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1. Jensen HA, Yourish HB, Bunaciu RP, Varner JD, Yen A: Induced myelomonocytic differentiation in leukemia cells is accompanied by noncanonical transcription factor expression. FEBS Open Bio; 2015;5:789-800
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  • [Title] Induced myelomonocytic differentiation in leukemia cells is accompanied by noncanonical transcription factor expression.
  • We investigated widely used, patient-derived myeloid leukemia cell lines with proclivity for differentiation into granulocytes by retinoic acid (RA) and/or monocytes by 1,25-dihyrdroxyvitamin D3 (D3).
  • Using K562 (FAB M1), HL60 (FAB M2), RA-resistant HL60 sublines, NB4 (FAB M3), and U937 (FAB M5), we correlated nuclear transcription factor expression to immunophenotype, G1/G0 cell cycle arrest and functional inducible oxidative metabolism.
  • Monocytic-lineage factor EGR1 was not induced by D3 (the monocytic inducer) but instead by RA (the granulocytic inducer) in lineage bipotent myeloblastic HL60.
  • In promyelocytic NB4 cells, EGR1 levels were increased by D3, while Gfi-1 expression (which promotes the granulocytic lineage) was upregulated during D3-induced monocytic differentiation in HL60, and by RA treatment in monocytic U937 cells.
  • Overall, the differentiation induction agents RA and D3 elicited cell-specific responses across these common FAB M1-M5 cell lines.

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  • (PMID = 26566473.001).
  • [ISSN] 2211-5463
  • [Journal-full-title] FEBS open bio
  • [ISO-abbreviation] FEBS Open Bio
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA033505; United States / NCI NIH HHS / CA / R01 CA152870
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ PMC4600856
  • [Keywords] NOTNLM ; AML, acute myeloid leukemia / APL, acute promyelocytic leukemia / AhR, aryl hydrocarbon receptor / C/EBPα, CCAAT-enhancer binding protein α / CD, cluster of differentiation [marker] / D3, 1,25-dihydroxyvitamin D3 / Differentiation / EGR1, early growth response protein 1 / FAB, French–American–British [myeloid leukemia classification] / Gfi-1, growth factor independent protein 1 / IRF-1, interferon regulatory factor 1 / Lineage selection / Myeloid leukemia / Oct4, octamer-binding transcription factor 4 / PU.1, binds PU-box, also called Spi-1 / RA, retinoic acid / RARα, retinoic acid receptor α / Retinoic acid / VDR, vitamin D receptor / Vitamin D3
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2. Link KA, Lin S, Shrestha M, Bowman M, Wunderlich M, Bloomfield CD, Huang G, Mulloy JC: Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation. Proc Natl Acad Sci U S A; 2016 Aug 09;113(32):9075-80
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  • Chromosomal translocation 8;21 is found in 40% of the FAB M2 subtype of acute myeloid leukemia (AML).
  • The resultant in-frame fusion protein AML1-ETO (AE) acts as an initiating oncogene for leukemia development.
  • This effect was recapitulated in the AE9a murine AML model.

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  • (PMID = 27457952.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA117846; United States / NCI NIH HHS / CA / U10 CA180861
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC4987773 [Available on 02/09/17]
  • [Keywords] NOTNLM ; AML / isoform / oncogene dosage / transformation
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3. Aurelius J, Thorén FB, Akhiani AA, Brune M, Palmqvist L, Hansson M, Hellstrand K, Martner A: Monocytic AML cells inactivate antileukemic lymphocytes: role of NADPH oxidase/gp91(phox) expression and the PARP-1/PAR pathway of apoptosis. Blood; 2012 Jun 14;119(24):5832-7
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  • [Title] Monocytic AML cells inactivate antileukemic lymphocytes: role of NADPH oxidase/gp91(phox) expression and the PARP-1/PAR pathway of apoptosis.
  • Dysfunction of T cells and natural killer (NK) cells has been proposed to determine the course of disease in acute myeloid leukemia (AML), but only limited information is available on the mechanisms of lymphocyte inhibition.
  • We aimed to evaluate to what extent human malignant AML cells use NADPH oxidase-derived reactive oxygen species (ROS) as an immune evasion strategy.
  • We report that a subset of malignant myelomonocytic and monocytic AML cells (French-American-British [FAB] classes M4 and M5, respectively), recovered from blood or BM of untreated AML patients at diagnosis, expressed the NADPH oxidase component gp91(phox).
  • Highly purified FAB M4/M5 AML cells produced large amounts of ROS on activation and triggered poly-[ADP-ribose] polymerase-1-dependent apoptosis in adjacent NK cells, CD4(+) T cells, and CD8(+) T cells.
  • In contrast, immature (FAB class M1) and myeloblastic (FAB class M2) AML cells rarely expressed gp91(phox), did not produce ROS, and did not trigger NK or T-cell apoptosis.
  • Microarray data from 207 AML patients confirmed a greater expression of gp91(phox) mRNA by FAB-M4/M5 AML cells than FAB-M1 cells (P < 10(-11)) or FAB-M2 cells (P < 10(-9)).
  • Our data are suggestive of a novel mechanism by which monocytic AML cells evade cell-mediated immunity.
  • [MeSH-major] Adenosine Diphosphate Ribose / metabolism. Apoptosis. Leukemia, Myeloid, Acute / pathology. Lymphocyte Activation / immunology. Membrane Glycoproteins / metabolism. NADPH Oxidase / metabolism. Poly(ADP-ribose) Polymerases / metabolism. T-Lymphocytes / pathology
  • [MeSH-minor] Antigens, CD14 / metabolism. Bone Marrow / pathology. Cell Differentiation / immunology. Cell Line, Tumor. Flow Cytometry. Humans. Killer Cells, Natural / immunology. Killer Cells, Natural / pathology. Monocytes / enzymology. Monocytes / immunology. Monocytes / pathology. Myeloid Cells / metabolism. Myeloid Cells / pathology. Protein Subunits / metabolism. Reactive Oxygen Species / metabolism. Signal Transduction

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  • (PMID = 22550344.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / CYBB protein, human; 0 / Membrane Glycoproteins; 0 / Protein Subunits; 0 / Reactive Oxygen Species; 20762-30-5 / Adenosine Diphosphate Ribose; EC 1.6.3.1 / NADPH Oxidase; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
  • [Other-IDs] NLM/ PMC3418695
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4. Ewerth D, Schmidts A, Hein M, Schnerch D, Kvainickas A, Greil C, Duyster J, Engelhardt M, Wäsch R: Suppression of APC/CCdh1 has subtype specific biological effects in acute myeloid leukemia. Oncotarget; 2016 Jul 26;7(30):48220-48230
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  • [Title] Suppression of APC/CCdh1 has subtype specific biological effects in acute myeloid leukemia.
  • We found a significant decrease of Cdh1 in primary acute myeloid leukemia (AML) blasts compared to normal CD34+ cells.
  • Indeed, knockdown (kd) of Cdh1 in HL-60 cell line (AML with maturation, FAB M2) led to less differentiated cells and a delay in PMA-induced differentiation.
  • Acute promyelocytic leukemia (APL, FAB M3) is an AML subtype which is highly vulnerable to differentiation therapy with all-trans retinoic acid (ATRA).
  • However, further depletion of Cdh1 in APL significantly reduced viability of leukemia cells upon ATRA-induced differentiation.
  • Thus, low Cdh1 expression may be important in AML biology by contributing to the differentiation block and response to therapy depending on differences in the microenvironment and the additional genetic background.

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  • (PMID = 27374082.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Cdh1 / acute myeloid leukemia / anaphase-promoting complex / differentiation / ubiquitin-ligase
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5. Nahajevszky S, Andrikovics H, Batai A, Adam E, Bors A, Csomor J, Gopcsa L, Koszarska M, Kozma A, Lovas N, Lueff S, Matrai Z, Meggyesi N, Sinko J, Sipos A, Varkonyi A, Fekete S, Tordai A, Masszi T: The prognostic impact of germline 46/1 haplotype of Janus kinase 2 in cytogenetically normal acute myeloid leukemia. Haematologica; 2011 Nov;96(11):1613-8
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  • [Title] The prognostic impact of germline 46/1 haplotype of Janus kinase 2 in cytogenetically normal acute myeloid leukemia.
  • BACKGROUND: Prognostic risk stratification according to acquired or inherited genetic alterations has received increasing attention in acute myeloid leukemia in recent years.
  • A germline Janus kinase 2 haplotype designated as the 46/1 haplotype has been reported to be associated with an inherited predisposition to myeloproliferative neoplasms, and also to acute myeloid leukemia with normal karyotype.
  • The aim of this study was to assess the prognostic impact of the 46/1 haplotype on disease characteristics and treatment outcome in acute myeloid leukemia.
  • DESIGN AND METHODS: Janus kinase 2 rs12343867 single nucleotide polymorphism tagging the 46/1 haplotype was genotyped by LightCycler technology applying melting curve analysis with the hybridization probe detection format in 176 patients with acute myeloid leukemia under 60 years diagnosed consecutively and treated with curative intent.
  • RESULTS: The morphological subtype of acute myeloid leukemia with maturation was less frequent among 46/1 carriers than among non-carriers (5.6% versus 17.2%, P = 0.018, cytogenetically normal subgroup: 4.3% versus 20.6%, P = 0.031), while the morphological distribution shifted towards the myelomonocytoid form in 46/1 haplotype carriers (28.1% versus 14.9%, P = 0.044, cytogenetically normal subgroup: 34.0% versus 11.8%, P = 0.035).
  • In cytogenetically normal cases of acute myeloid leukemia, the 46/1 carriers had a considerably lower remission rate (78.7% versus 94.1%, P = 0.064) and more deaths in remission or in aplasia caused by infections (46.8% versus 23.5%, P = 0.038), resulting in the 46/1 carriers having shorter disease-free survival and overall survival compared to the 46/1 non-carriers.
  • CONCLUSIONS: Janus kinase 2 46/1 haplotype influences morphological distribution, increasing the predisposition towards an acute myelomonocytoid form.
  • It may be a novel, independent unfavorable risk factor in acute myeloid leukemia with a normal karyotype.
  • [MeSH-major] Germ-Line Mutation. Janus Kinase 2 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Polymorphism, Single Nucleotide

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  • (PMID = 21791467.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ PMC3208678
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6. Lulli V, Romania P, Riccioni R, Boe A, Lo-Coco F, Testa U, Marziali G: Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation. Haematologica; 2010 Oct;95(10):1633-41
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  • [Title] Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation.
  • This study focuses on the role of Ets-1 during granulocytic differentiation of NB4 promyelocytic and HL60 myeloblastic leukemia cell lines induced by all-trans retinoic acid.
  • Expression of Ets-1 was also reduced during dimethylsulfoxide-induced differentiation and during granulocytic differentiation of human CD34(+) hematopoietic progenitor cells but not in NB4.R2 and HL60R cells resistant to all-trans retinoic acid.
  • In line with these observations, transduction of a transdominant negative molecule of Ets-1, which inhibited DNA binding and transcriptional activity of the wild-type Ets-1, significantly increased chemical-induced differentiation.
  • Interestingly, p51 Ets-1 over-expression was frequently observed in CD34(+) hematopoietic progenitor cells derived from patients with acute myeloid leukemia, as compared to its expression in normal CD34(+) cells.
  • CONCLUSIONS: Our results indicated that a decreased expression of Ets-1 protein generalizes to granulocytic differentiation and may represent a crucial event for granulocytic maturation.
  • [MeSH-minor] Cell Line, Tumor. HL-60 Cells. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Leukemia / pathology. Leukemia, Promyelocytic, Acute. RNA, Small Interfering / pharmacology


7. Lucena-Araujo AR, de Figueiredo-Pontes LL, de Oliveira FM, de Lourdes Chauffaille M, Falcao RP, Rego EM: Identification of a new translocation that disrupts the RUNX1 gene in a patient with de novo acute myeloid leukemia. Med Oncol; 2012 Jun;29(2):1114-8
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  • [Title] Identification of a new translocation that disrupts the RUNX1 gene in a patient with de novo acute myeloid leukemia.
  • Translocation (8;21)(q22;q22)/RUNX1-RUNX1T1 is a molecular marker that is usually associated with a favorable outcome in both pediatric and adult patients with acute myeloid leukemia (AML).
  • The present report describes the results of hematologic, cytogenetic, and fluorescence in situ hybridization analysis of a case of AML with maturation in a 23-year-old woman.
  • The patient was refractory to conventional and salvage chemotherapy regimens and early relapsed after unrelated donor bone marrow transplantation (BMT), dying of pneumonia, acute respiratory failure, and sepsis on day +80 after BMT, 1 year after diagnosis.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 21 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 21380778.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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8. Zhang X, Weissman SM, Newburger PE: Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells. RNA Biol; 2014;11(6):777-87
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  • [Title] Long intergenic non-coding RNA HOTAIRM1 regulates cell cycle progression during myeloid maturation in NB4 human promyelocytic leukemia cells.
  • HOTAIRM1 is a long intergenic non-coding RNA encoded in the human HOXA gene cluster, with gene expression highly specific for maturing myeloid cells.
  • Knockdown of HOTAIRM1 in the NB4 acute promyelocytic leukemia cell line retarded all-trans retinoid acid (ATRA)-induced granulocytic differentiation, resulting in a significantly larger population of immature and proliferating cells that maintained cell cycle progression from G1 to S phases.
  • Correspondingly, HOTAIRM1 knockdown resulted in retained expression of many otherwise ATRA-suppressed cell cycle and DNA replication genes, and abated ATRA induction of cell surface leukocyte activation, defense response, and other maturation-related genes.
  • The coupling of cell cycle progression with temporal dynamics in the expression patterns of these integrin genes suggests a regulated switch to control the transit from the proliferative phase to granulocytic maturation.
  • These results indicate that HOTAIRM1 provides a regulatory link in myeloid maturation by modulating integrin-controlled cell cycle progression at the gene expression level.

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  • (PMID = 24824789.001).
  • [ISSN] 1555-8584
  • [Journal-full-title] RNA biology
  • [ISO-abbreviation] RNA Biol
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK054369; United States / NIDDK NIH HHS / DK / DK054369
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11c; 0 / HOTAIR long untranslated RNA, human; 0 / RNA, Long Noncoding; 143198-26-9 / Integrin alpha4; 5688UTC01R / Tretinoin
  • [Other-IDs] NLM/ PMC4156508
  • [Keywords] NOTNLM ; HOX cluster / cell cycle / gene expression / granulocyte / integrin / long noncoding RNA / myeloid / myelopoiesis
  •  go-up   go-down


9. Schläfli AM, Isakson P, Garattini E, Simonsen A, Tschan MP: The autophagy scaffold protein ALFY is critical for the granulocytic differentiation of AML cells. Sci Rep; 2017 Oct 11;7(1):12980
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  • [Title] The autophagy scaffold protein ALFY is critical for the granulocytic differentiation of AML cells.
  • Acute myeloid leukemia (AML) is a malignancy of myeloid progenitor cells that are blocked in differentiation.
  • Acute promyelocytic leukemia (APL) is a rare form of AML, which generally presents with a t(15;17) translocation causing expression of the fusion protein PML-RARA.
  • Pharmacological doses of all-trans retinoic acid (ATRA) induce granulocytic differentiation of APL cells leading to cure rates of >80% if combined with conventional chemotherapy.
  • ATRA induces autophagy in ATRA-sensitive AML and APL cells and autophagy inhibition attenuates ATRA-triggered differentiation.
  • We found that ALFY mRNA levels increase significantly during the course of ATRA-induced differentiation of APL and AML cell lines.
  • Importantly ALFY depletion impairs ATRA-triggered granulocytic differentiation of these cells.
  • In summary, we present a crucial role for ALFY in retinoid triggered maturation of AML cells.

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  • (PMID = 29021535.001).
  • [ISSN] 2045-2322
  • [Journal-full-title] Scientific reports
  • [ISO-abbreviation] Sci Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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10. Hatta Y, Takagi N, Takei M: Lyn, a tyrosine kinase closely linked to the differentiation status of primary acute myeloid leukemia blasts, associates with negative regulation of all-trans retinoic acid (ATRA) and dihydroxyvitamin D3 (VD3)-induced HL-60 cells differentiation. Cancer Cell Int; 2016;16:37
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  • [Title] Lyn, a tyrosine kinase closely linked to the differentiation status of primary acute myeloid leukemia blasts, associates with negative regulation of all-trans retinoic acid (ATRA) and dihydroxyvitamin D3 (VD3)-induced HL-60 cells differentiation.
  • BACKGROUND: Lyn, an import member of Src family kinases (SFKs), is supposed to be implicated in acute myeloid leukemia (AML) pathogenesis and development by participation in AML differentiation, yet the details still remain incompletely understood.
  • METHODS: Primary AML blasts were obtained from 31 newly diagnosed AML patients with different French-American-British (FAB) subtypes.
  • RESULTS: Significant higher expression levels of total Lyn were observed in AML patients with favorable cytogenetics, higher MPO activity and FAB M2 subtype.
  • A clear positive correlation between the expression levels of Lyn and differentiation status of primary AML blasts was observed.
  • CONCLUSIONS: The expression level of total Lyn is closely linked to the differentiation status of AML blasts.
  • These results provide novel insights into a possible combinational therapeutic approach by targeting Lyn for AML patients, and offer new possibilities for the combination therapy with VD3 and dasatinib.

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  • (PMID = 27182202.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC4866426
  • [Keywords] NOTNLM ; Acute myeloid leukemia / All-trans retinoic acid / Dihydroxyvitamin D3 / Lyn / c-Myc / dasatinib
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