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1. Classen CF, Teigler-Schlegel A, Röttgers S, Reinhardt D, Döhner K, Debatin KM: AML bearing the translocation t(11;17)(q23;q21): involvement of MLL and a region close to RARA, with no differentiation response to retinoic acid. Ann Hematol; 2005 Nov;84(12):774-80
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  • [Title] AML bearing the translocation t(11;17)(q23;q21): involvement of MLL and a region close to RARA, with no differentiation response to retinoic acid.
  • We describe a case of acute myeloid leukemia (AML) bearing the translocation t(11;17)(q23;q21).
  • The morphological phenotype represented a monoblastic leukemia, AML French-American-British (FAB) M5a.
  • Further analysis of the translocation revealed an involvement of the mixed-lineage leukemia (MLL) gene and a region closely proximal to the retinoic acid (RA) receptor alpha (RARA) gene.
  • Rearrangements of the MLL (11q23) gene in AML are usually related to the morphological phenotype FAB M5.
  • In acute promyelocytic leukemia, the translocation (15;17)(q22;q11-21) involving the RARA leads to a maturation arrest that can be overcome by RA, often inducing remission.
  • In other forms of AML, however, the effects of RA are limited and diverse.
  • To study whether RA might have a therapeutical potential in our case, we performed an in vitro analysis of RA effects on AML cells.
  • Our data indicate that in AML cells bearing the t(11;17)(q23;q21), a differentiation arrest that is overcome by RA is not present.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic. Tretinoin / pharmacology
  • [MeSH-minor] Antigens, CD38 / biosynthesis. Cell Death / drug effects. Cell Death / genetics. Child. Drug Screening Assays, Antitumor. Female. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Leukemic / genetics. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Receptors, Retinoic Acid / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 16044313.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MLL protein, human; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5688UTC01R / Tretinoin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.2.2.5 / Antigens, CD38
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2. Klimek VM, Fircanis S, Maslak P, Guernah I, Baum M, Wu N, Panageas K, Wright JJ, Pandolfi PP, Nimer SD: Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes. Clin Cancer Res; 2008 Feb 1;14(3):826-32
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  • [Title] Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes.
  • PURPOSE: Epigenetic modulation of gene expression plays an important role in cancer, including leukemia.
  • The purpose of this study was to evaluate the toxicity, pharmacokinetic profile, and selected pharmacodynamic properties of the histone deacetylase inhibitor depsipeptide in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • EXPERIMENTAL DESIGN: Depsipeptide was administered to MDS or AML patients at a (solid tumor) phase I dose of 18 mg/m(2) i.v. on days 1 and 5 every 3 weeks.
  • RESULTS: Twelve patients (nine with AML, three with MDS) received one to five cycles of depsipeptide.
  • The best response of 11 assessed patients was one complete remission in a patient with AML, stable disease in six patients, and progression of disease in four patients.
  • Exploratory laboratory studies showed modest but rapid increases in apoptosis and changes in myeloid maturation marker expression.
  • Depsipeptide monotherapy has limited clinical activity in unselected AML/MDS patients.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Depsipeptides / pharmacokinetics. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


3. Villa O, Salido M, Pérez-Vila ME, Ferrer A, Arenillas L, Pedro C, Espinet B, Corzo C, Serrano S, Woessner S, Florensa L, Solé F: Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Aug;185(1):32-6
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  • [Title] Blast cells with nuclear extrusions in the form of micronuclei are associated with MYC amplification in acute myeloid leukemia.
  • We report three cases of acute myeloid leukemia without maturation [AML-M1 subtype according to the French-American-British classification (FAB)] with the presence of MYC oncogene amplification in form of double minutes (dmin) or homogeneously staining region (hsr).
  • [MeSH-major] Cell Nucleus / pathology. Genes, myc. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 18656691.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin
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4. Shah N, Leaker MT, Teshima I, Baruchel S, Abdelhaleem M, Ye CC: Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 May;50(5):1052-3
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  • [Title] Late-appearing Philadelphia chromosome in childhood acute myeloid leukemia.
  • A 3-year-old female was diagnosed with acute myeloid leukemia (AML-M2).
  • Cytogenetic analysis revealed a clone with trisomy 8 at diagnosis that was replaced by a clone containing a t(11;15) and del(20q) by the end of the second induction.
  • A new clone, characterized by a Philadelphia chromosome, with the minor BCR/ABL p190 transcript, emerged 14 months after diagnosis and remained to the end of disease course.
  • The late occurrence of the Philadelphia chromosome in AML has been documented rarely in adults.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Philadelphia Chromosome


5. Ghanem L, Steinman RA: p21Waf1 inhibits granulocytic differentiation of 32Dcl3 cells. Leuk Res; 2006 Oct;30(10):1285-92
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  • [Title] p21Waf1 inhibits granulocytic differentiation of 32Dcl3 cells.
  • Defining the molecular mechanisms that prevent myeloid progenitor cells from maturing is important because defects in maturation contribute to the development of myeloproliferative and myelodysplastic diseases.
  • IL-3 is an important developmental factor for myeloid progenitor cells in vivo and is required to maintain the undifferentiated state in the 32Dcl3 cell line.
  • 32Dcl3 cells are myeloid progenitor cells of murine origin with high basal levels of p21waf1/cip1 (p21) expression.
  • Our laboratory has previously reported that p21 levels decreased as CD34+-derived myeloid progenitor cells underwent terminal granulopoiesis in vitro.
  • The effect of p21 upon the expression of genes associated with granulocytic differentiation has been unexplored, however.
  • Since IL-3 maintains high levels of p21 in 32Dcl3 cells, we tested the hypothesis that p21 is an inhibitor of myeloid differentiation.
  • Rescue with human p21 in these cells suppressed premature granule protein expression. p21 knockdown was also found to accelerate morphologic granulocytic differentiation in 32Dcl3 cells stimulated with G-CSF.
  • Since high expression levels of p21 and overexpression of the IL-3 receptor have been correlated with poor outcomes in acute myeloid leukemias (AML), differentiation blockade by p21 may be one mechanism that contributes to AML pathogenesis.
  • [MeSH-minor] Animals. Base Sequence. Blotting, Northern. Cell Division / drug effects. Cell Line. Cell Survival / drug effects. DNA Primers. Gene Expression Regulation. Interleukin-3 / pharmacology. Leukemia, Myeloid, Acute / pathology. Mice. Molecular Sequence Data. Plasmids. Polymerase Chain Reaction. Transcription, Genetic

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  • (PMID = 16499966.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [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 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA Primers; 0 / Interleukin-3; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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6. Ozyurek E, Alioglu B, Coskun M, Ozbek N: Successful use of short-course high-dose methylprednisolone in a child with acute myeloblastic leukemia (FAB M2) and myeloid tumor. Leuk Lymphoma; 2006 May;47(5):923-5
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  • [Title] Successful use of short-course high-dose methylprednisolone in a child with acute myeloblastic leukemia (FAB M2) and myeloid tumor.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Methylprednisolone / therapeutic use. Sarcoma, Myeloid / drug therapy

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  • (PMID = 16753881.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] X4W7ZR7023 / Methylprednisolone
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7. Yamagata T, Maki K, Mitani K: Runx1/AML1 in normal and abnormal hematopoiesis. Int J Hematol; 2005 Jul;82(1):1-8
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  • Runx1 not only is critical for definitive hematopoiesis in the fetus but also is required for normal megakaryocytic maturation and T-lymphocyte and B-lymphocyte development in adult mice.
  • Runx1 has been identified in leukemia-associated chromosomal translocations, including t(8;21) (Runx1-ETO/MTG8), t(16;21) (Runx1-MTG16), t(3;21) (Runx1-Evi1), t(12;21) (TEL-Runx1), and t(X;21) (Runx1-Fog2).
  • However, expression of the fusion protein is not sufficient by itself to cause leukemia and likely requires additional events for leukemogenesis.
  • Point mutations in a Runx1 allele cause haploinsufficiency and a biallelic null for Runx1, which are associated with familial platelet disorder with a propensity for acute myeloid leukemia (FPD/AML) and AML-M0, respectively.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / physiology. Hematopoiesis / genetics. Hematopoiesis / physiology. Leukemia / genetics. Leukemia / physiopathology

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  • (PMID = 16105753.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
  • [Number-of-references] 81
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8. Yamagami T, Porada CD, Pardini RS, Zanjani ED, Almeida-Porada G: Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line. Cancer Biol Ther; 2009 Feb;8(4):331-7
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  • [Title] Docosahexaenoic acid induces dose dependent cell death in an early undifferentiated subtype of acute myeloid leukemia cell line.
  • Acute myeloid leukemia (AML) is the most frequently diagnosed adulthood leukemia, yet current therapies offer a cure rate of less than 30%.
  • This may be due in part to the fact that the leukemia-initiating cells in AML reside within the rare and highly primitive CD34(+)CD38(-) hematopoietic stem/progenitor cell (HSC) population that are often resistant to chemotherapy.
  • In the present studies, we investigated DHA's effect on the primitive and undifferentiated AML cell line KG1a, to explore the potential of this fatty acid to serve as adjuvant therapy for AML.
  • Treatment of KG1a cells with DHA for 96 hours did not lead to maturation or cell cycle modification when compared to an untreated KG1a control (n = 4).
  • Since we also show that DHA does not have a detrimental effect on normal hematopoiesis our results suggest that DHA could potentially serve as an well-tolerated adjuvant in the treatment of AML patients.

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  • (PMID = 19197149.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL070566; United States / NHLBI NIH HHS / HL / HL70566; United States / NHLBI NIH HHS / HL / R01 HL073737; United States / NHLBI NIH HHS / HL / HL052955-14A1; United States / NHLBI NIH HHS / HL / R01 HL052955; United States / NHLBI NIH HHS / HL / R01 HL052955-14A1; United States / NHLBI NIH HHS / HL / HL73737
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / bcl-2-Associated X Protein; 25167-62-8 / Docosahexaenoic Acids; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS122907; NLM/ PMC3954154
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9. Boyapati A, Yan M, Peterson LF, Biggs JR, Le Beau MM, Zhang DE: A leukemia fusion protein attenuates the spindle checkpoint and promotes aneuploidy. Blood; 2007 May 1;109(9):3963-71
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  • [Title] A leukemia fusion protein attenuates the spindle checkpoint and promotes aneuploidy.
  • The 8;21 chromosomal translocation occurs in 15% to 40% of patients with the FAB M2 subtype of acute myeloid leukemia (AML).
  • This chromosomal abnormality fuses part of the AML1/RUNX1 gene to the ETO/MTG8 gene and generates the AML1-ETO protein.
  • We previously identified a C-terminal truncated AML1-ETO protein (AEtr) in a mouse leukemia model.
  • AEtr is almost identical to the AML1-ETO exon 9a isoform expressed in leukemia patients.
  • Additionally, primary leukemia cells and cell lines expressing AEtr were aneuploid.
  • These results suggest that inactivation of the spindle checkpoint may contribute to the development of aneuploidy described in t(8;21) leukemia patients.

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  • (PMID = 17197431.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / U01 CA 84221; United States / NHLBI NIH HHS / HL / F32 HL079900; United States / NHLBI NIH HHS / HL / 5F32 HL 079900; United States / NCI NIH HHS / CA / R01 CA104509; United States / NCI NIH HHS / CA / CA 104509; United States / NCI NIH HHS / CA / CA 096735; United States / NCI NIH HHS / CA / R01 CA096735
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Bub1b protein, mouse; 0 / Cell Cycle Proteins; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / SPAG5 protein, human; EC 2.7.- / Protein Kinases; EC 2.7.11.1 / BUB1 protein, human; EC 2.7.11.1 / Bub1 spindle checkpoint protein; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; SH1WY3R615 / Nocodazole
  • [Other-IDs] NLM/ PMC1874577
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10. Babusíková O, Zelezníková T, Kirschnerová G, Kankuri E: Hematogones in acute leukemia during and after therapy. Leuk Lymphoma; 2008 Oct;49(10):1935-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematogones in acute leukemia during and after therapy.
  • After each leukemia therapy phase, characteristics of normal regenerating B-cells may be reminiscent of and mistaken for a relapse.
  • We compared the incidence and phenotypic characteristics of hematogone stages in a total of 669 bone marrow aspirates from 107 patients with B-ALL, 97 patients of AML, and 27 patients with T-ALL at diagnosis, during, and after therapy.
  • The three individual physiological maturation phases of B-lymphocytes (hematogone stages 1, 2, and 3) were studied by four-color flow cytometry in the course of bone marrow regeneration in leukemia patients.
  • Multiple stages of hematogones were observed twice as frequently in B-ALL (73.8%) and T-ALL (69.2%) samples as in AML aspirates (34.1%).
  • The hematogones had an extremely high phenotypic stability unaffected by disease or therapy or by their coincidence with leukemia cells.
  • [MeSH-major] B-Lymphocytes / cytology. Bone Marrow / physiology. Leukemia / immunology. Leukemia, Myeloid, Acute / immunology. Regeneration
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow Examination. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Infant. Infant, Newborn. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • [CommentIn] Leuk Lymphoma. 2009 Apr;50(4):523-4 [19373647.001]
  • (PMID = 18452085.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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11. Maha A, Cheong SK, Leong CF, Seow HF: Cell viability of acute myeloid leukaemia blasts in culture correlates with treatment outcome. Hematology; 2008 Feb;13(1):13-20
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  • [Title] Cell viability of acute myeloid leukaemia blasts in culture correlates with treatment outcome.
  • Despite the advances in understanding the pathophysiology of acute myeloid leukaemia (AML), the cure rate for acute myeloid leukaemia patients remains low.
  • However, many AML patients still die.
  • Acute myeloid leukaemia blasts demonstrated differing ability to survive in culture.
  • First, cells underwent maturation by increased expression of CD16 and down-regulated CD34 (a haemopoietic stem cell marker).
  • Thus, this study further supports the hypothesis that AML patients with poor survival may be related to having blasts with a biologically more immature or stem cell-like nature.
  • [MeSH-major] Cell Differentiation. Cell Proliferation. Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neoplastic Stem Cells / pathology

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  • (PMID = 18534060.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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12. Imataki O, Ohnishi H, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Isolated extramedullary relapse presenting as autologous lymphocyte response. Am J Hematol; 2008 Jun;83(6):512-4
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  • Isolated EMR in the CNS is a relatively rare form of recurrent leukemia.
  • We report here a case of a 38-year-old man with inv(16) acute myeloid leukemia (AML, M2) who suffered a central nervous system (CNS) relapse after allogeneic bone marrow transplantation (BMT) from a human leukocyte antigen (HLA)-matched sibling donor.
  • His leukemia relapsed in the CNS 2.5 years after the allogeneic BMT.
  • Lumbar puncture revealed 780/muL white blood cells with 67.3% leukemia cells and 32.7% mature lymphocytes.
  • Fluorescent in situ hybridization (FISH) using a probe for the Y chromosome demonstrated that both leukemia cells and lymphocytes in the cerebrospinal fluid (CSF) were derived from the recipient, although the bone marrow cells were from the donor.
  • No leukemia cells with inv(16) were detected by FISH in the bone marrow.
  • This observation suggests that the CNS is a "sanctuary" site not only from chemotherapy but also from the graft-versus-leukemia effect.
  • The present case contributes to our understanding of the possibility of immunological escape phenomenon of recurrent leukemia cells in extramedullary sites.
  • [MeSH-major] Central Nervous System Neoplasms / pathology. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adult. Bone Marrow Transplantation / methods. Humans. Male. Recurrence. Sarcoma, Myeloid. Transplantation Chimera

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  • [Copyright] Copyright 2008 Wiley-Liss, Inc.
  • (PMID = 18306363.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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13. Lee JJ, Park MS, Park JS, Kang HK, Kim SK, Nguyen Pham TN, Zhu XW, Cho D, Nam JH, Kim YJ, Rhee JH, Chung IJ, Kim HJ: Induction of leukemic-cell-specific cytotoxic T lymphocytes by autologous monocyte-derived dendritic cells presenting leukemic cell antigens. J Clin Apher; 2006 Oct;21(3):188-94
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  • We investigated the possibility of immunotherapy for AML using leukemic-cell-specific cytotoxic T lymphocytes that were stimulated in vitro by autologous DCs pulsed with tumor antigens.
  • On day 6, maturation of DCs was induced by addition of cytokine cocktail (TNF-alpha, IL-1beta, IL-6, and prostaglandin E(2)) for 2 days, and then the mature DCs were pulsed with whole leukemic cell lysates or apoptotic leukemic cells.
  • These results suggest that use of DCs pulsed with leukemic cell lysates or apoptotic leukemic cells is a feasible alternative immunotherapeutic approach to overcome the limitations of leukemic-DCs for the treatment of AML patients.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Dendritic Cells / cytology. Leukemia / immunology. Monocytes / cytology. T-Lymphocytes, Cytotoxic / cytology

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  • (PMID = 16570260.001).
  • [ISSN] 0733-2459
  • [Journal-full-title] Journal of clinical apheresis
  • [ISO-abbreviation] J Clin Apher
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 82115-62-6 / Interferon-gamma
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14. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • Conventional cytogenetic studies have shown a complex cytogenetic abnormality, notably and surprisingly, a t(8;21)(q22;q22) translocation.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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15. Leung J, Pang A, Yuen WH, Kwong YL, Tse EW: Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells. Blood; 2007 Jan 15;109(2):740-6
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  • [Title] Relationship of expression of aquaglyceroporin 9 with arsenic uptake and sensitivity in leukemia cells.
  • Arsenic trioxide (As2O3) is highly efficacious in acute promyelocytic leukemia (APL).
  • In 10 of 11 myeloid and lymphoid leukemia lines, quantitative polymerase chain reaction (Q-PCR) and Western blotting showed that AQP9 expression correlated positively with As2O3-induced cytotoxicity.
  • Similarly, the chronic myeloid leukemia line K562 expressed low levels of AQP9 and was As2O3 insensitive.
  • Pretreatment of the myeloid leukemia line HL-60 with all-trans retinoic acid (ATRA) up-regulated AQP9, leading to a significantly increased arsenic uptake and As2O3-induced cytotoxicity on incubation with As2O3, which might explain the synergism between ATRA and As2O3.
  • Q-PCR showed that primary APL cells expressed AQP9 significantly (2-3 logs) higher than other acute myeloid leukemias (AMLs), which might explain their exquisite As2O3 sensitivity.
  • However, APL and AML with maturation expressed comparable AQP9 levels, suggesting that AQP9 expression was related to granulocytic maturation.
  • [MeSH-major] Aquaporins / metabolism. Arsenicals / pharmacology. Leukemia, Myeloid / metabolism. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Oxides / pharmacology
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cell Proliferation / drug effects. Gene Expression Profiling. Humans. K562 Cells. Point Mutation. Reverse Transcriptase Polymerase Chain Reaction / methods. Sensitivity and Specificity. Tretinoin / pharmacology. Up-Regulation / drug effects

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  • (PMID = 16968895.001).
  • [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 / AQP9 protein, human; 0 / Aquaporins; 0 / Arsenicals; 0 / Oxides; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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16. Aguilera SB, Zarraga M, Rosen L: Leukemia cutis in a patient with acute myelogenous leukemia: a case report and review of the literature. Cutis; 2010 Jan;85(1):31-6
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  • [Title] Leukemia cutis in a patient with acute myelogenous leukemia: a case report and review of the literature.
  • Leukemia cutis is an infiltration of malignant neoplastic leukocytes or their precursors into the epidermis, dermis, or subcutis.
  • These neoplastic cells are derived from abnormal leukocytes in the bone marrow where maturation aberrations occur.
  • Acute myelogenous leukemia (AML) is the second most common cause of leukemia cutis and the most common leukemia among adults.
  • In the elderly population, AML presents a challenge to the medical community because of the number of preexisting comorbid conditions and the safety profile of useful chemotherapeutic agents.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Leukemic Infiltration. Skin / pathology


17. Studzinski GP, Wang X, Ji Y, Wang Q, Zhang Y, Kutner A, Harrison JS: The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway. J Steroid Biochem Mol Biol; 2005 Oct;97(1-2):47-55
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  • [Title] The rationale for deltanoids in therapy for myeloid leukemia: role of KSR-MAPK-C/EBP pathway.
  • The evidence for the promising potential for derivatives of Vitamin D (deltanoids) in the treatment of myeloid leukemias is increasing, but currently is not matched by the understanding of the precise mechanisms by which these anti-neoplastic effects are achieved.
  • Unlike solid tumors in which growth retardation by deltanoids appears to result from inhibition of cell proliferation and the promotion of cell death by apoptosis, control of myeloid leukemia proliferation by deltanoids results from the induction of differentiation of the immature myelo-monocytic cells towards functional monocytic cells.
  • We present here the accumulating evidence that a pathway that is initiated by deltanoid activation of Vitamin D receptor (VDR) and leads to monocytic differentiation of human myeloblastic HL60 cells, includes the MEK-ERK and JNK mitogen-activated protein kinases (MAPKs), their positive and negative regulators and a downstream effector C/EBPbeta.
  • Importantly, in freshly obtained acute myeloid leukemia (AML)-M2 cells exposed to PRI-2191, a novel deltanoid with a modified side chain, upregulation of C/EBPbeta paralleled the induction of monocytic differentiation.
  • These data provide a basis for the hypothesis that deltanoid-induced upregulation of C/EBPbeta bypasses the block to granulocytic differentiation in myeloid leukemia cells by redirecting the cells to monocytic differentiation.

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  • (PMID = 16046262.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA044722-15; United States / NCI NIH HHS / CA / R01 CA044722; United States / NCI NIH HHS / CA / R01 CA044722-15; United States / NCI NIH HHS / CA / R01 CA44722
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCAAT-Enhancer-Binding Protein-beta; 0 / Retinoblastoma Protein; 1406-16-2 / Vitamin D; EC 2.7.- / Protein Kinases; EC 2.7.1.- / KSR-1 protein kinase; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS169830; NLM/ PMC2814418
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18. Choi SW, Boxer LA, Pulsipher MA, Roulston D, Hutchinson RJ, Yanik GA, Cooke KR, Ferrara JL, Levine JE: Stem cell transplantation in patients with severe congenital neutropenia with evidence of leukemic transformation. Bone Marrow Transplant; 2005 Mar;35(5):473-7
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  • Severe congenital neutropenia (SCN) is a hematologic condition characterized by arrested maturation of myelopoiesis at the promyelocyte stage of development.
  • With appropriate treatment using recombinant human granulocyte-colony-stimulating factor (r-HuG-CSF), SCN patients are now surviving longer, but are at increased risk of developing myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML).
  • We report results for six patients with SCN who underwent HSCT for MDS or AML between 1997 and 2001 at two transplant centers.
  • Four patients, who all received induction chemotherapy for AML prior to HSCT, died.
  • Rapid transplantation should be the goal for the SCN patient once the diagnosis of MDS/AML is established.
  • SCN patients should be monitored carefully for progression to MDS in order to be treated with HSCT as soon as they have progressed and before developing AML.
  • For SCN patients who progress to AML, HSCT should still be considered, even though the risks appear to be greater.
  • [MeSH-major] Cell Transformation, Neoplastic. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Neutropenia / complications

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  • (PMID = 15640815.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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19. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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20. Trivedi PJ, Patel PS, Brahmbhatt MM, Patel BP, Gajjar SB, Iyer RR, Parikh EH, Shukla SN, Shah PM, Bakshi SR: A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21). Indian J Hum Genet; 2008 Jan;14(1):20-2
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  • [Title] A case of acute myeloid leukemia-M2 with trisomy 4 in addition to t(8;21).
  • t(8;21)(q22;q22) is the most frequently observed karyotypic abnormality associated with acute myeloid leukemia (AML), specifically in FAB-M2.
  • Short-term unstimulated bone marrow (BM) and peripheral blood lymphocyte culture showed 47,XX, +4,t(8;21) in all metaphase plates; and interphase and metaphase results of AML-ETO fusion was positive and trisomy of 4 was confirmed with WCP probes.
  • Trisomy 4 in AML with t(8;21) is a rare numerical abnormality.

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  • [Cites] Blood. 1986 May;67(5):1328-32 [3697508.001]
  • [Cites] Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2007 Aug;24(4):369-72 [17680522.001]
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  • (PMID = 20300287.001).
  • [ISSN] 0971-6866
  • [Journal-full-title] Indian journal of human genetics
  • [ISO-abbreviation] Indian J Hum Genet
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC2840780
  • [Keywords] NOTNLM ; Acute myeloid leukemia / cytogenetics / fluorescence in situ hybridization
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21. Wagner M, Schmelz K, Wuchter C, Ludwig WD, Dörken B, Tamm I: In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia. Int J Cancer; 2006 Sep 15;119(6):1291-7
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  • [Title] In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia.
  • To determine the expression and prognostic role of survivin in acute myeloid leukemia (AML), we investigated the mRNA expression pattern of survivin and of the splice variants survivin-2B and survivin-DeltaEx3 in adult (n = 74) and children (n = 31) with de novo AML using RT-PCR.
  • Survivin was the predominant transcript variant in AML cells, whereas significantly lower levels of survivin-2B and survivin-DeltaEx3 were observed (p < or = 0.0001).
  • Neither expression of survivin nor of any splice variant correlated with maturation stage (FAB subtypes, immunophenotype) or cytogenetic risk groups.
  • For AML cases treated according to AMLCG92 (adult) and AML-BFM93 (children) protocols, respectively, expression patterns were correlated with clinical data: in adult AML (n = 51), low expression of survivin-2B correlated with a better overall survival (p = 0.05; mean survival time 19 months vs. 9 months) and a better eventfree survival (p < or = 0.01; 27 months vs. 10 months).
  • In childhood AML (n = 31), high survivin-DeltaEx3 expression was associated with a shorter overall survival (p < or = 0.05; 24 months vs. 43 months).
  • We conclude that certain survivin splice variants have potential prognostic impact for long-term therapy outcome in adult as well as childhood de novo AML.
  • [MeSH-major] Alternative Splicing. Leukemia, Myeloid / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Apoptosis. Case-Control Studies. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Disease-Free Survival. Female. Humans. Immunophenotyping. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16619249.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / DNA, Neoplasm; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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22. Licciulli S, Cambiaghi V, Scafetta G, Gruszka AM, Alcalay M: Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation. Leukemia; 2010 Feb;24(2):429-37
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  • [Title] Pirin downregulation is a feature of AML and leads to impairment of terminal myeloid differentiation.
  • Terminal differentiation of blood cells requires the concerted action of a series of transcription factors that are expressed at specific stages of maturation and function in a cell-type and dosage-dependent manner.
  • Pirin (PIR) is a putative transcriptional regulator whose expression is silenced in cells bearing the acute myeloid leukemia-1 eight-twenty-one (AML1/ETO) and promyelocytic leukemia/retinoic acid receptor (PML/RAR) leukemogenic fusion proteins.
  • A role for PIR in myeloid differentiation has not to date been reported.
  • In this study we show that PIR expression is significantly repressed in a large proportion of acute myeloid leukemias (AMLs), regardless of subtype or underlying karyotypic abnormalities.
  • We show that PIR expression increases during in vitro myeloid differentiation of primary hematopoietic precursor cells, and that ablation of PIR in the U937 myelomonocytic cell line or in murine primary hematopoietic precursor cells results in impairment of terminal myeloid differentiation.
  • Our results suggest that PIR is required for terminal myeloid maturation, and its downregulation may contribute to the differentiation arrest associated with AML.
  • [MeSH-major] Carrier Proteins / genetics. Carrier Proteins / metabolism. Cell Differentiation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism


23. Han JS, Oh SY, Kim SH, Kwon HC, Hong SH, Han JY, Park KJ, Kim HJ: A case of pathologic splenic rupture as the initial manifestation of acute myeloid leukemia M2. Yonsei Med J; 2010 Jan;51(1):138-40
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  • [Title] A case of pathologic splenic rupture as the initial manifestation of acute myeloid leukemia M2.
  • A splenic rupture as the initial manifestation of acute myeloid leukemia is extremely rare.
  • In this study, we described a rare case of acute myeloid leukemia presenting principally as an acute abdomen due to a pathologic splenic rupture in a 35-year old male patient.
  • The oncologist should be aware of this rare initial presentation of acute myeloid leukemia (AML) M2, as the condition generally necessitates a prompt splenectomy.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Splenic Rupture / diagnosis

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  • [Cites] Cancer. 2000 Jan 15;88(2):480-90 [10640983.001]
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  • (PMID = 20046528.001).
  • [ISSN] 1976-2437
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2799964
  • [Keywords] NOTNLM ; Acute myeloid leukemia M2 / pathologic / splenic rupture
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24. Valente C, André S, Catarino A, Fradinho F, Gamboa F, Loureiro M, Fontes Baganha M: [Lymphangioleiomyomatosis - report of three cases]. Rev Port Pneumol; 2010 Jan-Feb;16(1):187-95
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  • [Transliterated title] Linfangioleiomiomatose - A propósito de três casos clínicos.
  • Pulmonary lymphangioleiomyomatosis (LAM) is a rare disease of unknown aetiology.
  • LAM may occur sporadically, in association with tuberous sclerosis complex (TSC) or inheritable multiorgan hamartomatosis.
  • In either situation, LAM occurs almost exclusively in women of reproductive age, and approximately one third of the patients with TSC have LAM2.
  • The authors review the cases of three female patients diagnosed with LAM based on clinical and radiological findings.

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  • (PMID = 20054519.001).
  • [ISSN] 2172-6825
  • [Journal-full-title] Revista portuguesa de pneumologia
  • [ISO-abbreviation] Rev Port Pneumol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Portugal
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25. Bund D, Buhmann R, Gökmen F, Kremser A, Dreyssig J, Kolb HJ, Schmetzer HM: Canine-DCs using different serum-free methods as an approach to provide an animal-model for immunotherapeutic strategies. Cell Immunol; 2010;263(1):88-98
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  • DC-quality and -quantity was determined by FACS studying the expression-profiles of DC-/costimulatory- and maturation-antigens before/after culture with canine and human monoclonal-antibodies (cmabs/hmabs).
  • AML-patients can be tested in the dog and estimated in clinical studies for DC-vaccination-strategies.

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20347071.001).
  • [ISSN] 1090-2163
  • [Journal-full-title] Cellular immunology
  • [ISO-abbreviation] Cell. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media, Serum-Free; 0 / Cytokines; 39325-01-4 / Picibanil; 56092-81-0 / Ionomycin
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26. Lewis RE, Cruse JM, Webb RN, Sanders CM, Beason K: Contrasting antigenic maturation patterns in M0-M2 versus M3 acute myeloid leukemias. Exp Mol Pathol; 2007 Oct;83(2):269-73
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  • [Title] Contrasting antigenic maturation patterns in M0-M2 versus M3 acute myeloid leukemias.
  • Acute myelogenous leukemia (AML) is divided into 8 FAB subgroups based on differentiation and maturation properties of the neoplastic cells.
  • Acute promyelocytic leukemia (APL), or M3 AML, is associated with disseminated intravascular coagulation (DIC).
  • Flow cytometric immunophenotyping differentiates among the AML subtypes.
  • Key markers in this classification include the myeloid antigens CD13 and CD33 and the hematopoietic precursor markers CD34 and HLA-DR.
  • The present study analyzes and compares differences in the expression of these markers in 27 M0-M2 cases and 8 M3 cases.
  • The M0-M2 cases generally expressed all four antigens.
  • Analysis of the M3 cases revealed a different immunophenotype as CD13 and CD33 were each positive in all 8 (100%) M3 AML cases while CD34 and HLA-DR were negative in 6 (75%) and 8 (100%) of the 8 M3 cases, respectively.
  • In contrast to expression of the early markers CD34 and HLA-DR in the M0-M2 group, these were negative in the M3 cases which were characterized by heterogeneous CD13 and generally homogeneous and bright CD33 expression.
  • [MeSH-major] Antigens, Neoplasm / analysis. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 17603036.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Neoplasm; 0 / HLA-DR Antigens
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27. Mardis ER, Ding L, Dooling DJ, Larson DE, McLellan MD, Chen K, Koboldt DC, Fulton RS, Delehaunty KD, McGrath SD, Fulton LA, Locke DP, Magrini VJ, Abbott RM, Vickery TL, Reed JS, Robinson JS, Wylie T, Smith SM, Carmichael L, Eldred JM, Harris CC, Walker J, Peck JB, Du F, Dukes AF, Sanderson GE, Brummett AM, Clark E, McMichael JF, Meyer RJ, Schindler JK, Pohl CS, Wallis JW, Shi X, Lin L, Schmidt H, Tang Y, Haipek C, Wiechert ME, Ivy JV, Kalicki J, Elliott G, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson MA, Baty J, Heath S, Shannon WD, Nagarajan R, Link DC, Walter MJ, Graubert TA, DiPersio JF, Wilson RK, Ley TJ: Recurring mutations found by sequencing an acute myeloid leukemia genome. N Engl J Med; 2009 Sep 10;361(11):1058-66
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  • [Title] Recurring mutations found by sequencing an acute myeloid leukemia genome.
  • BACKGROUND: The full complement of DNA mutations that are responsible for the pathogenesis of acute myeloid leukemia (AML) is not yet known.
  • METHODS: We used massively parallel DNA sequencing to obtain a very high level of coverage (approximately 98%) of a primary, cytogenetically normal, de novo genome for AML with minimal maturation (AML-M1) and a matched normal skin genome.
  • Four of the 64 mutations occurred in at least 1 additional AML sample in 188 samples that were tested.
  • Mutations in NRAS and NPM1 had been identified previously in patients with AML, but two other mutations had not been identified.
  • One of these mutations, in the IDH1 gene, was present in 15 of 187 additional AML genomes tested and was strongly associated with normal cytogenetic status; it was present in 13 of 80 cytogenetically normal samples (16%).
  • The other was a nongenic mutation in a genomic region with regulatory potential and conservation in higher mammals; we detected it in one additional AML tumor.
  • The AML genome that we sequenced contains approximately 750 point mutations, of which only a small fraction are likely to be relevant to pathogenesis.
  • CONCLUSIONS: By comparing the sequences of tumor and skin genomes of a patient with AML-M1, we have identified recurring mutations that may be relevant for pathogenesis.


28. Wong KF, Yuen HL, Siu LL, Pang A, Kwong YL: t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia. Hum Pathol; 2008 Nov;39(11):1702-7
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  • [Title] t(8;16)(p11;p13) predisposes to a transient but potentially recurring neonatal leukemia.
  • A Chinese girl presented with generalized papular rash and monocytic leukemia 19 days after birth.
  • Cytogenetic analysis showed t(8;16)(p11.2;p13.3) as the sole chromosomal abnormality.
  • Spontaneous regression of the leukemia was observed after 2 months, although the t(8;16) translocation persisted cytogenetically.
  • This was followed 7 months later by the development of acute myeloid leukemia with maturation and cytogenetic evolution with extra chromosomes 4 and 8.
  • Molecular study showed that the reciprocal MYST3 and CREBBP gene fusion characteristic of t(8;16) translocation persisted throughout the clinical course, even during spontaneous regression of the neonatal leukemia, and after chemotherapy-induced remission of the subsequent acute myeloid leukemia.
  • The possible role of MYST3 and CREBBP gene fusion in the pathogenesis of the leukemia is discussed.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 18657848.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CREBBP protein, human; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human
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29. Miao YQ, Chen ZX, He J, Cen JN, Bao XJ, Qiu QC, Zhang DE, Yan M: [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jan;28(1):27-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of AML1/ETO9a isoform in acute myeloid leukemia-M2 subtype].
  • OBJECTIVE: To investigate the expression of AML1/ETO9a isoform in the acute myeloid leukemia (AML)-M2 patients.
  • METHODS: Expressions of AML1/ETO fusion gene and AML1/ETO9a isoform were detected by using reverse transcriptase-polymerase chain reaction (RT-PCR) in leukemia patients, MDS patients, leukemia cell lines and healthy subjects.
  • RESULT: In 30 newly diagnosed AML-M2 patients 15 were found to express AML1/ETO9a isoform, while the rest including 20 AML-M2CR, 18 other subtypes of AML, 5 chronic myelogenous leukemia (CML), 3 myelodysplastic syndromes (MDS), 3 leukemia cell lines (NB4, KG-1, K562) and 5 healthy subjects were AML1/ETO9a negative.
  • Among the 15 AML/ETO9a isoform expressing cases, 13 were demonstrated t(8;21) translocation and AML1/ETO expression.
  • CONCLUSION: Isoform AML1/ETO9a was correlated to AML/M2, and it may promote the development of leukemia in combination with the AML1/ETO fusion gene.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 17649722.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms
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30. Tirado CA, Chena W, Valdez FJ, Henderson S, Smart RL, Doolittle J, Garcia R, Patel S, Holdridge S, Chastain C, Auchus M, Collins RH: A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation. J Assoc Genet Technol; 2009;35(3):88-92
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  • [Title] A Cryptic t(1;21;8)(p36;q22;q22) in a Case of Acute Myeloid Leukemia with Maturation.
  • The t(8;21)/RUNX1-RUNX1T1 is found in ~5 percent of cases of acute myeloid leukemia (AML) and in 10 percent of the prior AML with maturation (M2) category of the French-American-British (FAB) classification.
  • While AML with t(8;21) is considered a distinct entity with a favorable prognosis, the clinical consequence of variant translocations is less well defined.
  • In this report we described a 45 year-old male patient having a diagnosis of AML-M2 with morphologic and immunophenotypic features suggestive of t(8;21).

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  • (PMID = 19738329.001).
  • [ISSN] 1523-7834
  • [Journal-full-title] Journal of the Association of Genetic Technologists
  • [ISO-abbreviation] J Assoc Genet Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Kotru M, Batra M, Gomber S, Rusia U: Transient thrombocytosis with megathrombocytes in a case of acute myeloblastic leukemia. Indian J Pathol Microbiol; 2009 Jan-Mar;52(1):113-4
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  • [Title] Transient thrombocytosis with megathrombocytes in a case of acute myeloblastic leukemia.
  • It is rarely seen in acute leukemia.
  • A 12-year-old girl with acute myeloblastic leukemia (FAB M2) in remission presented with pyoderma.
  • This case has been presented because thrombocytosis is rare in AML and its appearance calls for a close follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / pathology. Thrombocytosis / pathology

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  • (PMID = 19136802.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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32. Obara H, Nishimura S, Hayashi N, Numagami Y, Inoue T, Kubo K, Kaimori M, Nishijima M: [Intracranial granulocytic sarcoma in a patient with acute myeloid leukemia]. No To Shinkei; 2006 Sep;58(9):797-801
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  • [Title] [Intracranial granulocytic sarcoma in a patient with acute myeloid leukemia].
  • Granulocytic sarcoma (GS) is extramedullary tumor composed of immature leukemic cells.
  • GS is presenting usually as a complication during the course of hematologic neoplasm, such as acute myeloblastic leukemia as well as myeloproliferative and myelodysplastic syndrome.
  • We report a 41-year-old man with acute leukemia type M7, who developed GS in the right occipital lobe after complete remission was achieved.
  • The majority of reported cases of GS in acute myeloid leukemia were M2 FAB classification and have chromosome translocation.
  • Our patient was M7 FAB classification, not have specific chromosome translocation.
  • GS occurrence in AML: M7 patient was extremely rare.
  • This is the first case report of AML: M7 with GS in the central nervous system.
  • [MeSH-major] Brain Neoplasms / complications. Leukemia, Myeloid, Acute / complications. Neoplasms, Multiple Primary / pathology. Occipital Lobe. Sarcoma, Myeloid / complications


33. Moore MA: Converging pathways in leukemogenesis and stem cell self-renewal. Exp Hematol; 2005 Jul;33(7):719-37
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  • Furthermore, the progression from chronic leukemia or myelodysplasia to acute leukemia involves accumulation of at least two mutational events that lead to enhancement of stem cell proliferation, or acquisition of stem cell behavior by a progenitor cell, coupled with maturation inhibition.
  • Translocations resulting in development of oncogenic fusion genes are found in AML and the transforming potential of two of these, AML1-ETO and NUP98-HOXA9, will be discussed.
  • Secondary, constitutively activating mutations of the Flt3 and c-kit receptors and of K- and N-ras are found with high frequency in AML, and the transforming potential of mutated FLT3 and the role of STAT5A activation in human stem cell transformation will be reviewed.
  • [MeSH-major] Hematopoiesis / physiology. Leukemia / physiopathology. Stem Cells / cytology. Stem Cells / physiology

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  • (PMID = 15963848.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 214
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34. Chen WL, Hsu YJ, Tsai WC, Tsao YT: An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen. J Natl Med Assoc; 2008 Aug;100(8):957-9
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  • [Title] An unusual case of febrile neutropenia: acute myeloid leukemia presenting as myeloid sarcoma of the spleen.
  • Differential diagnosis of a focal splenic lesion in the context of acute leukemia is quite challenging.
  • The results of hematological work-up were consistent with acute myeloblastic leukemia (M2, French-American-British classification).
  • Being susceptible to infection in this leukemic patient with severe neutropenia, a diagnosis of splenic abscess was straightforward, plausibly supported by the radiographic findings.
  • Histological sections from ultrasound-guided percutaneous core-needle biopsy of the spleen confirmed the diagnosis of myeloid sarcoma.
  • However, delayed leukemia-targeted therapy, unfortunately, resulted in catastrophic mortality.
  • It should be addressed that, even with the advent of modern imaging modalities, there can be a diagnostic pitfall when managing solitary splenic lesion in acute leukemic patients without histological examination.
  • [MeSH-major] Fever / etiology. Leukemia, Myeloid, Acute / diagnosis. Neutropenia / etiology. Sarcoma, Myeloid / diagnosis. Splenic Neoplasms / diagnosis
  • [MeSH-minor] Biopsy, Needle. Diagnosis, Differential. Diagnostic Errors. Fatal Outcome. Female. Humans. Middle Aged. Spleen / pathology. Tomography, X-Ray Computed


35. Peterson LF, Yan M, Zhang DE: The p21Waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO. Blood; 2007 May 15;109(10):4392-8
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  • The 8;21 translocation is a major contributor to acute myeloid leukemia (AML) of the M2 classification occurring in approximately 40% of these cases.
  • Thus, loss of p21(WAF1) facilitates AML1-ETO-induced leukemogenesis, suggesting that mutagenic events in the p21(WAF1) pathway to bypass the growth inhibitory effect from AML1-ETO-induced p21(WAF1) expression can be a significant factor in AML1-ETO-associated acute myeloid leukemia.

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  • (PMID = 17284535.001).
  • [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 / CA96735
  • [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 / AML1-ETO fusion protein, human; 0 / CDKN1A protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1885483
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36. 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).
  • 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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37. Merhi F, Auger J, Rendu F, Bauvois B: Allium compounds, dipropyl and dimethyl thiosulfinates as antiproliferative and differentiating agents of human acute myeloid leukemia cell lines. Biologics; 2008 Dec;2(4):885-95
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  • [Title] Allium compounds, dipropyl and dimethyl thiosulfinates as antiproliferative and differentiating agents of human acute myeloid leukemia cell lines.
  • Leukemia cells from patients with acute myeloid leukemia (AML) display high proliferative capacity and have a reduced capacity of undergoing apoptosis and maturation.
  • Whether the sulfur-containing molecules thiosulfinates (TS), diallyl TS (All(2)TS), dipropyl TS (Pr(2)TS) and dimethyl TS (Me(2)TS), are able to exert chemopreventative activity against AML is presently unknown.
  • The present study was an evaluation of proliferation, cytotoxicity, differentiation and secretion of AML cell lines (U937, NB4, HL-60, MonoMac-6) in response to treatment with these TS and their related sulfides (diallylsulfide, diallyl disulfide, dipropyl disulfide, dimethyl disulfide).
  • As assessed by flow cytometry, ELISA, gelatin zymogaphy and RT-PCR, we showed that Pr(2)TS and Me(2)TS, but not All(2)TS and sulfides, 1) inhibited cell proliferation in dose- and time-dependent manner and this process was neither due to cytotoxicity nor apoptosis, 2) induced macrophage maturation, and 3) inhibited the levels of secreted MMP-9 (protein and activity) and TNF-alpha protein, without altering mRNA levels.
  • By establishing for the first time that Pr(2)TS and Me(2)TS affect proliferation, differentiation and secretion of leukemic cell lines, this study provides the opportunity to explore the potential efficiency of these molecules in AML.

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  • (PMID = 19707466.001).
  • [ISSN] 1177-5475
  • [Journal-full-title] Biologics : targets & therapy
  • [ISO-abbreviation] Biologics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2727902
  • [Keywords] NOTNLM ; acute myeloid leukemia / differentiation / matrix metalloproteinase-9 / proliferation / thiosulfinate
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38. Gozzetti A, Crupi R, Rondoni M, Defina M, Bocchia M, Pietrini A, Raspadori D, Lauria F: A der(1)t(1;21)(p36.3;q22) in a patient with acute myelogenous leukemia M2. Acta Haematol; 2010;124(1):44-5
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  • [Title] A der(1)t(1;21)(p36.3;q22) in a patient with acute myelogenous leukemia M2.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20606416.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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39. Tabe Y, Konopleva M, Kondo Y, Contractor R, Jin L, Ruvolo V, Tsutsumi-Ishii Y, Miyake K, Miyake N, Ohsaka A, Nagaoka I, Issa JP, Andreeff M: PML-RARalpha and AML1-ETO translocations are rarely associated with methylation of the RARbeta2 promoter. Ann Hematol; 2006 Oct;85(10):689-704
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  • The acute promyelocytic leukemia-specific PML-RARalpha fusion protein is a dominant-negative transcriptional repressor of retinoic acid receptor (RAR) target genes, which recruits HDAC and corepressor proteins and inhibits coactivators.
  • Although DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine partially reversed RARbeta2 CpG methylation in these cells, it did not significantly enhance ATRA-induced RARbeta2 mRNA expression and induction of maturation.
  • However, the histone acetylase inhibitor SAHA combined with ATRA significantly reactivated RARbeta2 mRNA both in NB4 and MR2 cells with degradation of PML-RARalpha, which was associated with maturation.
  • In contrast, SAHA did not affect AML1-ETO levels and failed to induce RARbeta2 expression and maturation in Kasumi-1 cells.
  • In primary AML samples, RARbeta2 expression was uniformly low; however, no specific correlation was observed between the methylation of the RARbeta2 gene and expression of the fusion proteins, PML-RARalpha, and AML1-ETO.
  • These results demonstrate that oncogenic PML-RARalpha and AML1-ETO translocations are rarely associated with RARbeta2 promoter methylation in primary AML samples.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / biosynthesis. DNA Methylation. Leukemia, Promyelocytic, Acute / metabolism. Oncogene Proteins, Fusion / biosynthesis. Promoter Regions, Genetic. Receptors, Retinoic Acid / biosynthesis. Translocation, Genetic

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  • (PMID = 16832676.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / P01 CA49639; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / R01 CA89346
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / retinoic acid receptor beta; 5688UTC01R / Tretinoin; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
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40. Cleary ML: Regulating the leukaemia stem cell. Best Pract Res Clin Haematol; 2009 Dec;22(4):483-7
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  • [Title] Regulating the leukaemia stem cell.
  • Leukaemia stem cells (LSCs) are responsible for sustaining and propagating malignant disease, and, as such, are promising targets for therapy.
  • Studies of human LSCs have served an important role in defining the major tenets of the cancer stem cell model, which centre on the frequencies of cancer stem cells, their potential hierarchical organisation and their degree of maturation.
  • LSCs in acute myeloid leukaemia (AML) have recently been studied using mouse syngeneic models of leukaemia induced by MLL oncogenes.

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  • (PMID = 19959097.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116606; United States / NCI NIH HHS / CA / R01 CA055029-18; United States / NCI NIH HHS / CA / CA116606-05; United States / NCI NIH HHS / CA / R01 CA055029; United States / NCI NIH HHS / CA / CA055029-18; United States / NCI NIH HHS / CA / R01 CA116606-05
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 16
  • [Other-IDs] NLM/ NIHMS157679; NLM/ PMC2802107
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41. Satoh Y, Matsumura I, Tanaka H, Ezoe S, Fukushima K, Tokunaga M, Yasumi M, Shibayama H, Mizuki M, Era T, Okuda T, Kanakura Y: AML1/RUNX1 works as a negative regulator of c-Mpl in hematopoietic stem cells. J Biol Chem; 2008 Oct 31;283(44):30045-56
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  • Wild-type AML1 activated the c-mpl promoter through the proximal AML-binding site in luciferase assays using 293T and HeLa cells.
  • AML1dC dominant-negatively suppressed transcriptional activity of wild-type AML1.
  • Furthermore, we found that early hematopoietic cells that derived from AML1(+/-) ES cells expressed c-Mpl more intensely than those that developed from wild-type ES cells.
  • In contrast, AML1dC hardly affected c-Mpl expression and maturation of megakaryocytes.

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  • (PMID = 18687690.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Mpl protein, mouse; 0 / RUNX1 protein, human; 0 / Receptors, Thrombopoietin; 0 / Runx1 protein, mouse; 143641-95-6 / MPL protein, human
  • [Other-IDs] NLM/ PMC2662069
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42. Van Driessche A, Van de Velde AL, Nijs G, Braeckman T, Stein B, De Vries JM, Berneman ZN, Van Tendeloo VF: Clinical-grade manufacturing of autologous mature mRNA-electroporated dendritic cells and safety testing in acute myeloid leukemia patients in a phase I dose-escalation clinical trial. Cytotherapy; 2009;11(5):653-68
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  • [Title] Clinical-grade manufacturing of autologous mature mRNA-electroporated dendritic cells and safety testing in acute myeloid leukemia patients in a phase I dose-escalation clinical trial.
  • We report on a phase I dose-escalation trial using clinical-grade manufactured mature RNA-electroporated DC in acute myeloid leukemia (AML) patients.
  • To test product safety, increasing doses of DC were administered intradermally four times at 2-week intervals in 10 AML patients.
  • We also validated a simplified DC maturation protocol yielding a consistent phenotype, migration and allogeneic T-cell stimulatory capacity in AML patients in remission.
  • Despite a decreased cell recovery of mDC after a combination of mRNA electroporation and cryopreservation, successful vaccine preparations were obtained in all AML patients.
  • Intradermal injection of such DC vaccines in AML patients is safe.
  • [MeSH-major] Dendritic Cells / cytology. Electroporation. Immunotherapy, Adoptive / adverse effects. Immunotherapy, Adoptive / methods. Leukemia, Myeloid, Acute / therapy


43. Martino V, Bianchera A, Reia L, Bussolati O, Fazzina R, Marino F, Montemurro L, Tonelli R, Pession A, Gazzola GC, Sala R: Down-regulation of HOXA4, HOXA7, HOXA10, HOXA11 and MEIS1 during monocyte-macrophage differentiation in THP-1 cells. Mol Med Rep; 2009 Mar-Apr;2(2):241-4
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  • The translocation t(9;11)(p22;q23) generates the MLL-AF9 oncogene and is commonly associated with monocytic acute myeloid leukemia (AML-M5; FAB-classification).
  • We previously showed that the down-regulation of MLL-AF9 expression is not obligatory for monocyte-macrophage maturation in AML-M5 cells carrying t(9;11)(p22;q23).

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  • (PMID = 21475819.001).
  • [ISSN] 1791-2997
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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44. Saudemont A, Corm S, Wickham T, Hetuin D, Quesnel B: Induction of leukemia-specific CD8+ cytotoxic T cells with autologous myeloid leukemic cells maturated with a fiber-modified adenovirus encoding TNF-alpha. Mol Ther; 2005 Jun;11(6):950-9
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  • [Title] Induction of leukemia-specific CD8+ cytotoxic T cells with autologous myeloid leukemic cells maturated with a fiber-modified adenovirus encoding TNF-alpha.
  • Acute myeloid leukemia (AML) cells can be differentiated into dendritic cells (DCs) using appropriate combinations of cytokines but generation of autologous antileukemic cytotoxic T cells using leukemic DCs remains difficult.
  • Transduction by adenoviral vectors has been reported to induce efficient maturation of monocyte-derived DCs but AML cells are generally resistant to adenoviral gene transfer.
  • In this study we tested the effects of adenoviral TNF-alpha gene transfer on maturation of AML cells using the fiber-modified AdTNF.F(pK7) adenovirus.
  • AdTNF.F(pK7) induced significantly greater maturation of AML cells into antigen-presenting cells (APC) than did recombinant TNF-alpha or control adenoviral vector.
  • Maturation of leukemic cells into APCs was mediated at least partially via a PI3K/mTOR pathway, as the inhibitors LY294002, wortmannin, and rapamycin inhibited the maturation effect induced by the AdTNF.F(pK7) adenovirus.
  • In addition, CD8+ T cells expanded with AdTNF.F(pK7)-transduced AML cells showed greater expansion and specific CD8+ CTL activity against autologous AML cells than T cells expanded by other means.
  • Thus, fiber-modified adenoviral vectors encoding TNF-alpha are able to maturate AML cells into APCs with high efficacy and reproducibility, providing a useful tool to generate efficiently specific CD8+ CTLs against leukemic disease.
  • [MeSH-major] Adenoviridae / genetics. Cytotoxicity, Immunologic / immunology. Leukemia, Myeloid / immunology. T-Lymphocytes, Cytotoxic / immunology. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Acute Disease. Antigen-Presenting Cells / immunology. Capsid Proteins / genetics. Cell Differentiation. Coculture Techniques. Humans. Phenotype. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / physiology. Protein Kinase Inhibitors / pharmacology. Protein Kinases / physiology. Signal Transduction. TOR Serine-Threonine Kinases. Transduction, Genetic

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  • (PMID = 15922966.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / Protein Kinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 0 / hexon capsid protein, Adenovirus; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
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45. Wald DN, Vermaat HM, Zang S, Lavik A, Kang Z, Peleg G, Gerson SL, Bunting KD, Agarwal ML, Roth BL, Tse W: Identification of 6-benzylthioinosine as a myeloid leukemia differentiation-inducing compound. Cancer Res; 2008 Jun 1;68(11):4369-76
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  • [Title] Identification of 6-benzylthioinosine as a myeloid leukemia differentiation-inducing compound.
  • As the pathophysiology of acute myelogenous leukemia (AML) involves a block of myeloid maturation, a desirable therapeutic strategy is to induce leukemic cell maturation to increase the efficacy and to avoid the side effects of traditional chemotherapeutics.
  • 6BT induces monocytic differentiation of myeloid leukemia cell lines such as HL-60 and OCI-AML3, as well as primary patient samples as evidenced by morphology, immunophenotyping, and nitroblue tetrazolium reduction.
  • Not only can 6BT induce differentiation but a subset of AML cell lines such as MV4-11 and HNT34 instead undergo 6BT-mediated cell death.
  • 6BT is also able to synergize with currently used myeloid differentiation agents such as ATRA and decitabine.

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  • (PMID = 18519698.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA076917; United States / NCI NIH HHS / CA / P30 CA043703; United States / NCI NIH HHS / CA / R01 CA098916; United States / NCI NIH HHS / CA / CA98916
  • [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 / 6-benzylthioinosine; 0 / DNA Primers; 46S541971T / Thioinosine
  • [Other-IDs] NLM/ NIHMS502107; NLM/ PMC3896053
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46. Zhu YL, Zhang Y, Zhu P, Yang Y, Du JW, Liu J: [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia]. Beijing Da Xue Xue Bao; 2005 Jun 18;37(3):236-9
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  • [Title] [Role of molecular screening for common fusion genes in the diagnosis and classification of leukemia].
  • OBJECTIVE: To assess the value of common fusion genes analysis in the diagnosis and classification of leukemia by multiplex RT-PCR.
  • METHODS: The multiplex RT-PCR, including 8 parallel PCR reactions, could screen 86 mRNA breakpoints or splice variants at the same time, which was important for the diagnosis and prognosis of leukemia.
  • Bone marrow samples from 161 cases of leukemia and 8 cases of myelodysplastic syndrome (MDS) were involved in the study.
  • The distribution of common fusion genes in leukemia was analyzed by the method mentioned above in combination with clinical and morphological features.
  • RESULTS: Ten fusion genes were detected in 115 cases of leukemia, including AML1/ETO, PML/RAR alpha, PLZF/RAR alpha, dupMLL, MLL/AF6, MLL/AF10, CBFbeta/MYH11, BCR/ABL, Hox11, and EVI1 BCR/ABL was positive in all the 52 cases of chronic myeloid leukemia; PML/RAR alpha was found in 21 of 25 acute promyelocytic leukemia (APL), and PLZF/RAR alpha was detected in one case of APL.
  • Sixteen cases of 17 AML1/ETO-positive acute leukemia (AL) belonged to FAB-M2 subtype, and one case was mixed leukemia.
  • Furthermore, BCR/ABL was detected in 5 acute lymphoblastic leukemia (ALL) cases.
  • Fusion genes were also found in 2 MDS cases, of which AML1/ETO positive-MDS-RAEB progressed to AML rapidly.
  • CONCLUSION: Screening of common fusion genes by multiplex RT-PCR is an important tool which could provide useful and reliable molecular genetic information for the diagnosis and treatment of leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 15968309.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [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; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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47. Orelio C, Verkuijlen P, Geissler J, van den Berg TK, Kuijpers TW: SBDS expression and localization at the mitotic spindle in human myeloid progenitors. PLoS One; 2009;4(9):e7084
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  • [Title] SBDS expression and localization at the mitotic spindle in human myeloid progenitors.
  • The hematologic abnormalities include neutropenia, neutrophil chemotaxis defects, and an increased risk of developing Acute Myeloid Leukemia (AML).
  • Although several studies have suggested that SBDS as a protein plays a role in ribosome processing/maturation, its impact on human neutrophil development and function remains to be clarified.
  • METHODOLOGY/PRINCIPAL FINDINGS: We observed that SBDS RNA and protein are expressed in the human myeloid leukemia PLB-985 cell line and in human hematopoietic progenitor cells by quantitative RT-PCR and Western blot analysis.
  • Thus, the increased risk of myeloid malignancy in SDS remains unexplained.
  • [MeSH-major] Hematologic Diseases / metabolism. Leukemia, Myeloid, Acute / metabolism. Proteins / metabolism. Spindle Apparatus / metabolism


48. Lu G, Yin CC, Medeiros LJ, Abruzzo LV: Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature. Cancer Genet Cytogenet; 2009 Jan 15;188(2):118-23
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  • [Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.
  • Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).
  • We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).
  • Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).
  • The deletion was identified at initial diagnosis in one patient and at relapse in the other two.
  • Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.
  • The prognosis is poor, with survival similar to other AML cases with unfavorable cytogenetic changes.
  • [MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

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  • (PMID = 19100517.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 20
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49. Haferlach T, Kohlmann A, Schnittger S, Dugas M, Hiddemann W, Kern W, Schoch C: AML M3 and AML M3 variant each have a distinct gene expression signature but also share patterns different from other genetically defined AML subtypes. Genes Chromosomes Cancer; 2005 Jun;43(2):113-27
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  • [Title] AML M3 and AML M3 variant each have a distinct gene expression signature but also share patterns different from other genetically defined AML subtypes.
  • Acute promyelocytic leukemia (APL) with t(15;17) appears in two phenotypes: AML M3, with abnormal promyelocytes showing heavy granulation and bundles of Auer rods, and AML M3 variant (M3v), with non- or hypogranular cytoplasm and a bilobed nucleus.
  • We investigated the global gene expression profiles of 35 APL patients (19 AML M3, 16 AML M3v) by using high-density DNA-oligonucleotide microarrays.
  • Furthermore, a supervised pairwise comparison between M3 and M3v revealed differential expression of genes that encode for biological functions and pathways such as granulation and maturation of hematologic cells, explaining morphologic and clinical differences.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Promyelocytic, Acute / genetics

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15751046.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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50. Malaise M, Steinbach D, Corbacioglu S: Clinical implications of c-Kit mutations in acute myelogenous leukemia. Curr Hematol Malig Rep; 2009 Apr;4(2):77-82
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  • [Title] Clinical implications of c-Kit mutations in acute myelogenous leukemia.
  • This finding culminated in a two-class model integrating constitutive activating and maturation arrest-inducing mutations as key elements for the pathogenesis of acute myelogenous leukemia (AML).
  • c-Kit is expressed by myeloblasts in about 60% to 80% of patients, and the most frequently observed activating RTK mutations in AML (next to FLT3) are mutations or internal tandem duplications in c-Kit, with an overall incidence of 17%.
  • The identification of small-molecule tyrosine kinase inhibitors capable of blocking key kinase switches introduced a paradigm change in the treatment of diseases like gastrointestinal stromal tumors and chronic myelogenous leukemia.
  • Despite encouraging preclinical data, it appears that a complex clonal disease like AML will probably benefit from a synergistic approach of targeted drugs used (at least for now) in combination with conventional chemotherapy.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Gene Expression Regulation, Leukemic. Humans. Prognosis. Protein Kinase Inhibitors / administration & dosage. Protein Kinase Inhibitors / therapeutic use. Treatment Outcome


51. Nitta M, Hoshi A, Shinozaki T, Soeda S, Kawakami M, Kin H, Nakajima N, Hanai K, Kato S, Nomoto T, Usui Y, Terachi T: [Granulocytic sarcoma of the prostate]. Hinyokika Kiyo; 2010 Sep;56(9):521-5
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  • [Title] [Granulocytic sarcoma of the prostate].
  • Histological examination revealed leukemia-like cells, and bone-marrow examination (aspiration) was performed to determine the location of the original lesion.
  • However, no leukemia-like cells or any other form of malignant cells were identified.
  • Clinical imaging confirmed the absence of any other lesions, and granulocytic sarcoma of the prostate was subsequently diagnosed.
  • Four months after initial presentation, the patient developed acute myeloid leukemia [M2 by French-American-British classification].
  • [MeSH-major] Prostatic Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Aged. Humans. Leukemia, Myeloid, Acute / etiology. Male

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  • (PMID = 20940529.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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52. Putz G, Rosner A, Nuesslein I, Schmitz N, Buchholz F: AML1 deletion in adult mice causes splenomegaly and lymphomas. Oncogene; 2006 Feb 9;25(6):929-39
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  • AML1 is one of the most frequently mutated genes associated with human acute leukemia, suggesting that genetic alterations of the gene contribute to leukemogenesis.
  • AML1 was deleted in adult mice by inducing Cre activity to replicate AML1 deletions found in human MDS, familial platelet disorder and rare de novo human AML.
  • At a latency of 2 months after induction, the thymus was reduced in size and frequently populated by immature double negative thymocytes, indicating defective T-lymphocyte maturation, resulting in lymphatic diseases with 50% penetrance, including atypical hyperplasia and thymic lymphoma.
  • Mice also developed splenomegaly with an expansion of the myeloid compartment.


53. Dupret C, Asnafi V, Leboeuf D, Millien C, Ben Abdelali R, Preudhomme C, Beldjord K, Delabesse E, Macintyre E: IgH/TCR rearrangements are common in MLL translocated adult AML and suggest an early T/myeloid or B/myeloid maturation arrest, which correlates with the MLL partner. Leukemia; 2005 Dec;19(12):2337-8
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  • [Title] IgH/TCR rearrangements are common in MLL translocated adult AML and suggest an early T/myeloid or B/myeloid maturation arrest, which correlates with the MLL partner.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. B-Lymphocytes / pathology. Gene Rearrangement. Genes, T-Cell Receptor. Humans. Immunoglobulin Heavy Chains / genetics. Myeloid Cells / pathology. T-Lymphocytes / pathology

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  • (PMID = 16304577.001).
  • [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
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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54. Altucci L, Rossin A, Hirsch O, Nebbioso A, Vitoux D, Wilhelm E, Guidez F, De Simone M, Schiavone EM, Grimwade D, Zelent A, de Thé H, Gronemeyer H: Rexinoid-triggered differentiation and tumor-selective apoptosis of acute myeloid leukemia by protein kinase A-mediated desubordination of retinoid X receptor. Cancer Res; 2005 Oct 1;65(19):8754-65
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  • [Title] Rexinoid-triggered differentiation and tumor-selective apoptosis of acute myeloid leukemia by protein kinase A-mediated desubordination of retinoid X receptor.
  • Apart from PML-retinoic acid receptor-alpha (RARalpha) acute promyelocytic leukemia all other acute myeloid leukemias (AML) are unresponsive to retinoid differentiation therapy.
  • However, elevating the levels of cyclic AMP (cAMP) confers onto retinoid X receptor (RXR)-selective agonists ("rexinoids") the ability to induce terminal granulocyte differentiation and apoptosis of all-trans retinoic acid-resistant and insensitive AML cells and patients' blasts.
  • Immunohistochemistry confirmed induction of tumor necrosis factor-related apoptosis inducing ligand and DR5 in AML patient blasts cultured ex vivo.
  • AML patients' blasts responded to rexinoid-cAMP combination treatment with induction of maturation and apoptosis, independent of karyotype, immunophenotype, and French-American-British classification status.
  • Our results suggest that despite the genetic, morphologic, and clinical variability of this disease, the combination of rexinoids and cAMP-elevating drugs, such as phosphodiesterase inhibitors, might lead to a novel therapeutic option for AML patients by inducing a tumor-selective death pathway.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Phosphodiesterase Inhibitors / pharmacology. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors / agonists
  • [MeSH-minor] Acute Disease. Animals. Apoptosis / drug effects. Cell Differentiation / drug effects. Drug Synergism. HL-60 Cells. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Mice. Receptor Cross-Talk. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / physiology. U937 Cells

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  • (PMID = 16204045.001).
  • [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 / Phosphodiesterase Inhibitors; 0 / Receptors, Retinoic Acid; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Retinoid X Receptors; 0 / TNFRSF10B protein, human; 0 / Tnfrsf10b protein, mouse; 0 / retinoic acid receptor alpha; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
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55. Udayakumar AM, Pathare AV, Al-Kindi S, Khan H, Rehmen JU, Zia F, Al-Ghazaly A, Nusrut N, Khan MI, Wali YA, Al-Lamki Z, Dennison D, Raeburn JA: Cytogenetic, morphological, and immunophenotypic patterns in Omani patients with de novo acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Sep;177(2):89-94
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  • [Title] Cytogenetic, morphological, and immunophenotypic patterns in Omani patients with de novo acute myeloid leukemia.
  • Chromosome aberrations observed at diagnosis are considered to be the most valuable prognostic factors in acute myeloid leukemia (AML).
  • There are only limited studies on the role of such variability in AML patients.
  • Here, we report the results of a cytogenetic study on 63 ethnic Omani patients with de novo AML: 18 children (<or=16 years) and 45 adults.
  • By sex, 41 were male and 22 female; median age at diagnosis was 25 years.
  • The morphological diagnosis was based on the French-American-British (FAB) WHO criteria.
  • Karyotypes with a sole abnormality accounted for 20 of 63 patients (32%).
  • Chromosome abnormalities were more common in patients with the FAB-M2 subtype (15 of 22; 68%), which was also the most frequent subtype observed (22 of 63; 35%).
  • Among the normal karyotypes (24 of 63; 38%), M2 subtype was the also most frequent (7 of 24; 29%), followed by M4 (4 of 24; 17%).
  • Our population differed morphologically, with the M2 subtype as most common, whereas M4 and M3 were more commonly in those reports.
  • [MeSH-major] Antigens, CD / metabolism. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Aberrations. Chromosomes, Human / ultrastructure. Ethnic Groups / genetics. Female. Fluorescent Antibody Technique. Humans. Immunophenotyping. Infant. Karyotyping. Male. Middle Aged. Oman / ethnology

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  • (PMID = 17854660.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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56. Abdul-Nabi AM, Yassin ER, Varghese N, Deshmukh H, Yaseen NR: In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML. PLoS One; 2010 Aug 27;5(8):e12464
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  • [Title] In vitro transformation of primary human CD34+ cells by AML fusion oncogenes: early gene expression profiling reveals possible drug target in AML.
  • Different fusion oncogenes in acute myeloid leukemia (AML) have distinct clinical and laboratory features suggesting different modes of malignant transformation.
  • Here we compare the in vitro effects of representatives of 4 major groups of AML fusion oncogenes on primary human CD34+ cells.
  • They both caused erythroid hyperplasia and a clear block in erythroid and myeloid maturation.
  • On the other hand, AML1-ETO and PML-RARA had only modest effects on myeloid and erythroid differentiation.
  • These data show that differences among AML fusion oncogenes can be recapitulated in vitro using primary human CD34+ cells and that early gene expression profiling in these cells can reveal potential drug targets in AML.

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  • (PMID = 20805992.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL082549; United States / NCI NIH HHS / CA / T32CA009547; United States / NCI NIH HHS / CA / T32 CA009547; United States / NHLBI NIH HHS / HL / K02 HL084179; United States / NCI NIH HHS / CA / P30 CA091842; United States / NCI NIH HHS / CA / P30CA91842; United States / NHLBI NIH HHS / HL / R01HL082549; United States / NHLBI NIH HHS / HL / K02HL084179
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
  • [Other-IDs] NLM/ PMC2929205
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57. Khalil SH: Molecular hematology. Qualitative to quantitative techniques. Saudi Med J; 2005 Oct;26(10):1516-22
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  • The Section of Hematology, Department of Pathology and Laboratory Medicine at King Faisal Specialist Hospital and Research Center has shared this experience during the last 10 years with more than 6,546 samples submitted for the analysis of different gene rearrangements, fusion gene transcripts and gene mutations including Ig heavy chain gene rearrangement for B-cell malignancies, T-cell receptor gamma chain gene rearrangement for T-cell malignancies, BCR/ABL-P210 and P190 fusion gene transcripts, for chronic myeloid leukemia and Philadelphia positive acute lymphoblastic leukemia, PML/RARalpha fusion gene for promyelocytic leukemia, AML1/ETO for acute myeloid leukemia AML-M2 with t8;21, CBFB/MYH11 for AML M4E0 with inv 16, BCL-2 for follicular lymphoma, and BCL-1 for mantle cell lymphoma.
  • Hence, most molecular assays are qualitative in nature, quantitative assays are deemed necessary in the monitoring and follow-up of minimal residual disease in leukemia and lymphoma, and proved in our experience to serve as an essential tool to confirm complete remission CR post-chemotherapy and bone marrow transplantation, and to detect signs of early relapse for proper clinical intervention.
  • [MeSH-major] Hematologic Neoplasms / diagnosis. Molecular Biology / methods

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  • (PMID = 16228048.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Saudi Arabia
  • [Number-of-references] 36
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58. Gilles L, Guièze R, Bluteau D, Cordette-Lagarde V, Lacout C, Favier R, Larbret F, Debili N, Vainchenker W, Raslova H: P19INK4D links endomitotic arrest and megakaryocyte maturation and is regulated by AML-1. Blood; 2008 Apr 15;111(8):4081-91
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  • [Title] P19INK4D links endomitotic arrest and megakaryocyte maturation and is regulated by AML-1.
  • Chromatin immunoprecipitation assays performed in human MKs revealed that AML-1 binds in vivo the p19(INK4D) promoter.
  • Moreover, AML-1 inhibition led to the p19(INK4D) down-regulation in human MKs.

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  • (PMID = 18276842.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Platelet Glycoprotein GPIb-IX Complex; 0 / Platelet Membrane Glycoprotein IIb
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59. Thomas X, Elhamri M: [Farnesyltransferase inhibitors: preliminary results in acute myeloid leukemia]. Bull Cancer; 2005 Mar;92(3):227-38
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  • [Title] [Farnesyltransferase inhibitors: preliminary results in acute myeloid leukemia].
  • [Transliterated title] Inhibiteurs de farnésyl transférase: résultats cliniques dans la leucémie aiguë myéloïde.
  • Acute myeloid leukemias (AMLs) are appropriate disease targets in that they express relevant biologic targets such as Ras, MEK, AKT, and others that may depend upon farnesyl protein transferase activity to promote cell proliferation and survival.
  • Interruption of prenylation may prevent substrates from undergoing maturation which may result in the inhibition of cellular events that depend on the function of those substrates.
  • Phase I trials in AML and myelodysplasia have demonstrated biologic and clinical activities as determined by target enzyme inhibition, low toxicity, and both complete and partial responses.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myeloproliferative Disorders / drug therapy

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  • (PMID = 15820917.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / 7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / L 778,123; 0 / Piperidines; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / Quinolones; 12794-10-4 / Benzodiazepines; 192185-72-1 / tipifarnib; 193275-84-2 / lonafarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 3.6.5.2 / ras Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Number-of-references] 111
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60. Houtenbos I, Santegoets S, Westers TM, Waisfisz Q, Kipriyanov S, Denkers F, Scheper RJ, de Gruijl TD, Ossenkoppele GJ, van de Loosdrecht AA: The novel bispecific diabody alphaCD40/alphaCD28 strengthens leukaemic dendritic cell-induced T-cell reactivity. Br J Haematol; 2008 Jun;142(2):273-83
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  • We have recently shown the feasibility of generating fully functional DC from acute myeloid leukaemic (AML) blasts, but with varying expression levels of the important costimulatory molecule CD86.
  • To overcome this variability, we developed a novel bispecific diabody that simultaneously and agonistically targeted CD40 on AML-DC and CD28 on naïve T cells.
  • Beside optimization of CD28-mediated signalling, the resulting cellular cross-linking was also hypothesized to increase the strength and duration of T cell/AML-DC interactions, thus increasing T-cell responsiveness to AML antigens.
  • The alphaCD40/alphaCD28 diabody is capable of increasing T-cell proliferation induced by AML-DC as well as the induction of DC maturation.
  • Importantly, priming efficacy of tumour-specific cytotoxic T cells can also be improved by cross-linking AML-DC and T cells with the alphaCD40/alphaCD28 diabody.
  • We propose that the alphaCD40/alphaCD28-bispecific diabody can serve as a potent therapeutic tool to effectively augment anti-tumour T-cell responses elicited by AML-DC.
  • [MeSH-major] Antibodies, Bispecific / therapeutic use. Antigens, CD28 / immunology. Antigens, CD40 / immunology. Antigens, Neoplasm / immunology. Cancer Vaccines / immunology. Immunotherapy / methods. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 18492117.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antigens, CD28; 0 / Antigens, CD40; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines
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61. Pinel S, Barbault-Foucher S, Lott-Desroches MC, Astier A: [Inhibitors of aurora kinases]. Ann Pharm Fr; 2009 Mar;67(2):69-77
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  • They regulate the maturation of centrosomes, the separation and the condensation of chromosomes, mitotic checkpoint and cytokinesis.
  • The main indications are breast, colon, lung, pancreas and bladder cancers as well as hematologic tumors such as leukemia (ALL, AML, CML) and lymphoma.

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  • (PMID = 19298889.001).
  • [ISSN] 0003-4509
  • [Journal-full-title] Annales pharmaceutiques françaises
  • [ISO-abbreviation] Ann Pharm Fr
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Number-of-references] 56
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62. Klobusicka M, Kusenda J, Babusikova O: Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis. Neoplasma; 2005;52(3):211-8
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  • [Title] Myeloid enzymes profile related to the immunophenotypic characteristics of blast cells from patients with acute myeloid leukemia (AML) at diagnosis.
  • The purpose of this study was to assess the possible relationship between the cytochemical enzyme profile and immunophenotypic characteristics of distinct acute myeloid leukemia (AML) subtypes in discrete stages of leukemic cells maturation.
  • The immunophenotype was examined for the maturation dependent myeloid antigens CD13, CD33, CD11b, CD14, CD15, CD65, CD36, cytoplasmic MPO, non-lineage associated CD34 and HLA-DR antigens, lymphoid- associated antigens CD7, CD4, CD38 as well as natural killer cell associated marker CD56.
  • Flow cytometry by double marker staining and visualization of pathologic cells in dot plots reflected immunophenotypic aberrancy and degree of cell maturation.
  • The patients were classified into AML subtypes M0- M2, M3, M4 and M5 according to the main morphological, cytochemical and immunophenotypical features.
  • The cytochemical profile of blasts was in concordance with immunophenotype, particularly in more differentiated AML subtypes, M3, M4 and M5.
  • The findings of myeloid antigens expression and cytochemical features in poorly differentiated AML subtypes showed no practical relevance of cytochemical analysis.
  • Notwithstanding that the cytochemical analysis of AML subtypes not sufficiently identifies the distinct aberrancies in heterogeneous leukemic blast cell populations, evaluation of the cytochemical profile in connection with immunophenotyping may help to classify the AML patients to relevant subtypes with more accuracy.
  • [MeSH-major] Granulocyte Precursor Cells / enzymology. Immunophenotyping. Leukemia, Myeloid / classification. Leukemia, Myeloid / enzymology
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Azo Compounds. Carboxylic Ester Hydrolases / analysis. Child. Female. HLA-DR Antigens / analysis. Humans. Male. Naphthalenes. Peroxidase / analysis

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  • (PMID = 15875082.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Azo Compounds; 0 / HLA-DR Antigens; 0 / Naphthalenes; 9YDL1Q990E / Sudan Black B; EC 1.11.1.7 / Peroxidase; EC 3.1.1.- / Carboxylic Ester Hydrolases; EC 3.1.1.- / naphthylbutyrate esterase
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63. Choi Y, Elagib KE, Goldfarb AN: AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein. Crit Rev Eukaryot Gene Expr; 2005;15(3):207-16
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  • [Title] AML-1-ETO-Mediated erythroid inhibition: new paradigms for differentiation blockade by a leukemic fusion protein.
  • The chromosomal translocation t(8;21), generating the AML1-ETO fusion protein, is frequently associated with French-American-British (FAB) type M2 acute myeloid leukemia (AML).
  • Several mechanistic models for the role of AML1-ETO in leukemia development have emerged over the last decade.
  • Most of these models have emphasized the capacity of the fusion protein to redirect repressive cofactors, such as histone deacetylases (HDACs) and DNA methyltransferases (DNMTs), to RUNX target genes, thereby reversing the hematopoietic transcriptional program activated by wild-type RUNX1a phenomenon referred to collectively in this review as the "classical" corepressor model.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Animals. Cell Differentiation / genetics. Cells, Cultured. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Erythropoiesis / genetics. GATA1 Transcription Factor / physiology. Histone Deacetylases / genetics. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Signal Transduction / genetics. Translocation, Genetic

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  • (PMID = 16390317.001).
  • [ISSN] 1045-4403
  • [Journal-full-title] Critical reviews in eukaryotic gene expression
  • [ISO-abbreviation] Crit. Rev. Eukaryot. Gene Expr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Core Binding Factor Alpha 2 Subunit; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins, Fusion; EC 3.5.1.98 / Histone Deacetylases
  • [Number-of-references] 58
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64. Bacher U, Schnittger S, Kern W, Trenn G, Weisser M, Haferlach T, Schoch C: Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22). Cancer Genet Cytogenet; 2006 Jul 15;168(2):172-4
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  • [Title] Acute myeloid leukemia (AML) with t(8;21)(q22;q22) relapsing as AML with t(3;21)(q26;q22).
  • We here report on an 48-year-old male patient with a primary diagnosis of acute myeloid leukemia (AML)-M2 with t(8;21)(q22;q22), who developed complete hematologic and molecular remission after induction chemotherapy.
  • Thirteen months later, he relapsed and showed an AML-M2 with t(3;21)(q26;q22).
  • Retrospectively, polymerase chain reaction (PCR) for AML1-EVI1 and EVI1 overexpression was performed on bone marrow and peripheral blood samples taken at diagnosis and during the first year after the first manifestation of AML to quantify the AML1-EVI1-positive clone.
  • In a bone marrow sample taken 25 days from diagnosis, PCR for AML1-EVI1 was negative, and EVI1 expression, as assessed by quantitative real-time PCR, was within the same range as that of healthy controls.
  • These data suggest that this patient developed a secondary therapy-related AML rather than a relapse.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843110.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors
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65. Jiao B, Wu CF, Liang Y, Chen HM, Xiong SM, Chen B, Shi JY, Wang YY, Wang JH, Chen Y, Li JM, Gu LJ, Tang JY, Shen ZX, Gu BW, Zhao WL, Chen Z, Chen SJ: AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2. Leukemia; 2009 Sep;23(9):1598-604
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  • [Title] AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) acute myeloid leukemia-M2.
  • AML1-ETO fusion gene is generated from chromosomal translocation t(8;21) mainly in acute myeloid leukemia M2 subtype (AML-M2).
  • Its spliced variant transcript, AML1-ETO9a, rapidly induces leukemia in murine model.
  • To evaluate its clinical significance, AML1-ETO9a expression was assessed in 118 patients with t(8;21) AML-M2, using qualitative and nested quantitative reverse transcriptase (RT)-PCR methods.
  • Taken together, these data suggest that AML1-ETO9a is correlated with C-KIT overexpression/mutations and indicates poor disease outcome in t(8;21) AML-M2.
  • [MeSH-major] Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. Translocation, Genetic

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  • (PMID = 19458628.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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66. Gery S, Park DJ, Vuong PT, Virk RK, Muller CI, Hofmann WK, Koeffler HP: RTP801 is a novel retinoic acid-responsive gene associated with myeloid differentiation. Exp Hematol; 2007 Apr;35(4):572-8
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  • [Title] RTP801 is a novel retinoic acid-responsive gene associated with myeloid differentiation.
  • OBJECTIVE: Retinoids are crucial in the regulation of fundamental cellular processes including terminal differentiation of both normal and malignant myeloid progenitors.
  • Here we identified RTP801 as a novel early RA target gene in myeloid cells.
  • RTP801 mRNA levels are induced in acute myeloid leukemia (AML) cell lines during RA-dependent differentiation and are differentially expressed during maturation of normal CD34(+) cells.
  • The myeloid-specific, differentiation-related transcription factor C/EBPepsilon also induces RTP801 expression.
  • CONCLUSION: Taken together, our data suggest that RTP801 is an important RA-regulated gene involved in myeloid differentiation, which could represent a therapeutic target in leukemia.
  • [MeSH-major] Cell Differentiation / genetics. Leukemia, Myeloid / pathology. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Apoptosis. Cell Division. Granulocytes / cytology. Humans. Phosphorylation. Protein Kinases / metabolism. RNA, Messenger / genetics. TOR Serine-Threonine Kinases. U937 Cells

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  • (PMID = 17379067.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DDIT4 protein, human; 0 / RNA, Messenger; 0 / Transcription Factors; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases
  • [Other-IDs] NLM/ NIHMS20594; NLM/ PMC1922386
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67. Royer PJ, Bougras G, Ebstein F, Leveque L, Tanguy-Royer S, Simon T, Juge-Morineau N, Chevallier P, Harousseau JL, Gregoire M: Efficient monocyte-derived dendritic cell generation in patients with acute myeloid leukemia after chemotherapy treatment: application to active immunotherapy. Exp Hematol; 2008 Mar;36(3):329-39
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  • [Title] Efficient monocyte-derived dendritic cell generation in patients with acute myeloid leukemia after chemotherapy treatment: application to active immunotherapy.
  • OBJECTIVE: While complete remission in acute myeloid leukemia (AML) can be achieved after chemotherapy (CT), relapses occur for the majority of patients, underlying the need to eliminate residual disease.
  • Based on dendritic cell (DC) vaccination, the triggering of an immune response against residual leukemia cells after CT could maintain patients in remission.
  • The aim of our study was to assess, for vaccine preparation, generation of monocyte-derived DCs in AML patients after CT.
  • MATERIALS AND METHODS: We evaluated efficiency of the production, yields, maturation, and functional properties of DCs from 22 AML patients at different CT stages compared to those from 15 healthy donors.
  • CONCLUSION: In defining patient-sampling conditions, this preclinical study has direct implications for AML DC-based immunotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cancer Vaccines / therapeutic use. Dendritic Cells / cytology. Immunotherapy / methods. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Leukocytes, Mononuclear / cytology

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  • (PMID = 18207305.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CCR7 protein, human; 0 / Cancer Vaccines; 0 / Cytokines; 0 / Receptors, CCR7
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68. Nishizawa M, Hirayama F, Matsuyama N, Tada K, Kaneko H, Watanabe M, Miura Y, Tsudo M: [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate]. Rinsho Ketsueki; 2009 Jan;50(1):16-22
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  • [Title] [Transfusion-related acute lung injury with anti-leukocyte antibodies identified both in patient's serum and in red cell concentrate].
  • We report a fatal case of transfusion-related acute lung injury (TRALI) with anti-leukocyte antibodies detected both in the patient's serum and in the causative red cell concentrate (RC-M.A.P).
  • A 41-year-old Japanese woman diagnosed as having acute myeloid leukemia (AML, M2) developed TRALI caused by RC-M.A.P 15 days after the start of induction therapy for AML.
  • [MeSH-major] Acute Lung Injury / etiology. Autoantibodies / blood. Erythrocyte Transfusion / adverse effects. HLA Antigens / immunology. Leukemia, Myeloid, Acute / therapy. Leukocytes / immunology

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  • (PMID = 19225224.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / HLA Antigens
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69. Schanz J, Weiss B, Henrich D, Bohrer MH, Uppenkamp M: [30 year-old patient with multiple pelvic lesions and fecal incontinence]. Internist (Berl); 2009 Sep;50(9):1155, 1157-60
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  • The results of a bone marrow aspiration showed acute myeloid leukemia M2 with translocation t(8,21) associated with granulocytic sarcoma.
  • [MeSH-major] Fecal Incontinence / prevention & control. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Pelvic Neoplasms / diagnosis. Pelvic Neoplasms / surgery. Stem Cell Transplantation

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70. Bernardini P, Giannandrea F, Voso MT, Sica S: [Myeloproliferative disorders due to the use of gasoline as a solvent: report of three cases]. Med Lav; 2005 Mar-Apr;96(2):119-25
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  • METHODS: Clinical diagnosis was performed using standard immuno-phenotypic and morphological criteria; the hypothesis of an occupational origin was derived from analysis of the occupational histories.
  • RESULTS: The first case was a 59 year-old blacksmith suffering from acute myeloid leukaemia (AML) FAB M2, who had used petrol for 36 years to degrease the forged metal parts before painting them.
  • The second was a 53 year-old mechanic with AML FAB M3 who had used petrol for 15 years to degrease mechanical parts of tanker motors.
  • If it cannot, how many cases of benzene-related diseases escape aetiological diagnosis?
  • [MeSH-major] Gasoline / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Promyelocytic, Acute / chemically induced. Metallurgy. Motor Vehicles. Occupational Diseases / chemically induced. Primary Myelofibrosis / chemically induced. Solvents / adverse effects

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  • [CommentIn] Med Lav. 2005 Sep-Oct;96(5):447-51 [16711648.001]
  • [ErratumIn] Med Lav. 2005 Sep-Oct;96(5):418
  • (PMID = 16001511.001).
  • [ISSN] 0025-7818
  • [Journal-full-title] La Medicina del lavoro
  • [ISO-abbreviation] Med Lav
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Gasoline; 0 / Solvents; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1; EC 2.5.1.18 / glutathione transferase T1-1, human
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71. Elagib KE, Goldfarb AN: Oncogenic pathways of AML1-ETO in acute myeloid leukemia: multifaceted manipulation of marrow maturation. Cancer Lett; 2007 Jun 28;251(2):179-86
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  • [Title] Oncogenic pathways of AML1-ETO in acute myeloid leukemia: multifaceted manipulation of marrow maturation.
  • The leukemic fusion protein AML1-ETO occurs frequently in human acute myeloid leukemia (AML) and has received much attention over the past decade.
  • An initial model for its pathogenetic effects emphasized the conversion of a hematopoietic transcriptional activator, RUNX1 (or AML1), into a leukemogenic repressor which blocked myeloid differentiation at the level of target gene regulation.

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  • (PMID = 17125917.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA093735; United States / NCI NIH HHS / CA / CA100057-04; United States / NCI NIH HHS / CA / CA093735-05; United States / NCI NIH HHS / CA / R01 CA093735-05; United States / NCI NIH HHS / CA / R56 CA100057; United States / NCI NIH HHS / CA / R01 CA100057-04; United States / NCI NIH HHS / CA / CA 100057; United States / NCI NIH HHS / CA / R01 CA100057; United States / NCI NIH HHS / CA / CA 93735; United States / NCI NIH HHS / CA / T32 CA 009109; United States / NCI NIH HHS / CA / T32 CA009109
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 59
  • [Other-IDs] NLM/ NIHMS25324; NLM/ PMC1931834
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72. Manola KN, Georgakakos VN, Margaritis D, Stavropoulou C, Panos C, Kotsianidis I, Pantelias GE, Sambani C: Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer. Cancer Genet Cytogenet; 2008 Jan 1;180(1):37-42
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  • [Title] Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer.
  • We describe a case of treatment-induced acute myeloid leukemia M2 after breast cancer with a rare reciprocal t(12;12)(p13;q13) as a secondary cytogenetic abnormality in addition to the t(11;19)(q23;p13.1).
  • To the best of our knowledge, our patient represents the first report of the rare t(12;12)(p13;q13) described in treatment-induced leukemia and the possible formation of a new fusion gene.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms / drug therapy. Chromosomes, Human, Pair 12. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic


73. Riccioni R, Pasquini L, Mariani G, Saulle E, Rossini A, Diverio D, Pelosi E, Vitale A, Chierichini A, Cedrone M, Foà R, Lo Coco F, Peschle C, Testa U: TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL. Haematologica; 2005 May;90(5):612-24
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  • [Title] TRAIL decoy receptors mediate resistance of acute myeloid leukemia cells to TRAIL.
  • The present study was designed to evaluate the sensitivity to TRAIL-induced apoptosis in acute myeloblastic leukemias (AML).
  • DESIGN AND METHODS: TRAIL/TRAIL receptor (TRAIL-R) expression and sensitivity to TRAIL-mediated apoptosis were explored in 79 AML patients, including 17 patients with acute promyelocytic leukemia (APL).
  • RESULTS: In non-APL AML we observed frequent expression of TRAIL decoy receptors (TRAIL-R3 and TRAIL-R4), while TRAIL-R1 and TRAIL-R2 expression was restricted to AML exhibiting monocytic features.
  • Total leukemic blasts, as well as AML colony-forming units (AML-CFU), were invariably resistant to TRAIL-mediated apoptosis.
  • APL express membrane-bound TRAIL on their surface and exhibit a pattern of TRAIL-R expression similar to that observed in the other types of AML.
  • The induction of granulocytic maturation of APL cells by retinoic acid was associated with a marked decline of TRAIL expression.
  • We suggest that AML blasts, including APL blasts, are resistant to TRAIL-mediated apoptosis, a phenomenon seemingly related to the expression of TRAIL decoy receptors on these cells.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Leukemia, Myeloid / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand / physiology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antineoplastic Agents / pharmacology. Caspase 3 / analysis. Caspase 8 / analysis. Cell Differentiation / drug effects. Cell Membrane / metabolism. Cytarabine / pharmacology. Etoposide / pharmacology. Female. GPI-Linked Proteins. Granulocytes / drug effects. HL-60 Cells / pathology. Humans. Hydroxyurea / pharmacology. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Male. Middle Aged. Monocytes / drug effects. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Recombinant Fusion Proteins / pharmacology. Recombinant Fusion Proteins / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. U937 Cells / drug effects

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  • (PMID = 15921376.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GPI-Linked Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Fusion Proteins; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; X6Q56QN5QC / Hydroxyurea
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74. Harani MS, Adil SN, Shaikh MU, Kakepoto GN, Khurshid M: Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):26-9
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  • [Title] Frequency of fab subtypes in acute myeloid leukemia patients at Aga Khan University Hospital Karachi.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease.
  • The commonly used method for diagnosis and classification is based on FAB criteria using morphology and cytochemical stains.
  • The aim of present study is to determine the frequency of various sub types in acute myeloid leukemia using FAB criteria in our population.
  • This will aid in the correct diagnosis of acute leukemia and hence proper management of the patients.
  • The patients were diagnosed on the basis of bone marrow morphology using FAB classification.
  • AML-M4 was the predominant French-American-British (FAB) subtype (36.2%) followed by M2 (30.25%), M3 (10.4%), M1 (8.7%), M0 (7.7%), M5a (3.5%), M5b (2.5%) and M6 (0.8%).
  • CONCLUSIONS: The most common FAB subtype observed in our study was Acute myelomonocytic leukemia (M4) which is in accordance with studies reported from Saudia Arabia and a previous study reported from our institution.
  • However,other national and international studies have reported Myeloblastic Leukemia with maturation (M2) as the predominant subtype of AML.
  • [MeSH-major] Leukemia, Myeloid / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Child. Child, Preschool. Female. Hospitals, University. Humans. Infant. Male. Middle Aged. Pakistan

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  • (PMID = 15929522.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
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75. Roberson JR, Onciu M, Pounds S, Rubnitz JE, Pui CH, Razzouk BI: Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia. Pediatr Blood Cancer; 2008 Mar;50(3):542-8
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  • [Title] Prognostic significance of myeloperoxidase expression in childhood acute myeloid leukemia.
  • BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia (AML), but this association is unsubstantiated in pediatric AML.
  • PROCEDURE: We retrospectively compared cytochemical MPO results with outcome in 154 patients younger than 21 years treated on three consecutive institutional protocols for newly diagnosed AML (1987-2001).
  • Patients with FAB M0 and M7 AML (no MPO expression) or M3 AML (100% MPO expression) and Down's syndrome were excluded.
  • RESULTS: Median MPO expression was higher in FAB M2 subtype than in other subtypes (P < 0.0001) and differed significantly across cytogenetic risk groups (P = 0.002) with highest MPO expression among those with favorable karyotypes.
  • The percentage of MPO-positive blasts was not significantly associated with the probability of complete remission (P = 0.97), event-free survival (P = 0.72), or survival (P = 0.76) in multivariate analyses that accounted for age, FAB subtype, presenting WBC count, cytogenetic and protocol treatment risk group.
  • CONCLUSIONS: The percentage of MPO-positive blast cells is related to FAB subtype in pediatric AML but has limited prognostic relevance.
  • [MeSH-major] Leukemia, Myeloid / blood. Myeloid Cells / enzymology. Neoplastic Stem Cells / enzymology. Peroxidase / blood
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Biomarkers. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Prognosis. Retrospective Studies. Risk. Survival Analysis

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763467.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; EC 1.11.1.7 / Peroxidase
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76. Smits EL, Ponsaerts P, Van de Velde AL, Van Driessche A, Cools N, Lenjou M, Nijs G, Van Bockstaele DR, Berneman ZN, Van Tendeloo VF: Proinflammatory response of human leukemic cells to dsRNA transfection linked to activation of dendritic cells. Leukemia; 2007 Aug;21(8):1691-9
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  • Primary acute myeloid leukemia (AML) cells and AML cell lines markedly responded to poly(I:C) electroporation by apoptosis, upregulation of TLR3 expression, enhanced expression of major histocompatibility complex (MHC) and costimulatory molecules and by production of type I interferons (IFN).
  • Upon phagocytosis of poly(I:C)-electroporated AML cells, DC maturation and activation were induced as judged by an increased expression of MHC and costimulatory molecules, production of proinflammatory cytokines and an increase of T helper 1 (T(H)1)-polarizing capacity.
  • These immune effects were suboptimal when AML cells were passively pulsed with poly(I:C), indicating the superiority of poly(I:C) transfection over pulsing.
  • Our results demonstrate that poly(I:C) electroporation is a promising strategy to increase the immunogenicity of AML cells and to convert iDC into activated mature DC following the phagocytosis of AML cells.
  • [MeSH-major] Dendritic Cells / immunology. Leukemia, Myeloid / genetics. RNA, Double-Stranded / genetics. T-Lymphocytes / immunology. Toll-Like Receptor 3 / metabolism. Transfection
  • [MeSH-minor] Acute Disease. Cells, Cultured. Coculture Techniques. Cytokines / metabolism. Electroporation. Flow Cytometry. Humans. Interferon Type I / immunology. Interferon-gamma / immunology. Lymphocyte Activation. Poly I-C / metabolism. Th1 Cells / immunology

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  • (PMID = 17525722.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interferon Type I; 0 / RNA, Double-Stranded; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 24939-03-5 / Poly I-C; 82115-62-6 / Interferon-gamma
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77. Khanna-Gupta A: Sumoylation and the function of CCAAT enhancer binding protein alpha (C/EBP alpha). Blood Cells Mol Dis; 2008 Jul-Aug;41(1):77-81
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  • It is expressed at high levels throughout myeloid differentiation and binds to the promoters of multiple myeloid-specific genes at different stages of myeloid maturation.
  • Mutations in C/EBP alpha are present in a subset of patients with AML presenting with a normal karyotype.
  • In this review, the functional implications of post-translational modification, particularly sumoylation, of C/EBP alpha in normal granulopoiesis and leukemia are considered.

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  • (PMID = 18406180.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL063357-090008; United States / NHLBI NIH HHS / HL / P01 HL063357; United States / NHLBI NIH HHS / HL / P01 HL063357-090008; United States / NHLBI NIH HHS / HL / P01HL63357
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Small Ubiquitin-Related Modifier Proteins
  • [Number-of-references] 37
  • [Other-IDs] NLM/ NIHMS54847; NLM/ PMC2505045
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78. Ko RM, Kim HG, Wolff L, Klug CA: Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1101-11
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  • [Title] Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia.
  • Inactivation of p15(Ink4b) expression by promoter hypermethylation occurs in up to 80% of acute myeloid leukemia (AML) cases and is particularly common in the FAB-M2 subtype of AML, which is characterized by the presence of the RUNX1-ETO translocation in 40% of cases.
  • To establish whether the loss of p15(Ink4b) contributes to AML progression in association with RUNX1-ETO, we have expressed the RUNX1-ETO fusion protein from a retroviral vector in hematopoietic progenitor cells isolated from wild-type, p15(Ink4b) or p16(Ink4a) knockout bone marrow.
  • Loss of p15(Ink4b) alone resulted in increased myeloid progenitor cell frequencies in bone marrow by 10-month post-transplant and a 19-fold increase in the frequency of Lin(-)c-Kit(+)Sca-1(+) (LKS) cells that was not associated with expansion of long-term reconstituting HSC.
  • These results strongly suggest that p15(Ink4b) loss must be accompanied by additional oncogenic changes for RUNX1-ETO-associated AML to develop.

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  • (PMID = 18037485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096798; United States / NCI NIH HHS / CA / R01 CA087549; United States / NCI NIH HHS / CA / R01CA087549; United States / NCI NIH HHS / CA / CA096798-05; United States / NCI NIH HHS / CA / R01 CA096798-05; United States / NCI NIH HHS / CA / R01CA096798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ NIHMS49471; NLM/ PMC2430055
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79. Patroglu T, Torun YA, Karakukcu M, Gorozen F: A case of Turner syndrome associated with acute myeloid leukemia (M2). J Pediatr Hematol Oncol; 2006 Oct;28(10):682-3
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  • [Title] A case of Turner syndrome associated with acute myeloid leukemia (M2).
  • A 9-year-old girl was diagnosed as acute myeloid leukemia-M2 according to the French-American-British classification.
  • In addition, a diagnosis of Turner syndrome (TS) was made, on the basis of the presence of the chromosomal abnormality, ovarian failure, and abnormal physical features.
  • In particular, children with Down syndrome have increased risk of developing acute myeloblastic leukemia especially M7.
  • On the other hand, cases of myeloid leukemia that are complicated with TS are extremely rare.
  • This is the first report of TS with acute myeloid leukemia of M2 subtype and t (8;.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Turner Syndrome / genetics


80. Ayala RM, Martínez-López J, Albízua E, Diez A, Gilsanz F: Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia. Am J Hematol; 2009 Feb;84(2):79-86
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  • [Title] Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia.
  • The aim of this study was to evaluate the biological correlation and prognostic impact of Gata-1, Gata-2, EKLF, and c-MPL transcript level in a group of 41 acute myeloid leukemia (AML) patients.
  • Expression of c-MPL was associated with CD34+ AML and M2 FAB AML subtype.
  • A higher expression of EKLF was found in secondary AML versus primary AML.
  • Our study has identified expression of EKLF as a factor with a favorable impact on prognosis in AML.
  • [MeSH-major] GATA1 Transcription Factor / physiology. GATA2 Transcription Factor / physiology. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Receptors, Thrombopoietin / physiology

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  • (PMID = 19097174.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Receptors, Thrombopoietin; 0 / erythroid Kruppel-like factor; 143641-95-6 / MPL protein, human
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81. Gross SA, Zheng JH, Le AT, Kerzic PJ, Irons RD: PU.1 phosphorylation correlates with hydroquinone-induced alterations in myeloid differentiation and cytokine-dependent clonogenic response in human CD34(+) hematopoietic progenitor cells. Cell Biol Toxicol; 2006 Jul;22(4):229-41
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  • [Title] PU.1 phosphorylation correlates with hydroquinone-induced alterations in myeloid differentiation and cytokine-dependent clonogenic response in human CD34(+) hematopoietic progenitor cells.
  • The transcriptional regulatory factor PU.1 is important for the regulation of a diverse group of hematopoietic and myeloid genes.
  • In leukemia cells, differing patterns of PU.1 phosphorylation have been described among acute myelogenous leukemia (AML) subtypes.
  • Therefore, we hypothesized that modulation of PU.1-dependent gene expression might be a molecular mediator of alterations in myeloid cell growth and differentiation that have been demonstrated to be early events in benzene-induced leukemogenesis.
  • Maturation of granulocyte and monocyte lineages is also accompanied by distinct changes in PU.1-DNA binding patterns.
  • These results suggest that HQ induces a dysregulation in the external signals modulating PU.1 protein phosphorylation and this dysregulation may be an early event in the generation of benzene-induced AML.
  • [MeSH-major] Antigens, CD34 / biosynthesis. Cytokines / metabolism. Hematopoietic Stem Cells / cytology. Hydroquinones / chemistry. Myeloid Cells / cytology. Proto-Oncogene Proteins / physiology. Trans-Activators / physiology

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  • (PMID = 16642264.001).
  • [ISSN] 0742-2091
  • [Journal-full-title] Cell biology and toxicology
  • [ISO-abbreviation] Cell Biol. Toxicol.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES06258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Cytokines; 0 / Hydroquinones; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 123-31-9 / hydroquinone; EC 3.1.3.- / Phosphoric Monoester Hydrolases
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82. Abe T, Furukawa T, Masuko M, Sugimoto A, Okazuka K, Honma K, Fujimura T, Iguchi S, Nishi S, Ueno M, Nagahashi M, Watanabe G, Ajioka Y, Isahai N, Nagai K, Kazuyama Y, Aizawa Y: Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation. Int J Hematol; 2009 Oct;90(3):421-5
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  • [Title] Sequential adenovirus infection of type 14 hemorrhagic cystitis and type 35 generalized infection after cord blood transplantation.
  • We report a case of a 29-year-old male patient with a generalized adenovirus (AdV) infection after cord blood transplantation (CBT) for acute myelocytic leukemia with maturation at 2nd complete remission.
  • Molecular diagnosis using PCR-restriction fragment length polymorphism analysis demonstrated that AdV with the serotype 14 caused the cystitis.
  • [MeSH-major] Adenovirus Infections, Human / etiology. Cord Blood Stem Cell Transplantation / adverse effects. Cystitis / etiology. Hemorrhage / etiology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19763745.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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83. Lahortiga I, Belloni E, Vázquez I, Agirre X, Larrayoz MJ, Vizmanos JL, Valgañón M, Zudaire I, Sáez B, Mateos MC, Di Fiore PP, Calasanz MJ, Odero MD: NUP98 is fused to HOXA9 in a variant complex t(7;11;13;17) in a patient with AML-M2. Cancer Genet Cytogenet; 2005 Mar;157(2):151-6
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  • [Title] NUP98 is fused to HOXA9 in a variant complex t(7;11;13;17) in a patient with AML-M2.
  • This translocation has been associated with myeloid leukemias, predominantly acute myeloid leukemia (AML) M2 subtype with trilineage myelodysplastic features, and with a poor prognosis.
  • ;p1?2) in a patient with AML-M2 and poor prognosis.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 7. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Leukemia, Myeloid, Acute / genetics. Nuclear Pore Complex Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Translocation, Genetic

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  • [ErratumIn] Cancer Genet Cytogenet. 2005 Jun;159(2):194
  • (PMID = 15721637.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NUP98-HOXA9 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / homeobox protein HOXA9
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84. Chen JP, Chen L, Leek J, Lin C: Antisense c-myc fragments induce normal differentiation cycles in HL-60 cells. Eur J Clin Invest; 2006 Jan;36(1):49-57
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  • BACKGROUND: We have investigated the potential for using antisense technology as a means of delivering treatment for acute myeloblastic leukaemia (FAB-M2) by gene therapy.
  • Thus, we believe that further study of this construct is warranted as a potential gene therapy reagent for treatment of acute myeloblastic leukaemia.
  • [MeSH-major] Antisense Elements (Genetics). Leukemia, Myeloid, Acute / pathology. Proto-Oncogene Proteins c-myc / metabolism

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  • (PMID = 16403010.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antisense Elements (Genetics); 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Proto-Oncogene Proteins c-myc
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85. Welte K, Zeidler C, Dale DC: Severe congenital neutropenia. Semin Hematol; 2006 Jul;43(3):189-95
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  • One subtype of CN, Kostmann syndrome, is an autosomal recessive disorder, characterized histopathologically by early-stage maturation arrest of myeloid differentiation.
  • CN with similar clinical features occurs as an autosomal dominant disorder and many sporadic cases also have been reported.
  • Adverse events include mild splenomegaly, osteoporosis, and malignant transformation into myelodysplasia (MDS)/leukemia.
  • In recent analyses the influence of the G-CSF dose required to achieve neutrophil response (ANC >1,000/microL) in the risk of developing acute myeloid leukemia (AML) has been reported.

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  • (PMID = 16822461.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.4.21.37 / Leukocyte Elastase
  • [Number-of-references] 38
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86. Nebbioso A, Clarke N, Voltz E, Germain E, Ambrosino C, Bontempo P, Alvarez R, Schiavone EM, Ferrara F, Bresciani F, Weisz A, de Lera AR, Gronemeyer H, Altucci L: Tumor-selective action of HDAC inhibitors involves TRAIL induction in acute myeloid leukemia cells. Nat Med; 2005 Jan;11(1):77-84
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  • [Title] Tumor-selective action of HDAC inhibitors involves TRAIL induction in acute myeloid leukemia cells.
  • Inhibitors of histone deacetylases (HDACIs) induce proliferation arrest, maturation and apoptosis of cancer cells, but not normal cells, in vitro and in vivo, and are currently being tested in clinical trials.
  • We report that HDACIs induce, in addition to p21, expression of TRAIL (Apo2L, TNFSF10) by directly activating the TNFSF10 promoter, thereby triggering tumor-selective death signaling in acute myeloid leukemia (AML) cells and the blasts of individuals with AML.
  • HDACIs induced proliferation arrest, TRAIL-mediated apoptosis and suppression of AML blast clonogenicity irrespective of French-American-British (FAB) classification status, karyotype and immunophenotype.
  • [MeSH-major] Apoptosis / drug effects. Histone Deacetylase Inhibitors. Leukemia, Myeloid / drug therapy. Membrane Glycoproteins / metabolism. Receptors, Cell Surface / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins. Humans. TNF-Related Apoptosis-Inducing Ligand. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15619633.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53
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87. Sinha S, Aish L, Oo TH: Morphologic heterogeneity of acute promyelocytic leukemia: therapy-related acute promyelocytic leukemia presenting with FAB-M2 morphology. Am J Hematol; 2006 Jun;81(6):475-6
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  • [Title] Morphologic heterogeneity of acute promyelocytic leukemia: therapy-related acute promyelocytic leukemia presenting with FAB-M2 morphology.
  • [MeSH-major] Brachytherapy / adverse effects. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16680741.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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88. Moore MA, Dorn DC, Schuringa JJ, Chung KY, Morrone G: Constitutive activation of Flt3 and STAT5A enhances self-renewal and alters differentiation of hematopoietic stem cells. Exp Hematol; 2007 Apr;35(4 Suppl 1):105-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To model human leukemogenesis by transduction of human hematopoietic stem cells (HSC) with genes associated with leukemia and expressed in leukemic stem cells.
  • METHODS: Constitutive activation of Flt3 (Flt3-ITD) has been reported in 25 to 30% of patients with acute myeloid leukemia (AML).
  • Differentiation was biased to erythropoiesis, including erythropoietin independence, with myeloid maturation inhibition.
  • The phenotype of week-2 self-renewing CAFC also characterized primary Flt3-ITD(+) AML bone marrow samples.
  • Isolation of leukemic stem cells (LSC) with a CD34(+), CD38(-), HLA-DR(-) phenotype was undertaken with Flt3-ITD(+) AML samples resulting in co-purification of early CAFC.
  • Gene expression of LSC relative to the bulk leukemic population revealed upregulation of homeobox genes (HOXA9, HOXA5) implicated in leukemogenesis, and hepatic leukemia factor (HLF) involved in stem cell proliferation.
  • CONCLUSION: Myeloid leukemogenesis is a multi-stage process that can involve constitutively activated receptors and downstream pathways involving STAT5, HOX genes, and HLF.
  • [MeSH-major] Cell Differentiation. Cell Proliferation. Hematopoietic Stem Cells / metabolism. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / metabolism. STAT5 Transcription Factor / immunology. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 17379095.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; 0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / Tumor Suppressor Proteins; 0 / homeobox protein HOXA9; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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89. Kremser A, Dressig J, Grabrucker C, Liepert A, Kroell T, Scholl N, Schmid C, Tischer J, Kufner S, Salih H, Kolb HJ, Schmetzer H: Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods. J Immunother; 2010 Feb-Mar;33(2):185-99
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  • [Title] Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods.
  • Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
  • We studied the capability of 6 serum-free DC culture methods, chosen according to different mechanisms, to induce DC differentiation in 137 cases of AML and 52 cases of MDS.
  • The quality/quantity of DC generated was estimated by flow cytometry studying (co) expressions of "DC"antigens, costimulatory, maturation, and blast-antigens.
  • Comparing these methods on average 15% to 32% DC, depending on methods used, could be obtained from blast-containing mononuclear cells (MNC) in AML/MDS cases with a DC viability of more than 60%.
  • Average results of all culture methods tested were comparable, however not every given case of AML could be differentiated to DC with 1 selected method.
  • [MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology

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  • (PMID = 20139775.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil
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90. van Binsbergen E, de Weerdt O, Buijs A: A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review. Cancer Genet Cytogenet; 2007 Jul 1;176(1):72-5
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  • [Title] A new subtype of MLL-SEPT2 fusion transcript in therapy-related acute myeloid leukemia with t(2;11)(q37;q23): a case report and literature review.
  • The t(2;11)(q37;q23) is a rare recurrent cytogenetic abnormality associated with de novo and therapy-related acute myeloid leukemia, resulting in a MLL-SEPT2 fusion gene.
  • We report on a case of therapy-related acute myeloid leukemia M2 showing a t(2;11)(q37;q23) and resulting in a new subtype of a MLL-SEPT2 chimeric transcript.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 2. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion. Phosphoric Monoester Hydrolases / genetics. Translocation, Genetic

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  • (PMID = 17574968.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.1.3.- / Phosphoric Monoester Hydrolases
  • [Number-of-references] 9
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91. Runarsson G, Feltenmark S, Forsell PK, Sjöberg J, Björkholm M, Claesson HE: The expression of cytosolic phospholipase A2 and biosynthesis of leukotriene B4 in acute myeloid leukemia cells. Eur J Haematol; 2007 Dec;79(6):468-76
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  • [Title] The expression of cytosolic phospholipase A2 and biosynthesis of leukotriene B4 in acute myeloid leukemia cells.
  • Here, we have studied the expression and activity of the enzymes involved in the synthesis of leukotriene B4 (LTB4) in acute myeloid leukemia (AML) cells (16 clones) and G-CSF mobilized peripheral blood CD34+ cells.
  • CD34+ cells from patients with non-myeloid malignancies expressed cytosolic phospholipase A2 (cPLA2), 5-lipoxygenase activating protein (FLAP), and leukotriene A4 (LTA4) hydrolase but not 5-lipoxygenase (5-LO).
  • The enzyme cPLA2 was abundantly expressed in AML cells and the activity of the enzyme was high in certain AML clones.
  • The expression of 5-LO, FLAP, and LTA4 hydrolase in AML clones was in general lower than in healthy donor polymorphonuclear leukocytes (PMNL).
  • The calcium ionophore A23187-induced release of [14C] arachidonic acid (AA) in AML cells was low, compared with PMNL, and did not correlate with the expression of cPLA2 protein.
  • Biosynthesis of LTB4, upon calcium ionophore A23187 activation, was only observed in five of the investigated AML clones and only three of the most differentiated clones produced similar amounts of LTB4 as PMNL.
  • The capacity of various cell clones to produce LTs could neither be explained by the difference in [1-(14)C] AA release nor 5-LO expression.
  • Taken together, these results indicate that LT synthesis is under development during early myelopoiesis and the capacity to produce LTs is gained upon maturation.
  • High expression of cPLA2 in AML suggests a putative role of this enzyme in the pathophysiology of this disease.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / blood. Leukotriene B4 / biosynthesis. Phospholipases A2, Cytosolic / biosynthesis

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  • (PMID = 17976189.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Ionophores; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 1HGW4DR56D / Leukotriene B4; 37H9VM9WZL / Calcimycin; EC 1.13.11.34 / Arachidonate 5-Lipoxygenase; EC 3.1.1.4 / Phospholipases A2, Cytosolic
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92. Zeng LJ, Tan H: [In vitro anti-leukemia activity of cord blood original cytotoxic T lymphocytes]. Ai Zheng; 2005 Apr;24(4):419-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [In vitro anti-leukemia activity of cord blood original cytotoxic T lymphocytes].
  • BACKGROUND & OBJECTIVE: Cord blood transplantation (CBT) possesses graft-versus-leukemia (GVL) effect.
  • It is possible to cure leukemia if specific cytotoxic T lymphocytes (CTLs) can be induced from lymphocytes in cord blood (CB), and be used to eradicate minimal residual disease (MRD) in leukemia patients.
  • This study was to induce CTLs from cord blood, and explore its in vitro anti-leukemia activity.
  • Immature DCs were pulsed with apoptotic leukemia cells to present leukemic antigens to cord blood original lymphocytes to obtain CTLs.
  • The characteristics of maturation of DCs were evaluated by morphology and flow cytometry.
  • Anti-leukemia effect of CTLs was measured by lactate dehydrogenase release assay.
  • When E:T ratio was 50:1, CTLs showed far higher cytotoxicity to uncultured acute myeloid leukemia (AML) cells than to K562 cells, and to mononuclear cells of bone marrow from the corresponding patients in complete remission phase (CR-MNCs) [(52.6+/-21.0)% vs. (18.2+/-20.2)%, and (3.3+/-6.3)%, P < 0.05].
  • CONCLUSIONS: Mature DCs derived from cord blood, which loaded leukemia antigens, could induce leukemia-specific CTLs.
  • The CTLs have vigorous cytotoxicity to original leukemia cells rather than CR-MNCs.
  • [MeSH-major] Antigen Presentation / immunology. Dendritic Cells / immunology. Fetal Blood / immunology. Leukemia, Myeloid, Acute / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 15820063.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD1; 0 / Antigens, CD86; 0 / CD1a antigen; 0 / CD83 antigen; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Membrane Glycoproteins
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93. Eshel R, Ben-Zaken O, Vainas O, Nadir Y, Minucci S, Polliack A, Naparstek E, Vlodavsky I, Katz BZ: Leukomogenic factors downregulate heparanase expression in acute myeloid leukemia cells. Biochem Biophys Res Commun; 2005 Oct 7;335(4):1115-22
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  • [Title] Leukomogenic factors downregulate heparanase expression in acute myeloid leukemia cells.
  • Heparanase is a heparan sulfate-degrading endoglycosidase expressed by mature monocytes and myeloid cells, but not by immature hematopoietic progenitors.
  • Heparanase gene expression is upregulated during differentiation of immature myeloid cells.
  • PML-RARalpha and PLZF-RARalpha fusion gene products associated with acute promyelocytic leukemia abrogate myeloid differentiation and heparanase expression.
  • AML-Eto, a translocation product associated with AML FAB M2, also downregulates heparanase gene expression.
  • We found that retinoic acid that dissociates PML-RARalpha from the DNA, and which is used to treat acute promyelocytic leukemia patients, restores heparanase expression to normal levels in an acute promyelocytic leukemia cell line.
  • The retinoic acid effects were also observed in primary acute promyelocytic leukemia cells and in a retinoic acid-treated acute promyelocytic leukemia patient.
  • Histone deacetylase inhibitor reverses the downregulation of heparanase expression induced by the AML-Eto fusion gene product in M2 type AML.
  • In summary, we have characterized a link between leukomogenic factors and the downregulation of heparanase in myeloid leukemic cells.
  • [MeSH-major] Glucuronidase / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukocytes / metabolism. Proto-Oncogene Proteins / metabolism. Transcription Factors / metabolism

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  • (PMID = 16112651.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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94. Serrano E, Lasa A, Perea G, Carnicer MJ, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Acute myeloid leukemia subgroups identified by pathway-restricted gene expression signatures. Acta Haematol; 2006;116(2):77-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia subgroups identified by pathway-restricted gene expression signatures.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by abnormal proliferation of myeloid precursors and a maturation block.
  • Alternatively, we selected a pathway profiling strategy based on the current knowledge in order to stratify de novo AML patients and identify those cases which would potentially benefit from the use of new chemotherapeutic agents.
  • One hundred and thirty-two RNA samples obtained from de novo adult AML patients were tested for FLT3, FLT3-LG, NDST1, HDAC2, ATRX, FOS, DNMT1, DNMT3A, DNMT3B, NBS1, RAD50, MRE11A, Meis1 and Meis2 expression using quantitative PCR (qPCR) assays.
  • In accordance with previous results, Meis1 downregulation is a useful surrogate marker indicating a good prognosis in AML patients.
  • Simple qPCR platforms may help to identify different biologic subgroups in AML.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Karyotyping. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Prognosis. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. fms-Like Tyrosine Kinase 3 / genetics


95. Ressel A, Trümper L, Bäsecke J: [Occlusion of the femoral arteries in de novo AML]. Med Klin (Munich); 2007 May 15;102(5):388-92
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  • [Title] [Occlusion of the femoral arteries in de novo AML].
  • [Transliterated title] Femoralarterienverschluss bei De-novo-AML.
  • BACKGROUND: Leukemic emboli in acute (AML) and chronic myelocytic leukemia (CML) are associated with hyperleukocytosis (>100,000/microl leukocytes) and most frequently detected at autopsy.
  • CASE REPORT: A 53-year-old woman was admitted with hyperleukocytosis and acute pain in her right leg.
  • An occlusion of the right femoral arteries as the presenting symptom of a de novo AML (FAB M1/WHO: AML without maturation) with hyperleukocytosis was diagnosed.
  • CONCLUSION: Leukemic emboli of large vessels are uncommon in leukemia with hyperleukocytosis.
  • Leukemic emboli mainly occur in AML and CML in blast crisis and are rare in acute (ALL) and chronic lymphocytic leukemia (CLL).
  • [MeSH-major] Arterial Occlusive Diseases / etiology. Femoral Artery. Leukemia, Myeloid, Acute / diagnosis. Neoplastic Cells, Circulating
  • [MeSH-minor] Angiography. Blood Coagulation Tests. Diagnosis, Differential. Female. Granulocyte Precursor Cells / pathology. Humans. Leukocyte Count. Leukocytosis / diagnosis. Leukocytosis / pathology. Middle Aged

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  • (PMID = 17497090.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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96. Liu HC, Chen SH, Wang LY, Yeh TC, Chai IJ, Liang DC: In vitro cell growth stimulated by recombinant human cytokines can help to diagnose transient leukemia in neonates. J Formos Med Assoc; 2007 May;106(5):365-71
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  • [Title] In vitro cell growth stimulated by recombinant human cytokines can help to diagnose transient leukemia in neonates.
  • BACKGROUND/PURPOSE: In a previous study, we demonstrated that in vitro cell growth stimulated by human placental conditioned medium distinguished between transient leukemia (TL) and congenital acute myeloid leukemia (AML) in neonates.
  • METHODS: Eight neonates with features indistinguishable from AML were studied.
  • Cytospin smears of liquid suspension cultures all showed good myeloid or megakaryocytic maturation consistent with TL rather than AML.

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  • (PMID = 17561471.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-3; 0 / Recombinant Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 9014-42-0 / Thrombopoietin
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97. Zhou J, Meng R, Sui XH, Meng L, Yang BF: Effects of arsenic trioxide administration styles on leukocytosis. Chin Med Sci J; 2006 Jun;21(2):111-4
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  • METHODS: Three kinds of leukemia cells, NB4, K562, and acute promyelocytic leukemia (APL) cells, were cultured in the media with constant concentration and varying concentrations of As2O3 respectively for 24 hours.
  • RESULTS: The apoptosis rates of NB4, K562, and APL leukemia cells in the media with constant As2O3 concentration were 56.6% +/- 2.4%, 27.6% +/- 3.1%, and 52.2% +/- 2.8%, respectively, which were significantly higher than those with changing As2O3 concentration (23.2% +/- 2.1%, 11.0% +/- 2.5%, and 21.0% +/- 2.5%, respectively, P < 0.01).
  • The apoptosis rates of APL, M2 type acute myeloid leukemia (AML-M2), and chronic myeloid leukemia (CML) patients in the trial group (28.5% +/- 1.9%, 9.5% +/- 0.6%, and 12.5% +/- 1.8%) were also significantly higher than those in control group (8.5% +/- 2.2%, 2.

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  • (PMID = 16845799.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
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98. Tachikawa Y, Abe Y, Choi I, Ohtsuka R, Nagasawa E, Shibata K, Nishimura J, Nawata H, Muta K: [Second nonmyeloablative allogeneic peripheral blood stem cell transplantation with more immunosuppressive conditioning regimen for the late graft failure of the patient with acute myeloid leukemia]. Fukuoka Igaku Zasshi; 2005 Nov;96(11):378-82
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  • [Title] [Second nonmyeloablative allogeneic peripheral blood stem cell transplantation with more immunosuppressive conditioning regimen for the late graft failure of the patient with acute myeloid leukemia].
  • A 53-year-old woman with acute myeloid leukemia (M2; normal karyotype) in first remission underwent the nonmyeloablative allogeneic peripheral blood stem cell transplantation from her HLA-identical brother, with conditioning consisting of fludarabine and low dose total body irradiation (2Gy).
  • [MeSH-major] Immunosuppression / methods. Leukemia, Myeloid, Acute / therapy. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning / methods

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  • (PMID = 16502857.001).
  • [ISSN] 0016-254X
  • [Journal-full-title] Fukuoka igaku zasshi = Hukuoka acta medica
  • [ISO-abbreviation] Fukuoka Igaku Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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99. Secchiero P, Zerbinati C, Melloni E, Milani D, Campioni D, Fadda R, Tiribelli M, Zauli G: The MDM-2 antagonist nutlin-3 promotes the maturation of acute myeloid leukemic blasts. Neoplasia; 2007 Oct;9(10):853-61
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  • [Title] The MDM-2 antagonist nutlin-3 promotes the maturation of acute myeloid leukemic blasts.
  • The small-molecule inhibitor of murine double minute (MDM-2), Nutlin-3, induced variable apoptosis in primary acute myeloid leukemia (AML) blasts and promoted myeloid maturation of surviving cells, as demonstrated by analysis of CD11b and CD14 surface antigens and by morphologic examination.
  • Although the best-characterized activity of Nutlin-3 is activation of the p53 pathway, Nutlin-3 induced maturation also in one AML sample characterized by p53 deletion, as well as in the p53(-/-) human myeloblastic HL-60 cell line.
  • Taken together, these data disclose a novel, potentially relevant therapeutic role for Nutlin-3 in the treatment of both p53 wild-type and p53(-/-) AML, possibly in association with recombinant TRAIL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Imidazoles / pharmacology. Leukemia, Myeloid / drug therapy. Piperazines / pharmacology. Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Antigens, CD11b / drug effects. Antigens, CD11b / metabolism. Antigens, CD14 / drug effects. Antigens, CD14 / metabolism. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. E2F1 Transcription Factor / drug effects. E2F1 Transcription Factor / metabolism. Flow Cytometry. Humans. Immunoprecipitation. RNA, Small Interfering. Retinoblastoma Protein / biosynthesis. Retinoblastoma Protein / drug effects. TNF-Related Apoptosis-Inducing Ligand / drug effects. TNF-Related Apoptosis-Inducing Ligand / metabolism. Transfection. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / metabolism. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism

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