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1. 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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2. 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
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  • [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 better understand the cause of the marked heterogeneity in therapeutic response and to identify new prognostic markers and therapeutic targets a comprehensive list of the genetic mutations that underlie the pathogenesis of AML is needed.
  • 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.
  • Despite the low overall number of lesions across the patient cohort, novel recurring regions of genetic alteration were identified that harbor known, and potential new cancer genes.
  • 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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3. 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
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  • [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.
  • The World Health Organization (WHO) classification of lympho-hematopoietic neoplasms is increasingly based on genetic criteria.
  • 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.
  • These changes have greatly modified the approaches to diagnosis and prognostic stratification of AML patients.
  • To emphasize the need of various parameters for diagnosis, including myelodysplasia (MD)-related cytogenetic abnormalities, history of myelodysplasia or myelodysplasia/myeloproliferative neoplasm, and multilineage dysplasia, the category of "AML with multilineage dysplasia" was re-named AML with MD-related changes.
  • 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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4. 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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  • [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.
  • Other genetic abnormalities in t-MDS and t-AML comprise activating point mutations or internal tandem duplications of genes involved in signal transduction as tyrosine kinase receptors or genes more downstream in the RAS-BRAF pathway (class I mutations).
  • The alternative genetic pathways of t-MDS and t-AML can now be further characterized by a different clustering of six individual class I mutations and mutations of AML1 and p53 in the various pathways.
  • In addition, there is a significant association between class I and class II mutations possibly indicating cooperation in leukemogenesis, and between mutations of AML1 and RAS related to subsequent progression from t-MDS to t-AML.
  • 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


5. 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.
  • Currently, favorable risk AML patients are usually treated with contemporary chemotherapy while poor risk AML patients receive allogeneic stem cell transplantation if suitable stem cell donors exist.
  • The largest subgroup of AML patients (aproximately 40%) have no identifiable cytogenetic abnormalities and are classified as intermediate risk.
  • Recently, it is becoming increasingly evident that it is possible to identify a subgroup of poorer risk patients among those with normal cytogenic AML (NC-AML).
  • Molecular risk stratification for NC-AML patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q.
  • Further prospective studies are needed to confirm if poorer risk NC-AML patients have improved clinical outcomes after more aggressive therapy.
  • [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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6. 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.
  • The platelet count was higher and the rate of myeloperoxidase (MPO)-positive blasts was lower in AML with MLD than in the other WHO categories.
  • The 5-year survival rates for patients with favorable, intermediate, and adverse karyotypes were 63.4, 39.1, and 0.0%, respectively, and 35.5% for those with 11q23 abnormalities (P < 0.0001).
  • Overall survival (OS) did not significantly differ between nine patients with t(9;11) and 23 with other 11q23 abnormalities (P = 0.22).
  • Our results confirmed that the cytogenetic profile, MLD phenotype, and MPO-positivity of blasts are associated with survival in patients with AML, and showed that each category had the characteristics of the WHO classification such as incidence, clinical features, and OS.
  • [MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries


7. 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.
  • They constitute 10% to 12% of all AML patents, with the incidence of complex karyotypes increasing with the more advanced age.
  • 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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8. 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.
  • Patients presenting as t-MDS and patients presenting as overt t-AML cluster differently in these pathways.
  • Three types of gene mutations are observed in MDS and AML:.
  • At least 14 different genes have been identified as mutated in t-MDS and t-AML, clustering differently and characteristically in the eight genetic pathways.
  • 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.


9. 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).
  • Cytogenetic/FISH abnormalities were observed in 71% of subjects, FLT3-ITD mutations in 15%, and NPM1 mutations in 13%.
  • Six genes (AKT1, RUNX1, LTB, SDC1, RUNX1T1, and JAK2) from the imbalanced regions have been reported to be involved in AML, whereas other 30 cancer genes, not previously reported in an AML context, were identified as imbalanced.
  • They probably correspond to non passenger alterations that cooperate with the recurrent translocations.
  • The clinical data and genetic changes were tested to find out the possible association with prognosis.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid, Acute / genetics. Mutation
  • [MeSH-minor] Adolescent. Bone Marrow Cells / cytology. Child. Child, Preschool. Cytogenetics. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Karyotyping. Male. Polymerase Chain Reaction. Prognosis. Translocation, Genetic


10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
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  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • A substantial proportion of cases exhibiting recurrent reciprocal translocations at diagnosis, such as t(8;21) or t(15;17) have been exhaustively studied and are currently employed in clinical diagnosis.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • Here we review the differing technologies employed in generation of GEM of AML.
  • We discuss the relevance of GEM AML from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models; through to the valuable retroviral-mediated gene transfer models.
  • The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all AML cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
  • Finally, we comment on the emergence of newer transduction technologies, which can regulate the level of expression to defined cell lineages in both primary murine and human xenografts, and discuss how combining multiple genetic modalities, more relevant models of this complex disease are being generated.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis

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  • (PMID = 18264136.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 111
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12. 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.
  • AML with t(9;.
  • 11) (p22;q23); MLLT3-MLL, AML with t(6;9) (p23; q34); DEK-NUP214, AML with inv(3) (q21q26.2) or t(3;.
  • 3) (q21 ; q26.2); RPN1-EVI1 and AML (megakaryoblastic) with t(1;.
  • 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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13. 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".
  • HLV-AML leukemic clones are characterized by rate-limiting genomic mutations capable of conferring proliferation/survival advantage over a normal hematopoietic environment while in LLV-AML, the leukemic clones are not particularly proliferative or apoptosis-resistant, but are nevertheless selected against an impaired, previously damaged hematopoietic environment.
  • Such a pathogenesis-oriented classification might have therapeutic and prognostic implications, providing a theoretical basis for a further adaptation of the current standard treatment strategies to the individual characteristics of the AML patients.
  • [MeSH-major] Clone Cells. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology
  • [MeSH-minor] Apoptosis. Cell Lineage. Cell Proliferation. Cytogenetic Analysis. Humans. Kinetics. Models, Biological. Mutation. Prognosis. Selection, Genetic. Survival Analysis. World Health Organization

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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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14. 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.
  • This report discusses the diversity and relevance of clinical, pathologic, and genetic features and provides an update on the pathogenesis of these disorders.
  • 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.
  • Nevertheless, recognition of the diverse morphologic features is crucial as bone marrow morphologic examination remains the first and important step of patient evaluation.
  • 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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15. 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.
  • Here, we report the detection of a reciprocal translocation t(7;21)(p22;q22) in the marrow of two adults with MDS and AML, using conventional cytogenetic analysis and fluorescence-in situ-hybridization (FISH).
  • Combined cytomorphology and FISH studies in MDS marrow revealed abnormal RUNX1 signals within megakaryocytes, suggesting that the acquisition of t(7;21)(p22;q22) does not confer complete differentiation arrest and may represent an early genetic event in leukaemogenesis.
  • Molecular analysis of 100 MDS and AML marrow specimens by RT-PCR did not reveal new cases with the RUNX1-USP42 fusion.
  • 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


16. 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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17. 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).
  • We reviewed the cytogenetic and clinical findings of 215 pediatric patients (ages </=17) who were diagnosed with AML to check for abnormalities of 7q and/or 12p.
  • In connection with this, we prudently propose that downregulation of the HLXB9 expression may be a new treatment strategy for AML patients with t(7;12).
  • [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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18. 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.
  • In this study, we evaluated long-term outcomes of unselected AML patients categorized according to the new WHO classification.
  • Between 1990 and 2002, 109 adult AML cases were referred to our hospital.
  • 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.
  • These results indicate that outcomes for AML patients appear to be distinguished on the basis of the WHO classification, but the prognostic significance of multilineage dysplasia and prior therapy is lost after adjusting for cytogenetic risk and age.
  • Our findings suggest that the WHO classification may be strengthened by greater emphasis on genetic/cytogenetic information.
  • [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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19. 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.
  • Parallel analysis of gene expression helped delineate potential candidate genes, and unsupervised analysis of gene expression data revealed cell lines to cluster in part based on underlying cytogenetic abnormalities.
  • 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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20. Lu G, Gurevich I, Vo BT, Chen SS: t(10; 12) (q24; p13) as the sole abnormality in a case with refractory acute myeloid leukemia: The first case report and literature review. Beijing Da Xue Xue Bao; 2009 Aug 18;41(4):480-3
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  • [Title] t(10; 12) (q24; p13) as the sole abnormality in a case with refractory acute myeloid leukemia: The first case report and literature review.
  • Rearrangements involving chromosome region at 12p13 are common abnormalities in hematological malignancies, including myeloid and lymphoid types.
  • ETV6 rearrangements are more often observed in acute lymphoblastic leukemia than in acute myeloid leukemia (AML), where ETV6 gene deletions are more common than rearrangements.
  • Here, we report an AML case with the recurrent t(10;. 12) (q24;.
  • p13) as the sole abnormality.
  • In review of the literature, this is the first report of AML case with the novel abnormality as the sole change.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 12 / genetics. Gene Rearrangement / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 19727243.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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21. Lai YY, Qiu JY, Jiang B, Lu XJ, Huang XJ, Zhang Y, Liu YR, Shi HL, Lu DP: Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22). Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Oct;13(5):733-40
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  • [Title] Characteristics and prognostic factors of acute myeloid leukemia with t (8; 21) (q22; q22).
  • q22) frequently associated with additional chromosomal aberrations is one of the most recurrent chromosomal abnormalities in AML.
  • Clinically, this type of AML usually shows some specific characteristics and has a good response to chemotherapy with a high remission rate and a relatively long median survival.
  • On the other hand, some reports also showed poor prognosis in AML patients with t (8; 21), and the associated bad-prognosis factors have not been strongly established to date.
  • 21) AML in China, 75 Chinese AML patients with t (8;.
  • Cytogenetically, 62.5% cases had additional chromosomal abnormalities, and the main associated recurrent additional abnormalities were loss of a sex chromosome (LOS), trisomy 4, del (9q) and trisomy 8.
  • In multivariate analyses of prognostic factors, karyotype, extramedullary leukemia, age and post-remission therapy were of prognostic value for OS.
  • Extramedullary leukemia was an adverse prognostic factor (P = 0.012).
  • It is concluded that Chinese AML patients with t (8;.
  • 21) had some different characteristics as compared with patients from other countries, a relatively poor outcome was observed in our patients, especially in those with extramedullary leukemia or additional chromosomal abnormalities.
  • 21) AML in China, especially to those with adverse prognostic factors.

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  • (PMID = 16277833.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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22. 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.
  • Because of the defined molecular and cytogenetic features, AML has been a focus of gene expression profiling studies and identified differentially expressed genes in the different diagnostic and cytogenetic sub-groups.
  • [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
  • [MeSH-minor] Chromosome Aberrations. Chromosome Mapping. Genes, ras. Homeodomain Proteins / genetics. Humans. MicroRNAs / genetics. Nuclear Proteins / genetics. Prognosis. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics

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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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23. Park SH, Chi HS, Park SJ, Jang S, Park CJ: [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes]. Korean J Lab Med; 2010 Jun;30(3):231-8
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  • [Title] [Clinical importance of morphological multilineage dysplasia in acute myeloid leukemia with myelodysplasia related changes].
  • BACKGROUND: AML with myelodysplasia related changes (AML MRC) is known to show a poor prognosis compared with de novo AML, but controversies exist about the prognostic impact of multilineage dysplasia (MLD) among MRC.
  • We investigated the prognostic impact of MLD in AML MRC.
  • METHODS: A total of 357 patients newly diagnosed as AML at Asan Medical Center from January 2001 to December 2005 were analyzed.
  • They were diagnosed and classified as AML with recurrent genetic abnormalities, AML MRC, and AML not otherwise specified (AML NOS).
  • RESULTS: AML MRC patients showed a lower complete remission (CR) rate (44.7% vs. 64.9%, P=0.002) and shorter OS (297 vs. 561 days, P=0.004) and EFS (229 vs. 374 days, P=0.004) than AML NOS patients.
  • Patients with MLD among AML MRC also showed a lower CR rate (37.7%, P=0.001) and shorter OS (351 days, P=0.036) and EFS (242 days, P=0.076) than AML NOS patients.
  • However, among AML MRC patients, there were no differences in OS, EFS and CR between patients with and without MLD.
  • CONCLUSIONS: AML MRC patients showed a lower CR rate and shorter OS and EFS than AML NOS patients.
  • AML MRC patients with MLD showed similar results and their prognosis was not different from those without MLD.
  • MLD findings among AML MRC could be an independent poor prognostic factor in de novo AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / diagnosis

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  • (PMID = 20603581.001).
  • [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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24. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
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  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • The various aberrations observed were t(8;21)(q22;q22) (5.2%); t(15;17) (q22;q11-21) (9%); t(9;22)(q34;q11)(1.7%); t(14;17)(q32;q11.2)(0.5%); inv(16)(p13;q22)(1.7%); 11q23 rearrangements (4%); monosomy 7 (2.2%) and 22 (1.1%); deletion of 9q (q22q34) (5.1%), 5q (q13q33) (0.5%) and 13q (q13q31) (0.5%); common trisomies like +8 (5.6%), +16 (1.7%), +22 (1.1%), +21 (0.5%), +13 (0.5%), +11 (0.5%), +3 (0.5%); hyperdiploidy (3.4%); hypodiploidy (1.1%); complex karyotype (4%); and other structural abnormalities (4.5%).
  • Apart from these, three novel chromosomal abnormalities viz. t(8;18), t(7;14), t(13;15) were observed in the current study population.
  • CONCLUSION: This study confirms that the incidence of chromosomal abnormalities varies considerably.
  • Similarly, the frequency of other recurrent FAB associated abnormalities viz.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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25. Shali W, Hélias C, Fohrer C, Struski S, Gervais C, Falkenrodt A, Leymarie V, Lioure B, Raby P, Herbrecht R, Lessard M: Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH. Cancer Genet Cytogenet; 2006 Jul 15;168(2):133-45
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  • [Title] Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH.
  • We report a series of 43 consecutive therapy-related myelodysplastic syndromes (t-MDS) or acute myeloid leukemias (t-AML) observed for 6 years.
  • Conventional cytogenetic and fluorescent in situ hybridization (FISH)/ multiplex FISH (M-FISH) methods were used to analyze cytogenetic characteristics of secondary MDS/AML.
  • The features of chromosomal abnormalities were linked to the nature of the therapy and protocols used.
  • A considerable proportion of recurrent balanced translocations characterized t-AML secondary to therapy.
  • After treatment for lymphomas and chronic myeloproliferative diseases, there were more complex unbalanced abnormalities than the control group.
  • Compared to other series, recurrent translocations appeared to be more numerous (25%), probably reflecting an evolution of therapeutic modalities.
  • [MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Gene Amplification. Gene Deletion. Humans. Karyotyping. Male. Middle Aged. Translocation, Genetic


26. Yin CC, Medeiros LJ, Bueso-Ramos CE: Recent advances in the diagnosis and classification of myeloid neoplasms--comments on the 2008 WHO classification. Int J Lab Hematol; 2010 Oct;32(5):461-76
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  • [Title] Recent advances in the diagnosis and classification of myeloid neoplasms--comments on the 2008 WHO classification.
  • The fourth edition of the World Health Organization (WHO) classification of myeloid neoplasms refined the criteria for some previously described myeloid neoplasms and recognized several new entities based on recent elucidation of molecular pathogenesis, identification of new diagnostic and prognostic markers, and progress in clinical management.
  • Protein tyrosine kinase abnormalities, including translocations or mutations involving ABL1, JAK2, MPL, KIT, PDGFRA, PDGFRB, and FGFR1, have been used as the basis for classifying myeloproliferative neoplasms (MPN).
  • A list of cytogenetic abnormalities has been introduced as presumptive evidence of MDS in cases with refractory cytopenia but without morphologic evidence of dysplasia.
  • The subgroup 'acute myeloid leukemia (AML) with recurrent genetic abnormalities' has been expanded to include more molecular genetic aberrations.
  • The entity 'AML with multilineage dysplasia' specified in the 2001 WHO classification has been renamed 'AML with myelodysplasia-related changes' to include not only cases with significant multilineage dysplasia but also patients with a history of MDS or myelodysplasia-related cytogenetic abnormalities.
  • The term 'therapy-related myeloid neoplasms' is used to cover the spectrum of disorders previously known as t-AML, t-MDS, or t-MDS/MPN occurring as complications of cytotoxic chemotherapy and/or radiation therapy.
  • [MeSH-minor] Anemia, Refractory, with Excess of Blasts / classification. Humans. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / diagnosis. Protein-Tyrosine Kinases / genetics

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  • (PMID = 20626469.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Other-IDs] NLM/ NIHMS691453; NLM/ PMC4452117
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27. Chang ST, Hsieh YC, Lee LP, Tzeng CC, Chuang SS: Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up. Chang Gung Med J; 2006 Sep-Oct;29(5):532-7
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  • [Title] Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.
  • Acute myeloid leukemia (AML) with recurrent genetic abnormalities often carries a favorable prognosis.
  • AML with inv(16)(p13q22) occurs predominantly in younger patients and usually shows granulocytic and monocytic differentiation with abnormal eosinophils.
  • It is referred to as acute myelomonocytic leukemia with abnormal eosinophils (AMML Eo).
  • [MeSH-major] Eosinophils / pathology. Leukemia, Myelomonocytic, Acute / diagnosis

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  • (PMID = 17214400.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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28. McManus PM: Classification of myeloid neoplasms: a comparative review. Vet Clin Pathol; 2005 Sep;34(3):189-212
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  • [Title] Classification of myeloid neoplasms: a comparative review.
  • Classification of myeloid neoplasms in veterinary medicine was modeled in the early 1990s after French-American-British and National Cancer Institute systems used in human medicine.
  • WHO revisions lower the blast threshold from 30% to 20% for diagnosing acute myeloid leukemia (AML) and expand and redefine AML categories.
  • AML is now subdivided into 4 broad groups:.
  • 1) AML with recurrent genetic abnormalities, 2) AML with multilineage dysplasia, 3) AML with previous chemotherapy and/or radiation, and 4) AML, not otherwise categorized.
  • AML alphanumeric designations (M1, M2, etc) have been discontinued as numbers of subtypes have increased.
  • That threshold is 50% for diagnosing AML with multilineage dysplasia.
  • Chronic myelomonocytic leukemia has been removed from the MDS category and included in a new category of diseases that have features of both MDS and chronic leukemia.

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  • (PMID = 16134066.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 265
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29. Falini B, Mecucci C, Tiacci E, Alcalay M, Rosati R, Pasqualucci L, La Starza R, Diverio D, Colombo E, Santucci A, Bigerna B, Pacini R, Pucciarini A, Liso A, Vignetti M, Fazi P, Meani N, Pettirossi V, Saglio G, Mandelli F, Lo-Coco F, Pelicci PG, Martelli MF, GIMEMA Acute Leukemia Working Party: Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype. N Engl J Med; 2005 Jan 20;352(3):254-66
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  • [Title] Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
  • METHODS: We used immunohistochemical methods to study the subcellular localization of NPM in bone marrow-biopsy specimens from 591 patients with primary acute myelogenous leukemia (AML).
  • RESULTS: Cytoplasmic NPM was detected in 208 (35.2 percent) of the 591 specimens from patients with primary AML but not in 135 secondary AML specimens or in 980 hematopoietic or extrahematopoietic neoplasms other than AML.
  • It was associated with a wide spectrum of morphologic subtypes of the disease, a normal karyotype, and responsiveness to induction chemotherapy, but not with recurrent genetic abnormalities.
  • There was a high frequency of FLT3 internal tandem duplications and absence of CD34 and CD133 in AML specimens with a normal karyotype and cytoplasmic dislocation of NPM, but not in those in which the protein was restricted to the nucleus.
  • AML specimens with cytoplasmic NPM carried mutations of the NPM gene that were predicted to alter the protein at its C-terminal; this mutant gene caused cytoplasmic localization of NPM in transfected cells.
  • CONCLUSIONS: Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with AML who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy.
  • [MeSH-major] Bone Marrow / pathology. Cytoplasm / chemistry. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Nucleolus. DNA Mutational Analysis. Humans. Karyotyping. Middle Aged. Remission Induction. Transfection. Translocation, Genetic


30. Park TS, Cheong JW, Song J, Choi JR: Therapy-related myelodysplastic syndrome with der(17)t(12;17)(q13;p13) as a new recurrent cytogenetic abnormality after treatment for chronic lymphocytic leukemia. Leuk Res; 2009 Jul;33(7):1001-4
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  • [Title] Therapy-related myelodysplastic syndrome with der(17)t(12;17)(q13;p13) as a new recurrent cytogenetic abnormality after treatment for chronic lymphocytic leukemia.
  • He was initially diagnosed with chronic lymphocytic leukemia (CLL) and treated with six cycles of fludarabine, cyclophosphamide, and rituximab chemotherapy.
  • Therapy-related myelodysplastic syndrome (t-MDS) was suspected approximately 2 years later; in addition, complex karyotypic abnormalities including 5q deletion, monosomy 7, and der(17)t(12;17)(q13;p13) were found repeatedly in the patient's chromosome studies.
  • The chromosomal abnormality der(17)t(12;17)(q13;p13) is very rare in hematologic malignancies, and has been reported in only two patients with therapy-related acute myeloid leukemia (t-AML).
  • In addition, we suggest that der(17)t(12;17)(q13;p13) should be considered a new recurrent, nonrandom chromosomal abnormality in patients with t-MDS/AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Translocation, Genetic / genetics


31. Sanada M, Uike N, Ohyashiki K, Ozawa K, Lili W, Hangaishi A, Kanda Y, Chiba S, Kurokawa M, Omine M, Mitani K, Ogawa S: Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms. Leukemia; 2007 May;21(5):992-7
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  • [Title] Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms.
  • The unbalanced translocation, der(1;7)(q10;p10), is one of the characteristic cytogenetic abnormalities found in myelodysplastic syndromes (MDS) and other myeloid neoplasms.
  • Although described frequently with very poor clinical outcome and possible relationship with monosomy 7 or 7q- (-7/7q-), this recurrent cytogenetic abnormality has not been explored fully.
  • In contrast with other -7/7q- cases, where the abnormality tends to be found in one or more partial karyotypes, der(1;7)(q10;p10) represents the abnormality common to all the abnormal clones and usually appears as a sole chromosomal abnormality during the entire clinical courses, or if not, is accompanied only by a limited number and variety of additional abnormalities, mostly trisomy 8 and/or loss of 20q. der(1;7)(q10;p10)-positive MDS cases showed lower blast counts (P<0.0001) and higher hemoglobin concentrations (P<0.0075) at diagnosis and slower progression to acute myeloid leukemia (P=0.0043) than other -7/7q- cases. der(1;7)(q10;p10) cases showed significantly better clinical outcome than other -7/7q cases (P<0.0001).
  • In conclusion, der(1;7)(q10;p10) defines a discrete entity among myeloid neoplasms, showing unique clinical and cytogenetic characteristics.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Translocation, Genetic


32. Sazawal S, Kumar B, Hasan SK, Dutta P, Kumar R, Chaubey R, Mir R, Saxena R: Haematological & molecular profile of acute myelogenous leukaemia in India. Indian J Med Res; 2009 Mar;129(3):256-61
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  • [Title] Haematological & molecular profile of acute myelogenous leukaemia in India.
  • BACKGROUND & OBJECTIVE: Recurrent balanced translocations are generally recognized to be a major parameter for prognostication in acute myeloid leukaemia (AML).
  • Patients with these mutations have a good prognosis unlike abnormalities in chromosome 5 or 7 or FLT3 genes.
  • Therefore, we screened the AmL patients for known specific genetic abnormalities that could lead to more definitive prognoses.
  • METHODS: A total of 113 AML patients were evaluated at diagnosis based on routine morphology and cytochemistry and classified according to the WHO criteria.
  • The distribution of AML subtypes was M1(1), M2(32), M3(57), M4(14), M5(1), M6(1) and seven cases where morphological subtype could not be classified.
  • FLT3 internal tandem duplication (ITD) mutations were more frequent in patients with APL than in other AML subtypes (17.5 vs. 8.9%), the frequency greater in patients with bcr3 isoform (70%) than in those with in bcr1 isoform (30%).
  • FLT3 internal tandem duplication (ITD) mutation was predominant in acute promyelocytic leukaemia patients with bcr3 isoform.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Child. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Duplication. Genetic Predisposition to Disease / epidemiology. Humans. India / epidemiology. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Prevalence. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Young Adult. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19491417.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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33. Alvarez S, Cigudosa JC: Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel. Hematol Oncol; 2005 Mar;23(1):18-25
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  • [Title] Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel.
  • Complex karyotypes are seen in approximately 15% of de novo MDS/AML and in up to 50% of therapy-related MDS/AML.
  • Therefore, a large number of genetic studies using cytogenetic molecular techniques have been performed to better define the chromosomal abnormalities in this poor-prognosis group.
  • On the basis of the available data from several studies of AML with complex karyotypes, similar findings on recurrent breakpoints and frequently lost and gained chromosomal regions have been observed.
  • Interestingly, this non-random pattern of DNA gains and losses, that characterizes AML cases with complex karyotypes, affects the gene expression pattern, and a specific expression profile, characterized by the upregulation of genes involved in the DNA repair and chromosome segregation pathways, has been recently reported.
  • Therefore, a comprehensive genome-wide analysis of patients with AML or MDS with complex karyotypes has led to a better characterization of chromosomal aberrations.
  • [MeSH-major] Chromosomes, Human / genetics. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosome Segregation / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA Repair / genetics. Gene Amplification / genetics. Gene Expression Profiling / methods. Genome, Human / genetics. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm, Residual / genetics. Neoplasm, Residual / metabolism. Neoplasm, Residual / therapy. Risk Factors

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  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd.
  • (PMID = 16142824.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 53
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34. Phan CL, Megat Baharuddin PJ, Chin LP, Zakaria Z, Yegappan S, Sathar J, Tan SM, Purushothaman V, Chang KM: Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2008 Jan 1;180(1):60-4
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  • [Title] Amplification of BCR-ABL and t(3;21) in a patient with blast crisis of chronic myelogenous leukemia.
  • The Philadelphia (Ph) chromosome, or t(9;22), is the hallmark of chronic myelogenous leukemia (CML).
  • Blast crisis is characterized by the rapid expansion of a population of differentiation arrested blast cells (myeloid or lymphoid cells population), with secondary chromosomal abnormalities present.
  • We report a case of myeloid blast crisis of CML resistant to imatinib mesylate and chemotherapy.
  • The t(3;21)(q26;q22) is a recurrent chromosomal abnormality in some cases of CML blast phase and in treatment-related myelodysplastic syndrome and acute myeloid leukemia.
  • Amplification or copy number increase of RUNX1 has been reported in childhood acute lymphoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 3. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Translocation, Genetic

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  • (PMID = 18068536.001).
  • [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] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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35. Mansour S, Connell F, Steward C, Ostergaard P, Brice G, Smithson S, Lunt P, Jeffery S, Dokal I, Vulliamy T, Gibson B, Hodgson S, Cottrell S, Kiely L, Tinworth L, Kalidas K, Mufti G, Cornish J, Keenan R, Mortimer P, Murday V, Lymphoedema Research Consortium: Emberger syndrome-primary lymphedema with myelodysplasia: report of seven new cases. Am J Med Genet A; 2010 Sep;152A(9):2287-96
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  • Four reports have been published on an association between acute myeloid leukaemia (AML) and primary lymphedema, with or without congenital deafness.
  • We report seven new cases, including one extended family, confirming this entity as a genetic syndrome.
  • The lymphedema typically presents in one or both lower limbs, before the hematological abnormalities, with onset between infancy and puberty and frequently affecting the genitalia.
  • The AML is often preceded by pancytopenia or myelodysplasia with a high incidence of monosomy 7 in the bone marrow (five propositi and two relatives).
  • Associated anomalies included hypotelorism, epicanthic folds, long tapering fingers and/or neck webbing (four patients), recurrent cellulitis in the affected limb (four patients), generalized warts (two patients), and congenital, high frequency sensorineural deafness (one patient).
  • Children with lower limb and genital lymphedema should be screened for hematological abnormalities and immunodeficiency.

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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • (PMID = 20803646.001).
  • [ISSN] 1552-4833
  • [Journal-full-title] American journal of medical genetics. Part A
  • [ISO-abbreviation] Am. J. Med. Genet. A
  • [Language] ENG
  • [Grant] United Kingdom / British Heart Foundation / / PG/10/58/28477; United Kingdom / British Heart Foundation / /
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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36. Haferlach C, Mecucci C, Schnittger S, Kohlmann A, Mancini M, Cuneo A, Testoni N, Rege-Cambrin G, Santucci A, Vignetti M, Fazi P, Martelli MP, Haferlach T, Falini B: AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping biologic, pathologic, immunophenotypic, and prognostic features. Blood; 2009 Oct 1;114(14):3024-32
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  • [Title] AML with mutated NPM1 carrying a normal or aberrant karyotype show overlapping biologic, pathologic, immunophenotypic, and prognostic features.
  • Acute myeloid leukemia (AML) with mutated NPM1 usually carries normal karyotype (NK), but it may harbor chromosomal aberrations whose significance remains unclear.
  • We addressed this question in 631 AML patients with mutated/cytoplasmic NPM1.
  • An abnormal karyotype (AK) was present in 93 of 631 cases (14.7%), the most frequent abnormalities being +8, +4, -Y, del(9q), +21.
  • Chromosome aberrations in NPM1-mutated AML were similar to, but occurred less frequently than additional chromosome changes found in other AML with recurrent cytogenetic abnormalities according to WHO classification.
  • Four of the 31 NPM1-mutated AML patients karyotyped at different time points had NK at diagnosis but AK at relapse: del(9q) (n = 2), t(2;11) (n = 1), inv(12) (n = 1).
  • NPM1-mutated AML with NK or AK showed overlapping morphologic, immunophenotypic (CD34 negativity), and gene expression profile (down-regulation of CD34 and up-regulation of HOX genes).
  • No difference in survival was observed among NPM1-mutated AML patients independently of whether they carried a NK or an AK, the NPM1-mutated/FLT3-ITD negative cases showing the better prognosis.
  • Findings in our patients point to chromosomal aberrations as secondary events, reinforce the concept that NPM1 mutation is a founder genetic lesion, and indicate that NPM1-mutated AML should be clinically handled as one entity, irrespective of the karyotype.
  • [MeSH-major] Antigens, CD34 / metabolism. Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / immunology. Mutation / genetics. Nuclear Proteins / genetics

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  • [CommentIn] Blood. 2009 Nov 12;114(20):4601-2; author reply 4602-3 [19965707.001]
  • (PMID = 19429869.001).
  • [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, CD34; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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37. Roche-Lestienne C, Deluche L, Corm S, Tigaud I, Joha S, Philippe N, Geffroy S, Laï JL, Nicolini FE, Preudhomme C, Fi-LMC group: RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood; 2008 Apr 1;111(7):3735-41
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  • Acquired molecular abnormalities (mutations or chromosomal translocations) of the RUNX1 transcription factor gene are frequent in acute myeloblastic leukemias (AMLs) and in therapy-related myelodysplastic syndromes, but rarely in acute lymphoblastic leukemias (ALLs) and chronic myelogenous leukemias (CMLs).
  • Among 18 BCR-ABL+ leukemias presenting acquired trisomy of chromosome 21, we report a high frequency (33%) of recurrent point mutations (4 in myeloid blast crisis [BC] CML and one in chronic phase CML) within the DNA-binding region of RUNX1.
  • In addition, we also report a high frequency of cryptic chromosomal RUNX1 translocation to a novel recently described gene partner, PRDM16 on chromosome 1p36, for 3 (21.4%) of 14 investigated patients: 2 myeloid BC CMLs and, for the first time, 1 therapy-related BCR-ABL+ ALL.
  • These events are associated with a short survival and support the concept of a cooperative effect of BCR-ABL with molecular RUNX1 abnormalities on the differentiation arrest phenotype observed during progression of CML and in BCR-ABL+ ALL.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / genetics. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Transcription Factors / genetics. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Benzamides. Chromosomes, Human. Chronic Disease. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / mortality. Phenotype. Point Mutation. Retrospective Studies. Survival Rate. Translocation, Genetic / drug effects. Translocation, Genetic / genetics

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  • (PMID = 18202228.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / PRDM16 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RUNX1 protein, human; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [General-notes] NLM/ Investigator list not found.
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38. Peniket A, Wainscoat J, Side L, Daly S, Kusec R, Buck G, Wheatley K, Walker H, Chatters S, Harrison C, Boultwood J, Goldstone A, Burnett A: Del (9q) AML: clinical and cytological characteristics and prognostic implications. Br J Haematol; 2005 Apr;129(2):210-20
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  • [Title] Del (9q) AML: clinical and cytological characteristics and prognostic implications.
  • Del (9q) is a recurrent cytogenetic abnormality in acute myeloid leukaemia (AML).
  • We report an analysis of 81 patients with del(9q) as a diagnostic karyotypic abnormality entered into the Medical Research Council AML trials 10, 11 and 12.
  • (iii) Del(9q) in association with other cytogenetic abnormalities, 31 patients.
  • Patients with del(9q) in association with t(8;21) had a 5-year OS of 75%, which was significantly better than the groups with either sole del(9q) (40%) and del(9q) with other abnormalities (26%; P = 0.008).
  • It is likely that the deletion of single or multiple tumour suppressor genes located in this region may underlie the pathogenesis of del (9q) AML.
  • [MeSH-major] Gene Deletion. Genes, Tumor Suppressor. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis. Disease-Free Survival. Female. Genetic Markers. Humans. Male. Middle Aged. Survival Rate. Translocation, Genetic

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  • [CommentIn] Br J Haematol. 2005 Sep;130(6):969; author reply 969 [16156871.001]
  • (PMID = 15813849.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
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39. Davids MS, Steensma DP: The molecular pathogenesis of myelodysplastic syndromes. Cancer Biol Ther; 2010 Aug 15;10(4):309-19
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  • The myelodysplastic syndromes (MDS) are frequently associated with clonally restricted cytogenetic abnormalities, but until recently, the molecular pathobiology underlying this diverse group of neoplastic bone marrow disorders has been largely obscure.
  • During the last 10 years, many investigative groups have applied the formidable power of new molecular biology techniques to hunt for recurrent genetic alterations in MDS primary cells.
  • Several genetic abnormalities, including mutations in RUNX1 (AML1), TET2, ASXL1 and TP53, have been discovered in a substantial fraction of MDS cases; genes rearranged or mutated less commonly in MDS include IER3, ATRX, RAS and FLT3.
  • Abnormalities in iron regulation, microenvironment interactions, regulation of apoptosis and oxidative damage/DNA repair may all play an important pathobiological role.
  • [MeSH-minor] Apoptosis / genetics. DNA Repair / genetics. Hemoglobinuria, Paroxysmal / complications. Humans. Leukemia, Myeloid, Acute / complications. Oxidative Stress / genetics. Point Mutation. Protein Biosynthesis. Translocation, Genetic


40. Nimer SD: Is it important to decipher the heterogeneity of "normal karyotype AML"? Best Pract Res Clin Haematol; 2008 Mar;21(1):43-52
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  • [Title] Is it important to decipher the heterogeneity of "normal karyotype AML"?
  • Almost half of adult acute myelogenous leukemia (AML) is normal cytogenetically, and this subgroup shows a remarkable heterogeneity of genetic mutations at the molecular level and an intermediate response to therapy.
  • The finding of recurrent cytogenetic abnormalities has influenced, in a primary way, the understanding and treatment of leukemias.
  • Yet "normal karyotype AML" lacks such obvious abnormalities, but has a variety of prognostically important genetic abnormalities.
  • Although resistance to treatment is associated with specific mutations, the degree to which the leukemia resembles a stem cell in its functional properties may provide greater protection from the effects of treatment.
  • Although usually all of the circulating leukemia cells are cleared following treatment, a small residual population of leukemic cells in the bone marrow persists, making this disease hard to eradicate.
  • Increased understanding of the biological consequences of at least some of these mutations in "normal karyotype AML" is leading to more targeted approaches to develop more effective treatments for this disease.

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  • (PMID = 18342811.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052621; United States / NIDDK NIH HHS / DK / R01 DK052621-08; United States / NIDDK NIH HHS / DK / R56 DK052208-09A1; United States / NCI NIH HHS / CA / R01 CA102202-01; United States / NCI NIH HHS / CA / CA102202-01; United States / NIDDK NIH HHS / DK / R56 DK052208; United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / DK052208-09A1; United States / NIDDK NIH HHS / DK / DK052621-08
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 76
  • [Other-IDs] NLM/ NIHMS44325; NLM/ PMC2654590
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41. Haltrich I, Csóka M, Kovács G, Fekete G: [Cytogenetic and FISH findings are complementary in childhood ALL]. Magy Onkol; 2008 Sep;52(3):283-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary genetic abnormalities of leukemia cells have important prognostic significance in childhood acute leukemia.
  • In the last two years 30 newly diagnosed or recurrent childhood ALL bone marrow samples were analyzed for chromosomal abnormalities with conventional G-banding and interphase-fluorescence in situ hybridization (I-FISH) using probes to detect BCR/ABL fusions, cryptic TEL/AML1 and MLL rearrangements and p16(9p21) tumor suppressor gene deletions.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21. Gene Rearrangement. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Deletion. Histone-Lysine N-Methyltransferase. Humans. Interphase. Karyotyping / methods. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Predictive Value of Tests. Prognosis. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Risk Factors. Sensitivity and Specificity

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  • (PMID = 18845499.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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42. Liedtke M, Cleary ML: Therapeutic targeting of MLL. Blood; 2009 Jun 11;113(24):6061-8
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Treatment of hematologic malignancies is evolving from a uniform approach to targeted therapies directed at the underlying molecular abnormalities of disease.
  • The mixed lineage leukemia (MLL) proto-oncogene is a recurrent site of genetic rearrangements in acute leukemias; and since its discovery in 1992, many advances have been made in understanding its role in leukemogenesis.
  • Proteins associated with the MLL core complex or its fusion partners have been isolated and characterized for their critical roles in leukemia pathogenesis.
  • [MeSH-major] Leukemia / therapy. Myeloid-Lymphoid Leukemia Protein / metabolism

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  • (PMID = 19289854.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA120349
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 78
  • [Other-IDs] NLM/ PMC2699228
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43. Doubek M, Brychtova Y, Berkovcova J, Krejci M, Palasek I, Dvorakova D, Mayer J: Acute myeloid leukemias with recurrent genetic abnormalities: frequent assessment of minimal residual disease and treatment of molecular relapse with chemotherapy. Leukemia; 2005 May;19(5):885-8
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] Acute myeloid leukemias with recurrent genetic abnormalities: frequent assessment of minimal residual disease and treatment of molecular relapse with chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Neoplasm, Residual / drug therapy. Neoplasm, Residual / genetics

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  • (PMID = 15744338.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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