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1. Fitzgibbon J, Smith LL, Raghavan M, Smith ML, Debernardi S, Skoulakis S, Lillington D, Lister TA, Young BD: Association between acquired uniparental disomy and homozygous gene mutation in acute myeloid leukemias. Cancer Res; 2005 Oct 15;65(20):9152-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association between acquired uniparental disomy and homozygous gene mutation in acute myeloid leukemias.
  • Genome-wide single nucleotide polymorphism analysis has revealed large-scale cryptic regions of acquired homozygosity in the form of segmental uniparental disomy in approximately 20% of acute myeloid leukemias.
  • We have investigated whether such regions, which are the consequence of mitotic recombination, contain homozygous mutations in genes known to be mutational targets in leukemia.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Uniparental Disomy
  • [MeSH-minor] Acute Disease. Base Sequence. CCAAT-Enhancer-Binding Protein-alpha / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Genes, Wilms Tumor. Humans. Polymorphism, Single Nucleotide. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16230371.001).
  • [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
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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2. Park EK, Jeon JS, Noh HJ, Won JH, Park HS: Complete remission of IgA nephropathy after bone marrow transplantation for acute myeloid leukaemia. NDT Plus; 2008 Dec;1(6):420-422

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  • [Title] Complete remission of IgA nephropathy after bone marrow transplantation for acute myeloid leukaemia.
  • A 32-year-old woman was found to have IgA nephropathy and acute myeloid leukaemia.
  • We herein report a case of complete remission of IgA nephropathy after BMT for acute myeloid leukaemia.

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  • (PMID = 28657023.001).
  • [ISSN] 1753-0784
  • [Journal-full-title] NDT plus
  • [ISO-abbreviation] NDT Plus
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Keywords] NOTNLM ; IgA nephropathy / bone marrow transplantation
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3. Abbas S, Rotmans G, Löwenberg B, Valk PJ: Exon 8 splice site mutations in the gene encoding the E3-ligase CBL are associated with core binding factor acute myeloid leukemias. Haematologica; 2008 Oct;93(10):1595-7
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  • [Title] Exon 8 splice site mutations in the gene encoding the E3-ligase CBL are associated with core binding factor acute myeloid leukemias.
  • [MeSH-major] Exons / genetics. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Proto-Oncogene Proteins c-cbl / genetics. RNA Splice Sites / genetics

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  • (PMID = 18698078.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / RNA Splice Sites; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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4. Shirley S, Micheau O: The heme oxygenase-1 and c-FLIP in acute myeloid leukemias: two non-redundant but mutually exclusive cellular safeguards protecting cells against TNF-induced cell death? Oncotarget; 2010 Sep;1(5):317-9
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  • [Title] The heme oxygenase-1 and c-FLIP in acute myeloid leukemias: two non-redundant but mutually exclusive cellular safeguards protecting cells against TNF-induced cell death?
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism. Drug Resistance, Neoplasm. Heme Oxygenase-1 / metabolism. Leukemia, Myeloid, Acute / enzymology. Signal Transduction / drug effects. Tumor Necrosis Factor-alpha / pharmacology

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  • [CommentOn] Oncotarget. 2010 Sep;1(5):359-66 [21307400.001]
  • (PMID = 21307398.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Tumor Necrosis Factor-alpha; EC 1.14.99.3 / HMOX1 protein, human; EC 1.14.99.3 / Heme Oxygenase-1
  • [Other-IDs] NLM/ PMC3157731
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5. Maha A, Cheong SK, Leong CF, Seow HF: Molecular responses during chemotherapy in acute myeloid leukemias in predicting poor-response to standard chemotherapy. Malays J Pathol; 2009 Dec;31(2):81-91
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  • [Title] Molecular responses during chemotherapy in acute myeloid leukemias in predicting poor-response to standard chemotherapy.
  • It is postulated that in cells of chemo-sensitive patients, chemotherapy induces apoptotic signals leading to cell death while survival signals are maintained in cells of chemo-resistant patients.
  • We examined the expression pattern of proinflammatory cytokines, signaling molecules of the PI3K and MAPK pathways molecules and death receptor, DR5 on paired samples at diagnosis and during chemotherapy in acute myeloid leukaemia patients treated with cytosine arabinoside and daunorubicin.
  • Thus, expression of TNF-alpha, IL-6, DR5, phospho-p38 and phospho-Jnk may regulate cell death in chemo-sensitive cases.
  • IL-beta and IL-18 were also found to be higher in chemo-resistant cases at diagnosis and during chemotherapy.
  • Thus, expression of various cellular molecules in leukaemic blasts during chemotherapy may be useful in predicting treatment outcome.
  • These cellular molecules may also be potential targets for alternative therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Signal Transduction / drug effects

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  • (PMID = 20514850.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Elafin; 0 / PI3 protein, human; 0 / RNA, Messenger; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 04079A1RDZ / Cytarabine; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; ZS7284E0ZP / Daunorubicin
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6. Murati A, Adélaïde J, Quilichini B, Rémy V, Sainty D, Stoppa AM, Bernard P, Olschwang S, Birnbaum D, Chaffanet M, Mozziconacci MJ: New types of MYST3-CBP and CBP-MYST3 fusion transcripts in t(8;16)(p11;p13) acute myeloid leukemias. Haematologica; 2007 Feb;92(2):262-3
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  • [Title] New types of MYST3-CBP and CBP-MYST3 fusion transcripts in t(8;16)(p11;p13) acute myeloid leukemias.
  • The t(8;16)(p11;p13) translocation, associated with poor prognosis acute monocytic leukemia, fuses MYST3 on chromosome region 8p11 to CBP on chromosome region 16p13.
  • [MeSH-major] Carrier Proteins / genetics. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 8. Histone Acetyltransferases / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic

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  • (PMID = 17296583.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; W980KJ009P / Corticosterone
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7. Barouk-Simonet E, Soenen-Cornu V, Roumier C, Cosson A, Laï JL, Fenaux P, Preudhomme C: Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases. Cancer Genet Cytogenet; 2005 Mar;157(2):118-26
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  • [Title] Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases.
  • Chromosomal abnormalities are found by conventional cytogenetic (CC) analysis in about 50% of myelodysplastic syndromes (MDS) and 70% of acute myeloid leukemias (AML).
  • We studied by M-FISH 28 cases of MDS and AML with complex chromosomal abnormalities, 10 of them were therapy-related.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Humans. Karyotyping. Male. Middle Aged


8. 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
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  • [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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9. Hughes PJ, Brown G: A combination of 1α,25-dihydroxyvitamin D3, a plant-derived antioxidant and an inhibitor of the Cot1/Tlp2 oncogene as molecularly targeted weapons in the hematologist's battle against acute myeloid leukemias. Cell Cycle; 2010 Dec 1;9(23):4612-3
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  • [Title] A combination of 1α,25-dihydroxyvitamin D3, a plant-derived antioxidant and an inhibitor of the Cot1/Tlp2 oncogene as molecularly targeted weapons in the hematologist's battle against acute myeloid leukemias.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antioxidants / therapeutic use. Calcitriol / therapeutic use. Leukemia, Myeloid, Acute / enzymology. MAP Kinase Kinase Kinases / antagonists & inhibitors. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins / antagonists & inhibitors
  • [MeSH-minor] Cell Differentiation. Humans. Signal Transduction

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  • [CommentOn] Cell Cycle. 2010 Nov 15;9(22):4542-51 [21084834.001]
  • (PMID = 21260950.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comment; News
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP3K8 protein, human; FXC9231JVH / Calcitriol
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10. Martynkevich IS, Gritsaev SV, Moskalenko MV, Ivanova MP, Aksenova VIu, Tiranova SA, Abdulkadyrov KM: [FLT3 and NPM1 gene mutations in patients with acute myeloid leukemias and the impact of FLT3-ITD mutations on the survival of patients with a normal karyotype]. Ter Arkh; 2010;82(12):33-9
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  • [Title] [FLT3 and NPM1 gene mutations in patients with acute myeloid leukemias and the impact of FLT3-ITD mutations on the survival of patients with a normal karyotype].
  • AIM: To estimate the extent of FLT3 and NPM1 gene mutations and the impact of mutations of FLT3-ITD on the survival of patients with acute myeloid leukemias (AML).
  • MATERIALS AND METHODS: The nucleus-containing cells of bone marrow and blood were studied in 43 patients with AML.
  • In AML patients with a normal karyotype and the FLT3-ITD-/NPM1 and FLT3-ITD+/ NPM-T genotypes, median overall survival was 17.3 versus 8 months (p = 0.069); and event-free survival (EFS) was 11 versus 5 months (p = 0.026).
  • CONCLUSION: The findings allow AML patients with a normal karyotype and the FLT3-ITD-/NPM-genotypes to be identified as a poor prognosis group.
  • [MeSH-major] DNA / genetics. Genetic Predisposition to Disease. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 21516736.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 9007-49-2 / DNA; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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11. Dunphy CH, O'Malley DP, Perkins SL, Chang CC: Analysis of immunohistochemical markers in bone marrow sections to evaluate for myelodysplastic syndromes and acute myeloid leukemias. Appl Immunohistochem Mol Morphol; 2007 Jun;15(2):154-9
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  • [Title] Analysis of immunohistochemical markers in bone marrow sections to evaluate for myelodysplastic syndromes and acute myeloid leukemias.
  • BACKGROUND: Accurate bone marrow (BM) blast counts (BCs) are essential for diagnosis (dx) of myelodysplasia (MDS), MDS/myeloproliferative (MDS/MPD) disease, or acute myeloid leukemia (AML), and may be difficult in hemodiluted bone marrow aspirates (BMAs).
  • DESIGN: The initial BC (48), percentage (%) of Eps (38) (both based on initial 100 to 600-cell counts), and FC expressions of CD34, CD117, Glycophorin A(GLY A), and TdT (44) were tabulated from 50 BMs (MDS, MDS/MPD, or AML).
  • BMAs (48) and BMTPs (25) subsequently received 500-cell counts.
  • (1) Evaluation for MDS/AML requires 500-cell counts of BMAs and/or BMTPs. (2) CD34 and/or CD117 blasts by FC indicate IHC-BM may increase BC accuracy. (3) CD34 is more reliable than CD117 by IHC; however, in combination, they are most reliable and should be performed on BM clots/cores due to variable reactivity.

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  • (PMID = 17525626.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Biomarkers; 0 / Hemoglobin A, Glycosylated; EC 1.11.1.7 / Peroxidase; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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12. Serrano E, Carnicer MJ, Lasa A, Orantes V, Pena J, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias. Leuk Res; 2008 Jun;32(6):944-53
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  • [Title] Epigenetic-based treatments emphasize the biologic differences of core-binding factor acute myeloid leukemias.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by an abnormal proliferation of the myeloid precursors and a maturation block.
  • The most common chromosomal lesions in AML are the t(8;21) and inv(16).
  • To better understand the leukemogenic mechanism of these fusion proteins, we performed gene expression studies in samples from (8;21), AML1 mutated and inv(16) patients, as well as from the Kasumi-1 cell line and a U937 cell line expressing the AML1-ETO fusion gene.
  • To assess the influence of associated epigenetic lesions, we performed gene expression studies in Kasumi-1 cells and cells extracted from an Inv(16) patient, both treated with demethylating and HDAC inhibitor agents.
  • Shared deregulated genes in the different types of core-binding factor leukemias were identified.
  • Furthermore, some of the genes deregulated by the leukemogenic process reverted to their normal expression with demethylating and HDAC inhibitor treatment, highlighting the role of chromatin remodeling processes in AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. DNA Methylation. Enzyme Inhibitors / pharmacology. Epigenesis, Genetic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18206229.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFbeta-MYH11 fusion protein; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 3X2S926L3Z / trichostatin A; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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13. Veuillen C, Gravis G, Marcy M, Walz J, Bladou F, Salem N, Brunelle S, Olive D: Alterations of natural killer cells in metastatic prostate cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e16131

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  • Recently, our group have reported that patients with acute myeloid leukaemia have defective interactions receptor -ligand in NK cells due to a decreasing expression of Natural Cytotoxicity Receptors and it could be used as a evasion mechanism by leukaemia cells.
  • In ADPC and AIPC NK cells, the expression of NKRi and other NKRa did not differ from healthy donors.
  • In LPC NK cells, the expression of NKRi and NKRa did not differ from healthy donors.
  • Is it hormonal therapy or extension of the disease that is responsible of NK cells alterations?

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  • (PMID = 27963371.001).
  • [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] Journal Article
  • [Publication-country] United States
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14. Blum WG, Klisovic R, Liu S, Kefauver C, Grever MR, Schaaf L, Chan K, Byrd JC, Villalona-Calero M, Marcucci G: Efficacy of a novel schedule of decitabine in previously untreated AML, age 60 or older. J Clin Oncol; 2009 May 20;27(15_suppl):7010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of a novel schedule of decitabine in previously untreated AML, age 60 or older.
  • : 7010 Background: We established an optimal daily dose of decitabine in AML at 20mg/m<sup>2</sup>/day based on re-expression of epigenetically silenced genes, with promising clinical activity seen in poor risk older patients (pts) (Blum, J Clin Oncol. 2007).
  • METHODS: We designed a phase II study of decitabine for untreated AML pts of age≥60 who were not candidates for intensive chemotherapy (or who refused it).
  • Pts with persistent AML at the end of a cycle received a repeat of the 10 day course, but responding pts received maintenance with abbreviated courses of 3-5 days depending on degree and duration of neutropenia.
  • 15 pts had either secondary or t-AML.
  • 31/33 pts had at least 2 poor-risk factors of age ≥70, antecedent hematologic disorder, unfavorable karyotype, or ECOG 2, and 28/33 had HCT-CI scores of ≥2.
  • CR occurred in all subsets of disease and cytogenetic risk groups.
  • Median OS has not been reached; median f/u of 19 surviving pts is 8 months.
  • Though non-hematologic toxicities were infrequent, infection and/or febrile neutropenia were common (in 24/33 pts).

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  • (PMID = 27961371.001).
  • [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] Journal Article
  • [Publication-country] United States
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15. Ravandi Kashani F, Cortes J, Faderl S, Jones D, Byrd A, Brandt M, Garcia-Manero G, Levis M, Andreeff M, Kantarjian H: Phase I/II study of idarubicin (Ida), high-dose ara-C, and sorafenib (S) in patients (pts) younger than 65 years with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of idarubicin (Ida), high-dose ara-C, and sorafenib (S) in patients (pts) younger than 65 years with acute myeloid leukemia (AML).
  • It selectively induces apoptosis in FLT3-mutant human AML cell lines at nM concentrations.
  • METHODS: Objectives of this study are to determine the tolerability and efficacy of combination of S with chemotherapy.
  • In the phase I part, pts with relapsed AML were treated with escalating doses of S (400 mg qod, 400 mg daily, 400 mg bid) for 7 days during induction, and 400 mg bid was established as safe.
  • RESULTS: 10 pts (median age 34, range 21-58) with relapsed AML (median prior therapy 2, range 1-6) were treated in the phase I .
  • 5 pts have relapsed; median CR duration has not been reached, (range; 0.2+ - 10.6+ mo).
  • CONCLUSIONS: S can be safely combined with IA; it has a high CR rate in frontline therapy of younger pts with AML, in particular those with FLT3 mutations.
  • Correlative studies confirm potent activity of S against FLT3 signaling.

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  • (PMID = 27961390.001).
  • [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] Journal Article
  • [Publication-country] United States
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16. Steensma D, Kantarjian H, Wijermans P: Clinical experience with different dosing schedules of decitabine in patients with myelodysplastic syndromes (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7011

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Data from each clinical trial supporting overall improvement, duration of improvement, time to AML or death, progression-free survival (PFS), and transfusion independence was assessed.
  • RESULTS: Patients had IPSS classification scores of intermediate-2 or high-risk (D-0007, 70%; EORTC-06011, 93%; ID03-0180, 66%; DACO-020, 46%) and de novo MDS (D-0007, 87%; EORTC-06011, 88%; ID03-0180, 70%; DACO-020, 89%).
  • Comparable overall improvement (complete response [CR] + partial response [PR] + hematologic improvement [HI]), time to AML or death, and PFS was observed across all trials (Table).

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  • (PMID = 27961372.001).
  • [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] Journal Article
  • [Publication-country] United States
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17. Schiller GJ, O'Brien SM, Vey N, Pigneux A, DeAngelo DJ, Karp JE, Hudak D, Kell J, Stuart RK, Giles FJ: Comorbidity description using the hematopoietic cell transplantation-specific comorbidity index (HCT-CI) in elderly de novo poor-risk AML patients (pts) treated with laromustine. J Clin Oncol; 2009 May 20;27(15_suppl):7050

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comorbidity description using the hematopoietic cell transplantation-specific comorbidity index (HCT-CI) in elderly de novo poor-risk AML patients (pts) treated with laromustine.
  • : 7050 Background: Treatment of older pts with AML is often complicated by comorbidities and pts with comorbidities are often underrepresented in clinical trials.
  • The HCT-CI, which was developed in pts receiving allogeneic SCT, has been applied to pts receiving induction therapy for AML in an effort to assist in therapeutic and investigational decisions (Kantarjian 2006; Etienne 2007; Giles 2007).
  • HCT-CI scores have been shown to be predictive of early death and survival in pts ≥ 60 years receiving induction therapy for AML, with early death rates of 3%, 11%, and 29% for pts with HCT-CI scores of 0, 1-2, and ≥ 3, respectively (Giles 2007).
  • METHODS: 140 pts age ≥ 60 with poor risk de novo AML from two phase II studies were scored for comorbidity by HCT-CI.
  • CONCLUSIONS: The majority (81%) of these older poor risk AML pts treated with laromustine had a HCT-CI score ≥ 3, confirming the poor risk nature of this patient group.
  • The induction death rate for pts treated with laromustine and with HCT-CI score ≥ 3 was lower than that reported for a group of pts with HCT-CI score ≥ 3 treated with standard induction chemotherapy (14% vs 29%; Giles 2007).

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  • (PMID = 27961414.001).
  • [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] Journal Article
  • [Publication-country] United States
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18. Marcucci G, Maharry K, Whitman SP, Paschka P, Baldus CD, Langer C, Mrózek K, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B (CALGB): Improving the molecular risk classification for younger (&lt;60 years) de novo cytogenetically normal acute myeloid leukemia (CN AML) patients (pts). J Clin Oncol; 2009 May 20;27(15_suppl):7002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improving the molecular risk classification for younger (<60 years) de novo cytogenetically normal acute myeloid leukemia (CN AML) patients (pts).
  • : 7002 Background: CN AML pts are currently stratified into Low-risk [FLT3-ITD negative (neg)/NPM1 mutated (mut)] and High-risk [FLT3-ITD positive (pos) or NPM1 wild type (wt)] groups (FLT3-ITD/NPM1-only classification).
  • Here, we assess if adding CEBPA and WT1 mutation and ERG expression testing improves the currently used CN AML molecular risk classification.
  • METHODS: FLT3, NPM1, CEBPA and WT1 mutations and ERG and BAALC expression were tested at diagnosis in 143 CN AML adults enrolled on CALGB treatment protocols 9621 and 19808.
  • RESULTS: CALGB Group I (n=56) v Group II (n=87) had more complete remissions (CRs) (P=.005; 96% v 79%), and longer disease-free (DFS; P<.0001; 5 year (y) 69% v 21%) and overall (OS; P<.0001; 5 y 70% v 31%) survival [median follow-up for pts alive 6 y].
  • In contrast, for the same cohort of pts grouped by the FLT3-ITD/NPM1-only classification, CRs were 94% v 82% and 5 y DFS 59% v 32% and OS 67% v 36% in the Low- v High-risk groups.
  • CONCLUSIONS: Prognostic classification of younger de novo CN AML pts is improved by adding CEBPA and WT1 mutation and ERG expression testing.

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  • (PMID = 27961374.001).
  • [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] Journal Article
  • [Publication-country] United States
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19. Rao AV, Valk P, Metzeler KH, Acharya C, Rizzieri DA, Delwel R, Bohlander SH, Buske C, Potti A, Lowenberg B: Age-specific differences in oncogenic pathway deregulation and chemosensitivity in patients with acute myeloid leukemia: Strategies to maximize response to induction chemotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):7013

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Age-specific differences in oncogenic pathway deregulation and chemosensitivity in patients with acute myeloid leukemia: Strategies to maximize response to induction chemotherapy.
  • : 7013 Background: Despite all the advances made in understanding the poor prognosis of acute myeloid leukemia (AML) in the elderly, the underlying biology at a molecular signaling pathway level has yet to be defined.
  • METHODS: Clinically annotated, microarray data from 425 patients with newly diagnosed AML from two publicly available datasets GSE1159 and GSE12417 were analyzed.
  • Standard Kaplan-Meier survival curves were generated using the two-sided log-rank test and individual differences in the probability of oncogenic pathway deregulation between young vs. elderly were analyzed via the non-parametric Mann-Whitney U test and a one-sided p-value ≤ 0.05 was considered statistically significant.
  • RESULTS: Elderly AML patients had worse OS (median 8.8 months vs. 24.1 months in younger patients; p = 0.001) and EFS (median 7.1 months vs. 15.3 months in younger patients; p < 0.0001).
  • Older patients were also less sensitive to anthracycline compared to younger AML patients, p < 0.0001.
  • Unsupervised hierarchical clustering of younger AML patients revealed two clusters and clinically better survival for cluster 1 compared to cluster 2 (high Ras, Src, TNF pathway activation) and the latter were in turn less sensitive to adriamycin.
  • However, in elderly patients those in cluster 2 also had high Ras, Src, TNF but this did not translate into differences in survival or chemotherapy sensitivity.
  • CONCLUSIONS: AML arising in the elderly represents a distinct biologic entity characterized by unique patterns of deregulated signaling pathways that contributes to poor survival and resistance to adriamycin.

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  • (PMID = 27961386.001).
  • [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] Journal Article
  • [Publication-country] United States
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20. Queudeville M, Eckhoff SM, Debatin K, Meyer LH: Correlatoin of apoptosis signaling in primary pediatric BCP-ALL xenograft cells with the kinetics of engraftment in vivo in a NOD/SCID model and patient outcome. J Clin Oncol; 2009 May 20;27(15_suppl):10043

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 10043 Background: We previously identified the importance of intact apoptosis signaling for treatment response in pediatric ALL and AML by analyzing two key apoptogenic events, caspase-3 activation and cytochrome c release.
  • Using a NOD/SCID mouse model for pediatric BCP-ALL we found that short time from transplant to overt leukemia in the recipient mice (short time to leukemia, TTLshort) determines poor patient outcome.
  • METHODS: In this study we investigated the importance of deficient apoptosis signaling for leukemia engraftment in this model.
  • CONCLUSIONS: Our finding in the NOD/SCID/huALL model matches our results in pediatric ALL and AML to conclude that the functional integrity of a downstream apoptotic checkpoint is an important feature regulating leukemia biology.
  • Thus, deficient apoptosis signaling appears to determine rapid engraftment of leukemia cells in the NOD/SCID model in vivo and consequently poor patient outcome.

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  • (PMID = 27962469.001).
  • [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] Journal Article
  • [Publication-country] United States
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21. Raza A, Galili N, Borthakur G, Carter TH, Claxton DF, Erba HP, DeAngelo DJ, Berger MS, Schimmer A: A safety and schedule seeking trial of Bcl-2 inhibitor obatoclax in previously untreated older patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3579

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A safety and schedule seeking trial of Bcl-2 inhibitor obatoclax in previously untreated older patients with acute myeloid leukemia (AML).
  • : 3579 Background: Obatoclax (Ob) is a small-molecule inhibitor of all Bcl-2 prosurvival proteins.
  • In a previous study a 70 year old patient with untreated AML had a cytogenetic CR 8 days after receiving 20 mg/m<sup>2</sup> of Ob over 24 hrs.
  • This study evaluated the single-agent response rate in older patients with previously untreated AML.
  • Eligibility criteria included age ≥ 70, untreated AML (1 prior Rx allowed in Safety phase), ECOG PS ≤2, adequate renal and hepatic function.
  • Efficacy data after C2 show that 3 patients in the 20 mg 3-hr infusion cohort in the Safety phase and 1 at the same dose & schedule in the Schedule Seeking phase had ≥50% decrease in BM blasts after C2, which was not seen in the 60 mg 24-hr infusion cohort.
  • CONCLUSIONS: MTD for Ob as a 3-hr infusion administered in older patients with AML on 3 consecutive days is 20 mg/day, and both this regimen and 60 mg as a 24-hr infusion x 3 days were well tolerated.
  • Evidence of biological activity was seen with the 3-hr infusion schedule but not with the 24-hr infusion schedule, suggesting that efficacy may be improved with the 3-hr infusion schedule and may be related to PK differences.

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  • (PMID = 27961704.001).
  • [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] Journal Article
  • [Publication-country] United States
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22. Bloomfield CD: Importance of genetic heterogeneity in curing adult acute leukemia (AL). J Clin Oncol; 2009 May 20;27(15_suppl):s1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Importance of genetic heterogeneity in curing adult acute leukemia (AL).
  • Publication of the French-American-British classification 34 years ago resulted in acceptance that morphology and cytochemistry separated AL into two different diseases, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), that required separate treatment.
  • During the next 15-20 years the importance of cytogenetics in dissecting ALL and AML into entities requiring different therapies became widely accepted, resulting in 2001 in their first incorporation into the World Health Organization (WHO) classification of AL.
  • The most striking example of increased curability of AL is acute promyelocytic leukemia, in which targeted therapy combined with chemotherapy has increased survival from a 2-week median to an 80% cure rate.
  • Recognition of increased sensitivity of a genetic subtype of AML to high-dose cytarabine (HiDAC) has increased the cure rate of core-binding factor (CBF) AML from <10%-25% to 55%-60%.
  • Recent discovery of the adverse impact of KIT mutations in CBF AML may allow the addition of tyrosine kinase inhibitors to HiDAC to substantially further increase cure.
  • Among adult de novo AML 40%-45% are cytogenetically normal (CN); the striking molecular heterogeneity of CN-AML is now being recognized and promises to allow individualized approaches that improve substantially upon the current cure rate of 40%.
  • New approaches to studying the leukemia genome and epigenome should improve our understanding of AL heterogeneity, identify new therapeutic targets, and allow the cure of most patients.

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  • (PMID = 27962366.001).
  • [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] Journal Article
  • [Publication-country] United States
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23. Stuart RK, Stockerl-Goldstein K, Cooper M, Devetten M, Herzig R, Medeiros B, Schiller G, Wei A, Acton G, Rizzieri D: Randomized phase II trial of the nucleolin targeting aptamer AS1411 combined with high-dose cytarabine in relapsed/refractory acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7019

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized phase II trial of the nucleolin targeting aptamer AS1411 combined with high-dose cytarabine in relapsed/refractory acute myeloid leukemia (AML).
  • AS1411 has synergistic effects in combination with cytarabine on AML cell lines in vitro and in vivo.
  • METHODS: This open-label randomized phase II trial compared AS1411 plus high-dose cytarabine (HiDAC) with HiDAC alone in patients with primary refractory or relapsed AML who had received up to 3 previous lines of chemotherapy.
  • CONCLUSIONS: Data from this first phase II trial of an aptamer in oncology are encouraging.
  • The combination of AS1411 at 10 or 40 mg/kg/day with HiDAC appears well tolerated and shows promising signs of activity in patients with relapsed/refractory AML.

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  • (PMID = 27961391.001).
  • [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] Journal Article
  • [Publication-country] United States
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24. Duhoux F, Libouton J, Bahloula K, Ameye G, Poirel HA: Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):11037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies.
  • : 11037 Background: PRDM16 is a gene located on 1p36.32 that encodes for a zinc finger transcription factor and contains an N-terminal PR domain.
  • It has been shown to be involved in the reciprocal translocation t(1;3)(p36;q21) and more rarely the t(1;21)(p36;q22) which both occur in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML).
  • These translocations result in the overexpression of a truncated version of the PRDM16 protein that lacks the PR domain.
  • This overexpression might play an important role in the pathogenesis of MDS and AML in blocking myeloid differentiation.
  • METHODS: We studied 35 myeloid malignancies, 12 lymphoid malignancies and 3 undifferentiated acute leukemias with 1p36 abnormalities by fluorescent in situ hybridization (FISH) with a bacterial artificial chromosomes (BAC) contig containing 50 BAC probes on 1p36.
  • RESULTS: In addition to the known t(1;3)(p36;q21) (11 cases) and t(1;21)(p36;q22) (1 case) involving RPN1 andAML1/RUNX1 respectively in myeloid malignancies, we specifically found PRDM16 to be rearranged in 4 additional translocations : a t(1;12)(p36;p13) in an AML-M4, a t(1;7)(p36;p12) in a MDS, an add(1)(p36) in an AML-M2 and a t(1;2)(p36;p12) in a relapsed AML-M4.
  • We identified the respective candidate partner loci : TEL/ETV6, IKZF1, CDH4 and a non-coding unknown sequence.
  • CONCLUSIONS: In our series of 50 cases of hematological malignancies with 1p36 abnormalities, PRDM16 was involved in about 45% of myeloid malignancies, and was never involved in lymphoid malignancies.
  • PRDM16 is supposed to have similar oncogenic properties as MDS1/EVI-1(3q26), another gene encoding for a zinc finger protein and acting as a transcriptional regulatory factor with 2 isoforms.
  • Interestingly, the shortest isoform of MDS/EVI-1, lacking the PR domain, is supposed to have an oncogenic effect due to its translocation-induced upregulation in AML.
  • Further characterization of these new partner genes and functional studies should give us more insight into the pathogenesis of AML and MDS mediated by PRDM16, and the role of its partner genes.

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  • (PMID = 27964015.001).
  • [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] Journal Article
  • [Publication-country] United States
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25. Rausei-Mills V, Chang KL, Gaal KK, Weiss LM, Huang Q: Aberrant expression of CD7 in myeloblasts is highly associated with de novo acute myeloid leukemias with FLT3/ITD mutation. Am J Clin Pathol; 2008 Apr;129(4):624-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of CD7 in myeloblasts is highly associated with de novo acute myeloid leukemias with FLT3/ITD mutation.
  • Acute myeloid leukemia (AML) with normal cytogenetics represents approximately 40% to 50% of de novo AML.
  • This heterogeneous AML subgroup constitutes the single largest cytogenetic group with an intermediate prognosis.
  • Previous studies have suggested that the Fms-like tyrosine kinase-3 internal tandem duplication (FLT3/ITD) mutation-positive de novo AML may represent a distinctive subgroup of AML.
  • We analyzed the clinical and pathologic features of 15 cases of de novo AML with normal cytogenetics and with the FLT3/ITD mutation.
  • In comparison with patients with AML without the FLT3/ITD mutation, patients with FLT3/ITD+ AML are relatively younger, more often have marked peripheral leukocytosis with a higher number of circulating blasts at initial examination, more often have minimal differentiation morphologic features, more frequently have abnormal CD7 coexpression, and have poorer outcome.
  • Close association of aberrant CD7 expression and FLT3/ITD mutation in the myeloblasts of FLT3/ITD+ AML suggests that FLT3/ITD- mediated leukemic transformation occurs in the more early stage of myeloid progenitor cells.
  • [MeSH-major] Antigens, CD7 / metabolism. Granulocyte Precursor Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Mutation. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow Cells / chemistry. Bone Marrow Cells / pathology. California / epidemiology. Cell Transformation, Neoplastic. DNA, Neoplasm / analysis. Female. Humans. Male. Middle Aged. Survival Rate

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • [CommentIn] Am J Clin Pathol. 2008 Oct;130(4):644; author reply 645 [18825844.001]
  • (PMID = 18343790.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / DNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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26. Liu K, Kreuzer KA, Lass U, Schmidt CA: Assessment of chemosensitivity by monitoring bcl-2 transcript kinetics in acute myeloid leukemias. Hematol Oncol; 2005 Jun;23(2):68-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of chemosensitivity by monitoring bcl-2 transcript kinetics in acute myeloid leukemias.
  • Here we established a real time fluorescence PCR assay to analyze the association between the bcl-2 gene expression and clinical chemosensitivity in acute myeloid leukemia.
  • By applying real time PCR to clinical samples, we observed that although the bcl-2/beta-actin ratio was not related to FAB subtypes, the changing data following remission induction therapy clearly reflected drug-sensitivity.
  • These results suggest that RT-PCR assay monitored the efficacy of the chemotherapy by quantifying the bcl-2 gene transcript in AML.
  • [MeSH-major] Drug Monitoring / methods. Leukemia, Myeloid / diagnosis. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Acute Disease. Case-Control Studies. Humans. Kinetics. Neoplasm, Residual / diagnosis. RNA, Messenger / analysis. Reagent Kits, Diagnostic. Remission Induction. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16178036.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reagent Kits, Diagnostic
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27. Lyman GH, Dale DC, Culakova E, Poniewierski MS, Wolff D, Kuderer NM, Lambert K, Crawford J: Acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) and overall mortality with chemotherapy (CT) and granulocyte colony-stimulating factor (G-CSF): A meta-analysis of randomized controlled trials (RCTs). J Clin Oncol; 2009 May 20;27(15_suppl):9524

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) and overall mortality with chemotherapy (CT) and granulocyte colony-stimulating factor (G-CSF): A meta-analysis of randomized controlled trials (RCTs).
  • : 9524 Background: To evaluate the risk of AML/MDS and overall mortality in patients receiving CT ± G-CSF, a meta-analysis of RCTs were conducted.
  • Eligibility included RCTs of solid tumor or lymphoma patients randomized to CT ± primary G-CSF support, ≥2 years follow-up and reporting AML/MDS or all second malignancies.
  • Pre-specified study categories included: a)same dose/schedule, b)dose-dense or c)dose-escalated CT.
  • Primary outcomes were AML/MDS and mortality.
  • RR for AML/MDS with CT+G-CSF compared to control was 1.92 [P=.006] with ARD increase of 0.4% [P=.008].
  • RR for AML/MDS in study categories to receive the same, dose-dense or dose-escalated CT+G-CSF were 1.95 [P=.346], 1.20 [P=.666] and 2.47 [P=.006], respectively.
  • No differences in estimates of AML/MDS or mortality were observed between industry and non-industry-funded studies.
  • CONCLUSIONS: Risk of AML/MDS is increased with dose escalated CT+G-CSF.
  • Dose-dense regimens are associated with the greatest RR reduction in mortality and lowest risk of AML/MDS.
  • Further research is needed to differentiate any impact of G-CSF on the risk of AML/MDS from that due to increased CT intensity.

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  • (PMID = 27964513.001).
  • [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] Journal Article
  • [Publication-country] United States
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28. Gupta A, Singh M, Singh H, Kumar L, Sharma A, Bakhshi S, Raina V, Thulkar S: Febrile neutropenia during acute myeloid leukemia therapy: Single institution experience from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):e18000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Febrile neutropenia during acute myeloid leukemia therapy: Single institution experience from a developing country.
  • : e18000 Background: Febrile neutropenia poses a major challenge during treatment of acute myeloid leukaemia (AML).
  • METHODS: Episodes of febrile neutropenia in 104 consecutive patients of AML admitted to the medical oncology ward between May 2001 and December 2006 were studied.
  • RESULTS: 402 febrile episodes including 363 episodes of febrile neutropenia (180 in induction, 183 in consolidation) and 39 non-neutropenic episodes (18 in induction, 21 in consolidation) occurred.
  • Prompt and proper institution of antibiotics and antifungals besides considering alternative diagnosis peculiar to the region (e.g. tuberculosis, malaria) may aid in better management.

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  • (PMID = 27964014.001).
  • [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] Journal Article
  • [Publication-country] United States
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29. Schwind S, Marcucci G, Maharry K, Radmacher MD, Whitman SP, Paschka P, Mrózek K, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B (CALGB): MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML). J Clin Oncol; 2009 May 20;27(15_suppl):7001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML).
  • : 7001 Background: We showed recently that CEBPA mutations (mut) in CN AML are associated with better outcome and a unique microRNA expression profile, including miR-181a upregulation.
  • METHODS: We analyzed 187 de novo CN AML adult patients (pts) aged <60 years (y; median 45) similarly treated on CALGB 9621 and 19808.
  • Of these, 122 had molecular high risk [FLT3-ITD or NPM1 wild type (wt)] and 65 low risk (no FLT3-ITD, NPM1 mut) CN AML.
  • The mean of 2 miR-181a probe log intensities was used as a continuous variable for analyses.
  • RESULTS: Higher miR-181a levels (miR-181a↑) were associated with CEBPA mut, NPM1 wt, no FLT3-TKD, lower ERG expression, higher %FAB M1/M2, lower WBC and age, higher blood blasts, and lower % gum hypertrophy. miR-181a↑ tended to associate with more complete remissions (CRs; p = .07) and significantly associated with longer disease-free (DFS; p = .05) and overall (OS; p = .01) survival (median follow-up 6.5 y for pts alive).
  • CONCLUSIONS: miR-181a expression is a prognostic marker in CN AML, mainly in the molecular high risk group, where it predicts outcome independently of other variables including CEBPA mutations.
  • As miR-181a↑ confer better treatment response, novel approaches increasing miR-181a levels might benefit not only CN but also other AML pts.

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  • (PMID = 27961373.001).
  • [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] Journal Article
  • [Publication-country] United States
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30. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJ<sub>H</sub>) show more mature IgH status.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.
  • In contrast, none or a few of the CpG dinucleotides were methylated in the CD10-positive ALL, AML (M5) with MLL/AF9 or AML (M2) with AML1/ETO.

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  • (PMID = 27962471.001).
  • [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] Journal Article
  • [Publication-country] United States
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31. Vey N, Bourhis J, Dombret H, Bordessoule D, Prebet T, Charbonnier A, Squiban P, Damholt B, Blaise D, Olive D: A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML).
  • : 3015 Background: The outcome of the majority of patients with AML remains poor, especially in the oldest patients.
  • Allogeneic SCT is a curative approach for AML.
  • In some models, it has been shown that KIR mismatch is important for the anti-leukemic effect of the graft, most probably through unleashed NK cells towards AML blasts, as suggested by enhanced in vitro NK lytic activity of KIR-HLA mismatched donor NK against recipient blasts.
  • We present the results of the first-in-human phase I trial of this agent in patients with AML in complete remission (CR).
  • METHODS: Patients aged 60-80 years with non promyelocytic AML in first CR following induction and 1-6 cycles of consolidation chemotherapy, normal renal, and hepatic functions, KIR-expression on patient NK-cells and who signed informed consent were eligible.Dose escalation (0.0003, 0.003, 0.015, 0.075, 0.3, 1, 3 mg/kg) was studied using a 3+3 scheme.
  • As expected for an IgG4, NK cell numbers were unaffected by the treatment.
  • Upregulation of CD69 on NK cells and concomitant increases in TNF and MIP1b circulating cytokines were observed in some patients at the highest doses (0.075, 0.1, 0.3 mg/kg) but a dose dependency has not been reached yet.
  • At the 0.3mg/kg dose, MTD has not been reached, but a one week receptor blockade and signs of NK activation were observed.

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  • (PMID = 27962059.001).
  • [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] Journal Article
  • [Publication-country] United States
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32. Maris MB, Ravandi F, Stuart R, Stone R, Cripe L, Cooper M, Strickland S, Turturro F, Stock W, Berman C: A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML).
  • Interim results of REVEAL-1, a phase II study of single agent voreloxin in newly diagnosed elderly AML pts, are reported.
  • Eligibility: newly diagnosed AML (de novo or secondary AML), pts age ≥ 60 and ≥ 1 additional adverse risk factor (age ≥ 70, secondary AML, intermediate or unfavorable cytogenetics, or PS 2).
  • Median duration of remission has not been reached.
  • Voreloxin PK were similar to those in an earlier single agent phase I study in relapsed/refractory AML.
  • Ex-vivo sensitivity did not predict clinical response.
  • CONCLUSIONS: In REVEAL-1, voreloxin demonstrates clinical activity with 2 dosing schedules in previously untreated elderly (age ≥ 60) patients with AML who are unlikely to benefit from standard chemotherapy.

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  • (PMID = 27961427.001).
  • [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] Journal Article
  • [Publication-country] United States
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33. Hirte HW, McGuire W, Edwards R, Husain A, Hoskins P, Michels J, Matulonis U, Sexton C, Michelson G: A phase II trial of voreloxin in women with platinum-resistant ovarian cancer. J Clin Oncol; 2009 May 20;27(15_suppl):5559

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Clinical activity has been observed in ovarian cancer and AML.
  • METHODS: Pts may have received ≤ 3 prior platinum regimens plus one additional non-platinum regimen.

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  • (PMID = 27962535.001).
  • [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] Journal Article
  • [Publication-country] United States
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34. Ayan I, Kebudi R, Ozger H, Yaman Agaoglu F, Gorgun O, Bilgic B, Eralp L, Dizdar Y, Darendeliler E: Childhood osteosarcoma: Evaluation of 94 cases. A single institution study. J Clin Oncol; 2009 May 20;27(15_suppl):10040

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Between January 1990 and December 2006, 94 children (53 male, 41 female) with a median age of 13 (5-16) years and a histopathologic diagnosis of osteosarcoma were treated with an institutional chemotherapy regimen comprising of 6 courses (3 pre-, 3 postoperatively) of epirubicin (90 mg/m2), cisplatin(100 mg/m2), and ifosfamide(2 g/m2 × 3 days) every 3 weeks.
  • 26 patients died; 20 of disease, 5 of toxicity, and 1 of second malignancy (acute myeloid leukemia).
  • 5 and 10 year EFS for nonmetastatic patients was superior to those with metastatic disease [62.4 % (95% CI 49.9-79.9 %) vs. 6.9 % (95% CI 0-19.9 %)) (p<0.001).
  • 10 year OS for 18 patients (11 metastatic at diagnosis) who progressed during preoperative chemotherapy was 13 % vs. 75 % for those who didnot have progressive disease (p< 0.001).
  • Histologic response (<90 percent necrosis vs ≥90 percent) significantly correlated with 5 year EFS (31 % vs 67.6 %, p=0.023) but not with OS (57.7 % vs 76.5 %, p=0.13).
  • CONCLUSIONS: The presence of metastases at diagnosis was the most significant characteristic influencing outcome.

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  • (PMID = 27962466.001).
  • [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] Journal Article
  • [Publication-country] United States
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35. Plunkett W, Thomas DA, O'Brien SM, Federl S, Giles FJ, Nicol SJ, Gill J, Zhao L, Ravandi F, Kantarjian H: Phase I study of pemetrexed in patients with relapsed or refractory acute leukemia or lymphoid blast phase chronic myelogenous leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of pemetrexed in patients with relapsed or refractory acute leukemia or lymphoid blast phase chronic myelogenous leukemia.
  • The purpose of this phase I trial was to define the dose-limiting toxicity (DLT), maximum tolerated dose (MTD), and recommended phase II dose (RP2D) of pemetrexed given with vitamin supplementation to patients with relapsed or refractory leukemia.
  • METHODS: Patients ≥15 years of age were enrolled with relapsed or refractory leukemia, Eastern Cooperative Oncology Group performance status ≤2, adequate renal and hepatic function, and life expectancy of ≥6 weeks.
  • RESULTS: Twenty-two patients entered the trial; median age was 50 years (range: 18-75); 15 patients had acute myeloid leukemia and 7 patients had acute lymphocytic leukemia (ALL).
  • Two patients were ineligible and did not receive study drug.
  • At the 1,200 and 1,500 mg/m<sup>2</sup> dose levels, 1 patient per level developed grade (G) 3-4 liver enzyme and bilirubin elevations attributed to sepsis.
  • At the 3,600 mg/m<sup>2</sup> dose level, 1 patient had a G3 liver enzyme elevation and 2 added patients also had G3 liver toxicity.
  • In addition, 2 patients in the 3,600 mg/m<sup>2</sup> cohort developed G2 liver abnormalities.
  • Based on liver toxicities, the DLT dose level was established at 3,600 mg/m<sup>2</sup>.
  • Two patients died during the study due to disease progression and 1 patient discontinued due to a subdural hematoma of unknown cause.
  • PK and PD data were not available for this report.

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  • (PMID = 27961463.001).
  • [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] Journal Article
  • [Publication-country] United States
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36. Medeiros BC, Gotlib JR, Coutre SE, Jones C, Khan SA, Rajwanshi R, Rajwanshi R, Zehnder J, Zehnder J: Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia.
  • : 7052 Background: High treatment-related mortality and low response rates often discourage elderly patients with acute myeloid leukemia from receiving treatment.
  • METHODS: Phase II clinical trial of tailored temozolomide therapy to high-risk AML patients according to AGAT methylation promoter status.
  • Patients demonstrating evidence of AGAT promoter methylation were stratified to conventional doses of temozolomide at 200 mg/m2 orally x 7 days.
  • Patients demonstrating lack of AGAT promoter methylation (unmethylated) received protracted doses of temozolomide (100 mg/m2 orally x 14 days) followed by conventional doses of temozolomide.
  • De novo AML was diagnosed in eight patients and five patients had s-AML.
  • Drug-related hematologic toxicities were difficult to distinguish from disease-related cytopenias.
  • Seven patients have died from disease progression, while two patients died of neutropenic sepsis (early deaths).
  • CONCLUSIONS: These preliminary results suggest that temozolomide therapy may be individually tailored to elderly patients with AML according to AGAT promoter status.

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  • (PMID = 27961417.001).
  • [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] Journal Article
  • [Publication-country] United States
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37. Barret J, Dumontet C, Annereau J, Brel V, Breillout F, Guminski Y, Imbert T, Guilbaud N, Bailly C: A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512. J Clin Oncol; 2009 May 20;27(15_suppl):11087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512.
  • This system can be viewed as a suitable molecular gate to deliver selectively polyamine-based molecules into cancer cells.
  • This study was undertaken to investigate the potential of N-methyl-spermine-NBD, a proprietary fluorescent polyamine conjugate, designed to select patients with PTS-positive leukemic cells.
  • METHODS: The uptake of this probe was first measured by flow cytometry in a panel of human leukemia cell lines.
  • RESULTS: Data showed that high level of fluorescence was detected in F14512 -sensitive cancer cell lines whereas leukemia cells responding poorly to F14512 generally exhibited very low levels of PTS.
  • A panel of 50 fresh human acute myeloid leukemia samples showed a larger inter-individual variation and, interestingly, incorporation of the fluorescent probe was generally higher in leukemia blasts than in lymphocytes.
  • CONCLUSIONS: The data show that the PTS can easily be evaluated in fresh AML blasts and provides a simple means to identify patients for future enrollment in clinical trials with F14512.

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  • (PMID = 27963178.001).
  • [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] Journal Article
  • [Publication-country] United States
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38. Shepard RC, Talluto CC, Jacob G: Phase I study results of nanomolecular liposomal annamycin in refractory ALL. J Clin Oncol; 2009 May 20;27(15_suppl):7066

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7066 Background: There continues to be no effective second-line therapy for refractory AML or ALL and the cure rate with current therapy has not significantly improved in decades.
  • The first-line therapy for adult AML has remained the same 7 + 3 that it was a generation ago.
  • The MTD was determined to be 150 mg/m2/day for 3 days.
  • We are now testing it in a phase I study in children and young adults with refractory ALL or AML.

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  • (PMID = 27961442.001).
  • [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] Journal Article
  • [Publication-country] United States
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39. Giles FJ, O'Brien S, Rizzieri DA, Vey N, Krug U, Sekeres M, Jacobsen TF, Nilsson BI, Staudacher K: A phase II study with CP-4055 in patients with second salvage AML. J Clin Oncol; 2009 May 20;27(15_suppl):7047

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study with CP-4055 in patients with second salvage AML.
  • : 7047 Background: CP-4055 (cytarabine 5'-elaidic acid ester) is a novel derivative of cytarabine, independent of nucleoside transporters to enter the cell.
  • The aim of this study was to assess efficacy and safety of CP-4055 when given as second salvage therapy to patients (pts) with acute myeloid leukemia (AML).
  • METHODS: Adult pts who received two previous chemotherapy regimens and who had refractory/relapsed AML (CR after first salvage therapy lasting less than 6 months) were enrolled.
  • 6 pts had previous transplant, the majority of the pts had previous ara-C based therapy, 12 pts had not obtained CR1 or CR2.
  • Only 1 pt did not receive d1-5 dosing.
  • Most frequently reported related AE ≥ grade 3 (CTCAE v3.0) were myelosuppression, abdominal pain, colitis, diarrhoea, nausea, fatigue, liver function test (LFT) elevation.
  • Clinical activity (IWG criteria for AML), 2 CR (1 with no CR1 or CR2), and 1 CRp (CR rate 15%), were reported.
  • CONCLUSIONS: CP-4055 given as second salvage therapy to AML pts show manageable toxicity when administered at 2,000 mg/m<sup>2</sup>/d, 24 h CIV, in a d1-5 q3w schedule.
  • Clinical activity (2 CR and 1 CRp) has been reported among the first 20 late stage AML pts.

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  • (PMID = 27961426.001).
  • [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] Journal Article
  • [Publication-country] United States
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40. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • : e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.

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  • (PMID = 27963169.001).
  • [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] Journal Article
  • [Publication-country] United States
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41. Iliopoulou EG, Kountourakis P, Karamouzis MV, Doufexis D, Ardavanis A, Baxevanis CN, Rigatos G, Papamichail M, Perez SA: A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):3001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC).
  • : 3001 Background: HLA-mismatched NK cells have been found effective in acute myeloid leukemia pts.
  • RESULTS: Between 11/2007 and 11/2008 16 pts (performance status 0-1) were enrolled; 1 pt had rapid disease progression before treatment.
  • Pts characteristics: M/F 12/4; histology: adenocarcinoma/squamous cell carcinoma 13/3; stage IIIb/IV 2/14; 1<sup>st</sup>/2<sup>nd</sup> line treatment 13/3; median age 64 years (range, 50-71).
  • With a median follow-up of 6 months (range, 1-14) 3 pts with partial response and 7 pts with disease stabilization were recorded.

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  • (PMID = 27962051.001).
  • [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] Journal Article
  • [Publication-country] United States
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42. Raghavan M, Lillington DM, Skoulakis S, Debernardi S, Chaplin T, Foot NJ, Lister TA, Young BD: Genome-wide single nucleotide polymorphism analysis reveals frequent partial uniparental disomy due to somatic recombination in acute myeloid leukemias. Cancer Res; 2005 Jan 15;65(2):375-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide single nucleotide polymorphism analysis reveals frequent partial uniparental disomy due to somatic recombination in acute myeloid leukemias.
  • Genome-wide analysis of single nucleotide polymorphisms in 64 acute myeloid leukemias has revealed that approximately 20% exhibited large regions of homozygosity that could not be accounted for by visible chromosomal abnormalities in the karyotype.
  • Remission bone marrow was available from five patients showing UPD in their leukemias, and in all cases the homozygosity was found to be restricted to the leukemic clone.
  • These cryptic chromosomal abnormalities, which seem to be nonrandom, have the characteristics of somatic recombination events and may define an important new subclass of leukemia.
  • [MeSH-major] Leukemia, Myeloid / genetics. Polymorphism, Single Nucleotide. Uniparental Disomy
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Base Sequence. DNA Methylation. DNA, Neoplasm / genetics. Diploidy. Female. Genome, Human. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 15695375.001).
  • [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
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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43. Spadaro P, Ingemi M, Pitini V, Arrigo C, Soto Parra H: Myelodysplastic syndromes developing after imatinib therapy for GIST. J Clin Oncol; 2009 May 20;27(15_suppl):10532

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Between January 2007 and December 2008, bone marrow samples for morphologic analysis, FISH and classical cytogenetics were obtained from 49 pts. (30 male; 19 female, mean age 62) with unresectable or metastatic GIST before and during treatment with 400 mg/d of imatinib.
  • For pts. with progressive disease (15 pts.) or exon 9 mutant disease (5 pts.
  • All pathologic material was reviewed to identify pts. with MDS or AML according to the WHO classification.
  • One patient developed a RAEB-1 with monosomy 7 which rapidly transformed into AML.

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  • (PMID = 27963910.001).
  • [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] Journal Article
  • [Publication-country] United States
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44. Kunivayalil S, Jain A, Satheesh C, Tejinder S, Lakshmaiah K, Suresh TM, Lokanatha D, Babu G: A comparative study of single-dose pegfilgrastim versus daily filgrastim in patients with acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e18005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparative study of single-dose pegfilgrastim versus daily filgrastim in patients with acute myeloid leukemia.
  • It can be used during induction and consolidation chemotherapy in acute myeloid leukemia (AML).
  • Few studies addressed the use of pegylated filgrasim in AML.
  • Safety profile and complete remission status did not differ between the two groups.

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  • (PMID = 27964003.001).
  • [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] Journal Article
  • [Publication-country] United States
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45. Villano JL, Letarte N, Yu JM, Shakir AR, Bressler L: Hematologic adverse events associated with temozolomide (TMZ). J Clin Oncol; 2009 May 20;27(15_suppl):2053

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2053 Background: Secondary acute myeloid leukemia (AML) is reported to occur in 3%-10% of patients treated with alkylating agents for Hodgkin's lymphoma, non-Hodgkin's lymphoma, ovarian cancer, breast cancer, and multiple myeloma.
  • The incidence of secondary AML is greatest at 5-10 years after treatment, and AML often follows myelodysplastic syndrome (MDS).
  • Among these patients, we identified 140 cases that we labeled as major hematologic adverse events: agranulocytosis (8 cases), aplasia (42), aplastic anemia (52), leukemia (26), MDS (6), and lymphoma (6).
  • Risk of leukemia/MDS from our review may also be significant, but length of follow-up is insufficient and the real risk is likely still unknown.

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  • (PMID = 27964671.001).
  • [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] Journal Article
  • [Publication-country] United States
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46. Batty G, Kantarjian H, Issa JJ, Garcia-Manero G, Pierce S, O'Brien S, Jabbour E, Cortes J, Ravandi F: Feasibility of hypomethylating therapy in patients with renal insufficiency. J Clin Oncol; 2009 May 20;27(15_suppl):7089

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We investigated the outcomes of pts with RI and MDS, chronic myelomonocytic leukemia (CMML), or acute myeloid leukemia (AML) receiving therapy with HA.
  • We used the International Working Group criteria to evaluate the response rates.
  • RESULTS: Forty-two pts with sCr ≥ 1.5 mg/dL (including 17 with MDS, 16 with AML, and 9 with CMML) were treated with DAC or 5AZA alone or in combination with other agents (primarily histone deacetylase inhibitors).
  • The incidence of complications, DA, and the response rate were not significantly different for pts with sCr > 2.0 mg/dL.
  • CONCLUSIONS: The use of HA is well tolerated in pts with MDS and AML and RI who achieved comparable OR rates to those without RI.

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  • (PMID = 27961273.001).
  • [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] Journal Article
  • [Publication-country] United States
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47. Santos FP, Qiao W, Cortes JE, Jones D, Ravandi F, Verma D, Kantarjian H, Borthakur G: Prognostic value of FLT3 mutations among different cytogenetic subgroups in acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of FLT3 mutations among different cytogenetic subgroups in acute myeloid leukemia (AML).
  • : 7015 Background: Mutations of the FLT3 gene (in special internal tandem duplication -ITD) are common in normal karyotype AML (NK-AML) and are associated with shorter relapse free and overall survival (OS).
  • METHODS: The records of patients (pts) with newly diagnosed AML (from 2003 to 2007) were reviewed.
  • A Cox model was fit for OS, and non-significant variables were eliminated in a step-down fashion with a p- value cut-off of p = .10.
  • No difference was found in median OS between FLT3-mutated and FLT3- wild type pts in the good risk group (not reached (NR) vs NR, P = 0.57) nor in the poor risk group (55 vs 24 weeks, P = 0.44).
  • In intermediate risk, OS was worse in FLT3-ITD positive pts (33 vs 89 weeks, P < 0.0001) but not in FLT3-TKD positive pts (77 vs 70 weeks, P = 0.89).
  • CONCLUSIONS: In our cohort of pts, FLT3 mutations did not have a prognostic impact in AML with good and poor risk karyotype.

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  • (PMID = 27961388.001).
  • [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] Journal Article
  • [Publication-country] United States
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48. Popat UR, Saliba R, Hosing C, Khouri I, Alousi AM, Giralt SA, de Lima MJ, Qazilbash MH, Champlin R, Anderlini P: Age at diagnosis does not adversely affect outcome in patients with Hodgkin's Disease (HD) after autologous transplantation. J Clin Oncol; 2009 May 20;27(15_suppl):e19507

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Age at diagnosis does not adversely affect outcome in patients with Hodgkin's Disease (HD) after autologous transplantation.
  • : e19507 Background: Age at diagnosis is a poor prognostic factor for overall survival after standard therapy for HD.
  • Whether older age is a prognostic factor for outcome after autologous transplantation is not known.
  • We sought to evaluate the effect of older age at diagnosis on transplant outcome.
  • Seventy two patients (29%) were older than 40 years of age at the time of initial diagnosis.
  • At transplantation, 63 (25%) were in complete remission (CR); 148 (60%) were in partial remission (PR); and 37 (15%) had stable (SD) or progressive disease (PD).
  • Peripheral blood stem cells were used as stem cell source in 241 (97%) patients.
  • The cumulative incidence of non-relapse mortality at 1 year was 1.6%.
  • The cumulative incidence of secondary MDS or AML was 8%.
  • In univariate analysis, disease status (p<0.001) and number of prior chemotherapy regimens (p=0.007) were the only factors significantly predicting OS.
  • Disease status was the only factor significant (p<0.01) in a multivariate analysis with a hazard ratio of 2.7 (1.1-6.9) and 9.2 (3.4-25) for patients in PR, and SD/PD respectively (CR reference group).
  • Age at diagnosis was not a significant factor (see table ).
  • CONCLUSIONS: High-dose chemotherapy and autologous transplantation abrogate the adverse impact of age at diagnosis in patients with HD.

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  • (PMID = 27960864.001).
  • [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] Journal Article
  • [Publication-country] United States
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49. Becker H, Marcucci G, Maharry K, Margeson D, Radmacher MD, Whitman SP, Mrózek K, Baer MR, Larson RA, Bloomfield CD, for Cancer and Leukemia Group B (CALGB): NPM1 mutations as an independent prognosticator for older cytogenetically normal acute myeloid leukemia (CN AML). J Clin Oncol; 2009 May 20;27(15_suppl):7000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1 mutations as an independent prognosticator for older cytogenetically normal acute myeloid leukemia (CN AML).
  • : 7000 Background: In younger CN AML without FLT3-ITD, NPM1 mutations predict favorable outcome.
  • METHODS: Pretreatment marrow was studied in 189 older CN AML pts [median age 69 y (60 - 83 y); 162 de novo & 27 secondary (s; prior hematologic disorders) cases] enrolled on CALGB 9720 (n=106) & 10201 (n=83).
  • RESULTS: In de novo CN AML, NPM1 mutated (NPM1mut) pts (54%) had more CRs (85% v 45%, P<.0001) & longer relapse-free (RFS) (P=.02; 3 y rates 23% v 10%) & overall survival (OS) (P<.0001; 3 y 34% v 7%) than NPM1 wild-type (NPM1wt) pts.
  • CONCLUSIONS: NPM1 mutations independently predict better outcome in older CN AML.

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  • (PMID = 27963957.001).
  • [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] Journal Article
  • [Publication-country] United States
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50. Laille E, Ward R, Nasser A, Stoltz M, Cogle C, Gore S, Skikne BS, Garcia-Manero G: The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • : 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.
  • Few studies have evaluated the pharmacokinetics (PK) of AZA and the renal elimination of AZA has not been previously published to our knowledge.
  • METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m<sup>2</sup> AZA during their first treatment cycle.

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  • (PMID = 27961481.001).
  • [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] Journal Article
  • [Publication-country] United States
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51. Pratz KW, Cho E, Karp J, Levis M, Zhao M, Rudek M, Wright J, Smith BD: Phase I dose escalation trial of sorafenib as a single agent for adults with relapsed and refractory acute leukemias. J Clin Oncol; 2009 May 20;27(15_suppl):7065

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I dose escalation trial of sorafenib as a single agent for adults with relapsed and refractory acute leukemias.
  • Based on preclinical activity in FLT3 mutant AML, sorafenib was studied in refractory acute leukemia.
  • METHODS: The primary objective was to determine the safety and tolerability of sorafenib in refractory acute leukemias.
  • RESULTS: Fifteen patients (13 = AML, 2 = ALL) were enrolled (ages 37-85) and treated on three dosing schedules (400 mg BID x 14 d, 400 mg BID x 21 days, 600 mg BID x 21days) of single agent sorafenib.
  • No patients met criteria for complete or partial response, but 11 of 15 (73%) patients experienced stable disease as best response, with 6 showing a reduction in bone marrow blasts after only one cycle, half of who experienced a >50% reduction in bone marrow blasts.

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  • (PMID = 27961441.001).
  • [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] Journal Article
  • [Publication-country] United States
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52. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we report the results of a CTEP-sponsored phase I trial of SJG-136 administered on a daily x 5 schedule in pts with relapsed or refractory (R/R) leukemias.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • Thirteen (81%) pts had R/R AML, and 3 (19%) had R/R ALL of which 5 (31%) had diploid and 6 (38%) had adverse cytogenetics.
  • Other non-dose limiting toxicities included nausea, dyspnea, fatigue, bloating, and insomnia.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.
  • CONCLUSIONS: SJG-136 is safe and active in patients with advanced leukemias.

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  • (PMID = 27961262.001).
  • [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] Journal Article
  • [Publication-country] United States
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53. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.
  • In second case, a 4-year male we observed four copies of AML and two copies of TEL gene in more than 80% of cells.

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  • (PMID = 27960689.001).
  • [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] Journal Article
  • [Publication-country] United States
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54. McHayleh WM, Redner R, Sehgal R, Raptis A, Agha M, Natale J, Luong T, Schlesselman JJ, Foon K, Boyiadzis M: Etoposide and mitoxantrone in newly diagnosed acute myeloid leukemia patients with persistent leukemia after a course of induction therapy with cytarabine and idarubicin. J Clin Oncol; 2009 May 20;27(15_suppl):7073

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etoposide and mitoxantrone in newly diagnosed acute myeloid leukemia patients with persistent leukemia after a course of induction therapy with cytarabine and idarubicin.
  • : 7073 Background: The goal of induction chemotherapy in acute myeloid leukemia (AML) is complete remission with restoration of normal bone marrow.
  • If residual leukemia is present after the first course of induction therapy, patients receive a second course identical to the first or receive a non-cross resistant antileukemic regimen.
  • METHODS: In a retrospective study of adult patients with newly-diagnosed AML treated at the University of Pittsburgh Cancer Institute between December 2002 and May 2008, we evaluated the efficacy and toxicity of mitoxantrone (10 mg/m<sup>2</sup>/d) and etoposide (100 mg/m<sup>2</sup>/d), both administered intravenously within 5 days as second course therapy of patients not responding to first-course induction therapy with cytarabine and idarubicin.
  • RESULTS: 74 AML patients (mean age 56 years, range: 18-73 years) completed treatment with etoposide and mitoxantrone; 29 (39%) achieved CR.
  • Lower CR rate was associated with unfavorable cytogenetic risk status at diagnosis and higher percent blasts prior to treatment with mitoxantrone and etoposide.
  • CONCLUSIONS: Our study suggests that the combination of etoposide and mitoxantorne is an active and well-tolerated regimen as second-course therapy in newly diagnosed AML patients who have persistent leukemia after a first course of induction therapy with cytarabine and idarubicin.

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  • (PMID = 27961456.001).
  • [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] Journal Article
  • [Publication-country] United States
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55. Morgan MA, Reuter CW: Molecularly targeted therapies in myelodysplastic syndromes and acute myeloid leukemias. Ann Hematol; 2006 Mar;85(3):139-63
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] Molecularly targeted therapies in myelodysplastic syndromes and acute myeloid leukemias.
  • Although there has been significant progress in acute myeloid leukemia (AML) treatment in younger adults during the last decade, standard induction therapy still fails to induce remission in up to 40% of AML patients.
  • Additionally, relapses are common in 50-70% of patients who achieve a complete remission, and only 20-30% of patients enjoy long-term disease-free survival.
  • The natural history of myelodysplastic syndrome (MDS) is variable, with about half of the patients dying from cytopenic complications, and an additional 20-30% transforming to AML.
  • Presented here is an overview of molecularly targeted therapies currently being tested in AML and MDS patients, with a focus on FMS-like tyrosine kinase 3 inhibitors, farnesyltransferase inhibitors, antiangiogenesis agents, DNA hypomethylation agents, and histone deacetylase inhibitors.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Age Factors. Animals. Cell Proliferation / drug effects. DNA Methylation / drug effects. Disease-Free Survival. Histone Acetyltransferases / antagonists & inhibitors. Humans. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Protein Processing, Post-Translational / drug effects. Receptor, Macrophage Colony-Stimulating Factor / antagonists & inhibitors. Receptor, Macrophage Colony-Stimulating Factor / metabolism. Remission Induction / methods


56. Gu W, Hu S, Chen Z, Qiu G, Cen J, He B, He J, Wu W: High expression of WT1 gene in acute myeloid leukemias with more predominant WT1+17AA isoforms at relapse. Leuk Res; 2010 Jan;34(1):46-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High expression of WT1 gene in acute myeloid leukemias with more predominant WT1+17AA isoforms at relapse.
  • Real-time quantitative reverse transcriptase polymerase chain reaction method was established for detecting the expression levels of WT1 gene and WT1+17AA isoforms in 226 acute myeloid leukemia (AML) bone marrow (BM) cells.
  • The results showed that WT1 gene was 2-3 logarithms expressed more in AML BM cells at initial diagnosis or relapse than in normal BM cells (p<0.001), with predominant WT1+17AA isoforms expression (the ratio of WT1+17AA/WT1 more than 0.50).
  • Interestingly the ratio of WT1+17AA/WT1 was statistically higher in relapsed AMLs than in initially diagnosed (p=0.01), speculating that WT1+17AA isoforms might participate in AML relapse.
  • [MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics

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  • [Copyright] 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19414192.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers
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57. Santos J, Cerveira N, Bizarro S, Ribeiro FR, Correia C, Torres L, Lisboa S, Vieira J, Mariz JM, Norton L, Snijder S, Mellink CH, Buijs A, Shih LY, Strehl S, Micci F, Heim S, Teixeira MR: Expression pattern of the septin gene family in acute myeloid leukemias with and without MLL-SEPT fusion genes. Leuk Res; 2010 May;34(5):615-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression pattern of the septin gene family in acute myeloid leukemias with and without MLL-SEPT fusion genes.
  • Septins are proteins associated with crucial steps in cell division and cellular integrity.
  • In humans, 14 septin genes have been identified, of which five (SEPT2, SEPT5, SEPT6, SEPT9, and SEPT11) are known to participate in reciprocal translocations with the MLL gene in myeloid neoplasias.
  • We have recently shown a significant down-regulation of both SEPT2 and MLL in myeloid neoplasias with the MLL-SEPT2 fusion gene.
  • In this study, we examined the expression pattern of the other 13 known septin genes in altogether 67 cases of myeloid neoplasia, including three patients with the MLL-SEPT2 fusion gene, four with MLL-SEPT6 fusion, and three patients with the MLL-SEPT9 fusion gene.
  • When compared with normal controls, a statistically significant down-regulation was observed for the expression of both MLL (6.4-fold; p=0.008) and SEPT6 (1.7-fold; p=0.002) in MLL-SEPT6 leukemia.
  • Significant down-regulation of MLL was also found in MLL-MLLT3 leukemias.
  • In addition, there was a trend for SEPT9 down-regulation in MLL-SEPT9 leukemias (4.6-fold; p=0.077).
  • Using hierarchical clustering analysis to compare acute myeloid leukemia genetic subgroups based on their similarity of septin expression changes, we found that MLL-SEPT2 and MLL-SEPT6 neoplasias cluster together apart from the remaining subgroups and that PML-RARA leukemia presents under-expression of most septin family genes.
  • [MeSH-major] Cytoskeletal Proteins / genetics. GTP-Binding Proteins / genetics. Gene Expression. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Cluster Analysis. Humans. Infant. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748670.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / MLL-SEPT6 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.1.- / GTP-Binding Proteins
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58. Desmond JC, Raynaud S, Tung E, Hofmann WK, Haferlach T, Koeffler HP: Discovery of epigenetically silenced genes in acute myeloid leukemias. Leukemia; 2007 May;21(5):1026-34
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discovery of epigenetically silenced genes in acute myeloid leukemias.
  • The demethylating 5-aza-2'deoxycytidine (DAC) and the histone deacetylase inhibitor (HDACi) suberoyl anilide bishydroxamide (SAHA) possess potent antitumorigenic properties in myeloid disorders.
  • We analyzed the transcriptional effects of DAC and SAHA in the AML cell line KG-1.
  • We examined the expression level of these genes in 120 AML patient samples representing diverse karyotpyes.
  • Gas2l1, tfIIs, ehd3, enolase 2, mx1, dral, astml and pxdn were diminished across all AML karyotypes examined.
  • Ehd3 was methylated in 63% of AML patients examined.
  • This methylation was lost upon complete remission, and not observed in normal CD34+ cells.
  • CD34+ cells expressed ehd3 at approximately 10-fold higher levels than AML samples.
  • Analyses of 29 5q- AML/myelodysplastic syndrome (MDS) samples revealed marked decreases in expression of alpha-catenin, compared to non-5q- MDS samples (6.6+/-9-fold).
  • [MeSH-major] Epigenesis, Genetic. Genes, Tumor Suppressor. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 17330099.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / EHD3 protein, human; 0 / Hydroxamic Acids; 0 / alpha Catenin; 58IFB293JI / vorinostat; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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59. Parovichnikova EN, Savchenko VG, Kliasova GA, Isaev VG, Sokolov AN, Kulikov SM, Ustinova EN, Gribanova EO, Ryzhko VV, Khoroshko ND, Kravchenko SK, Galstian GM, Konstantinova TS, Zagoskina TP, Ziuzgin IS, Kaplanov KD, Moskov VI, Sokolova IV, Anchukova LV, Lapin VA, Loginov AB, Tumakov VA, Korobkin AV, Miliutina GI, Samoĭlova OS, Tikunova TS, Pristupa AS, Kondakova EV, Domnikova NP, Gavrilova LV, Obidina NA, Porokhina OV, Rekhtman GB, Mashchuk VN, Khuazheva NK, Kaporskaia TS, Golubeva ME, Maksimov AG, Ploskikh MA, Men'shakova SN, Mal'tsev VI, Rossiev VA, Pilipenko GI: [Toxicity of different treatment protocols for acute myeloid leukemias in adults: the results of four Russian multicenter studies]. Ter Arkh; 2010;82(7):5-11
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] [Toxicity of different treatment protocols for acute myeloid leukemias in adults: the results of four Russian multicenter studies].
  • AIM: To comparatively analyze the toxicity of 4 treatment protocols in patients with acute myeloid leukemia (AML), which were used in the Russian multicenter center in 1992 to 2009.
  • Randomization was made in 243 patients with AML (median age 38 years) in 1992-1995, 396 patients (median age 39 years) in 1995-1999, 392 patients (median age 39 years) in 2001-2006, and 137 patients (median age 40 years) in 2006-2009.
  • The analysis excluded patients with acute promyelocytic leukemias who were recruited in the AML-92 and AML-95 studies.
  • RESULTS: The baseline clinical and laboratory parameters in the patients enrolled in the studies in different years slightly differ in the count of leukocytes at the onset of the disease and in the level of lactate dehydrogenase (LDH): the recent studies revealed a larger number of high-risk group patients (leukocytes more than 30 10(9)(/l; LDH more than 500 units) possibly due to the later diagnosis of AML.
  • The long-term results of using the aggressive therapy did not differ from those obtained during the standard treatment protocols.
  • The incidence of invasive aspergillosis during the current programs from AML treatment was 10% (two induction courses), that of invasive candidiasis was 4.7% (two induction courses).
  • CONCLUSION; The long-term results of treatment for AML were virtually unchanged regardless significant therapy intensification.
  • The results of the analysis provide the basis for developing a new AML treatment protocol that should take into account all the merits and demerits of the previous protocols and provide a toxicity-treatment efficiency balance.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Leukocytes / cytology. Leukopenia / blood. Leukopenia / chemically induced. Leukopenia / epidemiology. Neutrophils / cytology. Opportunistic Infections / blood. Opportunistic Infections / epidemiology. Opportunistic Infections / etiology. Platelet Transfusion. Remission Induction. Russia

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  • (PMID = 20853602.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] EC 1.1.1.27 / L-Lactate Dehydrogenase
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60. Chen SW, Li CF, Chuang SS, Tzeng CC, Hsieh YC, Lee PS, Chen CH, Huang WT, Hwang WS, Tsao CJ: Aberrant co-expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan. Int J Lab Hematol; 2008 Apr;30(2):133-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant co-expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan.
  • Aberrant antigen expression in acute myeloid leukemia (AML) has been extensively studied in the West with limited reports from Taiwan.
  • We carried out this retrospective study to characterize the frequency and significance of aberrant antigen expression of AML in Taiwan.
  • Aberrant CD7 expression was observed in all non-AML-M3 subtypes, most frequently in AML-M7 (4/6, 67%); while CD19 expression was only observed in AML-M2 (5/36, 14%).
  • CD56 expression was most common in AML-M5 (4/8, 50%).
  • The relative frequency of CD19 and CD56 expression in AML with t(8;21) was higher than those with other chromosomal abnormalities or normal karyotype (P = 0.011 and 0.005, respectively).
  • In non-M3 AML, aberrant antigen expression was identified in 56/96 (58%) cases, in contrast to 2/15 (13%) AML-M3 cases (P = 0.001).
  • CD7, CD19 and CD56 expression was not correlated with remission rate.
  • We concluded that aberrant immunophenotype was more frequent in non-M3 leukemias in Taiwan.
  • The relative frequency of CD19 and/or CD56 expression in AML with t(8;21) was significantly higher than those without this translocation and co-expression of these two antigens may serve as the surrogate markers for AML with t(8;21).
  • [MeSH-major] Antigens, CD / metabolism. Antigens, CD19 / metabolism. Antigens, CD56 / metabolism. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 18333845.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD56
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61. Kappelmayer J, Simon A, Katona E, Szanto A, Nagy L, Kiss A, Kiss C, Muszbek L: Coagulation factor XIII-A. A flow cytometric intracellular marker in the classification of acute myeloid leukemias. Thromb Haemost; 2005 Aug;94(2):454-9
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] Coagulation factor XIII-A. A flow cytometric intracellular marker in the classification of acute myeloid leukemias.
  • This study was designed to study the sensitivity and specificity of factor XIII subunit A (FXIII-A) labelling in cultured myeloblastic and monoblastic cell lines and to investigate the intracytoplasmic expression of FXIII-A in de novo acute myeloid leukemia (AML) samples.
  • Myeloblastic and a monoblastic cell lines were cultured and investigated for lineage specific maturation markers and FXIII-A expression.
  • Furthermore, FXIII-A expression was investigated in 12 normal samples (7 bone marrow and 5 peripheral blood), 86 de novo AML samples and 6 chronic myelomonocytic leukemia (CMML) samples.
  • In the monoblastic MonoMac6 cell line the appearance of FXIII-A preceded that of CD14 while it remained negative in the myeloblastic PLB-985 cell line throughout its maturation period.
  • Among the AML samples the average frequency of FXIII-A positive cells in myeloblastic leukemia samples was below 10%, while in M4 and M5AML samples it was above 50% and was significantly higher than the generally used CD14 marker (p < 0.0001).
  • In the AML M4 and M5 cases, FXIII-A proved sensitive for the identification of monoblasts.
  • FXIII-A can be considered as a reliable intracytoplasmic marker for the monocytic and megakaryocytic series and its presence is highly predictive for mono- and megakaryocytic AML and for CMML.
  • [MeSH-major] Factor XIIIa / metabolism. Factor XIIIa / physiology. Flow Cytometry / methods. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / metabolism. Antigens, CD14 / biosynthesis. Cell Line. Cell Line, Tumor. Cell Lineage. Cells, Cultured. Cytoplasm / metabolism. Granulocytes / cytology. Humans. Leukocytes / metabolism. Megakaryocytes / cytology. Monocytes / cytology. Monocytes / metabolism. Myeloid Cells / cytology. Sensitivity and Specificity

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  • (PMID = 16113839.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD14; EC 2.3.2.13 / Factor XIIIa
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62. Goteri G, Zizzi A, Sabato S, Costagliola A, Stramazzotti D, Rubini C, Discepoli G, Capelli D, Leoni P: Immunostaining for nucleophosmin in bone marrow trephine biopsy specimens in acute myeloid leukemias. Anal Quant Cytol Histol; 2010 Aug;32(4):201-6
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] Immunostaining for nucleophosmin in bone marrow trephine biopsy specimens in acute myeloid leukemias.
  • STUDY DESIGN: Acute myeloid leukemia (AML) is a heterogeneous clonal disorder of hematopoietic progenitor cells that presents genetic abnormalities in several genes, including NPM.
  • Mutations of the NPM gene occur in 35% of patients with AML with normal karyotype, causing cytoplasmic rather than nuclear localization of the protein.
  • Because the NPM antibody recently became commercially available, we immunostained a series of diagnosed AML samples.
  • We performed NPM immunostaining in 48 AML cases.
  • CONCLUSION: NPM immunostaining is a feasible test, without problems of interpretation for pathologists, when the sections are optimally prepared and can be considered predictive of peculiar phenotypic and karyotype subtypes of AML, in addition to the well-known prognostic role.

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  • (PMID = 21434520.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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63. Cárdenas-Blanco A, Olariou E, Cameron I: Poster - Thurs Eve-28: New brain diffusion analysis method: White matter grey matter dissasociation. Med Phys; 2008 Jul;35(7Part2):3406

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The significance of the present diffusion decay study lies in the combination of three novel procedures to provide a better characterization of the diffusion decay: i) the acquisition of a large number of b-values (96 b-values up to 10,000 s/mm<sup>2</sup> ), ii) the application of a noise correction technique (3) to the acquired data, and iii) the use of a Non Negative Least Squares (NNLS) fitting algorithm to evaluate the diffusion coefficients.
  • The NNLS algorithm is used to fit the corrected data instead of the more commonly used Levenberg-Marquardt algorithm since the NNLS algorithm does not require the number of components to be specified, nor does it need initial estimates of the fitting parameters as input; thus giving it more versatility as a fitting tool for the diffusion decay.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28512828.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Brain / Diffusion / Medical imaging / Medical magnetic resonance imaging / Neural information
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64. Cheng PC, Crane J, Hunter T: Combination of bortezomib with a FLT3 inhibitor potentiates inhibition of proliferation and apoptosis of AML in vitro. J Clin Oncol; 2009 May 20;27(15_suppl):e14551

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination of bortezomib with a FLT3 inhibitor potentiates inhibition of proliferation and apoptosis of AML in vitro.
  • : e14551 Background: FLT3 receptor tyrosine kinase activating mutations contribute to leukemogenesis and poor prognosis in approximately 30% of acute myeloid leukemia (AML).
  • METHODS: In the course of conducting a synthetic lethality screen with a FLT3 inhibitor on the Ba/F3 murine cell line stably expressing human FLT3 or FLT3-ITD, we identified bortezomib, a proteasome inhibitor, as having potent activity against FLT3-ITD cells.
  • The effects of drugs on proliferation, apoptosis, and phosphosignaling were quantified in Ba/F3 cells and in the HL60 (WT FLT3) and MV4-11 (FLT3-ITD) human cell lines, using an MTS- based colorimetric assay, caspase 3 and 7 activity assays, and immunoblotting, respectively.
  • When the FLT3 inhibitor and bortezomib were used at IC25 concentrations, a more pronounced inhibition of cell proliferation was observed when they were used in combination than with either alone.
  • CONCLUSIONS: Bortezomib preferentially kills FLT3- ITD cells, showing a four-fold more potent inhibition of cell proliferation, induces apoptosis, and abrogates activation of FLT3 and its downstream effector pathways.

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  • (PMID = 27963616.001).
  • [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] Journal Article
  • [Publication-country] United States
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65. Lemez P, Urbánek V: Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients. Neoplasma; 2005;52(5):398-401
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy for acute myeloid leukemias with cytosine arabinoside, daunorubicin, etoposide, and mitoxantrone may cause permanent oligoasthenozoospermia or amenorrhea in middle-aged patients.
  • The aim was to follow-up gonadal functions in long-term survivors of acute myeloid leukemias (AML) after intensive chemotherapy based on high-doses of cytosine arabinoside (Ara-C) and anthracyclines in the study UHKT-911.
  • Adult patients were treated with at least 3 cycles of chemotherapy including 1-3 courses of Ara-C 10 x 2000 mg/m2/12 h and daunorubicin (DNR) 2 x 45 mg/m2/d.
  • The semen of a 49-year-old patient contained normal numbers of spermatozoa with decreased velocity when examined 1 year after chemotherapy but 4 years later exhibited oligoasthenozoospermia.
  • The patient received 4 cycles of Ara-C and DNR plus one cycle with etoposide 350 mg/m2 and mitoxantrone 30 mg/m2.
  • Semen examination of two patients 55- and 59-year-old showed permanent oligoasthenozoospermia with only sporadic progressively motile spermatozoa which might not be compatible with fertilization by sexual intercourse.
  • They received the same chemotherapy including cumulative doses of etoposide 500 mg/m2 and mitoxantrone 36 mg/m2.
  • Permanent amenorrhea developed in two women (42- and 46-year-old) during chemotherapy with DNR, Ara-C, etoposide, and mitoxantrone which was not the case in three women (29-40 years old) treated without etoposide and mitoxantrone.
  • Intensive chemotherapy with high-doses of Ara-C and DNR plus one cycle of etoposide and mitoxantrone may cause permanent gonadal dysfunction in middle-aged patients with AML.
  • [MeSH-major] Amenorrhea / chemically induced. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / drug therapy. Spermatozoa / drug effects
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Transplantation. Cytarabine / administration & dosage. Cytarabine / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Mitoxantrone / adverse effects. Oligospermia / chemically induced. Sperm Motility / drug effects

  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
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  • (PMID = 16151584.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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66. Lancet JE, Karp J, Cripe L, Roboz G, Wollman M, Berman C, Conroy A, Hawtin R, Fox J, Michelson G: Phase Ib/II pharmacokinetic/pharmacodynamic (PK/PD) study of combination voreloxin and cytarabine in relapsed or refractory AML patients. J Clin Oncol; 2009 May 20;27(15_suppl):7005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase Ib/II pharmacokinetic/pharmacodynamic (PK/PD) study of combination voreloxin and cytarabine in relapsed or refractory AML patients.
  • Clinical activity is observed in ovarian cancer and AML.
  • Interim results from a phase Ib/II study in relapsed or refractory AML are reported.
  • METHODS: Dose-escalation in relapsed/refractory AML patients (pts) with ≤ 3 prior induction regimens; phase II expansion in first-relapse pts (CR1 ≥ 3 months) at MTD.

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  • (PMID = 27961377.001).
  • [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] Journal Article
  • [Publication-country] United States
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67. Hollmig K, Waheed S, Nair B, Haessler J, Petty N, Pineda-Roman M, Alsayed Y, van Rhee F, Crowley J, Barlogie B: MDS-associated cytogenetic abnormalities (MDS-CA) after total therapy (TT) regimens for newly diagnosed multiple myeloma (MM): Apparent surge after introduction of post-transplant consolidation chemotherapy (CONS) in TT2 and TT3. J Clin Oncol; 2009 May 20;27(15_suppl):8595

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONCLUSIONS: Despite reduced induction chemotherapy prior to and CONS after tandem melphalan (200mg/m2)-based autotransplants from 4 in TT2 to 2 in TT3, overall and persistent MDS-CA increased significantly in TT3.
  • Clinical MDS and AML were rarely observed and a full account of hematopathologic findings will be presented.

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  • (PMID = 27962291.001).
  • [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] Journal Article
  • [Publication-country] United States
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68. Rangarajan B, Prabhash K, Nair R, Menon H, Jain P, Kannan S, Jeevangi NK, Bagal B, Parikh PM, Kurkure PA: Rater. J Clin Oncol; 2009 May 20;27(15_suppl):e20678

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Inclusion criteria were diagnosis of hematolymphoid malignancy, neutropenic febrile episode secondary to chemotherapy or during induction therapy of acute leukemia and more than 18 years of age All patients were risk stratified, hospitalized and treated with broad-spectrum, empiric, intravenous antibiotic therapy until recovery or outcome of the event.
  • We subsequently analyzed the subset of Acute Myeloid Leukemia (AML) patients as they were the majority comprising of 62/81 episodes.
  • The subset of AML patients risk stratified according to MASCC risk index showed sensitivity, specificity, PPV, NPV and accuracy of 71%, 25.5%, 11%, 87.5%, 31% respectively.
  • This trend is also seen in the subset analysis of AML patients.

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  • (PMID = 27961676.001).
  • [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] Journal Article
  • [Publication-country] United States
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69. Tsai DE, Wang W, Reshef R, Vogl D, Stadtmauer E, Andreadis C, Carlson A, Luger S: Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e20533

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia.
  • : e20533 Background: Bexarotene (Bex) is an oral retinoid X receptor agonist with activity against cutaneous T cell lymphoma and currently under investigation for other malignancies.
  • In patients receiving this agent for acute myeloid leukemia (AML), we noted increases in platelet counts.
  • METHODS: We analyzed platelet count data from 3 Bex clinical trials encompassing non-small cell lung cancer (NSCLC) and AML.
  • Similar findings were seen in a phase I monotherapy trial in AML where 5/18 (28%) patients achieved platelet transfusion independence with peak platelet counts of 40-91 K/uL.

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  • (PMID = 27960979.001).
  • [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] Journal Article
  • [Publication-country] United States
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70. Ghavamzadeh A, Allahyari A, Alimoghaddam K, Karimi A, Shamshiri A, Abolhasani R, Manookian A, Asadi M, Khatami F: Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders. J Clin Oncol; 2009 May 20;27(15_suppl):7042

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders.
  • : 7042 Background: High-dose chemotherapy with autologous stem cell support is utilized for the treatment of a variety of malignancies including Hodgkin/non-Hodgkins lymphoma and acute leukemias.
  • The aim of this study was to compare the time of engraftment and mortality rate and cost of neutropenic treatment in outpatient versus inpatient autologous stem cell transplantation (SCT).
  • METHODS: 9 outpatients (5 HL, 2 NHL, and 2 AML) were compared with 32 inpatients (15 HL, 8 NHL, and 9 AML; for whom the outpatient facilities were not ready) from May 2008 to December 2008.
  • They received conditioning regimen (CEAM for NHL and HL, busulfan and etoposide for AML) and stem cell infusion in hospital.
  • The day after SCT, outpatient group were discharged and followed by outpatient SCT team, and to be re-hospitalized in case of febrile neutropenia, after sepsis workup and performing chest x-ray, they were received the first dose of antibiotic in hospital and treatment continued in home.

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  • (PMID = 27961405.001).
  • [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] Journal Article
  • [Publication-country] United States
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71. Ritchie EK, Roboz G, Hinchcliff K, Curcio T, Scandura J, Feldman E: Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7054

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS.
  • : 7054 Background: Laromustine is a novel sulfonylhydrazine-alkylating agent with activity in acute myeloid leukemia (AML).
  • Laromustine in phase I and II trials shows activity in patients with relapsed/refractory leukemia (1) and elderly patients with new AML (2).
  • Based on this data, a phase I study to evaluate the safety and efficacy of combining escalating doses of laromustine with infusional ara-C in AML and MDS patients over 60.
  • METHODS: Laromustine 300 mg/m2 (cohort 1, n = 6), 400 mg/m2 (cohort 2, n = 5) and 500 mg/m2 (cohort 3) was administered by IV infusion over 1 hour on day 1 in combination with ara-C 100 mg/m2/day as a continuous infusion for 7 days.
  • Patients achieving CR after induction therapy were offered up to 2 cycles of consolidation therapy for a maximum cumulative laromustine dose of 1,000 mg/m2.

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  • (PMID = 27961420.001).
  • [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] Journal Article
  • [Publication-country] United States
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72. Singh T, Satheesh C, Ankit J, Sajeevan KV, Appaji L, Arunakumari B, Padma M, Mamatha HS: Use of Port-A-Cath in pediatric cancer patients: Experience from a tertiary cancer center in south India. J Clin Oncol; 2009 May 20;27(15_suppl):e20747

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Disease distribution included ALL(80%), AML(5%), NHL(5%), neuroblastoma (5%) and RMS (5%).

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  • (PMID = 27962033.001).
  • [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] Journal Article
  • [Publication-country] United States
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73. Ghavamzadeh A, Hashemi S, Alimoghaddam K, Nasri Moghaddam Z, Shadpour M, Jalili M: Phase II trial of old age acute myeloid leukemia treatment by arsenic trioxide and low-dose subcutaneous cytosin arabinoside. J Clin Oncol; 2009 May 20;27(15_suppl):7075

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of old age acute myeloid leukemia treatment by arsenic trioxide and low-dose subcutaneous cytosin arabinoside.
  • : 7075 Background: AML is a disease of old age, but unfortunately due to several factors standard treatment can not be delivered to these patients.
  • Patients couldn't tolerate standard treatment of AML due to old age or comorbid disorders.
  • CONCLUSIONS: Although prognosis of old age AML remain poor, but with this type of treatment RR is acceptable.
  • In this very high-risk group of very old AML, combination of ATO and ARA-C possibly could improve survival.

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  • (PMID = 27961458.001).
  • [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] Journal Article
  • [Publication-country] United States
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74. Jabbour E, Faderl S, Ravandi F, Konopleva M, Verstovsek S, Cortes J, Wierda W, Newsome WM, Yang H, Kantarjian H, Garcia-Manero G: Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML).
  • : 7004 Background: Standard induction therapy for pts with AML has not changed over the last 2 decades nor has the outcome of these pts.
  • We designed a phase II study of V with IA as front-line therapy for MDS/AML.
  • METHODS: Pts with untreated int-2/high-risk MDS or AML ages 15-65 with adequate liver and renal functions and PS, and EF ≥ 50% were eligible.
  • 3 pts with relapsed/refractory AML were treated in the run-in phase.
  • 8 (47%) had secondary disease.
  • The median PFS has not been reached.
  • CONCLUSIONS: The combination of IA and V is safe and active in AML/MDS.
  • Results will be compared with those of a parallel IA study at MDACC.

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  • (PMID = 27961376.001).
  • [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] Journal Article
  • [Publication-country] United States
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75. Tong W, Stevenson W, Cortes J, Needham L, Brotherton D, Davidson A, Drummond A, Garcia-Manero G: In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e14579

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia.
  • : e14579 Background: Histone deacetylase inhibitors alter gene expression and induce apoptosis in a wide range of cancer cells including those derived from human leukemias.
  • METHODS: We studied the in vitro and in vivo anti-leukemia activity of CHR-2845 using cell proliferation assay, annexin V binding assay, cell cycle analysis, western blot and in vitro primary leukemia cell culture.
  • RESULTS: Both U937 and THP1 cells express high levels of hCE-1 whereas the myeloid cell line, HL60, does not.
  • In comparison to vorinostat, CHR-2845 showed increased anti-proliferative potency (IC<sub>50</sub>) against monocytic cell lines (THP1, 30 nM vs 700 nM and U937, 30 nM vs 475 nM), compared to a myeloid cell line (HL60, 700nM vs 470 nM).
  • In a broad panel of leukemic cell lines, the potency of CHR-2845 over vorinostat correlated completely with hCE-1 expression.
  • In monocytic cell lines, CHR-2845 induced more apoptosis than vorinostat (THP1: 45±5% vs 11±1% and U937: 23±14% vs 6±1%), as measured by flow cytometry using Annexin V.
  • Biochemical assessment of histone H3 and H4 protein acetylation by Western blot also indicateed that CHR-2845 is at least 10 times more potent than vorinostat in monocytic cell lines but not in HL-60 cells.
  • We also studied the anti-leukemia activity of CHR-2845 in primary leukemia cells from 8 patients with acute or chronic myelomonocytic leukemia.
  • CONCLUSIONS: These results indicated that CHR-2845 has potential to be efficacious in the treatment of patients with monocytic leukemia.

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  • (PMID = 27963654.001).
  • [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] Journal Article
  • [Publication-country] United States
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76. Goldman S, Coiffier B, Reiter A, Younes A, Cairo MS, International TLS Expert Panel: A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel. J Clin Oncol; 2009 May 20;27(15_suppl):e17575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel.
  • METHODS: We convened an international panel (N = 17) of experts in pediatric and adult hematological malignancies and solid tumors (ST) to develop a medical decision tree for the P and T of TLS based on the risk classification (low, medium, high) and management recommendations of Coiffier et al (J Clin Oncol.
  • 2008) Results: Patients without evidence of LTLS were assigned to either low-risk disease (LRD), medium-risk (MRD), or high-risk (HRD).
  • Risk factors included pathological classification stage, bulk, disease burden (WBC/LDH) and renal impairment/involvement.
  • HRD was assigned to patients with either B-ALL, ALL/AML ≥100K/mm<sup>3</sup>, BL/LL stage III/IV, and/or high LDH, DLBCL/PTCL/MCL/ATL with bulky and elevated LDH and patients with MRD with renal impairment/involvement.
  • MRD consisted of ALL ≤100K/mm<sup>3</sup>, AML 25-100K/mm<sup>3</sup>, BL/LL stage I/II and low LDH, childhood ALCL, DLBCL/PTCL/MCL/ATL non-bulky but elevated LDH, CLL treated with targeted therapy, and LRD with renal impairment/involvement.
  • LRD consisted of ST (except bulky sensitive to cytotoxic therapy [MRD]), CML, MM, HL, other NHL and AML <25K/mm<sup>3</sup>.

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  • (PMID = 27963935.001).
  • [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] Journal Article
  • [Publication-country] United States
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77. Dutreix C, Huntsman Labed A, Roesel J, Lanza C, Wang Y: Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients. J Clin Oncol; 2009 May 20;27(15_suppl):e14540

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients.
  • : e14540 Background: Midostaurin is a multi-tyrosine-kinases inhibitor targeting class III tyrosine-protein-kinases, including Fms-like tyrosine kinase-3 (FLT3), involved in hematopoiesis and leukemia.
  • METHODS: The two studies presented here involved patients with wild-type or FLT3-mutated de novo (phase Ib) or relapsed (phase II) AML or MDS.
  • However, evaluation of available bone marrow blast (BM) response data revealed that a much higher midostaurin plasma would be needed for a satisfactory BM response.
  • These results support the ongoing phase III AML study in AML FLT3-mutated patients with midostaurin given in combination with chemotherapy.

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  • (PMID = 27963644.001).
  • [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] Journal Article
  • [Publication-country] United States
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78. Rubnitz J, Inaba H, Ribeiro R, Pounds S, Pui C, Leung W: Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10034

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pilot study of haploidentical natural killer cell transplantation in childhood acute myeloid leukemia.
  • : 10034 Background: In the setting of hematopoietic stem cell transplantation (HSCT), donor natural killer (NK) cells exhibit potent anti-leukemic effects without causing graft-versus-host disease.
  • We hypothesized that the transplantation of purified haploidentical NK cells may be a safe and effective form of consolidation therapy that will reduce the risk of relapse among children with acute myeloid leukemia (AML) who are not treated with HSCT.
  • In this pilot study, we assessed the safety, feasibility, and engraftment of NK cell infusions in 10 patients with AML in first remission.
  • RESULTS: The 10 patients had a median age of 2.5 years (range, 8 months to 21 years) and a median leukocyte count of 62 x 10<sup>9</sup>/L (range, 4 to 487) at diagnosis.
  • Leukemic cell genetic abnormalities included CBFβ-MYH11in 4 cases, RBM15-MKL1in 2 cases, MLL-ENL and MLL-AF9 in 1 case each; 2 cases had no detectable abnormalities.
  • All patients had detectable donor NK cells at one or more time points: donor NK cell chimerism ranged from 0% to 30% during the first 4 weeks after the infusions and was greater than 1% in 9 cases at week 1, 4 cases at week 2, 5 cases at week 3, and 3 cases at week 4.
  • One patient had prolonged NK engraftment (189 days), but no non-hematological toxicity.
  • Grade 3-4 non-hematological toxicity was limited to one respiratory viral infection and one episode of febrile neutropenia.
  • CONCLUSIONS: Haploidentical NK cells can be safely administered to AML patients who are in remission.
  • We have recently opened a new trial to evaluate the efficacy of NK cell therapy in children in first remission of AML.

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  • (PMID = 27962581.001).
  • [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] Journal Article
  • [Publication-country] United States
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79. Chamberlain MC, Raizer J: Extended exposure to alkylator chemotherapy: Delayed appearance of myelodysplasia. J Clin Oncol; 2009 May 20;27(15_suppl):e13030

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: A case series of gliomas treated with alkylator-based chemotherapy who subsequently developed myelodysplastic syndrome (tMDS) or acute myelocytic leukemia (AML).
  • The diagnosis of tMDS was determined by bone marrow biopsy in seven patients.
  • Three patients were diagnosed with AML as well (in two determined by bone marrow and one at autopsy).
  • Interval from last chemotherapy exposure to diagnosis of tMDS/AML ranged from 3 months to 31 months (median 24 months).
  • Five patients have died, two as a consequence of recurrent brain tumor, one as a complication of transplantation, and due due to AML.
  • CONCLUSIONS: Although rare, induction of tMDS/AML following extended use of alkylator-based chemotherapy may become more relevant with the evolving practice to treat gliomas for protracted periods.

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  • (PMID = 27962878.001).
  • [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] Journal Article
  • [Publication-country] United States
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80. Couronné L, Lippert E, Andrieux J, Kosmider O, Radford-Weiss I, Penther D, Dastugue N, Mugneret F, Lafage M, Gachard N, Nadal N, Bernard OA, Nguyen-Khac F: Analyses of TET2 mutations in post-myeloproliferative neoplasm acute myeloid leukemias. Leukemia; 2010 Jan;24(1):201-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analyses of TET2 mutations in post-myeloproliferative neoplasm acute myeloid leukemias.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Myeloproliferative Disorders / complications. Proto-Oncogene Proteins / genetics

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  • (PMID = 19710701.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor beta Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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81. Juncà J, Zamora L, Cabezón M, Marcè S, Nomdedéu J: Aberrant expression of CD7 in acute myeloid leukemias with FLT3-ITD. Am J Clin Pathol; 2008 Oct;130(4):644; author reply 645
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of CD7 in acute myeloid leukemias with FLT3-ITD.
  • [MeSH-major] Antigens, CD7 / biosynthesis. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism

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  • [CommentOn] Am J Clin Pathol. 2008 Apr;129(4):624-9 [18343790.001]
  • (PMID = 18825844.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Biomarkers, Tumor; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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82. Garcia-Manero G, Luger S, Venugopal P, Maness L, Wetzler M, Coutre S, Stock W, Borthakur G, Chiao J, Kantarjian H: A randomized phase II study of sapacitabine, an oral nucleoside analogue, in elderly patients with AML previously untreated or in first relapse or previously treated MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7021

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized phase II study of sapacitabine, an oral nucleoside analogue, in elderly patients with AML previously untreated or in first relapse or previously treated MDS.
  • : 7021 Background: Sapacitabine is a novel nucleoside analogue with a unique ability to cause irreparable single-strand DNA breaks and induce G2 cell cycle arrest.
  • It is orally administered and has demonstrated promising anti-leukemic activity against relapsed or refractory AML and MDS in a phase 1 trial.
  • METHODS: Eligible patients must be ≥70 years with AML previously untreated or in first relapse or ≥60 years with MDS previously treated with hypomethylating agents.
  • The planned sample size is 60 AML patients and 60 MDS patients.
  • RESULTS: As of December 2008, 60 AML and 13 MDS patients were enrolled and had ≥ 30 days of follow-up.
  • Preliminary efficacy data were available for the AML stratum.
  • Eight deaths of all causes occurred within 30 days of randomization and all were in the AML stratum (13%).

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  • (PMID = 27961383.001).
  • [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] Journal Article
  • [Publication-country] United States
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83. Bello CM, Yu D, Zhu W, Wetzstein GA, Lancet JE: Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors. J Clin Oncol; 2009 May 20;27(15_suppl):7088

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors.
  • : 7088 Background: Secondary acute myeloid leukemia (sAML) arising from myelodysplasia (MDS) or a myeloproliferative neoplasm (MPN) has a poor prognosis.
  • METHODS: Retrospective chart review of patients with untreated AML from MDS/MPN treated with standard induction therapy from January 2004 to September 2008.
  • Multivariable analysis indicated that the same three factors were significantly negatively associated with CR/CRp as well as OS: PR cytogenetics, prior treatment with DM/L, and long transformation to AML on log scale.
  • Only 32% of the group that received prior treatment with a DM/L achieved CR/CRp compared to 78% in non DM/L-treated patients (OR = 0.13, 95% CI: 0.04-0.42).
  • The median OS for those treated with a DM/L was 3.7 mo compared to 10.5 mo for non DM/L-treated patients (p < 0.0001).
  • CONCLUSIONS: Prior MDS treatment with a DM/L, PR cytogenetics and long transformation to AML are independent negative prognostic factors for response and OS in patients with sAML following induction therapy, suggesting that such patients may be better served by novel approaches, and that stratification for these risk factors should be considered in future clinical trials.

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  • (PMID = 27961482.001).
  • [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] Journal Article
  • [Publication-country] United States
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84. Meani N, Alcalay M: Role of nucleophosmin in acute myeloid leukemia. Expert Rev Anticancer Ther; 2009 Sep;9(9):1283-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of nucleophosmin in acute myeloid leukemia.
  • Mutations of the NPM1 gene leading to the expression of a cytoplasmic mutant protein, NPMc+, are the most frequent genetic abnormalities found in acute myeloid leukemias.
  • Acute myeloid leukemias with mutated NPM1 have distinct characteristics, including a significant association with a normal karyotype, involvement of different hematopoietic lineages, a specific gene-expression profile and clinically, a better response to induction therapy and a favorable prognosis.
  • In this review we summarize recent discoveries concerning NPM function, and discuss their possible impact on the pathogenesis of acute myeloid leukemias with mutated NPM1.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics

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  • (PMID = 19761432.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Number-of-references] 153
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85. Pemmaraju N, Kantarjian H, Ravandi F, O'Brien S, Wierda W, Thomas D, Garcia-Manero G, Borthakur G, Pierce S, Cortes J: Acute myeloid leukemia (AML) in adolescents and young adults (AYA): The M. D. Anderson Cancer Center (MDACC) experience. J Clin Oncol; 2009 May 20;27(15_suppl):7051

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML) in adolescents and young adults (AYA): The M. D. Anderson Cancer Center (MDACC) experience.
  • : 7051 Background: AML is a heterogeneous group of hematopoietic neoplasms demonstrating clonal proliferation of myeloid precursors and is typically a disease of older adults.
  • Little is known about outcomes of AYA with AML.
  • METHODS: We retrospectively analyzed all patients (pts) with AML treated at MDACC from 1965 to 2008.
  • RESULTS: Among 3,934 adult AML pts treated during this period, 163 pts (4%) were AYA with median age of 19 yrs.
  • This cohort included 27 (17%) pts with Core Binding Factor (CBF)-AML [inv(16), t(8:21)] and 19 pts (12%) with acute promyelocytic leukemia (APL).
  • Complete remission (CR) rates were 89% for CBF AML, 79% for APL, and 75% for all other pts.
  • Outcome is better for pts with CBF leukemia (3 yr survival 56%, sustained CR 49%) and APL (3 yr survival 51%, sustained CR 36%) compared to other AML (3 yr survival 28%, sustained CR 24%).
  • CONCLUSIONS: The outcome of AYA pts with AML is significantly better than for older adults with AML.
  • Despite the advances in treatments over time, there is still significant room for improvement, particularly among those AYA with AML other than CBF and APL.

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  • (PMID = 27961415.001).
  • [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] Journal Article
  • [Publication-country] United States
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86. Weight is a risk factor for treatment mortality in AML. Nurs Stand; 2005 Feb 16;19(23):10

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Weight is a risk factor for treatment mortality in AML.
  • Underweight or overweight children with acute myeloid leukaemia (AML) are more likely to succumb to treatment-related complications than their normal weight counterparts.

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  • (PMID = 28091019.001).
  • [ISSN] 2047-9018
  • [Journal-full-title] Nursing standard (Royal College of Nursing (Great Britain) : 1987)
  • [ISO-abbreviation] Nurs Stand
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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87. Lannert H, Lenze M, Able T, Park BJ, Lenze A, Meissner S, Eckstein V, Ho AD, Leicht S, Franz T: Changes in phosphorylation and dephosphorylation status of cytoskeleton and their regulator proteins in CD34+ stem cells after G-CSF stimulation and in AML. J Clin Oncol; 2009 May 20;27(15_suppl):e22067

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changes in phosphorylation and dephosphorylation status of cytoskeleton and their regulator proteins in CD34+ stem cells after G-CSF stimulation and in AML.
  • It is a dynamic structure that maintains cell shape, enables cellular motion.
  • In this study we investigated the expression of cytoskeleton proteins in native hematopoietic CD34+ stem cells from BM in comparison to mobilized peripheral blood stem cells (mPBSCs) from G-CSF stimulated donors as well as CD34+ cells from AML.
  • METHODS: An Auto-MACS (Miltenyi) and FACS Vantage SE cell sorter (Becton Dickinson) was used to process high enriched (>99%) CD34+ cells fractions from MNCs.
  • Stathmin is overexpressed in G-CSF mobilized hematopoietic stem cells and in AML in his active 'dephosphorylated' form.
  • Our results show, that mobilized stem cells "in vivo" and AML cells increase cytoskeleton proteins expression and cause a complex phosphorylation status, which may explain the regulation of migration and metastasis.

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  • (PMID = 27963210.001).
  • [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] Journal Article
  • [Publication-country] United States
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88. Suzuki R, Ohtake S, Takeuchi J, Nagai M, Kodera Y, Hamaguchi M, Miyawaki S, Karasuno T, Shimodaira S, Ohno R, Nakamura S, Naoe T: The clinical characteristics of CD7+ CD56+ acute myeloid leukemias other than M0. Int J Hematol; 2010 Mar;91(2):303-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical characteristics of CD7+ CD56+ acute myeloid leukemias other than M0.
  • Immunological phenotyping of acute leukemia have provided enormous and important information for the classification and lineage determination of leukemia.
  • Forty-nine patients with CD7(+) CD56(+) acute myeloid leukemia (AML) were analyzed.
  • There were 17 patients of M0, which corresponded to myeloid/NK cell precursor acute leukemia, and 32 patients of AML other than M0 (9 each for M1 and M2, one for M3, 3 for M4, 4 for M5 and 6 for M7).
  • Age distribution was similar between these two groups, but CD7(+) CD56(+) M0 showed significant male predominance than CD7(+) CD56(+) M1-M7 (M:F = 15:2 vs. 15:17, P = 0.006).
  • The disease localization and the hematological manifestations were different, showing fewer white blood cell counts and circulating leukemic blasts, less anemia, less thrombocytopenia and more frequent extramedullary involvement in M0 group.
  • These findings suggest that extramedullary involvement of myeloid/NK cell precursor acute leukemia is not directly derived from the presence of CD7 and CD56 antigens on leukemic cells.
  • The poor prognosis of CD7(+) CD56(+) M1-M7 suggests that this phenotype may act as a prognostic factor for AML, but this should be confirmed in further studies.
  • [MeSH-major] Antigens, CD56 / metabolism. Antigens, CD7 / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Leukemia, Myeloid, Acute
  • [MeSH-minor] Adolescent. Adult. Aged. Cyclophosphamide / therapeutic use. Data Collection. Disease-Free Survival. Doxorubicin / therapeutic use. Female. Flow Cytometry. Humans. Immunophenotyping. Leukocyte Count. Male. Middle Aged. Prednisone / therapeutic use. Prognosis. Remission Induction. Sex Distribution. Survival Analysis. Vincristine / therapeutic use. Young Adult

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  • (PMID = 20111912.001).
  • [ISSN] 1865-3774
  • [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 / Antigens, CD56; 0 / Antigens, CD7; 0 / Biomarkers, Tumor; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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89. Lennon PA, Abruzzo LV, Medeiros LJ, Cromwell C, Zhang X, Yin CC, Kornblau SM, Konopieva M, Lin P: Aberrant EVI1 expression in acute myeloid leukemias associated with the t(3;8)(q26;q24). Cancer Genet Cytogenet; 2007 Aug;177(1):37-42
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  • [Title] Aberrant EVI1 expression in acute myeloid leukemias associated with the t(3;8)(q26;q24).
  • EVI is a proto-oncogene that is activated in acute myeloid leukemia with chromosomal rearrangements that map to chromosome 3q26.
  • We previously reported the clinicopathologic features of five cases of acute myeloid leukemia carrying t(3;8)(q26;q24).
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. DNA-Binding Proteins / genetics. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Blotting, Western. Chromosome Mapping. Humans. In Situ Hybridization, Fluorescence. Proteins / genetics. Proto-Oncogene Proteins c-myc / genetics. RNA, Long Noncoding. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17693189.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 P50 CA100632; United States / NCI NIH HHS / CA / P01 CA-55164
  • [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 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / PVT1 long-non-coding RNA, human; 0 / Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Long Noncoding; 0 / Transcription Factors
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90. Carnicer MJ, Bernardini S, Bellincampi L, Noguera NI, Nuccetelli M, Ammatuna E, Breccia M, Lo-Coco F, Federici G: Role of gamma-glutamyl cysteine synthetase (gamma-GCS) gene expression as marker of drug sensitivity in acute myeloid leukemias. Clin Chim Acta; 2006 Mar;365(1-2):342-5
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  • [Title] Role of gamma-glutamyl cysteine synthetase (gamma-GCS) gene expression as marker of drug sensitivity in acute myeloid leukemias.
  • The aim of our study was to investigate gamma-GCS gene expression in patients affected by acute myeloid leukemia (AML).
  • METHODS: A total of 64 AML samples, including 23 acute promyelocytic leukemia (APL or M3) cases, were included in the study. gamma-GCS mRNA levels were determined by real-time quantitative RT-PCR.
  • All patients were evaluated at diagnosis, whereas post-treatment gamma-GCS mRNA levels were assessed at the end of the consolidation therapy in 16 cases.
  • RESULTS: Our data showed that variable degrees of gamma-GCS expression were detectable in AML, likely reflecting disease heterogeneity; in particular, APL cases, compared to the other AML subsets, showed both significantly lower basal levels of gamma-GCS mRNA at presentation and significantly increased mRNA levels after treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gene Expression. Glutamate-Cysteine Ligase / genetics. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16239001.001).
  • [ISSN] 0009-8981
  • [Journal-full-title] Clinica chimica acta; international journal of clinical chemistry
  • [ISO-abbreviation] Clin. Chim. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; EC 6.3.2.2 / Glutamate-Cysteine Ligase
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91. Nowbakht P, Ionescu MC, Rohner A, Kalberer CP, Rossy E, Mori L, Cosman D, De Libero G, Wodnar-Filipowicz A: Ligands for natural killer cell-activating receptors are expressed upon the maturation of normal myelomonocytic cells but at low levels in acute myeloid leukemias. Blood; 2005 May 1;105(9):3615-22
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  • [Title] Ligands for natural killer cell-activating receptors are expressed upon the maturation of normal myelomonocytic cells but at low levels in acute myeloid leukemias.
  • Natural killer (NK) cell-mediated cytolytic activity against tumors requires the engagement of activating NK receptors by the tumor-associated ligands.
  • Here, we have studied the role of NKG2D and natural cytotoxicity receptors (NCRs) in the recognition of human leukemia.
  • To detect as-yet-unknown cell-surface molecules recognized by NCRs, we developed soluble forms of NKp30, NKp44, and NKp46 as staining reagents binding the putative cognate ligands.
  • Analysis of UL16-binding protein-1 (ULBP1), ULBP2, and ULBP3 ligands for NKG2D and of potential ligands for NKp30, NKp44, and NKp46 in healthy hematopoietic cells demonstrated the ligand-negative phenotype of bone marrow-derived CD34(+) progenitor cells and the acquisition of cell-surface ligands during the course of myeloid differentiation.
  • In acute myeloid leukemia (AML), leukemic blasts from approximately 80% of patients expressed very low levels of ULBPs and NCR-specific ligands.
  • Treatment with differentiation-promoting myeloid growth factors, together with interferon-gamma, upregulated cell-surface levels of ULBP1 and putative NCR ligands on AML blasts, conferring an increased sensitivity to NK cell-mediated lysis.
  • We conclude that the ligand-negative/low phenotype in AML is a consequence of cell maturation arrest on malignant transformation and that defective expression of ligands for the activating NKG2D and NCR receptors may compromise leukemia recognition by NK cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / immunology. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Monocytes / pathology. Receptors, Immunologic / genetics
  • [MeSH-minor] Acute Disease. Case-Control Studies. Cell Differentiation. Humans. Ligands. Myeloid Cells / pathology. NK Cell Lectin-Like Receptor Subfamily K. Natural Cytotoxicity Triggering Receptor 1. Natural Cytotoxicity Triggering Receptor 2. Natural Cytotoxicity Triggering Receptor 3. Receptors, Natural Killer Cell

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  • (PMID = 15657183.001).
  • [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 / KLRK1 protein, human; 0 / Ligands; 0 / NCR1 protein, human; 0 / NCR2 protein, human; 0 / NCR3 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Natural Cytotoxicity Triggering Receptor 1; 0 / Natural Cytotoxicity Triggering Receptor 2; 0 / Natural Cytotoxicity Triggering Receptor 3; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell
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92. Lemez P, Gáliková J, Michalová K, Dvoráková D, MacWhannell A, Zemanová Z, Stejskal J: [Patients older than 80 years with de novo acute myeloid leukemias without erythroblastic and/or megakaryocytic dysplasia achieve complete remission and longer survival after classical chemotherapy 3 + 7]. Vnitr Lek; 2010 Jan;56(1):37-43
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  • [Title] [Patients older than 80 years with de novo acute myeloid leukemias without erythroblastic and/or megakaryocytic dysplasia achieve complete remission and longer survival after classical chemotherapy 3 + 7].
  • [Transliterated title] Nemocní starsí 80 let s de novo akutními myeloidními leukemiemi bez dysplazie v erytroblastické 8/nebo megakaryocytární radĕ dosahují kompletní remise a delsího prezlití po klasické chemoterapii 3+7.
  • Chemotherapy in most patients with AML over 80 years of age is not recommended because their median survival is about 1 month.
  • We report 9 consecutive patients with de novo AML diagnosed and treated in 1992-2008.
  • All bone marrow samples were hypercellular, classified as FAB types M2 in 2 cases, M4 in 6, and M5 in one case.
  • Two patients with a normal karyotype had resistant AML and survived 1.0 and 2.7 months; one patient with a complex karyotype died of septic shock on the 10th day of therapy.
  • All these three patients exhibited erythroblastic and/or megakaryocytic dysplasia (EMD) at presentation (two in more than 26% erythroblasts, all three in a half or more of megakaryocytes).
  • Three remaining patients with AML M4, a normal karyotype but without EMD, achieved complete remission in spite of co-morbidities and a poor performance status.
  • Very elderly AML patients without EMD appear to represent a favorable prognostic biological category (single-lineage AML) that show a good response to standard dose chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy

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  • (PMID = 20184110.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZS7284E0ZP / Daunorubicin
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93. Gruszka AM, Lavorgna S, Consalvo MI, Ottone T, Martinelli C, Cinquanta M, Ossolengo G, Pruneri G, Buccisano F, Divona M, Cedrone M, Ammatuna E, Venditti A, de Marco A, Lo-Coco F, Pelicci PG: A monoclonal antibody against mutated nucleophosmin 1 for the molecular diagnosis of acute myeloid leukemias. Blood; 2010 Sep 23;116(12):2096-102
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  • [Title] A monoclonal antibody against mutated nucleophosmin 1 for the molecular diagnosis of acute myeloid leukemias.
  • Mutations in the nucleophosmin 1 (NPM1) gene are the most frequent genetic aberrations of acute myeloid leukemia (AML) and define a clinically distinct subset of AML.
  • T26 recognized 10 of the 21 known NPM1 mutants, including the A, B, and D types, which cover approximately 95% of all cases, and did not cross-react with wild-type NPM1 or unrelated cellular proteins.
  • Within a series of consecutive de novo AML patients, 44 of 110 (40%) and 15 of 39 (38%) cases scored positive using the T26 antibody in immunofluorescence and flow cytometry assays, respectively.
  • T26 is the first antibody that specifically recognizes a leukemia-associated mutant protein.
  • Immunofluorescence or flow cytometry using T26 may thus become a new tool for a rapid, simple, and cost-effective molecular diagnosis of AMLs.
  • [MeSH-major] Antibodies, Monoclonal. Leukemia, Myeloid, Acute / diagnosis. Nuclear Proteins / genetics

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  • (PMID = 20538791.001).
  • [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 / Antibodies, Monoclonal; 0 / Mutant Proteins; 0 / Nuclear Proteins; 0 / Peptide Fragments; 117896-08-9 / nucleophosmin
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94. Woessner S: Transmission electron microscopy in hematological diagnosis. Ultrastruct Pathol; 2005 May-Aug;29(3-4):237-68
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  • [Title] Transmission electron microscopy in hematological diagnosis.
  • Transmission electron microscopy (TEM) is still a very useful adjunct for hematological diagnosis in the era of molecular techniques.
  • In this article, the main applications of TEM to the cellular identification of normal myeloid cells, the study of dyserythropoietic conditions, myelodysplastic syndromes, congenital dyserythropoietic anemias, acute myeloid leukemias, and lymphoproliferative disorders, as well as the application of ultrastructural cytochemical reactions in hematological diagnosis, are reviewed.
  • [MeSH-major] Hematologic Diseases / diagnosis. Microscopy, Electron, Transmission / methods

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  • (PMID = 16036879.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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95. Peterson LF, Boyapati A, Ahn EY, Biggs JR, Okumura AJ, Lo MC, Yan M, Zhang DE: Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts. Blood; 2007 Aug 1;110(3):799-805
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  • [Title] Acute myeloid leukemia with the 8q22;21q22 translocation: secondary mutational events and alternative t(8;21) transcripts.
  • Nonrandom and somatically acquired chromosomal translocations can be identified in nearly 50% of human acute myeloid leukemias.
  • One common chromosomal translocation in this disease is the 8q22;21q22 translocation.

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  • (PMID = 17412887.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096735; United States / NCI NIH HHS / CA / R01 CA104509; United States / NCI NIH HHS / CA / CA 104509; United States / NCI NIH HHS / CA / CA 96735
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 103
  • [Other-IDs] NLM/ PMC1924771
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96. Pardee TS, Zuber J, Lowe SW: Effects of the Flt3 ITD on response to chemotherapy in a murine model of acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7060

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the Flt3 ITD on response to chemotherapy in a murine model of acute myeloid leukemia.
  • : 7060 Background: Acute myeloid leukemia (AML) is an aggressive, genetically heterogeneous malignancy.
  • The Flt3 receptor tyrosine kinase containing an internal tandem duplication (Flt3 ITD) is a common mutation in AML and associated with a poor prognosis; however, its effect on chemotherapy response is currently unknown.
  • METHODS: Murine AML was generated by retroviral transduction of an MLL-ENL fusion protein into fetal liver cells and subsequent transplantation into syngeneic mice.
  • Blasts were harvested from moribund animals and myeloid lineage confirmed by immunophenotyping.
  • In contrast there was no difference in leukemic burden between Ara-C treated, dox treated or control animals in AML without Flt3 ITD (p = 0.2833).
  • These results suggest AML patients with Flt3 ITD may benefit more from high-dose cytarabine regimens then anthracyclines.

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  • (PMID = 27961434.001).
  • [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] Journal Article
  • [Publication-country] United States
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97. Foucar K: Myelodysplastic/myeloproliferative neoplasms. Am J Clin Pathol; 2009 Aug;132(2):281-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Myelodysplastic/myeloproliferative neoplasms (MDS/MPNs) are rare de novo myeloid neoplasms that exhibit hybrid dysplastic and proliferative features at presentation.
  • The borderline between MDS/MPNs and overt acute myeloid leukemias was also an issue, mainly related to the accurate and consistent delineation of blast equivalents such as promonocytes.
  • Aside from juvenile myelomonocytic leukemia, genetic features defining specific MDS/MPN subtypes have not been identified.
  • Consequently, there is little change in the 2008 World Health Organization classification of MDS/MPNs compared with the 2001 version.
  • [MeSH-major] Myelodysplastic-Myeloproliferative Diseases / classification. Myelodysplastic-Myeloproliferative Diseases / diagnosis

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  • (PMID = 19605822.001).
  • [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
  • [Number-of-references] 18
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98. Yoshida Y, Oguma S, Ohno H: John Auer and Auer rods; controversies revisited. Leuk Res; 2009 May;33(5):614-6
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  • John Auer first described needle or rod-shaped intracytoplasmic inclusion bodies in leukemia cells in 1906.
  • Auer rods can be seen in myeloid neoplasms ranging from acute myeloid leukemias (AML) to myelodysplasia, but not in normal or non-neoplastic reactive states.
  • This article briefly describes John Auer's experience and discusses debates on Auer rods, and criticizes their place in the definition of refractory anemia with excess of blasts-2 (RAEB-2) in the WHO classification of the myelodysplastic syndromes (MDS).
  • [MeSH-major] Biomarkers, Tumor. Leukemia / pathology

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  • (PMID = 18947869.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Biography; Historical Article; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Personal-name-as-subject] Auer J
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99. Hyde RK, Liu PP: RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1). J Cell Biochem; 2010 Aug 1;110(5):1039-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The core binding factor (CBF) acute myeloid leukemias (AMLs) are a prognostically distinct subgroup that includes patients with the inv(16) and t(8:21) chromosomal rearrangements.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Acute Disease. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myeloid / genetics. Models, Genetic

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  • [Copyright] Published 2010 Wiley-Liss, Inc.
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  • (PMID = 20589720.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / ZIA HG000030-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [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 / RUNX1 protein, human
  • [Other-IDs] NLM/ NIHMS360619; NLM/ PMC3298446
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100. Rocquain J, Gelsi-Boyer V, Adélaïde J, Murati A, Carbuccia N, Vey N, Birnbaum D, Mozziconacci MJ, Chaffanet M: Alteration of cohesin genes in myeloid diseases. Am J Hematol; 2010 Sep;85(9):717-9
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alteration of cohesin genes in myeloid diseases.
  • We have studied by array-comparative genomic hybridization (aCGH) a series of 167 samples including myelodysplastic syndromes, chronic myelomonocytic leukemias, and acute myeloid leukemias.
  • [MeSH-major] Antigens, Nuclear / genetics. Cell Cycle Proteins / genetics. Chromosomal Proteins, Non-Histone / genetics. Gene Deletion. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Phosphoproteins / genetics

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  • (PMID = 20687102.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / Antigens, Nuclear; 0 / Cell Cycle Proteins; 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins; 0 / RAD21 protein, human; 0 / Repressor Proteins; 0 / STAG2 protein, human; 0 / TET2 protein, human; 0 / cohesins
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