with disease characteristics described in previous studies.
  • CEBPA mutations were reported exclusively in acute myeloid leukemia (AML) (according to WHO classification criteria) and mutated patients preferentially belonged to M1, M2 and M4 FAB subtypes.
  • All but one case belonged to the 'intermediate' prognostic subgroup of MRC classification.
  • Systematic analysis of CEBPA mutations, in addition to that of alterations in master genes of hematopoiesis, may be useful to assess the prognosis of AML particularly in patients belonging to the 'intermediate' prognostic subgroup.

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  • (PMID = 15674366.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  • [Number-of-references] 39
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98. Moore MA, Chung KY, Plasilova M, Schuringa JJ, Shieh JH, Zhou P, Morrone G: NUP98 dysregulation in myeloid leukemogenesis. Ann N Y Acad Sci; 2007 Jun;1106:114-42
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  • [Title] NUP98 dysregulation in myeloid leukemogenesis.
  • It is mapped to 11p15.5 and is fused to a number of distinct partners, including nine members of the homeobox family as a consequence of leukemia-associated chromosomal translocations.
  • NUP98-HOXA9 is associated with the t(7;11)(p15;p15) translocation in acute myeloid leukemia (AML), myelodysplastic syndrome, and blastic crisis of chronic myeloid leukemia.
  • Expression of NUP98-HOXA9 in murine bone marrow resulted in a myeloproliferative disease progressing to AML by 7-8 months.
  • NUP98-HOXA9 expression inhibited erythroid and myeloid differentiation but enhanced serial progenitor replating.
  • In NUP98-HOX-transduced CD34(+) cells and cells from AML patients with t(7;11)(p15;p15) NUP98 was no longer associated with the nuclear pore complex but formed intranuclear aggregation bodies.
  • Analysis of NUP98 allelic expression in AML and myelodysplastic syndrome showed loss of heterozygosity observed in 29% of the former and 8% of the latter.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Nuclear Pore Complex Proteins / physiology
  • [MeSH-minor] Alleles. Animals. Antigens, CD34 / biosynthesis. Cell Nucleus / metabolism. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 7. Humans. Loss of Heterozygosity. Mice. Mice, Inbred NOD. Mice, SCID. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism

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  • (PMID = 17442773.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 92792; United States / NCI NIH HHS / CA / CA118085
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human
  • [Number-of-references] 103
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99. Bagrintseva K, Geisenhof S, Kern R, Eichenlaub S, Reindl C, Ellwart JW, Hiddemann W, Spiekermann K: FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L). Blood; 2005 May 1;105(9):3679-85
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  • [Title] FLT3-ITD-TKD dual mutants associated with AML confer resistance to FLT3 PTK inhibitors and cytotoxic agents by overexpression of Bcl-x(L).
  • FLT3 (fms-like tyrosine kinase 3) is constitutively activated in about 30% of patients with acute myeloid leukemia (AML) and represents a disease-specific molecular marker.
  • As molecular mechanisms of resistance, we found that FLT3-ITD-TKD mutants cause hyperactivation of STAT5 (signal transducer and activator of transcription-5), leading to upregulation of Bcl-x(L) and RAD51 and arrest in the G(2)M phase of the cell cycle.
  • Our data provide the molecular basis for understanding clinical FLT3 PTK inhibitor resistance and point to therapeutical strategies to overcome drug resistance in patients with AML.
  • [MeSH-major] Drug Resistance, Neoplasm / drug effects. Leukemia, Myeloid / drug therapy. Point Mutation. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Recombinant Fusion Proteins / pharmacology. Tandem Repeat Sequences
  • [MeSH-minor] Acute Disease. Animals. Cell Line. DNA-Binding Proteins / drug effects. DNA-Binding Proteins / genetics. Enzyme Inhibitors / pharmacology. Humans. Mice. Milk Proteins / drug effects. Proto-Oncogene Proteins c-bcl-2 / genetics. Rad51 Recombinase. STAT5 Transcription Factor. Trans-Activators / drug effects. Transfection. Up-Regulation / drug effects. bcl-X Protein. fms-Like Tyrosine Kinase 3

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  • (PMID = 15626738.001).
  • [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 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Milk Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / bcl-X Protein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.7.- / RAD51 protein, human; EC 2.7.7.- / Rad51 Recombinase; EC 2.7.7.- / Rad51 protein, mouse
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100. Chen Y, Liu K, Xu L, Chen H, Liu D, Zhang X, Shi H, Han W, Wang Y, Zhao T, Wang J, Wang J, Huang X: HLA-mismatched hematopoietic SCT without in vitro T-cell depletion for myelodysplastic syndrome. Bone Marrow Transplant; 2010 Aug;45(8):1333-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-mismatched hematopoietic SCT without in vitro T-cell depletion for myelodysplastic syndrome.
  • We have developed a new protocol for HLA-mismatched (including haploidentical) HSCT using G-CSF-primed BM plus G-CSF-mobilized PBSCs without in vitro T-cell depletion.
  • All patients achieved sustained myeloid engraftment.
  • The cumulative incidence of grades II-IV acute GVHD (aGVHD) was 60% and that of grades III and IV aGVHD was 15%.
  • The 2-year probability of leukemia-free survival (LFS) was 65%.
  • Patients transplanted within 7 months of diagnosis had better LFS (89 vs 43% ).
  • Severe aGVHD decreased the LFS significantly by increasing non-relapse mortality (NRM).
  • Patients with high-risk MDS benefit from receiving HSCT early in the course of the disease.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Histocompatibility. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adult. Bone Marrow Transplantation. Female. Graft Survival. Graft vs Host Disease. Granulocyte Colony-Stimulating Factor / therapeutic use. Histocompatibility Testing. Humans. Incidence. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Survival Analysis. Treatment Outcome. Young Adult






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