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1. Promsuwicha O, Auewarakul CU: Positive and negative predictive values of HLA-DR and CD34 in the diagnosis of acute promyelocytic leukemia and other types of acute myeloid leukemia with recurrent chromosomal translocations. Asian Pac J Allergy Immunol; 2009 Dec;27(4):209-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Positive and negative predictive values of HLA-DR and CD34 in the diagnosis of acute promyelocytic leukemia and other types of acute myeloid leukemia with recurrent chromosomal translocations.
  • The predictive value of HLA-DR and CD34 in the diagnosis of four distinct genetic entities of acute myeloid leukemia (AML) is presently not established.
  • The PPV and NPV of other myeloid markers such as CD117, MPO and CD11c to diagnose t(15;17) were much lower than those of HLA-DR and CD34.

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  • (PMID = 20232575.001).
  • [ISSN] 0125-877X
  • [Journal-full-title] Asian Pacific journal of allergy and immunology
  • [ISO-abbreviation] Asian Pac. J. Allergy Immunol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens
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2. Inaba H, Stewart CF, Crews KR, Yang S, Pounds S, Pui CH, Rubnitz JE, Razzouk BI, Ribeiro RC: Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia. Cancer; 2010 Jan 1;116(1):98-105
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  • [Title] Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia.
  • BACKGROUND: The prognosis after recurrence of pediatric acute myeloid leukemia (AML) is poor, and effective salvage regimens are urgently needed.
  • METHODS: In phase 1 and pilot studies, the authors evaluated the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of a 5-day course of cladribine followed by topotecan in pediatric patients with recurrent/refractory AML.

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  • [Copyright] Copyright 2010 American Cancer Society.
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  • (PMID = 19885837.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 7M7YKX2N15 / Topotecan
  • [Other-IDs] NLM/ NIHMS151111; NLM/ PMC2920745
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3. Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ: Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value. Blood; 2010 Sep 23;116(12):2122-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.
  • Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in acute myeloid leukemia (AML), but their prevalence and prognostic impact remain to be explored in large extensively characterized AML series, and also in various other hematologic malignancies.
  • Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of acute lymphoblastic leukemia (n = 96), and none in chronic myeloid leukemias (n = 81).
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 20538800.001).
  • [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] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2
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4. Bacher U, Kern W, Schnittger S, Hiddemann W, Haferlach T, Schoch C: Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia. Haematologica; 2005 Nov;90(11):1502-10
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  • [Title] Population-based age-specific incidences of cytogenetic subgroups of acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: It is well known that the different cytogenetic subgroups of acute myeloid leukemia (AML) show different age-specific frequencies.
  • There were also different age-specific incidences of some recurrent molecular mutations.
  • [MeSH-major] Cytogenetics. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16266897.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Genetic Markers
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5. Falini B, Mecucci C, Saglio G, Lo Coco F, Diverio D, Brown P, Pane F, Mancini M, Martelli MP, Pileri S, Haferlach T, Haferlach C, Schnittger S: NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia. Haematologica; 2008 Mar;93(3):439-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia.
  • Acute myeloid leukemia carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc(+) acute myeloid leukemia) represents one-third of adult AML (50-60% of all acute myeloid leukemia with normal karyotype) and shows distinct biological, pathological and clinical features.
  • We confirm in 2562 patients with acute myeloid leukemia our previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities.
  • Taken together, these findings make NPMc+ acute myeloid leukemia a good candidate for inclusion in the upcoming World Health Organization classification.
  • [MeSH-major] Cytoplasm / chemistry. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Bone Marrow / pathology. Cell Nucleus / chemistry. Chromosome Aberrations. Chromosome Inversion. Cohort Studies. DNA Mutational Analysis. Germany / epidemiology. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 18268276.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin
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6. Erkeland SJ, Verhaak RG, Valk PJ, Delwel R, Löwenberg B, Touw IP: Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia. Cancer Res; 2006 Jan 15;66(2):622-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Significance of murine retroviral mutagenesis for identification of disease genes in human acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with a variable response to treatment.
  • Recurrent cytogenetic defects and acquired mutations in regulatory genes are associated with AML subtypes and prognosis.
  • Here, we show that mouse leukemia genes identified by retroviral insertion mutagenesis are more frequently differentially expressed in distinct subclasses of adult and pediatric AML than randomly selected genes or genes located more distantly from a virus integration site.
  • Our data support the validity of retroviral insertion mutagenesis in mice for human disease and indicate that combining these murine screens for potential proto-oncogenes with GEP in human AML may help to identify critical disease genes and novel pathogenetic networks in leukemia.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid / genetics. Mutagenesis, Insertional. Proto-Oncogenes
  • [MeSH-minor] Acute Disease. Adult. Animals. Child. Humans. Mice. Retroviridae / genetics. Signal Transduction. Transcription, Genetic

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  • (PMID = 16423987.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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7. Ley TJ, Ding L, Walter MJ, McLellan MD, Lamprecht T, Larson DE, Kandoth C, Payton JE, Baty J, Welch J, Harris CC, Lichti CF, Townsend RR, Fulton RS, Dooling DJ, Koboldt DC, Schmidt H, Zhang Q, Osborne JR, Lin L, O'Laughlin M, McMichael JF, Delehaunty KD, McGrath SD, Fulton LA, Magrini VJ, Vickery TL, Hundal J, Cook LL, Conyers JJ, Swift GW, Reed JP, Alldredge PA, Wylie T, Walker J, Kalicki J, Watson MA, Heath S, Shannon WD, Varghese N, Nagarajan R, Westervelt P, Tomasson MH, Link DC, Graubert TA, DiPersio JF, Mardis ER, Wilson RK: DNMT3A mutations in acute myeloid leukemia. N Engl J Med; 2010 Dec 16;363(25):2424-33
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  • [Title] DNMT3A mutations in acute myeloid leukemia.
  • BACKGROUND: The genetic alterations responsible for an adverse outcome in most patients with acute myeloid leukemia (AML) are unknown.
  • We sequenced the exons of DNMT3A in 280 additional patients with de novo AML to define recurring mutations.
  • CONCLUSIONS: DNMT3A mutations are highly recurrent in patients with de novo AML with an intermediate-risk cytogenetic profile and are independently associated with a poor outcome. (Funded by the National Institutes of Health and others.).


8. Bedekovics J, Rejto L, Telek B, Udvardy M, Ujfalusi A, Oláh E, Hevessy Z, Kappelmayer J, Kajtár B, Méhes G: [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression]. Orv Hetil; 2009 May 31;150(22):1031-5
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  • [Title] [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression].
  • [Transliterated title] Mutáns nucleophosmin fehérje kimutatása akut myeloid leukaemiában: az NPMc+ AML biológiai és klinikai jellemzôi.
  • The mutation of the nucleophosmin gene (NPM1) is the most frequently occurring genetic aberration in acute myeloid leukemia (AML).
  • All but one were female patients, and were diagnosed as de novo AML with no recurrent cytogenetic aberrations (6/23, 26.1%).
  • [MeSH-major] Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Bone Marrow / chemistry. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / analysis. Nuclear Proteins / genetics

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  • (PMID = 19465351.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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9. Yang L, Zhang Y, Zhang MR, Xiao ZJ: [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations]. Zhonghua Yi Xue Za Zhi; 2005 Aug 31;85(33):2312-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].
  • OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.
  • METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.
  • [MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16321221.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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10. Sarvis JA, Auge BK: Myeloid (granulocytic) sarcoma of epididymis as rare manifestation of recurrent acute myelogenous leukemia. Urology; 2009 May;73(5):1163.e1-3
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  • [Title] Myeloid (granulocytic) sarcoma of epididymis as rare manifestation of recurrent acute myelogenous leukemia.
  • Myeloid sarcoma involving the genitourinary system is a rare complication associated with acute myelogenous leukemia or other myeloproliferative disorders.
  • We report the second known case of myeloid sarcoma involving the epididymis in a patient with a history of acute myelogenous leukemia.
  • [MeSH-major] Epididymis / pathology. Leukemia, Myeloid, Acute / diagnosis. Sarcoma, Myeloid / diagnosis. Testicular Neoplasms / diagnosis


11. Dang L, Jin S, Su SM: IDH mutations in glioma and acute myeloid leukemia. Trends Mol Med; 2010 Sep;16(9):387-97
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  • [Title] IDH mutations in glioma and acute myeloid leukemia.
  • The systematic sequencing of glioblastoma multiforme (GBM) genomes has identified the recurrent mutation of IDH1, a gene encoding NADP(+)-dependent isocitrate dehydrogenase 1 (IDH1) that catalyzes the oxidative decarboxylation of isocitrate yielding alpha-ketoglutarate (alpha-KG).
  • Subsequent studies have confirmed recurrent IDH1 and IDH2 mutations in up to 70% of low-grade glioma and secondary GBM, as well as in 10% of acute myeloid leukemia (AML) cases.
  • [MeSH-major] Brain Neoplasms / enzymology. Glioma / enzymology. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / enzymology. Mutation


12. Suela J, Alvarez S, Cigudosa JC: DNA profiling by arrayCGH in acute myeloid leukemia and myelodysplastic syndromes. Cytogenet Genome Res; 2007;118(2-4):304-9
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  • [Title] DNA profiling by arrayCGH in acute myeloid leukemia and myelodysplastic syndromes.
  • Acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) represent two distinct but related myeloid haematological neoplasms.
  • Both types of genomic studies have confirmed that recurrent genomic losses and gains can almost exclusively be found in cases with complex karyotype.
  • Recently, single- nucleotide-polymorphism based arrays have been used in AML showing that loss of heterozygosity (LOH) is a common feature in normal karyotype leukemia.
  • [MeSH-major] DNA, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Nucleic Acid Hybridization


13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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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14. Verhaak RG, Valk PJ: Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia. Cancer Treat Res; 2010;145:67-83
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  • [Title] Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia.
  • The pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision making in acute myeloid leukemia (AML).
  • The World Health Organization (WHO) has recognized this important information by including, besides clinical, cytological, cytochemical, and immunophenotypical features, recurrent cytogenetic abnormalities in its classification (Table 1).
  • [MeSH-major] Genes, Neoplasm. Leukemia, Myeloid, Acute / genetics


15. Pedersen-Bjergaard J, Andersen MT, Andersen MK: Genetic pathways in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2007;:392-7
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  • [Title] Genetic pathways in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia.
  • In therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML), at least eight alternative genetic pathways have been defined based on characteristic recurrent chromosome abnormalities.
  • Class I and Class II mutations are significantly associated, indicating their cooperation in leukemogenesis The chromosome aberrations and gene mutations detected in the therapy-related and in the de novo subsets of MDS and AML are identical, although the frequencies with which they are observed may differ.
  • Hence, therapy-related and de novo MDS and AML are identical diseases and should be subclassified and treated similarly.


16. Panani AD: Gain of an isochromosome 5p: a rare recurrent abnormality in acute myeloid leukemia. In Vivo; 2006 May-Jun;20(3):359-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gain of an isochromosome 5p: a rare recurrent abnormality in acute myeloid leukemia.
  • Chromosomal abnormalities characterize the biological behavior of acute myeloid leukemia (AML), also facilitating the identification of genes responsible for its development and/or progression.
  • [MeSH-major] Chromosome Disorders / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 8 / genetics. Isochromosomes / genetics. Leukemia, Myeloid, Acute / genetics


17. Landrette SF, Kuo YH, Hensen K, Barjesteh van Waalwijk van Doorn-Khosrovani S, Perrat PN, Van de Ven WJ, Delwel R, Castilla LH: Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11. Blood; 2005 Apr 1;105(7):2900-7
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  • [Title] Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11.
  • Recurrent chromosomal rearrangements are associated with the development of acute myeloid leukemia (AML).
  • This fusion protein inhibits the core-binding factor (CBF), resulting in a block of hematopoietic differentiation, and induces leukemia upon the acquisition of additional mutations.
  • In this study, we demonstrate that Plag1 and Plagl2 independently cooperate with CBF beta-SMMHC in vivo to efficiently trigger leukemia with short latency in the mouse.
  • Overall, this study shows that Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Animals. Female. G1 Phase / immunology. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / cytology. Humans. Male. Mice. Mice, Mutant Strains. Middle Aged. Mutagenesis, Insertional. Retroviridae / genetics. S Phase / immunology

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  • (PMID = 15585652.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096983-01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / PLAG1 protein, human; 0 / PLAGL2 protein, human; 0 / RNA-Binding Proteins; 0 / Transcription Factors
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18. Haferlach T: Molecular genetic pathways as therapeutic targets in acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2008;:400-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular genetic pathways as therapeutic targets in acute myeloid leukemia.
  • The heterogeneity of acute myeloid leukemia (AML) results from a complex network of cytogenetic aberrations and molecular mutations.
  • Clinical variances within distinct genetically defined subgroups could in part be linked to the interaction of diverse mutation classes, and the subdivision of normal karyotype AML on the basis of recurrent molecular mutations gains increasing relevance for therapeutic decisions.

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  • (PMID = 19074117.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Genetic Markers; 0 / Oxides; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 111
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19. Su YC, Chen CB, Chang YT, Tung YT, Li DK: hSNF5 /INI1 mutation analysis in acute myeloid leukemia. Int J Hematol; 2008 Mar;87(2):172-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] hSNF5 /INI1 mutation analysis in acute myeloid leukemia.
  • Previous studies indicated that region 11.2 of the long arm of chromosome 22 (22q11.2) might be a locus encoding a tumor suppressor gene, since its deletion is a recurrent genetic characteristic of aggressive pediatric cancer.
  • To investigate whether the hSNF5/INI1 gene is involved in leukemogenesis, mutation analysis of the hSNF5/INI1 gene was performed in the present study using 5 hematopoietic cell lines, acute myeloid leukemia (AML) specimen and normal control.
  • [MeSH-major] Chromosomal Proteins, Non-Histone / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide / genetics. Transcription Factors / genetics

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  • (PMID = 18266055.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / SMARCB1 protein, human; 0 / Transcription Factors
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20. Gupta M, Raghavan M, Gale RE, Chelala C, Allen C, Molloy G, Chaplin T, Linch DC, Cazier JB, Young BD: Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia. Genes Chromosomes Cancer; 2008 Sep;47(9):729-39
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia.
  • The acquisition of uniparental disomy (aUPD) in acute myeloid leukemia (AML) results in homozygosity for known gene mutations.
  • Novel recurrent regions of aUPD were uncovered at 2p, 17p, 2q, 17q, 1p, and Xq.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Uniparental Disomy / genetics

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  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 18506749.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789; United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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21. Niparuck P, Chuncharunee S, Ungkanont A, Udomtrupayakul U, Aungchaisuksiri P, Rerkamnuatchoke B, Jootar S, Atichartakarn V: Long-term outcomes of de novo acute myeloid leukemia in Thai patients. J Med Assoc Thai; 2009 Sep;92(9):1143-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes of de novo acute myeloid leukemia in Thai patients.
  • BACKGROUND: Acute myeloid leukemia (AML) is the heterogeneous disease.
  • MATERIAL AND METHOD: The authors performed a retrospective analysis of 106 adults with newly diagnosed de novo AML at Ramathibodi Hospital between 2003 and 2007.
  • AML with recurrent cytogenetic translocations, complex chromosome, trisomy 8, polyploidy, del 5q and del 7q were found in 16.8, 6.3, 5.3, 5.3, 2.1 and 3.2%, respectively.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19772172.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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22. Radtke I, Mullighan CG, Ishii M, Su X, Cheng J, Ma J, Ganti R, Cai Z, Goorha S, Pounds SB, Cao X, Obert C, Armstrong J, Zhang J, Song G, Ribeiro RC, Rubnitz JE, Raimondi SC, Shurtleff SA, Downing JR: Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12944-9
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic analysis reveals few genetic alterations in pediatric acute myeloid leukemia.
  • Pediatric de novo acute myeloid leukemia (AML) is an aggressive malignancy with current therapy resulting in cure rates of only 60%.
  • To approach this goal, we examined diagnostic leukemic samples from a cohort of 111 children with de novo AML using single-nucleotide-polymorphism microarrays and candidate gene resequencing.
  • Our data demonstrate that, in contrast to pediatric acute lymphoblastic leukemia (ALL), de novo AML is characterized by a very low burden of genomic alterations, with a mean of only 2.38 somatic copy-number alterations per leukemia, and less than 1 nonsynonymous point mutation per leukemia in the 25 genes analyzed.
  • Even more surprising was the observation that 34% of the leukemias lacked any identifiable copy-number alterations, and 28% of the leukemias with recurrent translocations lacked any identifiable sequence or numerical abnormalities.
  • The only exception to the presence of few mutations was acute megakaryocytic leukemias, with the majority of these leukemias being characterized by a high number of copy-number alterations but rare point mutations.
  • These data reflect a remarkably low burden of genomic alterations within pediatric de novo AML, which is in stark contrast to most other human malignancies.

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  • (PMID = 19651601.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / PHS HHS / / 21765
  • [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 / CCDC26 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLLT4 protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; EC 3.6.1.- / Kinesin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2716382
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23. Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A: Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma. Leukemia; 2007 Jun;21(6):1183-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
  • Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.
  • [MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
  • [MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods


24. Lin P, Medeiros LJ, Yin CC, Abruzzo LV: Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Apr 1;166(1):82-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia.
  • We identified a reciprocal translocation between chromosomes 3 and 8, with breakpoints at bands 3q26 and 8q24, in five patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).
  • We conclude that the t(3;8)(q26;q24) is a recurrent translocation associated with therapy-related MDS/AML or de novo AML, and is frequently associated with monosomy 7.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Recurrence, Local / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Humans. Karyotyping. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Male. Middle Aged. Sarcoma / drug therapy. Sarcoma / pathology


25. Walter MJ, Payton JE, Ries RE, Shannon WD, Deshmukh H, Zhao Y, Baty J, Heath S, Westervelt P, Watson MA, Tomasson MH, Nagarajan R, O'Gara BP, Bloomfield CD, Mrózek K, Selzer RR, Richmond TA, Kitzman J, Geoghegan J, Eis PS, Maupin R, Fulton RS, McLellan M, Wilson RK, Mardis ER, Link DC, Graubert TA, DiPersio JF, Ley TJ: Acquired copy number alterations in adult acute myeloid leukemia genomes. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12950-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired copy number alterations in adult acute myeloid leukemia genomes.
  • Cytogenetic analysis of acute myeloid leukemia (AML) cells has accelerated the identification of genes important for AML pathogenesis.
  • To complement cytogenetic studies and to identify genes altered in AML genomes, we performed genome-wide copy number analysis with paired normal and tumor DNA obtained from 86 adult patients with de novo AML using 1.85 million feature SNP arrays.
  • Twenty-four percent of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were recurrent.
  • The mRNA expression levels of 57 genes were significantly altered in 27 of 50 recurrent CNA regions <5 megabases in size.

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  • (PMID = 19651600.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL083012; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHLBI NIH HHS / HL / T32 HL007088; United States / NCI NIH HHS / CA / U10 CA101140
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / NSD1 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Nup98 protein, human
  • [Other-IDs] NLM/ PMC2716381
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26. Pedersen-Bjergaard J, Christiansen DH, Desta F, Andersen MK: Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2006 Nov;20(11):1943-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia.
  • Alternative genetic pathways were previously outlined in the pathogenesis of therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML) based on cytogenetic characteristics.
  • Some of the chromosome aberrations, the recurrent balanced translocations or inversions, directly result in chimeric rearrangement of genes for hematopoietic transcription factors (class II mutations) which disturb cellular differentiation.
  • Therapy-related and de novo myelodysplasia and acute myeloid leukemia seem to share genetic pathways, and surprisingly gene mutations were in general not more frequent in patients with t-MDS or t-AML as compared to similar cases of de novo MDS and AML studied previously.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Humans. Mutation


27. Palmqvist L, Argiropoulos B, Pineault N, Abramovich C, Sly LM, Krystal G, Wan A, Humphries RK: The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia. Blood; 2006 Aug 1;108(3):1030-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia.
  • Here, we demonstrate that overexpression of the wild-type (wt) Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions (NUP98-HOXA10 and NUP98-HOXD13) to induce aggressive acute myeloid leukemia (AML).
  • Furthermore, our data support the finding that Meis1 overexpression leads to marked elevation in Flt3 transcription and extend it to the context of NUP98-HOX-induced leukemia.
  • Together, these results support a multistep model where the synergism between NUP98-HOX and wt-Flt3 is the result of the ability of Flt3 to increase proliferation of myeloid progenitors blocked in differentiation by NUP98-HOX fusions and reveal a direct role for wt-Flt3 in the pathobiology of AML.
  • Given the similarities in the leukemogenic role of native HOX and NUP98-fused HOX genes, our results underscore the clinical significance of the recurrent co-overexpression of wt-FLT3 and HOX in human leukemia and suggest that specific FLT3 inhibitors could be useful in treatment of HOX-induced AML or acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia, Myeloid / etiology. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion
  • [MeSH-minor] Acute Disease. Animals. Bone Marrow Cells. Bone Marrow Transplantation. Cell Differentiation. Cell Line. Cell Proliferation. Gene Expression Regulation, Neoplastic. Mice. Transcription Factors. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16861351.001).
  • [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 / Homeodomain Proteins; 0 / Hoxd13 protein, mouse; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 140441-81-2 / HOXA10 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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28. Falini B, Tiacci E, Martelli MP, Ascani S, Pileri SA: New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues. Discov Med; 2010 Oct;10(53):281-92
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues.
  • Here, we focus on changes that, as compared to the 2001 edition, were introduced into the 2008 WHO classification of acute myeloid leukemia (AML) and related precursor neoplasms.
  • The category of AML with recurrent genetic abnormalities was expanded to account for 60% of AML by adding three distinct entities, i.e., AML with t(6,9), inv(3), or t(1;22), and two provisional entities, i.e., AML with mutated NPM1 or CEBPA.
  • Finally, we describe the unique characteristics of myeloid proliferations associated with Down syndrome and blastic plasmacytoid dendritic cell neoplasm.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / pathology. Lymphoproliferative Disorders / classification. Lymphoproliferative Disorders / pathology. Medical Oncology / trends. Neoplasms / classification. Neoplasms / pathology

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  • (PMID = 21034669.001).
  • [ISSN] 1944-7930
  • [Journal-full-title] Discovery medicine
  • [ISO-abbreviation] Discov Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
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29. Murata M, Ishikawa Y, Ohashi H, Terakura S, Ozeki K, Kiyoi H, Naoe T: Donor cell leukemia after allogeneic peripheral blood stem cell transplantation: a case report and literature review. Int J Hematol; 2008 Jul;88(1):111-5
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  • [Title] Donor cell leukemia after allogeneic peripheral blood stem cell transplantation: a case report and literature review.
  • A 49-year-old male developed recurrent acute myeloid leukemia 27 months after allogeneic peripheral blood stem cell transplantation (PBSCT) from an HLA-identical brother.
  • Thus, this recipient developed donor cell leukemia (DCL).
  • [MeSH-major] Leukemia, Myeloid, Acute. Living Donors. Peripheral Blood Stem Cell Transplantation

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  • (PMID = 18470599.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha
  • [Number-of-references] 27
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30. Levine RL, Loriaux M, Huntly BJ, Loh ML, Beran M, Stoffregen E, Berger R, Clark JJ, Willis SG, Nguyen KT, Flores NJ, Estey E, Gattermann N, Armstrong S, Look AT, Griffin JD, Bernard OA, Heinrich MC, Gilliland DG, Druker B, Deininger MW: The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood; 2005 Nov 15;106(10):3377-9
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  • [Title] The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia.
  • Recently, we and others identified a single recurrent somatic activating mutation (JAK2V617F) in the Janus kinase 2 (JAK2) tyrosine kinase in the myeloproliferative disorders (MPDs) polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis.
  • We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML)/atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B-lineage acute lymphoblastic leukemia (ALL), T-cell ALL, and chronic lymphocytic leukemia (CLL).
  • These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies.


31. Trost D, Hildebrandt B, Beier M, Müller N, Germing U, Royer-Pokora B: Molecular cytogenetic profiling of complex karyotypes in primary myelodysplastic syndromes and acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Feb;165(1):51-63
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  • [Title] Molecular cytogenetic profiling of complex karyotypes in primary myelodysplastic syndromes and acute myeloid leukemia.
  • Complex chromosomal aberrations are present in < or =30% of patients with primary myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) and are associated with a poor prognosis.
  • To obtain a more comprehensive view of the recurrent aberrations, we performed spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) with selected probes on bone marrow samples from 17 patients with primary MDS and 3 with primary AML.
  • A detailed analysis of specific breakpoints and deletions revealed recurrent involvement of specific chromosomal bands harboring known tumor suppressor genes or oncogenes.
  • [MeSH-major] Karyotyping / methods. Leukemia, Myeloid / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Aged. Chromosome Mapping. Cytogenetics / methods. Female. Genetic Markers. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged


32. Wieser R, Scheideler M, Hackl H, Engelmann M, Schneckenleithner C, Hiden K, Papak C, Trajanoski Z, Sill H, Fonatsch C: microRNAs in acute myeloid leukemia: expression patterns, correlations with genetic and clinical parameters, and prognostic significance. Genes Chromosomes Cancer; 2010 Mar;49(3):193-203
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  • [Title] microRNAs in acute myeloid leukemia: expression patterns, correlations with genetic and clinical parameters, and prognostic significance.
  • Acute myeloid leukemia (AML) is a malignant disease of hematopoietic cells whose emergence, course, and prognosis is affected by specific recurrent genetic alterations like chromosome aberrations and point mutations, as well as by changes in the expression of certain genes.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. MicroRNAs / genetics. RNA, Neoplasm / genetics
  • [MeSH-minor] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Hematopoietic Stem Cells / pathology. Hematopoietic Stem Cells / physiology. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis. Survival Analysis. Transcription, Genetic

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  • (PMID = 20013895.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 19795; Austria / Austrian Science Fund FWF / / P 20920; Austria / Austrian Science Fund FWF / / P 21401
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm
  • [Number-of-references] 72
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33. Quentmeier H, Schneider B, Röhrs S, Romani J, Zaborski M, Macleod RA, Drexler HG: SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines. J Hematol Oncol; 2009;2:3
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  • [Title] SET-NUP214 fusion in acute myeloid leukemia- and T-cell acute lymphoblastic leukemia-derived cell lines.
  • BACKGROUND: SET-NUP214 fusion resulting from a recurrent cryptic deletion, del(9)(q34.11q34.13) has recently been described in T-cell acute lymphoblastic leukemia (T-ALL) and in one case of acute myeloid leukemia (AML).
  • RESULTS: Of 141 human leukemia/lymphoma cell lines tested, only the T-ALL cell line LOUCY and the AML cell line MEGAL expressed the SET(TAF-Ibeta)-NUP214 fusion gene transcript.
  • [MeSH-major] Histone Chaperones / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics


34. Lee MY, Tan TD, Feng AC: Clinicopathologic analysis of acute myeloid leukemia in a single institution: biphenotypic acute myeloid leukemia may not be an aggressive subtype. J Chin Med Assoc; 2007 Jul;70(7):269-73
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  • [Title] Clinicopathologic analysis of acute myeloid leukemia in a single institution: biphenotypic acute myeloid leukemia may not be an aggressive subtype.
  • BACKGROUND: Most acute leukemias are classified as lymphoid or myeloid lineages by standard microscopic morphology, cytochemistry and a panel of immunologic markers.
  • The World Health Organization classification of acute leukemia incorporates morphologic, cytogenetic, immunologic and clinical features to define the entities that are biologically homogeneous and that have clinical relevance.
  • The purpose of this study was to determine the clinicopathologic characteristics of acute myeloid leukemia (AML) in Taiwan.
  • There were 9 cases (13%) with recurrent cytogenetic abnormality, 7 (10%) multilineage dysplasia-related, 7 (10%) therapy-related, 39 (56%) not other categorized and 8 (11%) of ambiguous lineage.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology

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  • (PMID = 17631462.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
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35. Armengol G, Canellas A, Alvarez Y, Bastida P, Toledo JS, Pérez-Iribarne Mdel M, Camós M, Tuset E, Estella J, Coll MD, Caballín MR, Knuutila S: Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia. Leuk Lymphoma; 2010 Jan;51(1):114-24
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  • [Title] Genetic changes including gene copy number alterations and their relation to prognosis in childhood acute myeloid leukemia.
  • We studied a series of 68 subjects diagnosed with childhood acute myeloid leukemia (AML) using conventional cytogenetics and fluorescence in situ hybridization (FISH), polymerase chain reaction (PCR) to analyze mutations in FLT3 and NPM1 genes, and/or array comparative genomic hybridization (CGH).
  • They probably correspond to non passenger alterations that cooperate with the recurrent translocations.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation


36. Carnicer MJ, Lasa A, Buschbeck M, Serrano E, Carricondo M, Brunet S, Aventin A, Sierra J, Di Croce L, Nomdedeu JF: K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML). Ann Hematol; 2008 Oct;87(10):819-27
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  • [Title] K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML).
  • The CEBPA gene codes for a transcription factor that has a pivotal role in controlling proliferation and differentiation of myeloid progenitors.
  • Acquired CEBPA mutations have been found in acute myeloid leukemias (AML) with a good prognosis, and most of these patients have a normal karyotype.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 18587575.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Receptors, Antigen, T-Cell, gamma-delta
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37. Pereira FG, Metze K, Costa FP, Lima CS, Lorand-Metze I: Phenotypic quantitative features of patients with acute myeloid leukemia. Neoplasma; 2006;53(2):155-60
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  • [Title] Phenotypic quantitative features of patients with acute myeloid leukemia.
  • The recent WHO classification for acute myeloid leukemias (AML) separates entities by recurrent cytogenetic abnormalities and immunophenotypic features presenting prognostic impact.
  • We have examined the expression of several lineage and maturation linked antigens used in routine immunophenotyping of patients with de novo AML, using a 3-color two-step panel.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal. Antigens, CD / metabolism. Female. Flow Cytometry. Humans. Male. Middle Aged. Neoplasm, Residual. Phenotype. Prognosis. Survival Analysis

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  • (PMID = 16575472.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Biomarkers, Tumor
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38. Kuriyama K: [Classification of myeloid leukemias]. Nihon Rinsho; 2009 Oct;67(10):1853-62
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  • [Title] [Classification of myeloid leukemias].
  • Myeloid leukemia in this series corresponds to the myeloid neoplasms of the 4th WHO classification of pathology and genetics of tumor of haematopoietic and lymphoid tissue.
  • The myeloid neoplasms are composed of six categories, which are 1) myeloproliferative neoplasms (MPN), a new category of 2) myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB or FGFR1, 3) myelodysplastic syndrome (MDS)/MPN, 4) MDS, 5) acute myeloid leukemia (AML) and related precursor neoplasms, and 6) acute leukemias of ambiguous lineage.
  • In MPNs without chronic myelogenous leukemia, the genetic marker of JAK2 V617F is added to the diagnostic criteria for polycythemia vera, essential thrombocythemia and primary myelofibrosis.
  • 22) (p13; q13); RBM15-MKL1 are added to the subtype of AML with recurrent genetic abnormalities, and AML with gene mutations of NPM1 and CEBPA are also added as provisional entities of it.
  • The myeloid neoplasms of the 4th WHO classification are comprehensive and seem to be dynamic by incorporating the results of leukemia researches.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Eosinophilia. Humans. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor beta / genetics. World Health Organization

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  • (PMID = 19860179.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Number-of-references] 14
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39. Verra WC, Snijders TJ, Seute T, Han KS, Nieuwenhuis HK, Rutten GJ: Myeloid sarcoma presenting as a recurrent, multifocal nerve root entrapment syndrome. J Neurooncol; 2009 Jan;91(1):59-62
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  • [Title] Myeloid sarcoma presenting as a recurrent, multifocal nerve root entrapment syndrome.
  • BACKGROUND: Myeloid sarcoma is an extramedullary manifestation of haematologic malignancy, most commonly acute myeloid leukemia (AML), which can cause neurological symptoms.
  • After surgically removing the tumour pathologic examination yielded a myeloid sarcoma.
  • Five months later the patient developed a thoracal (Th10-Th11) radiculopathy due to a relapse of the myeloid sarcoma, followed by C8-Th1-radiculopathy caused by leptomeningeal spread.
  • CONCLUSION: This case forms the first description of recurrent, multifocal and progressive radiculopathy due to myeloid sarcoma.
  • This diagnosis should be considered in patients with radiculopathy with previous haematological malignancy and/or signs or symptoms of such disease; the absence of systemic disease activity does not rule out myeloid sarcoma.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Nerve Compression Syndromes / etiology. Sarcoma, Myeloid / complications

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  • (PMID = 18712278.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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40. Gregory TK, Wald D, Chen Y, Vermaat JM, Xiong Y, Tse W: Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics. J Hematol Oncol; 2009;2:23
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  • [Title] Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.
  • Acute myeloid leukemia (AML) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation.
  • In approximately 60% of cases, specific recurrent chromosomal aberrations can be identified by modern cytogenetic techniques.
  • [MeSH-major] Genetic Markers. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 19490647.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 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
  • [Number-of-references] 65
  • [Other-IDs] NLM/ PMC2700131
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41. Olcay L, Dingil G, Yildirim E, Dilek G, Dirim E: Splenic abscesses in therapy-resistant acute myeloblastic leukemia presenting as recurrent febrile neutropenia and unresolved splenomegaly. Turk J Pediatr; 2007 Jul-Sep;49(3):315-8
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  • [Title] Splenic abscesses in therapy-resistant acute myeloblastic leukemia presenting as recurrent febrile neutropenia and unresolved splenomegaly.
  • A 14 7/12-year-old boy with acute myeloblastic leukemia M3v was admitted with disseminated intravascular coagulation, otitis media, lobar pneumonia, and splenomegaly.
  • He developed acute appendicitis and was operated.
  • [MeSH-major] Abscess / complications. Leukemia, Myeloid, Acute / complications. Neutropenia / diagnosis. Splenic Diseases / complications

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  • (PMID = 17990589.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Turkey
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42. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

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  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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43. Morerio C, Acquila M, Rapella A, Tassano E, Rosanda C, Panarello C: Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Dec;171(2):122-5
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  • [Title] Inversion (11)(p15q22) with NUP98-DDX10 fusion gene in pediatric acute myeloid leukemia.
  • The inv(11)(p15q22), a rare but recurrent chromosome abnormality that creates a NUP98-DDX10 fusion gene, is associated with de novo or secondary myeloid malignancies.
  • We report a case of acute monocytic leukemia presenting this rearrangement, studied using fluorescence in situ hybridization (FISH) and reverse transcriptase-PCR (RT-PCR).
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DEAD-box RNA Helicases / genetics. Gene Fusion. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / genetics

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  • (PMID = 17116492.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AB040537/ AB040538
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; EC 3.6.1.- / DDX10 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Number-of-references] 12
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44. Troke PJ, Kindle KB, Collins HM, Heery DM: MOZ fusion proteins in acute myeloid leukaemia. Biochem Soc Symp; 2006;(73):23-39
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  • [Title] MOZ fusion proteins in acute myeloid leukaemia.
  • MOZ (monocytic leukaemia zinc finger protein; also known as ZNF220 or MYST3) is a member of the MYST family of protein acetyltransferases.
  • Chromosomal translocations involving the MOZ gene are associated with AML (acute myeloid leukaemia), suggesting that it has a role in haematopoiesis.
  • Recurrent reciprocal translocations fuse the MOZ gene [or the gene encoding MORF (MOZ-related factor); also known as MYST4] to genes encoding the nuclear receptor co-activators CBP [CREB (cAMP response element-binding protein)-binding protein], p300 or the p160 protein TIF2 (transcription intermediary factor 2).
  • [MeSH-major] Histone Acetyltransferases / metabolism. Leukemia, Myeloid, Acute / etiology. Oncogene Proteins, Fusion / metabolism

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  • (PMID = 16626284.001).
  • [ISSN] 0067-8694
  • [Journal-full-title] Biochemical Society symposium
  • [ISO-abbreviation] Biochem. Soc. Symp.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Trans-Activators; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
  • [Number-of-references] 67
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45. Cucuianu A: Dominant and opportunistic leukemic clones: proposal for a pathogenesis-oriented classification in acute myeloid leukemia. Med Hypotheses; 2005;65(1):107-13
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  • [Title] Dominant and opportunistic leukemic clones: proposal for a pathogenesis-oriented classification in acute myeloid leukemia.
  • Despite the common clinical, hematological and prognostic features that define acute myeloid leukemia (AML) there is considerable heterogeneity among individual cases, suggesting different pathogenic pathways.
  • Based on a simple theoretical model, according to the vital characteristics of the leukemic clone (proliferative rate and resistance to apoptosis), I propose a classification of AML into two broad categories: (a) high leukemic clone vitality (HLV) AML or "dominant type" AML, corresponding roughly to the World Health Organization (WHO) classification group of entities "AML with recurrent cytogenetic abnormalities" and (b) low leukemic clone vitality (LLV) or "opportunistic type" AML corresponding to the WHO groups "AML with multilineage dysplasia" and "alkylating agent-related AML".
  • [MeSH-major] Clone Cells. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology

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  • (PMID = 15893127.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
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46. MacKinnon RN, Patsouris C, Chudoba I, Campbell LJ: A FISH comparison of variant derivatives of the recurrent dic(17;20) of myelodysplastic syndromes and acute myeloid leukemia: Obligatory retention of genes on 17p and 20q may explain the formation of dicentric chromosomes. Genes Chromosomes Cancer; 2007 Jan;46(1):27-36
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  • [Title] A FISH comparison of variant derivatives of the recurrent dic(17;20) of myelodysplastic syndromes and acute myeloid leukemia: Obligatory retention of genes on 17p and 20q may explain the formation of dicentric chromosomes.
  • The dic(17;20) is a recurrent unbalanced translocation occurring rarely in myelodysplastic syndromes and acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 20. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Chromosomal Instability. Chromosome Deletion. Humans. In Situ Hybridization, Fluorescence. Karyotyping


47. Dombret H, Preudhomme C, Boissel N: Core binding factor acute myeloid leukemia (CBF-AML): is high-dose Ara-C (HDAC) consolidation as effective as you think? Curr Opin Hematol; 2009 Mar;16(2):92-7
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  • [Title] Core binding factor acute myeloid leukemia (CBF-AML): is high-dose Ara-C (HDAC) consolidation as effective as you think?
  • PURPOSE OF REVIEW: Core binding factor acute myeloid leukemia (CBF-AML) corresponds to two distinct subtypes of AML characterized by recurrent favorable chromosome translocations, namely t(8;21) and inv(16)/t(16;16).
  • [MeSH-major] Core Binding Factors / genetics. Cytarabine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics


48. Czader M, Orazi A: Therapy-related myeloid neoplasms. Am J Clin Pathol; 2009 Sep;132(3):410-25
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  • [Title] Therapy-related myeloid neoplasms.
  • Session 5 of 2007 Workshop of the Society for Hematopathology/European Association for Haematopathology focused on therapy-related myeloid neoplasms.
  • We highlight common diagnostic issues such as the differentiation between therapy-related myelodysplastic syndrome and therapy-related acute erythroid leukemia.
  • As similar therapeutic interventions are frequently considered for patients with either of these diagnoses, in the current World Health Organization classification, regardless of morphologic presentation, therapy-related myeloid neoplasms are considered together as a unique clinicopathologic syndrome of therapy-related myelodysplastic syndrome/acute myeloid leukemia.
  • We also present examples of therapy-related acute myeloid leukemias with recurrent cytogenetic abnormalities.
  • [MeSH-major] Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary

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  • (PMID = 19687318.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 97
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49. Sakai I, Tamura T, Narumi H, Uchida N, Yakushijin Y, Hato T, Fujita S, Yasukawa M: Novel RUNX1-PRDM16 fusion transcripts in a patient with acute myeloid leukemia showing t(1;21)(p36;q22). Genes Chromosomes Cancer; 2005 Nov;44(3):265-70
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  • [Title] Novel RUNX1-PRDM16 fusion transcripts in a patient with acute myeloid leukemia showing t(1;21)(p36;q22).
  • The t(1;21)(p36;q22) is a recurrent chromosome abnormality associated with therapy-related acute myeloid leukemia (AML).
  • It is suggested that PRDM16 and MDS1/EVI1 share a common molecular mechanism for the leukemogenesis of RUNX1-associated leukemia.
  • Characterization of the RUNX1-PRDM16 fusion protein and comparison with the RUNX1-MDS1/EVI1 protein will facilitate the understanding of the mechanisms underlying RUNX1-associated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 21 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Leukemia, Myelomonocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16015645.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / PRDM16 protein, human; 0 / RNA, Neoplasm; 0 / RUNX1 protein, human; 0 / Transcription Factors
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50. Malinge S, Ragu C, Della-Valle V, Pisani D, Constantinescu SN, Perez C, Villeval JL, Reinhardt D, Landman-Parker J, Michaux L, Dastugue N, Baruchel A, Vainchenker W, Bourquin JP, Penard-Lacronique V, Bernard OA: Activating mutations in human acute megakaryoblastic leukemia. Blood; 2008 Nov 15;112(10):4220-6
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  • [Title] Activating mutations in human acute megakaryoblastic leukemia.
  • Oncogenic activation of tyrosine kinase signaling pathway is recurrent in human leukemia.
  • To gain insight into the oncogenic process leading to acute megakaryoblastic leukemia (AMKL), we performed sequence analyses of a subset of oncogenes known to be activated in human myeloid and myeloproliferative disorders.
  • [MeSH-major] Down Syndrome / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Mutation. Neoplasm Proteins / genetics


51. Kornblau SM, McCue D, Singh N, Chen W, Estrov Z, Coombes KR: Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia. Blood; 2010 Nov 18;116(20):4251-61
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  • [Title] Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia.
  • We hypothesized that comprehensive profiling of C&Ckine expression in leukemia would provide greater insight compared with individual analyses.
  • We used multiplex array technology to simultaneously measure the level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndrome (MDS) patients and 19 normal controls.
  • In conclusion, C&Ckine expression in AML and MDS differs from normal, is similar with one another, and forms recurrent patterns of expression with prognostic relevance.
  • [MeSH-major] Chemokines / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / diagnosis


52. McHayleh W, Foon K, Redner R, Sehgal R, Raptis A, Agha M, Luong TM, Schlesselman JJ, Boyiadzis M: Gemtuzumab ozogamicin as first-line treatment in patients aged 70 years or older with acute myeloid leukemia. Cancer; 2010 Jun 15;116(12):3001-5
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  • [Title] Gemtuzumab ozogamicin as first-line treatment in patients aged 70 years or older with acute myeloid leukemia.
  • BACKGROUND: Elderly patients with acute myeloid leukemia (AML) are generally unable to withstand the rigors of intensive induction chemotherapy and its attendant complications.
  • Gemtuzumab ozogamicin (GO) is an immunoconjugate that had demonstrated activity in recurrent AML.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20564405.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab
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53. Kakihana K, Kubo F, Wakabayashi S, Kurosu T, Miki T, Murakami N, Miura O: A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Jul 15;184(2):109-12
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  • [Title] A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia.
  • MLL located at 11q23 is fused with a variety of partner genes by recurrent chromosomal translocations in acute leukemias.
  • Here we report a case of chronic myelomonocytic leukemia (CMML) with a 46,XY,t(11;19)(q23;p13.1) karyotype that transformed to acute myeloid leukemia (AML) without showing any karyotypic evolution.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic


54. Carella C, Bonten J, Rehg J, Grosveld GC: MN1-TEL, the product of the t(12;22) in human myeloid leukemia, immortalizes murine myeloid cells and causes myeloid malignancy in mice. Leukemia; 2006 Sep;20(9):1582-92
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  • [Title] MN1-TEL, the product of the t(12;22) in human myeloid leukemia, immortalizes murine myeloid cells and causes myeloid malignancy in mice.
  • MN1-TEL is the product of the recurrent t(12;22)(p12;q11) associated with human myeloid malignancies.
  • MN1-TEL-transduced BM showed increased self-renewal capacity of primitive progenitors in vitro, and prolonged in vitro culture of MN1-TEL-expressing BM produced immortalized myeloid, interleukin (IL)-3/stem cell factor-dependent cell lines with a primitive morphology.
  • Three months after transplantation, all mice succumbed to promonocytic leukemia.
  • Transplantation of freshly MN1-TEL-transduced BM into lethally irradiated mice also caused acute myeloid leukemia within 3 months of transplantation.
  • We infer that MN1-TEL is a hematopoietic oncogene that stimulates the growth of hematopoietic cells, but depends on secondary mutations to cause leukemia in mice.
  • [MeSH-major] Cell Transformation, Neoplastic. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 22. Hematopoietic Stem Cells / pathology. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • (PMID = 16810199.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA72999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MN1-TEL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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55. Wang Y, Xue Y, Chen S, Wu Y, Pan J, Zhang J, Shen J: [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)]. Zhonghua Yi Xue Yi Chuan Xue Za Zhi; 2010 Feb;27(1):34-7
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  • [Title] [A clinical and laboratory study on acute myeloid leukemia with t(6;9)(p23;q34)].
  • OBJECTIVE: To explore the clinical and laboratory features of 6 cases of acute myeloid leukemia (AML) with t(6;9)(p23;q34).
  • CONCLUSION: The t(6;9)(p23;q34) is a rare recurrent abnormity.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 20140864.001).
  • [ISSN] 1003-9406
  • [Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics
  • [ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.4.11.2 / Antigens, CD13
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56. Jones L, Wei G, Sevcikova S, Phan V, Jain S, Shieh A, Wong JC, Li M, Dubansky J, Maunakea ML, Ochoa R, Zhu G, Tennant TR, Shannon KM, Lowe SW, Le Beau MM, Kogan SC: Gain of MYC underlies recurrent trisomy of the MYC chromosome in acute promyelocytic leukemia. J Exp Med; 2010 Nov 22;207(12):2581-94
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  • [Title] Gain of MYC underlies recurrent trisomy of the MYC chromosome in acute promyelocytic leukemia.
  • Gain of chromosome 8 is the most common chromosomal gain in human acute myeloid leukemia (AML).
  • In a mouse model of promyelocytic leukemia in which the MRP8 promoter drives expression of the PML-RARA fusion gene in myeloid cells, a Myc allele is gained in approximately two-thirds of cases as a result of trisomy for mouse chromosome 15.
  • MYC retroviruses cooperated in myeloid leukemogenesis and suppressed gain of chromosome 15.
  • In addition, we found that human myeloid leukemias with trisomy 8 have increased MYC.

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  • (PMID = 21059853.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221; United States / NCI NIH HHS / CA / R01 CA095274-07; United States / NCI NIH HHS / CA / CA095274-07; United States / NCI NIH HHS / CA / R01 CA095274; United States / NCI NIH HHS / CA / CA95274; United States / NCI NIH HHS / CA / R37 CA072614
  • [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 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  • [Other-IDs] NLM/ PMC2989761
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57. Lucena-Araujo AR, Panepucci RA, dos Santos GA, Jácomo RH, Santana-Lemos BA, Lima AS, Garcia AB, Araújo AG, Falcão RP, Rego EM: The expression of DeltaNTP73, TATP73 and TP53 genes in acute myeloid leukaemia is associated with recurrent cytogenetic abnormalities and in vitro susceptibility to cytarabine cytotoxicity. Br J Haematol; 2008 Jul;142(1):74-8
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  • [Title] The expression of DeltaNTP73, TATP73 and TP53 genes in acute myeloid leukaemia is associated with recurrent cytogenetic abnormalities and in vitro susceptibility to cytarabine cytotoxicity.
  • We compared TATP73 and DeltaNTP73 expression in acute myeloid leukaemia (AML) samples and normal CD34(+) progenitors.
  • Amongst AML blasts, TATP73 was more expressed in AML harbouring the recurrent genetic abnormalities (RGA): PML-RARA, RUNX1-RUNX1T1 and CBFB-MYH11, whereas higher DeltaNTP73 expression was detected in non-RGA cases.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. DNA-Binding Proteins / genetics. Genes, p53 / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 18422993.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 04079A1RDZ / Cytarabine
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58. Ferguson EC, Talley P, Vora A: Translocation (6;17)(q23;q11.2): a novel cytogenetic abnormality in congenital acute myeloid leukemia? Cancer Genet Cytogenet; 2005 Nov;163(1):71-3
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  • [Title] Translocation (6;17)(q23;q11.2): a novel cytogenetic abnormality in congenital acute myeloid leukemia?
  • Congenital leukemia occurring within 4 weeks of birth is extremely rare and, excluding transient neonatal myeloproliferation associated with Down syndrome, makes up approximately 1% of childhood leukemias.
  • It is usually seen as acute myeloid leukemia (AML), most frequently French-American-British (FAB) types M4 and M5.
  • Recurrent cytogenetic abnormalities have been reported in this group, and in approximately one third of cases the MLL gene at 11q23 is involved.
  • We present a case of congenital leukemia (AML FAB type M1) with an acquired translocation between chromosomes 6 and 17.
  • [MeSH-major] Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 6. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 16271959.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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59. Stevens SJ, Meers LE, Albrechts JC, Mebis-Verhees K, Bos GM, Engelen JJ, Janssen JW: A translocation in acute lymphoblastic leukemia that cytogenetically mimics the recurrent MLL-AFF1 translocation and fuses SEPT11 to MLL. Cancer Genet Cytogenet; 2010 Aug;201(1):48-51
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  • [Title] A translocation in acute lymphoblastic leukemia that cytogenetically mimics the recurrent MLL-AFF1 translocation and fuses SEPT11 to MLL.
  • A 55-year-old man sought care for aggressive acute lymphoblastic leukemia (ALL), which developed 8 years after he had received chemotherapeutic treatment for nephrotic syndrome.
  • However, subsequent reverse transcriptase-polymerase chain reaction for the expected mixed lineage leukemia [trithorax homolog, Drosophila] (MLL)-AFF1 fusion transcript was negative.
  • This MLL-SEPT11 fusion is cytogenetically indistinguishable from the recurrent t(4;11)(q21;q23).
  • Thus, it is crucial to characterize cytogenetic aberrations in leukemia by molecular methods, even in cases where a known recurrent translocation is presumed.
  • Five septins have been identified thus far as MLL fusion partners in leukemia.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Gene Fusion. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633769.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.1.- / SEPT11 protein, human; EC 3.6.1.- / Septins
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60. Trubia M, Albano F, Cavazzini F, Cambrin GR, Quarta G, Fabbiano F, Ciambelli F, Magro D, Hernandezo JM, Mancini M, Diverio D, Pelicci PG, Coco FL, Mecucci C, Specchia G, Rocchi M, Liso V, Castoldi G, Cuneo A: Characterization of a recurrent translocation t(2;3)(p15-22;q26) occurring in acute myeloid leukaemia. Leukemia; 2006 Jan;20(1):48-54
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  • [Title] Characterization of a recurrent translocation t(2;3)(p15-22;q26) occurring in acute myeloid leukaemia.
  • Six patients with de novo acute myeloid leukemia (AML) and a t(2;3)(p15-21;q26-27) were identified among approximately 1000 cases enrolled in the GIMEMA trial.
  • The patients showed dysplasia of at least two myeloid cell lineages in all cases; they had a low-to-normal platelet count and displayed an immature CD34+ CD117+ immunophenotype.
  • We arrived at the following conclusions: (a) the t(2;3) is a recurrent translocation having an approximate 0.5% incidence in adult AML;.
  • [MeSH-major] Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Myeloid / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Cytogenetic Analysis / methods. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Polymerase Chain Reaction. Predictive Value of Tests. Prognosis. Trisomy

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  • (PMID = 16619048.001).
  • [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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61. Foster N, Paulsson K, Sales M, Cunningham J, Groves M, O'Connor N, Begum S, Stubbs T, McMullan DJ, Griffiths M, Pratt N, Tauro S: Molecular characterisation of a recurrent, semi-cryptic RUNX1 translocation t(7;21) in myelodysplastic syndrome and acute myeloid leukaemia. Br J Haematol; 2010 Mar;148(6):938-43
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  • [Title] Molecular characterisation of a recurrent, semi-cryptic RUNX1 translocation t(7;21) in myelodysplastic syndrome and acute myeloid leukaemia.
  • A proportion of cytogenetic abnormalities in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML) may escape detection by high-resolution genomic technologies, but can be identified by conventional cytogenetic and molecular analysis.
  • Thus, our studies have identified t(7;21)(p22;q22) as a rare but recurrent abnormality in MDS/AML, with the existence of alternative spliced forms of the RUNX1-USP42 transcript in different patients.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 7 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic


62. Herry A, Douet-Guilbert N, Morel F, Le Bris MJ, Guéganic N, Berthou C, De Braekeleer M: Isochromosome 5p and related anomalies: a novel recurrent chromosome abnormality in myeloid disorders. Cancer Genet Cytogenet; 2010 Jul 15;200(2):134-9
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  • [Title] Isochromosome 5p and related anomalies: a novel recurrent chromosome abnormality in myeloid disorders.
  • Loss of material from chromosome arm 5q is a common finding in patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML).
  • Isochromosome of the short arm of chromosome 5 and its related abnormalities such as idic(5)(q11) and structurally rearranged i(5)(p10) are rare but recurrent abnormalities; their identification requires a combination of conventional and molecular cytogenetic techniques.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5. Isochromosomes. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


63. Mrózek K: Cytogenetic, molecular genetic, and clinical characteristics of acute myeloid leukemia with a complex karyotype. Semin Oncol; 2008 Aug;35(4):365-77
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  • [Title] Cytogenetic, molecular genetic, and clinical characteristics of acute myeloid leukemia with a complex karyotype.
  • Patients with acute myeloid leukemia (AML) harboring three or more acquired chromosome aberrations in the absence of the prognostically favorable t(8;21)(q22;q22), inv(16)(p13q22)/t(6;16)(p13;q22), and t(15;17)(q22;q21) aberrations form a separate category - AML with a complex karyotype.
  • The emerging nonrandom pattern of abnormalities includes relative paucity, but not absence, of balanced rearrangements (translocations, insertions, or inversions), predominance of aberrations leading to loss of chromosome material (monosomies, deletions, and unbalanced translocations) that involve, in decreasing order, chromosome arms 5q, 17p, 7q, 18q, 16q, 17q, 12p, 20q, 18p, and 3p, and the presence of recurrent, albeit less frequent and often hidden (in marker chromosomes and unbalanced translocations) aberrations leading to overrepresentation of segments from 8q, 11q, 21q, 22q, 1p, 9p, and 13q.

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  • (PMID = 18692687.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 77658; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA 16058; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / CA 101140; United States / NCI NIH HHS / CA / P30 CA016058
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 83
  • [Other-IDs] NLM/ NIHMS66054; NLM/ PMC3640813
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64. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Dalal EN, Shukla SN, Shah PM, Bakshi SR: A new recurring chromosome 13 abnormality in two older patients with de novo acute myeloid leukemia: An Indian experience. Indian J Hum Genet; 2009 Sep;15(3):137-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new recurring chromosome 13 abnormality in two older patients with de novo acute myeloid leukemia: An Indian experience.
  • We report here two cases of trisomy 13 in acute myeloid leukemia M1 subtype. short-term unstimulated bone marrow and peripheral blood lymphocyte culture showed 47, XY, +13 in all metaphase plates and trisomy 13 was confirmed with whole chromosome paint probes.

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  • (PMID = 21088719.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2922630
  • [Keywords] NOTNLM ; Acute myeloid leukemia-M1 / recurrent / sole abnormality / trisomy 13
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65. Hejlik DP, Nagarajan L: Deletion of 5q in myeloid leukemia cells HL-60: an L1 element-mediated instability. Cancer Genet Cytogenet; 2005 Jan 15;156(2):97-103
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  • [Title] Deletion of 5q in myeloid leukemia cells HL-60: an L1 element-mediated instability.
  • Complete and partial deletions of chromosome 5 are recurrent anomalies associated with refractory myelogenous leukemia.
  • We have analyzed a complex rearrangement of chromosome band 5q both in the primary leukemic cells of the patient from whom the acute myelogenous leukemia (AML) cell line HL-60 was derived and in the HL-60 cells in culture.
  • The resulting genomic fragment is found inserted into a telomeric locus (D5S89), with loss of 4.1 Mbp of in-between sequences, encoding one or more candidate myeloid leukemia suppressor genes.

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  • (PMID = 15642388.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA66982
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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66. Cashen AF, Devine H, DiPersio J: Second complete remission in an elderly patient with acute myeloid leukemia retreated with decitabine. Am J Hematol; 2006 Jul;81(7):543-5
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  • [Title] Second complete remission in an elderly patient with acute myeloid leukemia retreated with decitabine.
  • A 67-year-old man with acute myeloid leukemia (AML) was treated with low-dose decitabine.
  • He developed recurrent AML after discontinuation of decitabine.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / prevention & control

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  • (PMID = 16755561.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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67. Wakui M, Kuriyama K, Miyazaki Y, Hata T, Taniwaki M, Ohtake S, Sakamaki H, Miyawaki S, Naoe T, Ohno R, Tomonaga M: Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol. Int J Hematol; 2008 Mar;87(2):144-51
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  • [Title] Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol.
  • We reviewed and categorized 638 of 809 patients who were registered in the Japan Adult Leukemia Study Group acute myeloid leukemia (AML)-97 protocol using morphological means.
  • According to the WHO classification, 171 patients (26.8%) had AML with recurrent genetic abnormalities, 133 (20.8%) had AML with multilineage dysplasia (MLD), 331 (51.9%) had AML not otherwise categorized, and 3 (0.5%) had acute leukemia of ambiguous lineage.
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries


68. Akasaka T, Balasas T, Russell LJ, Sugimoto KJ, Majid A, Walewska R, Karran EL, Brown DG, Cain K, Harder L, Gesk S, Martin-Subero JI, Atherton MG, Brüggemann M, Calasanz MJ, Davies T, Haas OA, Hagemeijer A, Kempski H, Lessard M, Lillington DM, Moore S, Nguyen-Khac F, Radford-Weiss I, Schoch C, Struski S, Talley P, Welham MJ, Worley H, Strefford JC, Harrison CJ, Siebert R, Dyer MJ: Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Blood; 2007 Apr 15;109(8):3451-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • CCAAT enhancer-binding protein (CEBP) transcription factors play pivotal roles in proliferation and differentiation, including suppression of myeloid leukemogenesis.
  • Mutations of CEBPA are found in a subset of acute myeloid leukemia (AML) and in some cases of familial AML.
  • Here, using cytogenetics, fluorescence in situ hybridization (FISH), and molecular cloning, we show that 5 CEBP gene family members are targeted by recurrent IGH chromosomal translocations in BCP-ALL.
  • Our findings implicate the CEBP gene family as novel oncogenes in BCP-ALL, and suggest opposing functions of CEBP dysregulation in myeloid and lymphoid leukemogenesis.

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  • (PMID = 17170124.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Immunoglobulin Heavy Chains
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69. Oda M, Isoyama K, Ito E, Inoue M, Tsuchida M, Kigasawa H, Kato K, Kato S: Survival after cord blood transplantation from unrelated donor as a second hematopoietic stem cell transplantation for recurrent pediatric acute myeloid leukemia. Int J Hematol; 2009 Apr;89(3):374-82
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  • [Title] Survival after cord blood transplantation from unrelated donor as a second hematopoietic stem cell transplantation for recurrent pediatric acute myeloid leukemia.
  • The Japan Cord Blood Bank Network (JCBBN) reports the treatment of 22 children with acute myeloid leukemia (AML) who received umbilical cord blood transplantation from unrelated donors (CBT) as their second hematopoietic stem cell transplantation (HSCT).
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / surgery. Tissue Donors


70. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
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  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Recurrent pancytopenia subsequently led to diagnosis of myelodysplastic syndrome (MDS) with deletion of the long arm of chromosome 5 (MDS 5q-).
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


71. Rücker FG, Sander S, Döhner K, Döhner H, Pollack JR, Bullinger L: Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations. Leukemia; 2006 Jun;20(6):994-1001
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  • [Title] Molecular profiling reveals myeloid leukemia cell lines to be faithful model systems characterized by distinct genomic aberrations.
  • To model and investigate different facets of leukemia pathogenesis, a widely accepted approach is to use immortalized leukemia cell lines.
  • To improve the molecular characterization of these model systems, we analyzed 17 myeloid leukemia cell lines using DNA microarray technology.
  • By array-based comparative genomic hybridization, we identified recurrent genomic DNA gains and losses, as well as high-level amplifications.
  • Comparison with clinical leukemia specimens showed that key signatures were retained, as myeloid cell lines with characteristic cytogenetic aberrations co-clustered with leukemia samples carrying the respective abnormality.
  • Thus, our analyses demonstrate myeloid cell lines to exhibit conserved and stable signatures reflecting the underlying primary cytogenetic aberrations.
  • Our refined molecular characterization of myeloid cell lines supports the utility of cell lines as faithful and powerful model systems and provides additional insights into the molecular mechanisms of leukemogenesis.
  • [MeSH-major] Chromosome Aberrations. Gene Expression Profiling. Leukemia, Myeloid / genetics. Models, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cluster Analysis. Gene Expression Regulation, Leukemic. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 16721385.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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72. Tomizawa D, Koh K, Hirayama M, Miyamura T, Hatanaka M, Saikawa Y, Ishii E: Outcome of recurrent or refractory acute lymphoblastic leukemia in infants with MLL gene rearrangements: A report from the Japan Infant Leukemia Study Group. Pediatr Blood Cancer; 2009 Jul;52(7):808-13
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  • [Title] Outcome of recurrent or refractory acute lymphoblastic leukemia in infants with MLL gene rearrangements: A report from the Japan Infant Leukemia Study Group.
  • BACKGROUND: Despite the poor outcome of recurrent or refractory acute lymphoblastic leukemia (ALL) in infants with MLL gene rearrangement, few studies have focused on this specific group.
  • We conducted a retrospective analysis of infants with recurrent or refractory ALL from two previous consecutive Japanese studies to clarify the characteristics and prognostic factors among these patients PROCEDURE: All recurrent or refractory ALL infants with MLL gene rearrangement (MLL-R) who were registered in two consecutive Japanese nation-wide multicentric trials (MLL96 and MLL98; between 1995 and 2001) were eligible for the study.
  • CONCLUSIONS: The prognosis of infants with recurrent or refractory MLL-R ALL is extremely poor despite alternative treatments including HSCT; therefore, it is necessary to develop novel treatment strategies.
  • [MeSH-major] Drug Resistance, Neoplasm. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19229974.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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73. Steensma DP, McClure RF, Karp JE, Tefferi A, Lasho TL, Powell HL, DeWald GW, Kaufmann SH: JAK2 V617F is a rare finding in de novo acute myeloid leukemia, but STAT3 activation is common and remains unexplained. Leukemia; 2006 Jun;20(6):971-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JAK2 V617F is a rare finding in de novo acute myeloid leukemia, but STAT3 activation is common and remains unexplained.
  • Recently, several groups identified a recurrent somatic point mutation constitutively activating the hematopoietic growth factor receptor-associated JAK2 tyrosine kinase in diverse chronic myeloid disorders - most commonly classic myeloproliferative disorders (MPD), especially polycythemia vera.
  • We hypothesized that the JAK2 V617F mutation might also be present in samples from patients with acute myeloid leukemia (AML), especially erythroleukemia (AML-M6) or megakaryoblastic leukemia (AML-M7), where it might mimic erythropoietin or thrombopoietin signaling.
  • We then analyzed genomic DNA from 162 AML, 30 B-cell lymphoma, and 10 chronic lymphocytic leukemia (CLL) samples for JAK2 mutations, and assayed a subset for SOCS1 and FLT3 mutations.
  • Janus kinase2 V617F was present in 13/162 AML samples (8%): 10/13 transformed MPD, and three apparent de novo AML (one of 12 AML-M6, one of 24 AML-M7, and one AML-M2 - all mixed clonality).
  • Thus, while JAK2 V617F is uncommon in de novo AML and probably does not occur in lymphoid malignancy, unexplained STAT3 activation is common in AML.
  • [MeSH-major] Leukemia, Myeloid / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. STAT3 Transcription Factor / metabolism
  • [MeSH-minor] Acute Disease. Blotting, Western. Humans. Janus Kinase 2. Phosphorylation. Point Mutation. Signal Transduction / genetics. Suppressor of Cytokine Signaling Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16598306.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12 CA90628; United States / NCI NIH HHS / CA / P50 CA97274; United States / NCI NIH HHS / CA / R01 CA69008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / SOCS1 protein, human; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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74. Fischbach NA, Rozenfeld S, Shen W, Fong S, Chrobak D, Ginzinger D, Kogan SC, Radhakrishnan A, Le Beau MM, Largman C, Lawrence HJ: HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo. Blood; 2005 Feb 15;105(4):1456-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HOXB6 overexpression in murine bone marrow immortalizes a myelomonocytic precursor in vitro and causes hematopoietic stem cell expansion and acute myeloid leukemia in vivo.
  • Dysregulated HOX gene expression profoundly effects the proliferation and differentiation of hematopoietic stem cells (HSCs) and committed progenitors, and aberrant activation of HOX genes is a common event in human myeloid leukemia.
  • HOXB6 is frequently overexpressed in human acute myeloid leukemia (AML).
  • We also explored structure-function relationships using mutant HOXB6 proteins unable to bind to DNA or a key HOX-binding partner, pre-B-cell leukemia transcription factor-1 (PBX1).
  • Additionally, we investigated the potential cooperative interaction with myeloid ecotropic viral integration site 1 homolog (MEIS1).
  • In vivo, HOXB6 expanded HSCs and myeloid precursors while inhibiting erythropoiesis and lymphopoiesis.
  • Cytogenetic analysis of a subset of HOXB6-induced AMLs revealed recurrent deletions of chromosome bands 2D-E4, a region frequently deleted in HOXA9-induced AMLs.
  • [MeSH-major] Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Transformation, Neoplastic / pathology. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics. Leukemia, Myeloid / blood. Myeloid Progenitor Cells / metabolism. Myeloid Progenitor Cells / pathology
  • [MeSH-minor] Acute Disease. Animals. Cell Differentiation / genetics. Cell Line, Transformed. Cell Proliferation. Erythropoiesis / genetics. Female. Karyotyping. Lymphopoiesis / genetics. Mice. Mice, Congenic. Mice, Inbred C57BL. Neoplasm Proteins / physiology. Phenotype. Time Factors

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  • (PMID = 15522959.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK48642
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxb6 protein, mouse; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein
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75. Kaltenbach S, Soler G, Barin C, Gervais C, Bernard OA, Penard-Lacronique V, Romana SP: NUP98-MLL fusion in human acute myeloblastic leukemia. Blood; 2010 Sep 30;116(13):2332-5
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  • [Title] NUP98-MLL fusion in human acute myeloblastic leukemia.
  • H3K4 (histone H3 lysine 4) methylation by the SET domain of the trithorax-group protein MLL (mixed-lineage leukemia) is important for the control of homeobox (HOX) gene expression during development.
  • MLL fusion proteins associated with human leukemia contain the menin interaction peptide and frequently recruit H3K79 (histone H3 lysine 79) methylation activity.
  • We have characterized a novel recurrent chromosomal aberration, inv(11)(p15q23), as an isolated chromosomal abnormality in 2 patients with acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20558618.001).
  • [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 Primers; 0 / DNA, Neoplasm; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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76. Fagnoni P, Limat S, Hintzy-Fein E, Martin F, Deconinck E, Cahn JY, Arveux P, Dussaucy A, Woronoff-Lemsi MC: [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification]. Bull Cancer; 2006 Aug;93(8):813-9
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  • [Title] [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification].
  • [Transliterated title] Coûts hospitaliers de prise en charge des leucémies aiguës myéloïdes: de la comptabilité analytique à la T2A.
  • The confrontation of the macro- and micro-economic approaches of hospital costs is a recurrent question, in particular for pathologies where length of stay is highly variable, like acute myeloid leukemias (AML).
  • [MeSH-major] Hospital Costs. Leukemia, Myeloid / economics. Prospective Payment System / economics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Diagnosis-Related Groups / economics. Female. France. Humans. Length of Stay / economics. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies

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  • (PMID = 16935786.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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77. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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78. Huang KP, Chase AJ, Cross NC, Reiter A, Li TY, Wang TF, Chu SC, Lu XY, Li CC, Kao RH: Evolutional change of karyotype with t(8;9)(p22;p24) and HLA-DR immunophenotype in relapsed acute myeloid leukemia. Int J Hematol; 2008 Sep;88(2):197-201
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  • [Title] Evolutional change of karyotype with t(8;9)(p22;p24) and HLA-DR immunophenotype in relapsed acute myeloid leukemia.
  • The rare recurrent translocation of (8;9)(p22;p24) with PCM1-JAK2 fusion was recently characterized in diverse hematological malignancies.
  • Most of them are atypical chronic myeloid leukemia (CML) or other myeloproliferative disorders (MPD), and are predominantly in the male.
  • We report a female patient with acute myeloid leukemia (AML) initially presenting with normal karyotype and negative HLA-DR expression who achieved complete remission after standard chemotherapy.
  • [MeSH-major] Autoantigens / genetics. Cell Cycle Proteins / genetics. HLA-DR Antigens / genetics. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18594780.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / HLA-DR Antigens; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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79. Kim H, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ: [A Case of Acute Myeloid Leukemia with Masked t(8;21).]. Korean J Lab Med; 2006 Oct;26(5):338-42

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  • [Title] [A Case of Acute Myeloid Leukemia with Masked t(8;21).].
  • We report a case that revealed the characteristics of acute myeloblastic leukemia with maturation (AML-M2) on the morphology of the bone marrow biopsy and 45,X,-Y in conventional cytogenetic study, but was confirmed to have a typical AML1/ETO translocation by molecular studies using reverse transcriptase polymerase chain reaction and fluorescence in situ hybridization.
  • In case typical morphologic features compatible with recurrent cytogenetic abnormalities are shown, molecular studies in addition to conventional cytogenetic study might be required to confirm the diagnosis.

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  • (PMID = 18156748.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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80. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
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  • [Title] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • We conclude that human autoantigen pericentriolar material (PCM1)-JAK2 is a novel, recurrent fusion gene in hematologic malignancies.
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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81. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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82. Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T: Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia. Cancer Genet Cytogenet; 2009 Oct;194(1):38-43
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  • [Title] Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
  • Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in acute lymphoblastic leukemia.
  • We describe here a novel case of acute myeloid leukemia (AML) with double idic(21)(p11.2).
  • A 35-year-old man was diagnosed as having de novo AML with multilineage dysplasia because of 30% myeloperoxidase-positive blasts and trilineage dysplasia in the bone marrow.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping

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  • (PMID = 19737652.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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83. Park J, Kim M, Lim J, Kim Y, Han K, Lee J, Chung NG, Cho B, Kim HK: Three-way complex translocations in infant acute myeloid leukemia with t(7;12)(q36;p13): the incidence and correlation of a HLXB9 overexpression. Cancer Genet Cytogenet; 2009 Jun;191(2):102-5
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  • [Title] Three-way complex translocations in infant acute myeloid leukemia with t(7;12)(q36;p13): the incidence and correlation of a HLXB9 overexpression.
  • The t(7;12)(q36;p13) is one of the recurrent cytogenetic abnormalities that involves the ETV6 gene.
  • It is found in patients suffering with infantile acute myeloid leukemia (AML).
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Homeodomain Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

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  • (PMID = 19446746.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / Transcription Factors
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84. Yanada M, Suzuki M, Kawashima K, Kiyoi H, Kinoshita T, Emi N, Saito H, Naoe T: Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience. Eur J Haematol; 2005 May;74(5):418-23
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  • [Title] Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience.
  • The actual utility of a new classification system of acute myeloid leukemia (AML) recently introduced by the World Health Organization (WHO) has not been thoroughly investigated yet.
  • AML with recurrent genetic abnormalities accounted for 26%, AML with multilineage dysplasia for 29%, therapy-related AML for 13%, and AML not otherwise categorized for 32% of classifiable cases.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / therapy

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  • (PMID = 15813916.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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85. Strehl S, Nebral K, König M, Harbott J, Strobl H, Ratei R, Struski S, Bielorai B, Lessard M, Zimmermann M, Haas OA, Izraeli S: ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations. Clin Cancer Res; 2008 Feb 15;14(4):977-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations.
  • Cytogenetic analysis of six cases of childhood acute lymphoblastic leukemia revealed a novel recurrent t(8;12)(q13;p13), suggesting involvement of ETV6.
  • RESULTS: We have identified a novel recurrent t(8;12)(q13;p13), which results in a fusion between the transcriptional repressor ETV6 (TEL) and the transcriptional coactivator NCOA2 (TIF2) in six cases of childhood leukemia expressing both T-lymphoid and myeloid antigens.
  • In addition, ETV6-NCOA2 leukemia shows a high frequency of heterozygous activating NOTCH1 mutations, which disrupt the heterodimerization or the PEST domains.
  • CONCLUSIONS: The ETV6-NCOA2 fusion may define a novel subgroup of acute leukemia with T-lymphoid and myeloid features, which is associated with a high prevalence of NOTCH1 mutations.
  • [MeSH-major] Nuclear Receptor Coactivator 2 / genetics. Oncogene Fusion / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 18281529.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / NCOA2 protein, human; 0 / NOTCH1 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Receptor, Notch1; 0 / Repressor Proteins
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86. Pilatrino C, Cilloni D, Messa E, Morotti A, Giugliano E, Pautasso M, Familiari U, Cappia S, Pelicci PG, Lo Coco F, Saglio G, Guerrasio A: Increase in platelet count in older, poor-risk patients with acute myeloid leukemia or myelodysplastic syndrome treated with valproic acid and all-trans retinoic acid. Cancer; 2005 Jul 1;104(1):101-9
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  • [Title] Increase in platelet count in older, poor-risk patients with acute myeloid leukemia or myelodysplastic syndrome treated with valproic acid and all-trans retinoic acid.
  • BACKGROUND: The authors investigated the efficacy and safety of the histone deacetylase inhibitors valproic acid (VPA) and all-trans retinoic acid (ATRA) as differentiation agents in a cohort of older, poor-risk patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • METHODS: Twenty older patients with recurrent or refractory AML or MDS were treated in a Phase II protocol with sequential VPA and ATRA therapy.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Platelet Count. Tretinoin / therapeutic use. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Aged. Female. Humans. Male. Middle Aged. Risk


87. Bunin NJ, Davies SM, Aplenc R, Camitta BM, DeSantes KB, Goyal RK, Kapoor N, Kernan NA, Rosenthal J, Smith FO, Eapen M: Unrelated donor bone marrow transplantation for children with acute myeloid leukemia beyond first remission or refractory to chemotherapy. J Clin Oncol; 2008 Sep 10;26(26):4326-32
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  • [Title] Unrelated donor bone marrow transplantation for children with acute myeloid leukemia beyond first remission or refractory to chemotherapy.
  • PURPOSE: Identify prognostic factors that influence outcome after unrelated donor bone marrow transplantation in children with acute myeloid leukemia (AML).
  • RESULTS: In this analysis, the only risk factor that predicted leukemia recurrence and overall and leukemia-free survival was disease status at transplantation.
  • The 5-year probabilities of leukemia-free survival were 45%, 20%, and 12% for patients who underwent transplantation at second complete remission, relapse, and primary induction failure, respectively.
  • As expected, risk of acute but not chronic graft-versus-host disease (GVHD) was lower with T-cell-depleted bone marrow grafts; T-cell-depleted grafts were not associated with higher risks of leukemia recurrence.
  • We observed similar risks of leukemia relapse in patients with and without acute and chronic GVHD.
  • Nevertheless, 20% of children who underwent transplantation in relapse are long-term survivors, suggesting that unrelated donor bone marrow transplantation is an effective therapy in a significant proportion of children with recurrent or primary refractory AML.

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  • [Cites] Hematol Oncol Clin North Am. 1999 Oct;13(5):1091-112, viii-ix [10553263.001]
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  • (PMID = 18779619.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U24 CA076518; United States / NCI NIH HHS / CA / U24-CA76518
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC2653120
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88. Bullinger L, Krönke J, Schön C, Radtke I, Urlbauer K, Botzenhardt U, Gaidzik V, Carió A, Senger C, Schlenk RF, Downing JR, Holzmann K, Döhner K, Döhner H: Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis. Leukemia; 2010 Feb;24(2):438-49
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  • [Title] Identification of acquired copy number alterations and uniparental disomies in cytogenetically normal acute myeloid leukemia using high-resolution single-nucleotide polymorphism analysis.
  • As acute myeloid leukemia (AML) represents a genetically heterogeneous disease, this technology might prove helpful, especially for cytogenetically normal AML (CN-AML) cases.
  • Furthermore, we identified two cases with a cryptic t(6;11) as well as several non-recurrent aberrations pointing to leukemia-relevant regions.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Polymorphism, Single Nucleotide / genetics. Uniparental Disomy / genetics

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  • (PMID = 20016533.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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89. Tempescul A, Guillerm G, Douet-Guilbert N, Morel F, Le Bris MJ, De Braekeleer M: Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia. Cancer Genet Cytogenet; 2007 Jan 1;172(1):74-6
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  • [Title] Translocation (10;17)(p15;q21) is a recurrent anomaly in acute myeloblastic leukemia.
  • We report here two cases of patients with acute myeloblastic leukemia, type M1 (FAB classification), associated with a t(10;17)(p15;q21).
  • Four other patients with this translocation have been reported, three of them having acute undifferentiated or poorly differentiated leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 17175384.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / retinoic acid receptor alpha; 143220-95-5 / PML protein, human
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90. Chou WC, Hou HA, Chen CY, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Chang YC, Lee FY, Liu MC, Liu CW, Tseng MH, Huang CF, Tien HF: Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation. Blood; 2010 Apr 8;115(14):2749-54
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  • [Title] Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation.
  • Recent genome-wide screening also revealed IDH1 mutation as a recurrent event in acute myeloid leukemia (AML), but its clinical implications in AML are largely unknown.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Neoplasm Proteins / genetics

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  • [CommentIn] Blood. 2010 Jul 22;116(3):495-6 [20651083.001]
  • (PMID = 20097881.001).
  • [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 / Antigens, CD14; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.4.11.2 / Antigens, CD13
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91. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


92. Moreno Tejero ML, Lassaletta Atienza A, García Salido A, Sevilla Navarro J, Madero López L: [Arsenic trioxide treatment in a patient with recurrent acute promyelocytic leukemia (APL)]. An Pediatr (Barc); 2010 Jul;73(1):39-41
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  • [Title] [Arsenic trioxide treatment in a patient with recurrent acute promyelocytic leukemia (APL)].
  • [Transliterated title] Tratamiento con trióxido de arsénico en paciente con recaída de leucemia promielocítica aguda.
  • Acute promyelocytic leukemia (APL) is a special subtype of acute myeloid leukemia (AML) with M3 morphology and specific chromosomal translocation t(15;17) with resultant leukemogenic PML-RARalpha fusion gene.
  • Its main characteristics are therapy response using all-trans-retinoic acid (ATRA) and its high rate of recovery; higher than other subtypes of acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia, Promyelocytic, Acute / drug therapy. Oxides / therapeutic use

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  • [Copyright] 2010 Asociación Española de Pediatría. Published by Elsevier Espana. All rights reserved.
  • (PMID = 20605542.001).
  • [ISSN] 1695-9531
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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93. Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F: AML M1 presenting with recurrent acute large arterial vessel thromboembolism. Leuk Res; 2007 Jun;31(6):869-71
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  • [Title] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
  • Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).
  • We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.
  • Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology
  • [MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 17011031.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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94. Herry A, Douet-Guilbert N, Guéganic N, Morel F, Le Bris MJ, Berthou C, De Braekeleer M: Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association. Ann Hematol; 2006 Apr;85(4):244-9
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  • [Title] Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association.
  • We report here a 71 year-old female presenting with acute myeloblastic leukemia (FAB-M1) after treatment of essential thrombocythemia with Vercyte.
  • Twenty-one cases, including ours, of myelodysplastic syndromes and acute myelogenous leukemia with MLL amplification present in hsr or dmin were found in the literature.
  • Most of these patients shared some characteristics: they were old, they had de novo acute myeloid leukemia (AML) with a complex karyotype and a short survival, 90% of them having also a del(5q).
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Amplification. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 16425025.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6Q99RDT97R / Pipobroman; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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95. Sperr WR, Mitterbauer M, Mitterbauer G, Kundi M, Jäger U, Lechner K, Valent P: Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse. Clin Cancer Res; 2005 Sep 15;11(18):6536-43
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  • [Title] Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse.
  • PURPOSE: Recent data suggest that tryptase is produced by blast cells in a group of patients with acute myeloid leukemia (AML).
  • In 61 patients with de novo AML exhibiting elevated serum tryptase (>15 ng/mL) at diagnosis, tryptase levels were measured serially during and after chemotherapy by a fluoroenzyme immunoassay.
  • In all patients with continuous hematologic CR, tryptase levels remained constantly normal, whereas a recurrent elevation of tryptase in CR was invariably followed by a hematologic relapse.
  • [MeSH-major] Leukemia, Myeloid / pathology. Neoplasm, Residual / pathology. Serine Endopeptidases / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Recurrence, Local. Oncogene Proteins, Fusion / genetics. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Survival Analysis. Time Factors. Tryptases

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  • (PMID = 16166430.001).
  • [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
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases
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96. van Binsbergen E, de Weerdt O, Buijs A: A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review. Cancer Genet Cytogenet; 2007 Jul 1;176(1):72-5
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  • [Title] A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review.
  • The t(2;11)(q37;q23) is a rare recurrent cytogenetic abnormality associated with de novo and therapy-related acute myeloid leukemia, resulting in a MLL-SEPT2 fusion gene.
  • We report on a case of therapy-related acute myeloid leukemia M2 showing a t(2;11)(q37;q23) and resulting in a new subtype of a MLL-SEPT2 chimeric transcript.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion. Phosphoric Monoester Hydrolases / genetics. Translocation, Genetic

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  • (PMID = 17574968.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
  • [Number-of-references] 9
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97. Kai T, Kimura H, Shiga Y, Ogawa K, Sato H, Maruyama Y: Recurrent extramedullary relapse of acute promyelocytic leukemia after allogeneic stem cell transplantation: successful treatment by arsenic trioxide in combination with local radiotherapy. Int J Hematol; 2006 May;83(4):337-40
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  • [Title] Recurrent extramedullary relapse of acute promyelocytic leukemia after allogeneic stem cell transplantation: successful treatment by arsenic trioxide in combination with local radiotherapy.
  • Isolated extramedullary relapse is rare in patients with acute promyelocytic leukemia (APL) after allogeneic stem cell transplantation (SCT), and an optimal therapy for it has not been established.
  • In the present case, the bone marrow was in morphologic and molecular remission during the course of recurrent EMD.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Arsenicals / administration & dosage. Leukemia, Promyelocytic, Acute / therapy. Oxides / administration & dosage. Sarcoma, Myeloid / therapy. Stem Cell Transplantation. Tretinoin / administration & dosage

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  • (PMID = 16757435.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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98. Boissel N, Nibourel O, Renneville A, Gardin C, Reman O, Contentin N, Bordessoule D, Pautas C, de Revel T, Quesnel B, Huchette P, Philippe N, Geffroy S, Terre C, Thomas X, Castaigne S, Dombret H, Preudhomme C: Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group. J Clin Oncol; 2010 Aug 10;28(23):3717-23
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  • [Title] Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group.
  • PURPOSE: Recently, whole-genome sequencing in acute myeloid leukemia (AML) identified recurrent isocitrate dehydrogenase enzyme isoform (IDH1) mutations (IDH1m), previously reported to be involved in gliomas as well as IDH2 mutations (IDH2m).
  • PATIENTS AND METHODS: The prevalence and the prognostic impact of R132 IDH1 and R172 IDH2 mutations were evaluated in a cohort of 520 adults with AML homogeneously treated in the French Acute Leukemia French Association (ALFA) -9801 and -9802 trials.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20625116.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00880243/ NCT00931138
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
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99. Mills K: Gene expression profiling for the diagnosis and prognosis of acute myeloid leukaemia. Front Biosci; 2008;13:4605-16
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  • [Title] Gene expression profiling for the diagnosis and prognosis of acute myeloid leukaemia.
  • Acute myeloid leukaemia (AML) is a heterogeneous disease covering a range of morphological lineages and differentiation stages, but also has number of recurrent chromosomal abnormalities and mutations associated with prognosis.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gene Expression Profiling. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis

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  • (PMID = 18508532.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MicroRNAs; 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
  • [Number-of-references] 110
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100. von Neuhoff C, Reinhardt D, Sander A, Zimmermann M, Bradtke J, Betts DR, Zemanova Z, Stary J, Bourquin JP, Haas OA, Dworzak MN, Creutzig U: Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98. J Clin Oncol; 2010 Jun 1;28(16):2682-9
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  • [Title] Prognostic impact of specific chromosomal aberrations in a large group of pediatric patients with acute myeloid leukemia treated uniformly according to trial AML-BFM 98.
  • PURPOSE: Because cytogenetic data are essential for risk stratification of childhood acute myeloid leukemia (AML), the impact of chromosomal aberrations is crucial.
  • CONCLUSION: Because the prognostic value of rare recurrent chromosomal aberrations still has to be elucidated, these data will contribute to future risk stratification for the treatment of pediatric AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Chromosome Aberrations. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 20439630.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin; ICE protocol 4
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