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1. Salmon JM, Slater NJ, Hall MA, McCormack MP, Nutt SL, Jane SM, Curtis DJ: Aberrant mast-cell differentiation in mice lacking the stem-cell leukemia gene. Blood; 2007 Nov 15;110(10):3573-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant mast-cell differentiation in mice lacking the stem-cell leukemia gene.
  • The stem cell leukemia (SCL) gene encodes a basic helix-loop-helix transcription factor expressed in erythroid, megakaryocyte, and mast-cell lineages.
  • Fractionation of bone marrow myeloid progenitors demonstrated that these MCPs were present in the megakaryocyte-erythroid-restricted cell fraction.
  • In part, this may be due to a requirement for SCL in normal mast-cell maturation: SCL(-/Delta) mast cells had reduced expression of the high-affinity IgE receptor and mast cell proteases, MCP-5 and MCP-6.
  • [MeSH-minor] Animals. Cell Count. Cells, Cultured. Erythroid Cells / cytology. GATA2 Transcription Factor / genetics. Humans. Leukemia / genetics. Macrophages / cytology. Megakaryocytes / cytology. Mice. Mice, Inbred C57BL. Mice, Transgenic. Stem Cells / cytology. Transfection. Up-Regulation


2. Choschzick M, Bacher U, Ayuk F, Lebeau A: Immunohistochemistry and molecular analyses in myeloid sarcoma of the breast in a patient with relapse of NPM1-mutated and FLT3-mutated AML after allogeneic stem cell transplantation. J Clin Pathol; 2010 Jun;63(6):558-61
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  • [Title] Immunohistochemistry and molecular analyses in myeloid sarcoma of the breast in a patient with relapse of NPM1-mutated and FLT3-mutated AML after allogeneic stem cell transplantation.
  • Myeloid sarcoma of the breast is a rare manifestation of acute myeloid leukaemia (AML).
  • This report describes a patient who was diagnosed with AML FAB M2.
  • Core needle biopsy of the lesion resulted in diagnosis of myeloid sarcoma.
  • The myeloid sarcoma showed complete transient resolution following treatment with the kinase inhibitor sorafenib.
  • However, the patient developed bone marrow relapse and died in fatal cerebral haemorrhage 1 year after initial diagnosis of AML.
  • In summary, combined molecular and immunohistochemical examination of NPM1 and FLT3 is helpful in the diagnosis of extramedullary manifestations of AML in core needle biopsies.
  • [MeSH-major] Breast Neoplasms / genetics. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Sarcoma, Myeloid / genetics. fms-Like Tyrosine Kinase 3 / genetics


3. 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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4. Desouki MM, Post GR, Cherry D, Lazarchick J: PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. Clin Med Res; 2010 Jul;8(2):84-8
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  • [Title] PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms.
  • OBJECTIVE: Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression.
  • PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.
  • RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).
  • PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).
  • [MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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  • [Cites] Br J Haematol. 2001 Sep;114(4):881-3 [11564080.001]
  • [Cites] Immunity. 2001 Jun;14(6):779-90 [11420047.001]
  • [Cites] Leuk Lymphoma. 2002 Dec;43(12):2335-41 [12613521.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4620-5 [12907641.001]
  • [Cites] Am J Clin Pathol. 2003 Nov;120(5):767-77 [14608905.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):1839-46 [15155532.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7399-404 [15492262.001]
  • [Cites] Genomics. 1991 Oct;11(2):424-34 [1685142.001]
  • [Cites] Blood. 1992 Jul 15;80(2):470-7 [1378322.001]
  • [Cites] Genes Dev. 1992 Sep;6(9):1589-607 [1516825.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1308-16 [9694719.001]
  • [Cites] Clin Cancer Res. 1999 Mar;5(3):611-5 [10100713.001]
  • [Cites] Arch Pathol Lab Med. 2005 Jan;129(1):32-8 [15628906.001]
  • [Cites] Am J Surg Pathol. 2005 May;29(5):687-92 [15832095.001]
  • [Cites] Mod Pathol. 2005 Dec;18(12):1542-9 [16056244.001]
  • [Cites] Mod Pathol. 2006 Jul;19(7):1010-8 [16648862.001]
  • [Cites] Am J Clin Pathol. 2006 Aug;126(2):235-40 [16891199.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):534-44 [16938666.001]
  • [Cites] Oncol Rep. 2006 Nov;16(5):1003-8 [17016584.001]
  • [Cites] Am J Clin Pathol. 2006 Nov;126(5):798-804 [17050077.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1127-38 [17577776.001]
  • [Cites] Mod Pathol. 2007 Aug;20(8):871-7 [17529924.001]
  • [Cites] Lab Invest. 2009 Mar;89(3):301-14 [19139719.001]
  • [Cites] Am J Surg Pathol. 2009 May;33(5):775-80 [19145202.001]
  • [Cites] J Clin Pathol. 2007 Jun;60(6):709-14 [16837628.001]
  • [Cites] Am J Surg Pathol. 2002 Oct;26(10):1343-50 [12360049.001]
  • (PMID = 20660931.001).
  • [ISSN] 1554-6179
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ PMC2910102
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5. Veyret C, Levy C, Chollet P, Merrouche Y, Roche H, Kerbrat P, Fumoleau P, Fargeot P, Clavere P, Chevallier B: Inflammatory breast cancer outcome with epirubicin-based induction and maintenance chemotherapy: ten-year results from the French Adjuvant Study Group GETIS 02 Trial. Cancer; 2006 Dec 1;107(11):2535-44
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  • [Title] Inflammatory breast cancer outcome with epirubicin-based induction and maintenance chemotherapy: ten-year results from the French Adjuvant Study Group GETIS 02 Trial.
  • In the lenograstim group, 1 patient developed acute myeloblastic leukemia M2, and 1 patient developed myelodysplastic syndrome.
  • CONCLUSIONS: FEC-HD induction chemotherapy followed by FEC 75 maintenance regimen had moderate and acute long-term toxicities and lead to high DFS and OS rates in patients with IBC.

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 17054108.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Placebos; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 6WS4C399GB / lenograstim; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; FEC protocol
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6. Endersby R, Majewski IJ, Winteringham L, Beaumont JG, Samuels A, Scaife R, Lim E, Crossley M, Klinken SP, Lalonde JP: Hls5 regulated erythroid differentiation by modulating GATA-1 activity. Blood; 2008 Feb 15;111(4):1946-50
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  • Hemopoietic lineage switch (Hls) 5 and 7 were originally isolated as genes up-regulated during an erythroid-to-myeloid lineage switch.
  • Here we show that Hls5 impedes erythroid maturation by restricting proliferation and inhibiting hemoglobin synthesis; however, Hls5 does not influence the morphology of erythroid cells.
  • We conclude that Hls5 and Hls7/Mlf1 act cooperatively to induce biochemical and phenotypic changes associated with erythroid/myeloid lineage switching.
  • [MeSH-minor] Cell Cycle. Cell Line. Cell Line, Tumor. DNA Primers. Erythropoietin / pharmacology. Globins / genetics. Humans. Leukemia, Erythroblastic, Acute. Nuclear Proteins / physiology. Transcription Factors / physiology

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  • (PMID = 18063753.001).
  • [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 / Apoptosis Regulatory Proteins; 0 / DNA Primers; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Nuclear Proteins; 0 / TRIM35 protein, human; 0 / Transcription Factors; 0 / ZFPM1 protein, human; 11096-26-7 / Erythropoietin; 9004-22-2 / Globins
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7. Jin Y, Mancuso JJ, Uzawa S, Cronembold D, Cande WZ: The fission yeast homolog of the human transcription factor EAP30 blocks meiotic spindle pole body amplification. Dev Cell; 2005 Jul;9(1):63-73
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  • Centrosome aberrations caused by misregulated centrosome maturation result in defective spindle and genomic instability.
  • Here we report that the fission yeast homolog of the human transcription factor EAP30, Dot2, negatively regulates meiotic spindle pole body (SPB, the yeast equivalent of centrosome) maturation. dot2 mutants show excess electron-dense material accumulating near SPBs, which we refer to as aberrant microtubule organization centers (AMtOCs).
  • Our findings, therefore, uncover meiosis-specific regulation of SPB maturation and provide evidence that a member of the conserved EAP30 family is required for maintenance of genome stability through regulation of SPB maturation.
  • EAP30 is part of a transcription factor complex associated with acute myeloid leukemia, so these results may have relevance to human cancer.


8. Jegalian AG, Facchetti F, Jaffe ES: Plasmacytoid dendritic cells: physiologic roles and pathologic states. Adv Anat Pathol; 2009 Nov;16(6):392-404
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  • Demonstrating potential for neoplastic transformation reflective of varying stages of maturation, clonal proliferations range from PDC nodules most commonly associated with chronic myelomonocytic leukemia to the rare but highly aggressive malignancy now known as blastic plasmacytoid dendritic cell neoplasm (BPDCN).
  • Acute leukemia therapy regimens may lead to sustained clinical remission of BPDCN, with bone marrow transplantation in first complete remission potentially curative in adult patients.
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / pathology. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Male. Toll-Like Receptors / immunology

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  • (PMID = 19851130.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Toll-Like Receptors
  • [Number-of-references] 151
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9. Gibson SE, Dong HY, Advani AS, Hsi ED: Expression of the B cell-associated transcription factors PAX5, OCT-2, and BOB.1 in acute myeloid leukemia: associations with B-cell antigen expression and myelomonocytic maturation. Am J Clin Pathol; 2006 Dec;126(6):916-24
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  • [Title] Expression of the B cell-associated transcription factors PAX5, OCT-2, and BOB.1 in acute myeloid leukemia: associations with B-cell antigen expression and myelomonocytic maturation.
  • The aberrant expression of the B-cell transcription factor PAX5 has been described in a subset of acute myeloid leukemia (AML) with t(8;21)(q22;q22) in association with B-cell antigen expression.
  • However, the expression of other B cell-associated transcription factors, particularly OCT-2 and its B cell-specific coactivator BOB.1, has not been described in AML.
  • In this study, expression of PAX5, OCT-2 and BOB.1 was evaluated by immunohistochemical staining of bone marrow samples from 83 cases of AML.
  • The expression patterns were correlated with t(8;21)(q22;q22), B cell-associated antigen expression, and AML subtype.
  • We confirmed the expression of PAX5 in AML with t(8;21)(q22;q22), but also demonstrated its expression in cases that express B-cell antigens but lack this translocation.
  • Although OCT-2 and BOB.1 were not associated with PAX5 expression, we report expression of OCT-2 in AML with myelomonocytic/monocytic maturation and BOB.1 in normal hematopoietic elements.
  • [MeSH-major] Antigens, CD / metabolism. B-Cell-Specific Activator Protein / metabolism. Leukemia, Myeloid / metabolism. Octamer Transcription Factor-2 / metabolism. Trans-Activators / metabolism
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Bone Marrow / metabolism. Bone Marrow / pathology. Cell Differentiation. Flow Cytometry. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Monocytes / metabolism. Monocytes / pathology. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Tissue Array Analysis

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  • (PMID = 17074681.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Octamer Transcription Factor-2; 0 / PAX5 protein, human; 0 / POU2AF1 protein, human; 0 / Trans-Activators
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10. 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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11. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
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  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • A 2-year-old domestic shorthair cat was presented to us with decreased activity and anorexia.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.

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  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
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12. Del Principe MI, Del Poeta G, Venditti A, Buccisano F, Maurillo L, Mazzone C, Bruno A, Neri B, Irno Consalvo M, Lo Coco F, Amadori S: Apoptosis and immaturity in acute myeloid leukemia. Hematology; 2005 Feb;10(1):25-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis and immaturity in acute myeloid leukemia.
  • The primary cause of treatment failures in acute myeloid leukemia (AML) is the emergence of both resistant disease and early relapse.
  • The flow cytometric quantitative measurement of bcl-2 and bax expression for the determination of bax/bcl-2 ratio provided crucial clinical information in AML: in our hands, lower bax/bcl-2 ratio conferred a very poor prognosis with decreased rates of complete remission (CR) and overall survival (OS).
  • Moreover, striking correlations were found between lower bax/bcl-2 ratio and higher progenitor marker expression, such as CD34, CD117 and CD133 antigens, confirming the link between this apoptotic index and the maturation pathways.
  • CDDOMe, bcl-2 antisense oligonucleotides, CEP-701, etc), confirming the key role of apoptotic mechanisms on the outcome of AML patients.
  • [MeSH-major] Apoptosis / drug effects. Cell Differentiation. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Humans. Mitochondrial Proteins / physiology. Proto-Oncogene Proteins c-bcl-2 / physiology. Signal Transduction / drug effects

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  • (PMID = 16019442.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mitochondrial Proteins; 0 / Proto-Oncogene Proteins c-bcl-2
  • [Number-of-references] 89
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13. Rosato RR, Almenara JA, Maggio SC, Atadja P, Craig R, Vrana J, Dent P, Grant S: Potentiation of the lethality of the histone deacetylase inhibitor LAQ824 by the cyclin-dependent kinase inhibitor roscovitine in human leukemia cells. Mol Cancer Ther; 2005 Nov;4(11):1772-85
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  • [Title] Potentiation of the lethality of the histone deacetylase inhibitor LAQ824 by the cyclin-dependent kinase inhibitor roscovitine in human leukemia cells.
  • Interactions between the novel histone deacetylase inhibitor LAQ824 and the cyclin-dependent kinase inhibitor roscovitine were examined in human leukemia cells.
  • Pretreatment (24 hours) with a subtoxic concentration of LAQ824 (30 nmol/L) followed by a minimally toxic concentration of roscovitine (10 micromol/L; 24 hours) resulted in greater than additive effects on apoptosis in U937, Jurkat, and HL-60 human leukemia cells and blasts from three patients with acute myelogenous leukemia.
  • Collectively, these findings suggest that combined treatment of human leukemia cells with LAQ824 and roscovitine disrupts maturation and synergistically induces apoptosis, lending further support for an antileukemic strategy combining novel histone deacetylase and cyclin-dependent kinase inhibitors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Leukemia / drug therapy. Leukemia / enzymology. Purines / pharmacology
  • [MeSH-minor] Apoptosis. Apoptosis Inducing Factor / metabolism. Blotting, Western. Cell Cycle. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cytochromes c / metabolism. Cytosol / metabolism. Down-Regulation. Flow Cytometry. HL-60 Cells. Humans. Jurkat Cells. Membrane Potentials. Mitochondria / pathology. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Protein Conformation. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reactive Oxygen Species. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. U937 Cells. X-Linked Inhibitor of Apoptosis Protein / metabolism

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  • (PMID = 16275999.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA61774; United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / CA93738
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Inducing Factor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / LAQ824; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Purines; 0 / Reactive Oxygen Species; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / roscovitine; 9007-43-6 / Cytochromes c
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14. 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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  • [Cites] Biochem J. 2005 Nov 15;392(Pt 1):93-102 [16008523.001]
  • [Cites] J Biol Chem. 2003 Jul 18;278(29):27053-8 [12736248.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):5834-45 [15988001.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):9769-72 [15632201.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]
  • [Cites] Oncogene. 2005 Feb 10;24(7):1138-49 [15592522.001]
  • [Cites] Nat Genet. 2005 Jan;37(1):19-24 [15624019.001]
  • [Cites] Blood. 2004 Dec 15;104(13):3911-7 [15308577.001]
  • [Cites] Genes Dev. 2004 Dec 1;18(23):2879-92 [15545626.001]
  • [Cites] Genes Dev. 2004 Dec 1;18(23):2893-904 [15545625.001]
  • [Cites] J Clin Invest. 1999 May 15;103(10):1399-408 [10330422.001]
  • [Cites] Blood. 1992 May 15;79(10):2733-40 [1586720.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1926-45 [15314020.001]
  • [Cites] Annu Rev Nutr. 2004;24:201-21 [15189119.001]
  • [Cites] Curr Cancer Drug Targets. 2004 May;4(3):285-98 [15134535.001]
  • [Cites] Onkologie. 2004 Feb;27(1):83-90 [15007254.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(1):58-70 [14673143.001]
  • [Cites] Cell. 2003 Oct 31;115(3):305-18 [14636558.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7305-15 [14576840.001]
  • [Cites] Cancer Biol Ther. 2003 Jul-Aug;2(4 Suppl 1):S150-6 [14508093.001]
  • [Cites] Curr Treat Options Oncol. 2006 Jul;7(4):285-94 [16916489.001]
  • [Cites] Blood. 2006 Jan 15;107(2):698-707 [16166593.001]
  • [Cites] Nat Cell Biol. 2000 Aug;2(8):515-20 [10934472.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):700-5 [11212271.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(7):2283-93 [11884613.001]
  • [Cites] Blood. 2002 Nov 15;100(10):3553-60 [12411319.001]
  • [Cites] Mol Cell. 2002 Nov;10(5):995-1005 [12453409.001]
  • [Cites] J Biol Regul Homeost Agents. 2003 Jan-Mar;17(1):46-65 [12757021.001]
  • [Cites] Clin Cancer Res. 2005 Oct 15;11(20):7243-54 [16243794.001]
  • (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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15. Wang XB, Liu J, Wu JS, Sun ZM, Huang SA: [Effects of soluble secreted by acute myeloid leukemia cells on differentiation, maturation, apoptosis, and functions of dendritic cells]. Ai Zheng; 2007 Feb;26(2):142-7
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  • [Title] [Effects of soluble secreted by acute myeloid leukemia cells on differentiation, maturation, apoptosis, and functions of dendritic cells].
  • This study was to investigate the effects of soluble factors secreted by acute myeloid leukemia (AML) cells on the differentiation, maturation, apoptosis, and functions of DCs derived from normal mononuclear cells.
  • METHODS: Mononuclear cells were cultured with interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF), in the presence or absence of 24-hour culture supernatants from fresh primary AML cells, to generate immature DCs.
  • The maturation of DCs was induced by cytokines IL-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), and prostaglandin-2 (PGE-2).
  • RESULTS: AML cell supernatant-treated DCs showed significantly lower expression of co-stimulatory molecules CD80 and CD86, and reduced response to cytokines IL-1beta, IL-6, TNF-alpha, and PGE-2.
  • The apoptosis rate was significantly lower in AML cell supernatant-treated DCs than in control DCs [(29.4+/-9.5)% vs. (15.1+/-4.2)%, P<0.01].
  • The allostimulatory effects of AML cell supernatant-treated DCs on CD4+ and CD8+ T cells were significantly lower than those of normal mature DCs [PF: (1.8+/-0.5)% vs. (5.2+/-1.6)% for CD4+ T cells, (2.1+/-0.6)% vs. (6.5+/-2.0)% for CD8+ T cells, P<0.01].
  • CONCLUSION: Soluble factors derived from AML cells could inhibit development and functions of DCs.
  • [MeSH-major] Apoptosis. Cell Differentiation. Dendritic Cells. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 17298742.001).
  • [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, CD80; 0 / Antigens, CD86; 0 / Culture Media; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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16. Cui W, Kong NR, Ma Y, Amin HM, Lai R, Chai L: Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia. Mod Pathol; 2006 Dec;19(12):1585-92
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  • [Title] Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia.
  • Previously, we reported that SALL4 was constitutively expressed in acute myeloid leukemia and SALL4 transgenic mice developed acute myeloid leukemia.
  • In this study, we aimed to survey SALL4 protein expression in benign and neoplastic hematopoietic tissues in addition to acute myeloid leukemia using immunostaining with a polyclonal anti-SALL4 antibody.
  • Reverse transcription-polymerase chain reaction was also performed to detect SALL4 mRNA expression on eight precursor B-cell lymphoblastic leukemia/lymphomas, 10 benign hematopoietic tissues, and seven hematopoietic cancer cell lines.
  • In neoplastic tissues, only precursor B-cell lymphoblastic leukemia/lymphomas had detectable SALL4 (12/16 at protein level, 7/8 at RNA level), similar to that observed in acute myeloid leukemia.
  • Of the seven cell lines examined, only those derived from acute myeloid leukemia and precursor B-cell lymphoblastic leukemia/lymphomas were positive.
  • The persistence of SALL4 expression in leukemic blasts in precursor B-cell lymphoblastic leukemia/lymphomas resembles to what we observed in acute myeloid leukemia, and correlates with the maturation arrest of these cells.
  • We have shown in our previous study that the constitutive expression of SALL4 in mice can lead to acute myeloid leukemia development.
  • The similar expression pattern of SALL4 in acute myeloid leukemia and B-cell lymphoblastic leukemia/lymphomas suggests that these two disease entities may share similar biological features and/or mechanisms of leukemogenesis.
  • More definite studies to investigate the role of SALL4 in the pathogenesis of B-cell lymphoblastic leukemia/lymphomas are needed in the future to address this question.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma / genetics. Plasmacytoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

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  • (PMID = 16998462.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK063220
  • [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 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / SALL4 protein, human; 0 / Transcription Factors
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17. Skokowa J, Germeshausen M, Zeidler C, Welte K: Severe congenital neutropenia: inheritance and pathophysiology. Curr Opin Hematol; 2007 Jan;14(1):22-8
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  • PURPOSE OF REVIEW: Severe congenital neutropenia is a heterogeneous disorder of hematopoiesis characterized by a maturation arrest of granulopoiesis at the level of promyelocytes with peripheral blood absolute neutrophil counts below 0.5 x 10/l.
  • This genetic heterogeneity suggests that several pathologic mechanisms may lead to the same phenotype due to downregulation of common myeloid transcription factors.
  • Congenital neutropenia is considered as a preleukemic syndrome, since after 10 years of observation the cumulative incidence for leukemia is 21%.
  • Acquired granulocyte colony-stimulating factor receptor mutations are detected in approximately 80% of congenital neutropenia patients who developed acute myeloid leukemia.
  • SUMMARY: Congenital neutropenia is a congenital disorder of hematopoiesis inherited by autosomal dominant or recessive traits.
  • Congenital neutropenia patients with acquired granulocyte colony-stimulating factor receptor mutations define a group with high risk for development of leukemia.

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  • [ErratumIn] Curr Opin Hematol. 2007 Mar;14(2):181
  • (PMID = 17133096.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lymphoid Enhancer-Binding Factor 1; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.4.21.37 / Leukocyte Elastase
  • [Number-of-references] 54
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18. Henrich S, Crossett B, Christopherson RI: Differentially expressed nuclear proteins in human CCRF-CEM, HL-60, MEC-1 and Raji cells correlate with cellular properties. Proteomics Clin Appl; 2007 Oct;1(10):1252-65
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  • The human cell lines CCRF-CEM (T-cell acute lymphocytic leukemia), HL-60 (acute myeloid leukemia), MEC-1 (B-cell chronic lymphocytic leukemia) and Raji (Burkitt's B-cell lymphoma) have been analysed for differences in their nuclear proteomes.
  • Proteins uniquely over-expressed between myeloid and lymphoid cell lines include those that may have use as markers for diagnosis, disease progression and B-cell maturation and differentiation.
  • Expression of various proliferation-associated nuclear proteins correlated with relative growth rates of the cell lines, giving these proteins potential diagnostic applications for distinction of chronic versus acute subtypes of haematological malignancies.
  • The nuclear expression profiles should enable classification of subtypes of leukemia, and identify potential nuclear protein targets for development of diagnostic and therapeutic strategies.

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  • [Copyright] Copyright © 2007 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
  • (PMID = 21136623.001).
  • [ISSN] 1862-8346
  • [Journal-full-title] Proteomics. Clinical applications
  • [ISO-abbreviation] Proteomics Clin Appl
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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19. Kim H, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ: [A Case of Acute Myeloid Leukemia with Masked t(8;21).]. Korean J Lab Med; 2006 Oct;26(5):338-42
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  • [Title] [A Case of Acute Myeloid Leukemia with Masked t(8;21).].
  • We report a case that revealed the characteristics of acute myeloblastic leukemia with maturation (AML-M2) on the morphology of the bone marrow biopsy and 45,X,-Y in conventional cytogenetic study, but was confirmed to have a typical AML1/ETO translocation by molecular studies using reverse transcriptase polymerase chain reaction and fluorescence in situ hybridization.
  • In case typical morphologic features compatible with recurrent cytogenetic abnormalities are shown, molecular studies in addition to conventional cytogenetic study might be required to confirm the diagnosis.

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  • (PMID = 18156748.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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20. 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


21. 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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22. 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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  • [Cites] Dev Cell. 2004 Nov;7(5):637-51 [15525526.001]
  • [Cites] Nat Med. 2006 Aug;12(8):945-9 [16892037.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Cell. 2000 Oct 27;103(3):375-86 [11081625.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(1):156-63 [11113190.001]
  • [Cites] Nature. 2001 Jan 18;409(6818):355-9 [11201745.001]
  • [Cites] Leuk Res. 2001 Apr;25(4):313-22 [11248328.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9889-95 [11150306.001]
  • [Cites] Cell. 2001 May 18;105(4):445-57 [11371342.001]
  • [Cites] Leuk Lymphoma. 2000 Dec;40(1-2):67-77 [11426630.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6470-83 [11533236.001]
  • [Cites] Mol Endocrinol. 2001 Nov;15(11):1870-9 [11682618.001]
  • [Cites] Dev Cell. 2001 Aug;1(2):227-37 [11702782.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5187-93 [11729202.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2985-91 [11929790.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Curr Biol. 2002 Aug 20;12(16):1368-78 [12194817.001]
  • [Cites] FEBS Lett. 2002 Sep 25;528(1-3):246-50 [12297314.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] Blood. 2003 Jan 1;101(1):289-91 [12393441.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4574-9 [12672959.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):440-5 [14744753.001]
  • [Cites] Oncogene. 2004 Mar 15;23(11):2016-27 [15021889.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4459-64 [15070740.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2825-37 [15077146.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 8;101(23):8699-704 [15159543.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] Cancer Genet Cytogenet. 1986 Aug;22(4):331-8 [3460687.001]
  • [Cites] Eur J Immunol. 1988 Jan;18(1):97-104 [2831066.001]
  • [Cites] Cancer Genet Cytogenet. 1990 Feb;44(2):169-79 [2297675.001]
  • [Cites] Blood. 1991 May 1;77(9):2031-6 [2018839.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Cancer Genet Cytogenet. 1993 Oct 1;70(1):6-11 [8221614.001]
  • [Cites] Leukemia. 1994 Mar;8(3):465-75 [7907395.001]
  • [Cites] J Tongji Med Univ. 1994;14(1):35-7 [7877191.001]
  • [Cites] Leuk Lymphoma. 1994 Dec;16(1-2):51-6 [7696931.001]
  • [Cites] Br J Haematol. 1995 Apr;89(4):805-11 [7772516.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] Genes Dev. 1996 Dec 15;10(24):3081-93 [8985178.001]
  • [Cites] Leuk Lymphoma. 1996 Oct;23(3-4):227-34 [9031103.001]
  • [Cites] Nat Genet. 1997 Mar;15(3):303-6 [9054947.001]
  • [Cites] Blood. 1998 May 1;91(9):3134-43 [9558367.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3604-11 [9584201.001]
  • [Cites] Cell. 1998 Jun 12;93(6):1067-76 [9635435.001]
  • [Cites] Clin Lab Haematol. 1999 Feb;21(1):17-20 [10197258.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] Science. 1999 Jul 16;285(5426):418-22 [10411507.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1456-66 [15522959.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2452-61 [15972450.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):773-85 [16195750.001]
  • [Cites] Nature. 2005 Oct 13;437(7061):1043-7 [16222300.001]
  • [Cites] Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2005 Oct;13(5):733-40 [16277833.001]
  • [Cites] PLoS Biol. 2005 Dec;3(12):e416 [16292982.001]
  • [Cites] Cancer Treat Rev. 2006 May;32(3):166-79 [16527420.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17186-91 [15569932.001]
  • (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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23. Babusikova O, Stevulova L, Fajtova M: Immunophenotyping parameters as prognostic factors in T-acute leukemia patients. Neoplasma; 2009;56(6):508-13
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  • [Title] Immunophenotyping parameters as prognostic factors in T-acute leukemia patients.
  • The main aim of this study represents the extension of our studies using multiparametric flow cytometry analysis for exact definition of membrane and intracellular (cytoplasmic and nuclear) markers of acute leukemia cells of T-phenotype.
  • The main aim was concerned to more proper T-ALL diagnosis and stage definition and identification of the prognostic factors and the useful markers for the follow-up of T-ALL in remission.
  • New knowledge of the T-cell maturation stages of hematopoietic cells in bone marrow and thymus has been applied, as each T-acute leukemia clone is representative of one blocked stage through maturation.
  • Patients with more favorable prognosis (i. e. those of cortical stage) could have been already differentiated at diagnosis from those, allocated to pro-T stage, with very immature phenotypes and of an unfavorable clinical course.
  • These patients had very distinctive immunophenotes, CD1a and CD8 markers completely negative, CD7 and cCD3 positive; CD5 was weakly expressed and myeloid markers CD33 and CD13 were coexpressed, or immature markers CD34, HLA-DR were coexpressed, together with myeloid markers CD13 and CD33 of weak positivity.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, T-Lymphocyte / immunology. Biomarkers, Tumor / immunology. HLA-DR Antigens / analysis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19728759.001).
  • [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 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / HLA-DR Antigens
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24. Nowbakht P, Ionescu MC, Rohner A, Kalberer CP, Rossy E, Mori L, Cosman D, De Libero G, Wodnar-Filipowicz A: Ligands for natural killer cell-activating receptors are expressed upon the maturation of normal myelomonocytic cells but at low levels in acute myeloid leukemias. Blood; 2005 May 1;105(9):3615-22
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  • [Title] Ligands for natural killer cell-activating receptors are expressed upon the maturation of normal myelomonocytic cells but at low levels in acute myeloid leukemias.
  • Here, we have studied the role of NKG2D and natural cytotoxicity receptors (NCRs) in the recognition of human leukemia.
  • Analysis of UL16-binding protein-1 (ULBP1), ULBP2, and ULBP3 ligands for NKG2D and of potential ligands for NKp30, NKp44, and NKp46 in healthy hematopoietic cells demonstrated the ligand-negative phenotype of bone marrow-derived CD34(+) progenitor cells and the acquisition of cell-surface ligands during the course of myeloid differentiation.
  • In acute myeloid leukemia (AML), leukemic blasts from approximately 80% of patients expressed very low levels of ULBPs and NCR-specific ligands.
  • Treatment with differentiation-promoting myeloid growth factors, together with interferon-gamma, upregulated cell-surface levels of ULBP1 and putative NCR ligands on AML blasts, conferring an increased sensitivity to NK cell-mediated lysis.
  • We conclude that the ligand-negative/low phenotype in AML is a consequence of cell maturation arrest on malignant transformation and that defective expression of ligands for the activating NKG2D and NCR receptors may compromise leukemia recognition by NK cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / immunology. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Monocytes / pathology. Receptors, Immunologic / genetics
  • [MeSH-minor] Acute Disease. Case-Control Studies. Cell Differentiation. Humans. Ligands. Myeloid Cells / pathology. NK Cell Lectin-Like Receptor Subfamily K. Natural Cytotoxicity Triggering Receptor 1. Natural Cytotoxicity Triggering Receptor 2. Natural Cytotoxicity Triggering Receptor 3. Receptors, Natural Killer Cell

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  • (PMID = 15657183.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KLRK1 protein, human; 0 / Ligands; 0 / NCR1 protein, human; 0 / NCR2 protein, human; 0 / NCR3 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily K; 0 / Natural Cytotoxicity Triggering Receptor 1; 0 / Natural Cytotoxicity Triggering Receptor 2; 0 / Natural Cytotoxicity Triggering Receptor 3; 0 / Receptors, Immunologic; 0 / Receptors, Natural Killer Cell
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25. 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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26. Pereira FG, Metze K, Costa FP, Lima CS, Lorand-Metze I: Phenotypic quantitative features of patients with acute myeloid leukemia. Neoplasma; 2006;53(2):155-60
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  • [Title] Phenotypic quantitative features of patients with acute myeloid leukemia.
  • The recent WHO classification for acute myeloid leukemias (AML) separates entities by recurrent cytogenetic abnormalities and immunophenotypic features presenting prognostic impact.
  • We have examined the expression of several lineage and maturation linked antigens used in routine immunophenotyping of patients with de novo AML, using a 3-color two-step panel.
  • Predominant FAB types were M2 and M4.
  • In Cox univariate analysis, age, peripheral leukocytes (WBC) at diagnosis, MFI of CD45, and MPO were significant for worse a survival.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal. Antigens, CD / metabolism. Female. Flow Cytometry. Humans. Male. Middle Aged. Neoplasm, Residual. Phenotype. Prognosis. Survival Analysis

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  • (PMID = 16575472.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Biomarkers, Tumor
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27. 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


28. Wang H, Yang W, Shao H, Zhang J, Qi L, Liao A, Li Y, Liu Z: Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2). Cancer Genet Cytogenet; 2009 Jan 15;188(2):95-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complex t(2;21;8)(p12;q22;q22): a variant t(8;21) in a patient with acute myeloid leukemia (AML-M2).
  • Acute myeloid leukemia with maturation (AML-M2 based on the French-American-British classification) is often accompanied by typical chromosomal changes such as t (8;21)(q22;q22).
  • The role of this complex variant translocation, as well as the possible formation mechanism, prognostic factors, and morphologic changes are discussed.
  • [MeSH-major] Chromosomes, Human, Pair 2. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • [RetractionIn] Cancer Genet Cytogenet. 2009 Jul;192(1):54 [19489159.001]
  • (PMID = 19100512.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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29. 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


30. Bertagnolo V, Brugnoli F, Mischiati C, Sereni A, Bavelloni A, Carini C, Capitani S: Vav promotes differentiation of human tumoral myeloid precursors. Exp Cell Res; 2005 May 15;306(1):56-63
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  • [Title] Vav promotes differentiation of human tumoral myeloid precursors.
  • In T and B cells, it appears crucial for both development and functions, while, in non-lymphoid hematopoietic cells, Vav seems not involved in cell maturation, but rather in the response of mature cells to agonist-dependent proliferation and phagocytosis.
  • We have previously demonstrated that the amount and the tyrosine phosphorylation of Vav are up-regulated in both whole cells and nuclei of tumoral promyelocytes induced to granulocytic maturation by ATRA and that tyrosine-phosphorylated Vav does not display any ATRA-induced GEF activity but contributes to the regulation of PI 3-K activity.
  • In this study, we report that Vav accumulates in nuclei of ATRA-treated APL-derived cells and that the down-modulation of Vav prevents differentiation of tumoral promyelocytes, indicating that it is a key molecule in ATRA-dependent myeloid maturation.
  • On the other hand, the overexpression of Vav induces an increased expression of surface markers of granulocytic differentiation without affecting the maturation-related changes of the nuclear morphology.
  • Our data support the unprecedented notion that Vav plays crucial functions in the maturation process of myeloid cells, and suggest that Vav can be regarded as a potential target for the therapeutic treatment of myeloproliferative disorders.
  • [MeSH-major] Cell Cycle Proteins / physiology. Cell Differentiation / physiology. Myeloid Progenitor Cells / metabolism. Proto-Oncogene Proteins / physiology
  • [MeSH-minor] Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Gene Expression / genetics. Gene Expression / physiology. Gene Expression Regulation, Leukemic / drug effects. Granulocytes / physiology. HL-60 Cells. Humans. Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Phosphorylation. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-vav. RNA, Small Interfering / genetics. Stilbenes / pharmacology. Transfection. Tretinoin / pharmacology. Tumor Cells, Cultured

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  • (PMID = 15878332.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Stilbenes; 0 / VAV1 protein, human; 4339-71-3 / 3,3',4,5'-tetrahydroxystilbene; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Protein-Tyrosine Kinases
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31. Kufner S, Zitzelsberger H, Kroell T, Pelka-Fleischer R, Salem A, de Valle F, Schweiger C, Nuessler V, Schmid C, Kolb HJ, Schmetzer HM: Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions. Scand J Immunol; 2005 Jul;62(1):86-98
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  • [Title] Leukemia-derived dendritic cells can be generated from blood or bone marrow cells from patients with acute myeloid leukaemia: a methodological approach under serum-free culture conditions.
  • Functional dendritic cells (DC) are professional antigen-presenting cells (APC) and can be generated in vitro from healthy as well as from leukaemic cells from acute myeloid leukemia (AML) patients giving rise to APC of leukaemic origin-presenting leukaemic antigens.
  • We describe the generation and characterization of DC from different mononuclear cell (MNC) fractions from 50 AML patients under different serum-free culture conditions, determine the optimal culture conditions and compare the results with that from 23 healthy donors.
  • In detail, we could show that AML-DC harvests were higher after 10-14 days culture (healthy DC: 7 days); total or adherent PB or BM-MNC fractions yield comparable DC counts, however, from magnetic cell sorting (MACS)-depleted MNC fractions or thawn MNC lower DC counts can be generated.
  • Whereas the addition of FL increases the DC harvest, the addition of autologous plasma in many cases has inhibitory influence on DC maturation.
  • Optimal harvest of vital and mature DC from AML samples was obtained with a granulocyte/macrophage-colony stimulating factor, interleukin-4, FL and tumour necrosis factor-alpha-containing serum-free Xvivo medium after 10-14 days of culture (36/26% DC; 38/64% vital DC; 46/51% mature DC were generated from AML/healthy MNC samples).
  • Surface marker profiles (e.g. costimulatory antigen expressing) of DC obtained from AML samples were comparable with that of healthy DC.
  • The leukaemic derivation of AML-DC was demonstrated by the persistence of the clonal cytogenetic aberration in the DC or by coexpression of leukaemic antigens on DC.
  • Autologous T-cell activation of leukaemia-derived DC was demonstrated in cases with AML.
  • We demonstrate that the generation of leukaemia-derived DC is feasable in AML under serum-free culture conditions giving rise to DC with comparable characteristics as healthy DC and offering an anti-leukaemia-directed immunotherapeutical vaccination strategy in AML.
  • [MeSH-major] Bone Marrow Cells / immunology. Cell Culture Techniques. Dendritic Cells / immunology. Leukemia, Myeloid / immunology. Leukocytes, Mononuclear / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Culture Media, Serum-Free. Female. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-4 / pharmacology. Lymphocyte Activation. Male. Middle Aged. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / pharmacology. Vaccination / methods

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  • (PMID = 16091128.001).
  • [ISSN] 0300-9475
  • [Journal-full-title] Scandinavian journal of immunology
  • [ISO-abbreviation] Scand. J. Immunol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Culture Media, Serum-Free; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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32. 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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33. Nguyen S, Beziat V, Dhedin N, Kuentz M, Vernant JP, Debre P, Vieillard V: HLA-E upregulation on IFN-gamma-activated AML blasts impairs CD94/NKG2A-dependent NK cytolysis after haplo-mismatched hematopoietic SCT. Bone Marrow Transplant; 2009 May;43(9):693-9
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  • [Title] HLA-E upregulation on IFN-gamma-activated AML blasts impairs CD94/NKG2A-dependent NK cytolysis after haplo-mismatched hematopoietic SCT.
  • Natural killer (NK) cells generated after haploidentical hematopoietic SCT in patients with AML are characterized by specific phenotypic features and impaired functioning that may affect transplantation outcome.
  • We show that IFN-gamma produced by immature CD56(bright) NK cells upregulates cell surface expression of HLA-E on AML blasts and that this upregulation protects leukemic cells from NK-mediated cell lysis through the mediation of CD94/NKG2A, an inhibitory receptor overexpressed on NK cells after haploidentical SCT.
  • This implies that maturation of NK cells is the key to improved immune responses and transplantation outcome.
  • [MeSH-major] HLA Antigens / genetics. Hematopoietic Stem Cell Transplantation. Histocompatibility Antigens Class I / genetics. Interferon-gamma / pharmacology. Interferon-gamma / physiology. Killer Cells, Natural / immunology. Leukemia, Myeloid, Acute / pathology. NK Cell Lectin-Like Receptor Subfamily C / immunology. NK Cell Lectin-Like Receptor Subfamily D / immunology

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  • (PMID = 19011664.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-E antigen; 0 / Histocompatibility Antigens Class I; 0 / KLRC1 protein, human; 0 / KLRD1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily C; 0 / NK Cell Lectin-Like Receptor Subfamily D; 82115-62-6 / Interferon-gamma
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34. Schnittger S, Haferlach C, Ulke M, Alpermann T, Kern W, Haferlach T: IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status. Blood; 2010 Dec 16;116(25):5486-96
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  • [Title] IDH1 mutations are detected in 6.6% of 1414 AML patients and are associated with intermediate risk karyotype and unfavorable prognosis in adults younger than 60 years and unmutated NPM1 status.
  • Mutations in the IDH1 gene at position R132 coding for the enzyme cytosolic isocitrate dehydrogenase are known in glioma and have recently been detected also in acute myeloid leukemia (AML).
  • To further clarify the role of this mutation in AML, we have analyzed IDH1R132 in 1414 AML patients.
  • IDH1-mutated cases more often had AML without maturation/French-American-British M1 (P < .001), an immature immunophenotype, and female sex (8.7% vs 4.7% in male, P = .003) compared with IDH1wt cases.
  • In conclusion, these data show that IDH1R132 may significantly add information regarding characterization and prognostication in AML.
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics

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  • (PMID = 20805365.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human
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35. Gozzini A, Santini V: Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts. Ann Hematol; 2005 Dec;84 Suppl 1:54-60
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  • [Title] Butyrates and decitabine cooperate to induce histone acetylation and granulocytic maturation of t(8;21) acute myeloid leukemia blasts.
  • In leukemic cells, hypermethylation of CpG islands in the promoter region of genes critical for cell cycle and maturation is frequent, and DNMTs were found to be overexpressed, findings paralleled by evidence of transcriptional repression of downstream genes.
  • Therefore, the combination of HDAC and DNMT inhibitors has been considered to be a possible therapeutic approach to restore normal gene expression in acute myeloid leukemia (AML) and other diseases.
  • Thus, treatment of AML with HDAC inhibitors such as D1 and DNMT inhibitors such as decitabine might have clinical benefit for patients, especially these presenting subtypes of AML, like AML1/ETO, in which the leukemogenic mechanism involves corepressor protein complexes containing HDAC and DNMT.
  • [MeSH-major] Azacitidine / analogs & derivatives. Butyrates / pharmacology. DNA Modification Methylases / antagonists & inhibitors. Histone Deacetylase Inhibitors. Leukemia, Myeloid, Acute / genetics. Mannose / analogs & derivatives

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  • (PMID = 16228241.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Butyrates; 0 / Histone Deacetylase Inhibitors; 0 / O-n-butanoyl-2,3-O-isopropylidenemannofuranoside; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine; PHA4727WTP / Mannose
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36. 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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  • [Cites] Cancer Res. 2004 Jan 1;64(1):370-7 [14729647.001]
  • [Cites] J Cell Physiol. 2004 Mar;198(3):333-42 [14755538.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):233-8 [15225777.001]
  • [Cites] J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):365-70 [15225802.001]
  • [Cites] Exp Cell Res. 2004 Aug 15;298(2):339-58 [15265684.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5425-33 [15289351.001]
  • [Cites] Steroids. 2004 Sep;69(10):629-35 [15465107.001]
  • [Cites] Blood. 1979 Sep;54(3):713-33 [288488.001]
  • [Cites] J Biol Chem. 2000 Jun 9;275(23):17276-80 [10764733.001]
  • [Cites] Exp Cell Res. 2000 Aug 1;258(2):425-37 [10896794.001]
  • [Cites] J Cell Biochem. 2001;80(4):471-82 [11169731.001]
  • [Cites] Cancer Res. 2001 Feb 1;61(3):963-9 [11221891.001]
  • [Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]
  • [Cites] J Cell Sci. 2001 May;114(Pt 9):1609-12 [11309192.001]
  • [Cites] J Cell Biochem. 2001 Apr 2-27;82(1):68-77 [11400164.001]
  • [Cites] Exp Cell Res. 2001 Aug 15;268(2):294-300 [11478855.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 15;93(16):1224-33 [11504768.001]
  • [Cites] Biol Signals Recept. 2001 Nov-Dec;10(6):341-9 [11721090.001]
  • [Cites] Steroids. 2002 Aug;67(9):789-98 [12123791.001]
  • [Cites] Acta Biochim Pol. 2002;49(2):393-406 [12362981.001]
  • [Cites] Cell Cycle. 2002 Mar-Apr;1(2):103-10 [12429916.001]
  • [Cites] Cell Cycle. 2002 Nov-Dec;1(6):410-5 [12548017.001]
  • [Cites] J Cell Biochem. 2003 Mar 1;88(4):695-705 [12577303.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9402-6 [12522135.001]
  • [Cites] Cancer Res. 2003 Mar 15;63(6):1325-32 [12649194.001]
  • [Cites] J Cell Biochem. 2003 Aug 15;89(6):1087-101 [12898508.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52651-9 [14517214.001]
  • [Cites] Biochemistry. 1990 Jan 9;29(1):190-6 [2322540.001]
  • [Cites] J Biol Chem. 1990 Sep 15;265(26):15823-31 [2394750.001]
  • [Cites] J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):231-40 [1314073.001]
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27489-94 [7499206.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]
  • [Cites] J Natl Cancer Inst. 1997 Aug 20;89(16):1199-206 [9274914.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):12792-6 [9371754.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23242-8 [10438498.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):472-87 [15601867.001]
  • (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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37. Bennett CL, Evens AM, Andritsos LA, Balasubramanian L, Mai M, Fisher MJ, Kuzel TM, Angelotta C, McKoy JM, Vose JM, Bierman PJ, Kuter DJ, Trifilio SM, Devine SM, Tallman MS: Haematological malignancies developing in previously healthy individuals who received haematopoietic growth factors: report from the Research on Adverse Drug Events and Reports (RADAR) project. Br J Haematol; 2006 Dec;135(5):642-50
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  • Pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) and granulocyte colony-stimulating factor (G-CSF) promote haematopoietic progenitor cell maturation.
  • Mantle cell, diffuse large B-cell lymphoma and chronic lymphocytic leukaemia were diagnosed 1-5 years after PEG-rHuMGDF exposure among three volunteers.
  • Acute myeloid leukaemia was diagnosed 4 and 5 years after G-CSF mobilisation in two donors who underwent peripheral blood stem cell donation for sibling allogeneic haematopoietic stem cell transplantation.
  • Following intensive chemotherapy, one died from acute leukaemia and the second is in complete remission.
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Autoantibodies / immunology. Clinical Trials as Topic. Female. Granulocyte Colony-Stimulating Factor / adverse effects. Humans. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / etiology. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / etiology. Leukemia, Monocytic, Acute / genetics. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / etiology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / etiology. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Polyethylene Glycols / adverse effects. Recombinant Proteins / adverse effects. Thrombopoietin / adverse effects. Thrombopoietin / immunology

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  • [CommentIn] Br J Haematol. 2007 Apr;137(1):77-8; author reply 79-80 [17359373.001]
  • [CommentIn] Br J Haematol. 2007 Apr;137(1):78-9; author reply 79-80 [17359374.001]
  • [CommentIn] Br J Haematol. 2006 Dec;135(5):651-2 [17054429.001]
  • (PMID = 17054431.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA 102713-01; United States / NCI NIH HHS / CA / K23 CA109613-A1; United States / NCI NIH HHS / CA / P 30 CA60553
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Hematopoietic Cell Growth Factors; 0 / Recombinant Proteins; 0 / polyethylene glycol-recombinant human megakaryocyte growth and development factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 30IQX730WE / Polyethylene Glycols; 9014-42-0 / Thrombopoietin
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38. Walter RB, Gooley TA, van der Velden VH, Loken MR, van Dongen JJ, Flowers DA, Bernstein ID, Appelbaum FR: CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy. Blood; 2007 May 15;109(10):4168-70
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  • [Title] CD33 expression and P-glycoprotein-mediated drug efflux inversely correlate and predict clinical outcome in patients with acute myeloid leukemia treated with gemtuzumab ozogamicin monotherapy.
  • Studying patients undergoing GO monotherapy for relapsed acute myeloid leukemia (AML), we now find that AML blasts of responders have a significantly higher mean CD33 level and lower P-glycoprotein (Pgp) activity compared with nonresponders.
  • The inverse relationship between CD33 and Pgp suggests a maturation-stage-dependent expression of both proteins, and offers the rationale for using cell differentiation-promoting agents to enhance GO-induced cytotoxicity.

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  • [Cites] Leukemia. 1999 Dec;13(12):1943-53 [10602414.001]
  • [Cites] Exp Hematol. 2006 Jan;34(1):54-65 [16413391.001]
  • [Cites] Blood. 2001 May 15;97(10):3197-204 [11342449.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3244-54 [11432892.001]
  • [Cites] Blood. 2001 Aug 15;98(4):988-94 [11493443.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1544-53 [11587212.001]
  • [Cites] Leukemia. 2002 May;16(5):813-9 [11986941.001]
  • [Cites] Am J Clin Pathol. 2002 Oct;118(4):560-6 [12375643.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1466-73 [12689934.001]
  • [Cites] Cancer. 2003 Nov 15;98(10):2095-104 [14601078.001]
  • [Cites] Leukemia. 2004 Feb;18(2):316-25 [14614514.001]
  • [Cites] Cancer. 2004 Feb 1;100(3):441-54 [14745859.001]
  • [Cites] Haematologica. 2004 May;89(5):634-6 [15136240.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4276-84 [14962898.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Blood. 1999 Aug 1;94(3):1086-99 [10419902.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 6):2-8 [10530710.001]
  • [Cites] Haematologica. 2005 Jan;90(1):54-9 [15642669.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1295-302 [15454492.001]
  • [Cites] Leukemia. 2005 Feb;19(2):176-82 [15592433.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1442-52 [16116598.001]
  • [Cites] Glycobiology. 2006 Jan;16(1):1R-27R [16014749.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1436-43 [10942240.001]
  • (PMID = 17227830.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA091 316
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / P-Glycoprotein; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
  • [Other-IDs] NLM/ PMC1885511
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39. 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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40. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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41. 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]
  • [Cites] Leukemia. 2003 Apr;17(4):731-7 [12682630.001]
  • [Cites] Leuk Res. 1998 Oct;22(10):899-903 [9766750.001]
  • (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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42. 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]
  • [Cites] J Assoc Physicians India. 2002 Nov;50:1435-7 [12583479.001]
  • [Cites] Ann Hematol. 2003 Apr;82(4):231-5 [12707726.001]
  • [Cites] Am J Hematol. 2007 May;82(5):405-8 [17133422.001]
  • [Cites] Bildgebung. 1994 Mar;61(1):37-9 [8193516.001]
  • [Cites] Ann Hematol. 1996 Dec;73(6):297-302 [9003161.001]
  • [Cites] Haematologica. 1998 Aug;83(8):760-1 [9793269.001]
  • [Cites] Jpn J Med. 1987 May;26(2):234-6 [3476781.001]
  • (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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43. 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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44. 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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  • [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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45. Reynaud S, Malissein E, Donnard M, Bordessoule D, Turlure P, Trimoreau F, Denizot Y: Functional platelet-activating factor receptors in immature forms of leukemic blasts. Leuk Res; 2007 Mar;31(3):399-402
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  • We highlight, for the first time, Gq transcripts, PAF receptor (PAF-R) transcripts and protein in blast cells of acute myeloid (AML) and lymphoid (ALL) leukemia patients.
  • In conclusion, functional PAF-R are present in blast cells of patients with acute leukemia; a result that could be of physiologic importance regarding the important effect of PAF on leukocytes maturation and functions.
  • [MeSH-major] Blast Crisis. Leukemia, Lymphoid / metabolism. Leukemia, Lymphoid / pathology. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Platelet Membrane Glycoproteins / metabolism. Receptors, G-Protein-Coupled / metabolism
  • [MeSH-minor] Acute Disease. Calcium / metabolism. Humans. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription, Genetic

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  • (PMID = 16837045.001).
  • [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 / Platelet Membrane Glycoproteins; 0 / Receptors, G-Protein-Coupled; 0 / platelet activating factor receptor; SY7Q814VUP / Calcium
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46. Yoshida H, Ichikawa H, Tagata Y, Katsumoto T, Ohnishi K, Akao Y, Naoe T, Pandolfi PP, Kitabayashi I: PML-retinoic acid receptor alpha inhibits PML IV enhancement of PU.1-induced C/EBPepsilon expression in myeloid differentiation. Mol Cell Biol; 2007 Aug;27(16):5819-34
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  • [Title] PML-retinoic acid receptor alpha inhibits PML IV enhancement of PU.1-induced C/EBPepsilon expression in myeloid differentiation.
  • PML and PU.1 play important roles in myeloid differentiation.
  • PML-deficient mice have an impaired capacity for terminal maturation of their myeloid precursor cells.
  • We showed that PU.1 directly activates the transcription of the C/EBPepsilon gene that is essential for granulocytic differentiation.
  • The type IV isoform of PML interacted with PU.1, promoted its association with p300, and then enhanced PU.1-induced transcription and granulocytic differentiation.
  • In contrast to PML IV, the leukemia-associated PML-retinoic acid receptor alpha fusion protein dissociated the PU.1/PML IV/p300 complex and inhibited PU.1-induced transcription.
  • These results suggest a novel pathogenic mechanism of the PML-retinoic acid receptor alpha fusion protein in acute promyelocytic leukemia.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / metabolism. Cell Differentiation. Myeloid Cells / cytology. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism. Transcription Factors / metabolism. Tumor Suppressor Proteins / metabolism

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  • [Cites] Nat Genet. 1999 Nov;23(3):287-95 [10610177.001]
  • [Cites] Mol Cell Biol. 1997 Mar;17(3):1375-86 [9032264.001]
  • [Cites] Nat Cell Biol. 2000 May;2(5):E85-90 [10806494.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3349-56 [10828015.001]
  • [Cites] Blood. 2000 Aug 15;96(4):1297-308 [10942371.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1314-20 [11222375.001]
  • [Cites] Stem Cells. 2001;19(2):125-33 [11239167.001]
  • [Cites] Leuk Res. 2001 Nov;25(11):981-95 [11597733.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7178-85 [11704846.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7186-203 [11704847.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7216-22 [11704849.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jun 10;94(12):6462-7 [9177240.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Nov 25;94(24):13187-92 [9371821.001]
  • [Cites] Stem Cells. 1998;16(1):25-37 [9474745.001]
  • [Cites] Science. 1998 Mar 6;279(5356):1547-51 [9488655.001]
  • [Cites] Oncogene. 1999 Feb 18;18(7):1495-501 [10050886.001]
  • [Cites] Blood. 1999 May 15;93(10):3167-215 [10233871.001]
  • [Cites] J Clin Invest. 1999 May 15;103(10):1399-408 [10330422.001]
  • [Cites] Blood. 1999 Jul 15;94(2):560-71 [10397723.001]
  • [Cites] Blood. 2005 Jan 1;105(1):292-300 [15331439.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12513-8 [16113082.001]
  • [Cites] Cancer Cell. 2006 Feb;9(2):81-94 [16473276.001]
  • [Cites] J Exp Med. 2006 Apr 17;203(4):821-8 [16549595.001]
  • [Cites] Oncogene. 2001 Oct 29;20(49):7223-33 [11704850.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3377-90 [12032776.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4406-12 [12036869.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1141-8 [12393450.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3265-73 [12515729.001]
  • [Cites] EMBO J. 2003 Nov 3;22(21):5806-16 [14592978.001]
  • [Cites] Blood. 2003 Nov 15;102(10):3727-36 [12893766.001]
  • [Cites] Nat Genet. 2004 Jun;36(6):624-30 [15146183.001]
  • [Cites] Cell. 1990 Apr 6;61(1):113-24 [2180582.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1257-66 [1708811.001]
  • [Cites] Cell. 1991 Aug 23;66(4):663-74 [1652368.001]
  • [Cites] Cell. 1991 Aug 23;66(4):675-84 [1652369.001]
  • [Cites] Science. 1994 Sep 9;265(5178):1573-7 [8079170.001]
  • [Cites] Oncogene. 1995 Oct 19;11(8):1549-60 [7478579.001]
  • [Cites] Immunity. 1995 Dec;3(6):703-14 [8777716.001]
  • [Cites] Cancer Res. 1996 Jul 1;56(13):2945-8 [8674046.001]
  • [Cites] EMBO J. 1996 Oct 15;15(20):5647-58 [8896458.001]
  • [Cites] Blood. 2000 May 1;95(9):2748-52 [10779416.001]
  • (PMID = 17562868.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / Cebpe protein, mouse; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / proto-oncogene protein Spi-1; 142805-41-2 / CEBPE protein, human; 143220-95-5 / PML protein, human; EC 2.3.1.48 / E1A-Associated p300 Protein; EC 2.3.1.48 / EP300 protein, human
  • [Other-IDs] NLM/ PMC1952121
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47. 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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48. 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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49. Florian S, Sonneck K, Hauswirth AW, Krauth MT, Schernthaner GH, Sperr WR, Valent P: Detection of molecular targets on the surface of CD34+/CD38-- stem cells in various myeloid malignancies. Leuk Lymphoma; 2006 Feb;47(2):207-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of molecular targets on the surface of CD34+/CD38-- stem cells in various myeloid malignancies.
  • Recent data suggest that myeloid neoplasms are organized hierarchically in terms of self-renewal and maturation of early progenitor cells, similar to normal myelopoiesis.
  • In acute myeloid leukemia (AML), the NOD/SCID mouse-repopulating leukemic stem cells usually co-express CD123 with CD34, but lack CD38.
  • In the present study, expression of target antigens on CD34+/CD38- cells was analysed by multi-color flow cytometry in patients with AML (n = 18), myelodysplastic syndromes (MDS, n = 6), chronic myeloid leukemia (CML, n = 8) and systemic mastocytosis (SM, n = 9).
  • Independent of the type of disease, the vast majority of these stem cells co-expressed aminopeptidase-N (CD13) and CD44 in all patients.
  • In conclusion, neoplastic stem cells in various myeloid neoplasms appear to express a similar phenotype including target antigens such as CD13, CD33 and CD44.
  • [MeSH-major] Antigens, CD34 / analysis. Antigens, CD38 / analysis. Leukemia, Myeloid / diagnosis. Mastocytosis, Systemic / diagnosis. Myelodysplastic Syndromes / diagnosis. Stem Cells / immunology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Chronic Disease. Female. Flow Cytometry. Gene Expression Regulation, Leukemic / genetics. Humans. Immunophenotyping. Male. Middle Aged


50. 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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51. 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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  • [Cites] Methods Mol Biol. 2007;407:177-208 [18453257.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4403-11 [10969785.001]
  • [Cites] Leuk Res. 1998 Mar;22(3):221-39 [9619914.001]
  • [Cites] Biosci Biotechnol Biochem. 2004 Nov;68(11):2415-7 [15564688.001]
  • [Cites] Ann N Y Acad Sci. 2004 Dec;1030:361-8 [15659818.001]
  • [Cites] Urol Oncol. 2005 Jan-Feb;23(1):36-48 [15885582.001]
  • [Cites] J Cell Physiol. 2005 Sep;204(3):881-8 [15795939.001]
  • [Cites] Nutr Cancer. 2005;52(2):121-9 [16201843.001]
  • [Cites] Leuk Res. 2006 Mar;30(3):296-302 [16112192.001]
  • [Cites] Bioorg Med Chem Lett. 2006 Jun 1;16(11):2974-7 [16563756.001]
  • [Cites] Biotechnol J. 2006 Apr;1(4):420-39 [16892270.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):3942-7 [10632323.001]
  • [Cites] Cytometry. 2000 Apr 15;42(2):83-94 [10797445.001]
  • [Cites] Mol Pharmacol. 2007 Dec;72(6):1545-56 [17878267.001]
  • [Cites] Blood. 2003 Jun 15;101(12):4990-7 [12609832.001]
  • [Cites] Breast Cancer Res. 2004;6(4):R291-9 [15217495.001]
  • [Cites] Int J Oncol. 2004 Sep;25(3):737-44 [15289877.001]
  • [Cites] Int J Cancer. 2004 Nov 20;112(4):707-12 [15382055.001]
  • [Cites] Blood. 1983 Oct;62(4):709-21 [6192859.001]
  • [Cites] Biochem Pharmacol. 1993 May 5;45(9):1881-7 [8494547.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8707-11 [7690969.001]
  • [Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]
  • [Cites] Blood. 1995 Nov 15;86(10):3745-53 [7579341.001]
  • [Cites] Chem Biol Interact. 2006 Aug 25;162(2):140-8 [16857180.001]
  • [Cites] Nutr Cancer. 2007;58(2):178-87 [17640164.001]
  • [Cites] Toxicol In Vitro. 2007 Dec;21(8):1678-85 [17604596.001]
  • [Cites] Trends Mol Med. 2007 Nov;13(11):470-81 [17981087.001]
  • [CommentIn] Cancer Biol Ther. 2009 Feb;8(4):338-9 [19197147.001]
  • (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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52. 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


53. Leger DY, Liagre B, Beneytout JL: Role of MAPKs and NF-kappaB in diosgenin-induced megakaryocytic differentiation and subsequent apoptosis in HEL cells. Int J Oncol; 2006 Jan;28(1):201-7
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  • Apoptosis is the physiological fate of normal megakaryocyte after differentiation and maturation.
  • [MeSH-minor] Diosgenin / pharmacology. Humans. Leukemia, Myeloid, Acute / pathology. Signal Transduction. Tumor Cells, Cultured


54. 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


55. 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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56. Savaşan S, Buck S, Raimondi SC, Becton DL, Weinstein H, Chang M, Ravindranath Y: CD36 (thrombospondin receptor) expression in childhood acute megakaryoblastic leukemia: in vitro drug sensitivity and outcome. Leuk Lymphoma; 2006 Oct;47(10):2076-83
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  • [Title] CD36 (thrombospondin receptor) expression in childhood acute megakaryoblastic leukemia: in vitro drug sensitivity and outcome.
  • The outcome for children with acute megakaryoblastic leukemia (AMKL) remains poor, except for cases associated with Down syndrome (DS).
  • CD36 expression in acute myeloid leukemia cases other than AMKL was not associated with increased in vitro drug sensitivity.
  • CD36 expression in AMKL may be an indicator of megakaryoblast maturation and chemotherapy sensitivity.
  • [MeSH-major] Antigens, CD36 / biosynthesis. Gene Expression Regulation, Neoplastic. Leukemia, Megakaryoblastic, Acute / complications. Leukemia, Megakaryoblastic, Acute / metabolism

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  • [CommentIn] Leuk Lymphoma. 2006 Oct;47(10):2004-5 [17071466.001]
  • (PMID = 17071479.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / U10 CA 30969
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Biomarkers, Tumor; 04079A1RDZ / Cytarabine; ZS7284E0ZP / Daunorubicin
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57. 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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  • [Cites] Science. 1997 Sep 26;277(5334):1996-2000 [9302295.001]
  • [Cites] Leukemia. 1997 Oct;11(10):1696-9 [9324291.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3707-13 [9345056.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1812-7 [9465099.001]
  • [Cites] Blood. 1998 May 1;91(9):3134-43 [9558367.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4028-37 [9596646.001]
  • [Cites] Leukemia. 1998 Jun;12(6):893-8 [9639417.001]
  • [Cites] Gene. 1998 May 28;212(1):103-9 [9661669.001]
  • [Cites] EMBO J. 1999 Mar 1;18(5):1223-34 [10064589.001]
  • [Cites] Blood. 1999 Mar 15;93(6):2067-74 [10068680.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1259-67 [10096557.001]
  • [Cites] Genes Dev. 1999 Jun 15;13(12):1501-12 [10385618.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4055-62 [10435586.001]
  • [Cites] Oncogene. 1999 Sep 23;18(39):5381-92 [10498892.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2890-904 [15024077.001]
  • [Cites] Mol Cell Biol. 1996 Jun;16(6):2987-97 [8649410.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17186-91 [15569932.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(6):2419-30 [15743834.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4523-6 [15705784.001]
  • [Cites] J Clin Invest. 2005 Aug;115(8):2159-68 [16025155.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1357-60 [15936816.001]
  • [Cites] Gene Ther. 2005 Oct;12(19):1444-52 [15877047.001]
  • [Cites] Cell Cycle. 2005 Aug;4(8):1113-9 [16082198.001]
  • [Cites] Mol Cell Biol. 2005 Dec;25(23):10205-19 [16287839.001]
  • [Cites] Am J Hematol. 2005 Dec;80(4):282-7 [16315255.001]
  • [Cites] Leukemia. 2006 Feb;20(2):224-9 [16357831.001]
  • [Cites] J Cell Physiol. 2006 Jun;207(3):582-93 [16250015.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3303-12 [16380455.001]
  • [Cites] Cancer Cell. 2006 Apr;9(4):249-60 [16616331.001]
  • [Cites] J Cell Physiol. 2006 Sep;208(3):594-601 [16741927.001]
  • [Cites] J Biol Chem. 1996 Jun 28;271(26):15782-6 [8663132.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4255-62 [15156181.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4547-54 [15231665.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] Blood. 1984 Jul;64(1):318-20 [6329379.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10431-4 [1720541.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6336-45 [8413232.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):4004-8 [8171026.001]
  • [Cites] Nature. 1994 Jun 16;369(6481):574-8 [7911228.001]
  • [Cites] Nature. 1994 Oct 6;371(6497):534-7 [7935768.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4917-21 [7761424.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5545-9 [7777546.001]
  • [Cites] Cell. 1995 Aug 25;82(4):675-84 [7664346.001]
  • [Cites] Oncogene. 1995 Nov 2;11(9):1761-9 [7478604.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3444-9 [8622955.001]
  • [Cites] Proc Assoc Am Physicians. 1995 Jul;107(2):175-80 [8624850.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):651-6 [10617663.001]
  • [Cites] Science. 2000 Mar 10;287(5459):1804-8 [10710306.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2676-86 [10733570.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2511-22 [10851050.001]
  • [Cites] J Biol Chem. 2000 Jun 23;275(25):18794-800 [10764767.001]
  • [Cites] Blood. 2000 Jul 15;96(2):655-63 [10887131.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5577-90 [11463839.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5660-79 [11607817.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] Leukemia. 2002 May;16(5):874-85 [11986950.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] J Exp Med. 2002 Nov 4;196(9):1227-40 [12417632.001]
  • [Cites] J Biol Chem. 2002 Dec 6;277(49):47338-47 [12354776.001]
  • [Cites] Cell Cycle. 2002 Sep-Oct;1(5):343-50 [12461297.001]
  • [Cites] Gene. 2003 Jan 16;303:1-10 [12559562.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3157-63 [12480707.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1665-6 [12886257.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9506-11 [12881486.001]
  • [Cites] Oncogene. 2003 Aug 28;22(36):5646-57 [12944913.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1751-61 [14660751.001]
  • [Cites] Blood. 2004 Jan 15;103(2):743-6 [14702288.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):825-30 [14561740.001]
  • [Cites] Mol Pharmacol. 2004 Mar;65(3):571-81 [14978235.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Mar 26;316(1):85-92 [15003515.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):14059-64 [8943060.001]
  • [Cites] J Immunol. 1997 Mar 1;158(5):2251-8 [9036972.001]
  • [Cites] Nat Genet. 1997 Mar;15(3):303-6 [9054947.001]
  • [Cites] Leuk Lymphoma. 1997 Jun;26(1-2):35-41 [9250785.001]
  • (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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58. Huang YC, Shieh HR, Chen YJ: Midostaurin (PKC412) modulates differentiation and maturation of human myeloid dendritic cells. Toxicol In Vitro; 2010 Sep;24(6):1705-10
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  • [Title] Midostaurin (PKC412) modulates differentiation and maturation of human myeloid dendritic cells.
  • Midostaurin, a tyrosine kinase inhibitor, has been shown efficacy against acute myeloid leukemia and various other malignancies in clinical trials.
  • To understand the effect of midostaurin on human myeloid dendritic cells (DCs), we conducted an ex vivo study using immature DCs differentiated from CD14(+) monocytes and further maturated using lipopolysaccharide.
  • Moreover, midostaurin affected DC differentiation and maturation patterns; CD83 expression levels decreased, whereas CD14 and CD80 expressions increased.

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20685248.001).
  • [ISSN] 1879-3177
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Biomarkers; 0 / Lipopolysaccharides; 120685-11-2 / 4'-N-benzoylstaurosporine; EC 2.7.11.13 / Protein Kinase C; H88EPA0A3N / Staurosporine
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59. 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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60. Ansa-Addo EA, Lange S, Stratton D, Antwi-Baffour S, Cestari I, Ramirez MI, McCrossan MV, Inal JM: Human plasma membrane-derived vesicles halt proliferation and induce differentiation of THP-1 acute monocytic leukemia cells. J Immunol; 2010 Nov 1;185(9):5236-46
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  • [Title] Human plasma membrane-derived vesicles halt proliferation and induce differentiation of THP-1 acute monocytic leukemia cells.
  • The myeloid-differentiating agents all-trans retinoic acid/PMA and histamine, the inflammatory mediator that inhibits promonocyte proliferation, induced an intracellular Ca(2+)-mediated PMV (as opposed to exosome) release from THP-1 promonocytes.
  • Use of the TGF-β receptor antagonist SB-431542 and anti-TGF-β1 Ab showed that this was due to TGF-β1 carried on PMvs. Although TGF-β1 levels have been shown to increase in cell culture supernatants during macrophage differentiation and dendritic cell maturation, the presence of TGF-β1 in PMVs is yet to be reported.
  • In this study, to our knowledge we show for the first time that TGF-β1 is carried on the surface of PMVs, and we confirm the presence within PMVs of certain leaderless proteins, with reported roles in myeloid cell differentiation.
  • Our in vitro findings support a model in which TGF-β1-bearing PMVs, released from promonocytic leukemia cells (THP-1) or primary peripheral blood monocytes on exposure to sublytic complement or after treatment with a differentiation therapy agent, such as all-trans retinoic acid, significantly reduce proliferation of THP-1 cells.
  • [MeSH-minor] Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Cell Proliferation. Cell Separation. Electrophoresis, Polyacrylamide Gel. Enzyme-Linked Immunosorbent Assay. Exocytosis. Flow Cytometry. Fluorescent Antibody Technique. Humans. Leukemia, Monocytic, Acute / metabolism. Microscopy, Electron, Transmission

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  • (PMID = 20921526.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1
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61. Bertagnolo V, Grassilli S, Bavelloni A, Brugnoli F, Piazzi M, Candiano G, Petretto A, Benedusi M, Capitani S: Vav1 modulates protein expression during ATRA-induced maturation of APL-derived promyelocytes: a proteomic-based analysis. J Proteome Res; 2008 Sep;7(9):3729-36
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  • [Title] Vav1 modulates protein expression during ATRA-induced maturation of APL-derived promyelocytes: a proteomic-based analysis.
  • Overexpression of Vav1 promotes the overcoming of the differentiation blockade that characterizes acute promyelocytic leukemia cells.
  • At variance, down-modulation of Vav1 prevents ATRA-induced maturation, and in particular, the inhibition of its tyrosine phosphorylation prevents the neutrophil differentiation-related changes of cell morphology.
  • We have performed high-resolution 2-DE coupled with mass spectra analysis of HL-60 and NB4 promyelocytic cell lines induced to differentiate with ATRA when the amounts or the tyrosine phosphorylation of Vav1 were forcedly reduced.
  • In particular, the expression of 14-3-3epsilon, alpha-enolase, alpha-tubulin and splice isoform 2 of alpha3 proteasome subunit changed as a consequence of the down-modulation of Vav1 during the differentiation of both HL-60 and NB4 cell lines, suggesting that these proteins may constitute a common part of the ATRA-induced pathway during maturation of APL-derived promyelocytes.
  • These results indicate an unprecedented role for Vav1 in the maturation of myeloid cells as a regulator of protein expression.

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  • (PMID = 18642942.001).
  • [ISSN] 1535-3893
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-vav; 0 / VAV1 protein, human; 5688UTC01R / Tretinoin
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62. Olsen RJ, Chang CC, Herrick JL, Zu Y, Ehsan A: Acute leukemia immunohistochemistry: a systematic diagnostic approach. Arch Pathol Lab Med; 2008 Mar;132(3):462-75
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  • [Title] Acute leukemia immunohistochemistry: a systematic diagnostic approach.
  • CONTEXT: The diagnosis and classification of leukemia is becoming increasingly complex.
  • Current classification schemes incorporate morphologic features, immunophenotype, molecular genetics, and clinical data to specifically categorize leukemias into various subtypes.
  • Detailed blast immunophenotyping can be performed with lineage- and maturation-specific markers.
  • Although no one marker is pathognomonic for one malignancy, a well-chosen panel of antibodies can efficiently aid the diagnosis and classification of acute leukemias.
  • General immunohistochemical staining patterns of the most commonly encountered lymphoid and myeloid leukemias are emphasized.
  • The goal is to discuss the immunostaining of acute leukemias when flow cytometry and genetic studies are not available.
  • CONCLUSIONS: Immunophenotyping of blasts using an immunohistochemical approach to lymphoid and myeloid malignancies is presented.
  • Initial and subsequent additional antibody panels are suggested to confirm or exclude each possibility in the differential diagnosis and a general strategy for diagnostic evaluation is discussed.
  • When performed in an optimized laboratory and combined with a careful morphologic examination, the immunohistochemical approach represents a useful laboratory tool for classifying various leukemias.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia / classification. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Flow Cytometry. Humans. Immunohistochemistry

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  • (PMID = 18318587.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 110
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63. Pendino F, Hillion J, Dudognon C, Delaunay J, Mourah S, Podgorniak MP, Lafon I, Chomienne C, Lanotte M, Dombret H, Rousselot P, Ségal-Bendirdjian E: Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL. Leukemia; 2006 Apr;20(4):599-603
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  • [Title] Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL.
  • Recently, we have shown that long-term treatment with all-trans retinoic acid (ATRA), a compound clinically approved for differentiation therapy of acute promyelocytic leukemia (APL), represses hTERT in differentiation-resistant APL cell lines leading to telomere shortening and death.
  • In contrast to differentiation-therapy, which is only successful in this subtype of leukemia, the telomerase-targeted pathway could also be of use in non-APL.
  • Here, we demonstrate that repression of hTERT occurs in fresh blasts cells from patients with myeloid leukemias of various subtypes exposed ex vivo to ATRA or synthetic retinoids.
  • These results support the idea that, by hTERT targeting, retinoids can induce telomere shortening and cell death and their integration in therapy protocols for myeloid leukemias refractory to maturation should be considered.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Retinoids / pharmacology. Telomerase / antagonists & inhibitors

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  • (PMID = 16482212.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Retinoids; EC 2.7.7.49 / Telomerase
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64. Baldus CD, Martus P, Burmeister T, Schwartz S, Gökbuget N, Bloomfield CD, Hoelzer D, Thiel E, Hofmann WK: Low ERG and BAALC expression identifies a new subgroup of adult acute T-lymphoblastic leukemia with a highly favorable outcome. J Clin Oncol; 2007 Aug 20;25(24):3739-45
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  • [Title] Low ERG and BAALC expression identifies a new subgroup of adult acute T-lymphoblastic leukemia with a highly favorable outcome.
  • PURPOSE: Expression of the genes ERG (v-ets erythroblastosis virus E26 oncogene homolog) and BAALC (brain and acute leukemia, cytoplasmic) shows similarity during hematopoietic maturation and predicts outcome in acute myeloid leukemia.
  • We hypothesized that like ERG, BAALC expression might be of prognostic significance in acute T-lymphoblastic leukemia (T-ALL) and that ERG and BAALC expression together would better identify the patient's risk profile.
  • RESULTS: High BAALC expression correlated with a higher frequency of early T-ALL (P < .0001), CD34 positivity (P < .0001), coexpression of myeloid markers (P = .0001), and high ERG expression (P = .03).
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Expression. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Trans-Activators / genetics

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  • (PMID = 17646667.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAALC protein, human; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Neoplasm Proteins; 0 / Organotechnetium Compounds; 0 / Oximes; 0 / Trans-Activators; 0 / technetium Tc 99m 4,9-diaza-3,3,10,10-tetramethyldodecan-2,11-dione dioxime
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65. Jácomo RH, Figueiredo-Pontes LL, Rego EM: [From the molecular model to the impact on prognosis: an overview on acute promyelocytic leukemia]. Rev Assoc Med Bras (1992); 2008 Jan-Feb;54(1):82-9
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  • [Title] [From the molecular model to the impact on prognosis: an overview on acute promyelocytic leukemia].
  • [Transliterated title] Do paradigma molecular ao impacto no prognóstico: uma visão da leucemia promielocítica aguda.
  • Acute promyelocytic leukemia (APL) is a model of clinical applicability of the knowledge of molecular physiopathology.
  • The consequence is a protein with low sensibility to its ligand and a myeloid maturation arrest.
  • Epidemiologically, it differs from other acute myeloid leukemia due to a higher incidence in young adults and in countries of "Latin" colonization.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis. Leukemia, Promyelocytic, Acute / genetics

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  • [ErratumIn] Rev Assoc Med Bras. 2008 May-Jun;54(3):282
  • (PMID = 18392492.001).
  • [ISSN] 0104-4230
  • [Journal-full-title] Revista da Associação Médica Brasileira (1992)
  • [ISO-abbreviation] Rev Assoc Med Bras (1992)
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  • [Number-of-references] 66
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66. 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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67. 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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68. Brugnoli F, Lambertini E, Varin-Blank N, Piva R, Marchisio M, Grassilli S, Miscia S, Capitani S, Bertagnolo V: Vav1 and PU.1 are recruited to the CD11b promoter in APL-derived promyelocytes: role of Vav1 in modulating PU.1-containing complexes during ATRA-induced differentiation. Exp Cell Res; 2010 Jan 1;316(1):38-47
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  • Vav1 plays an important role in the all-trans retinoic acid (ATRA)-induced completion of the differentiation program of acute promyelocytic leukemia (APL)-derived cells, in which it strengthens the drug effects and is involved in the regulation of maturation-related proteins, such as the CD11b surface antigen.
  • In both myeloid and lymphoid cells, accumulating data attribute to the multidomain protein Vav1 a functional relevance in the control of gene expression, by direct interaction with chromatin remodeling and/or transcriptional proteins.
  • [MeSH-minor] Cell Line, Tumor. Cell Nucleus / metabolism. Chromatin Immunoprecipitation. DNA / genetics. DNA / metabolism. Electrophoretic Mobility Shift Assay. Gene Expression Regulation, Neoplastic / physiology. Humans. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Intracellular Signaling Peptides and Proteins / metabolism. Leukemia, Promyelocytic, Acute / pathology. Neutrophils / cytology. Neutrophils / metabolism. Phosphorylation / drug effects. Protein Binding / drug effects. Protein Binding / physiology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. RNA, Small Interfering / genetics. Stilbenes / pharmacology

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  • (PMID = 19747912.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / ITGAM protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Stilbenes; 0 / Trans-Activators; 0 / VAV1 protein, human; 0 / proto-oncogene protein Spi-1; 4339-71-3 / 3,3',4,5'-tetrahydroxystilbene; 5688UTC01R / Tretinoin; 9007-49-2 / DNA; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase
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69. Song LP, Zhang J, Wu SF, Huang Y, Zhao Q, Cao JP, Wu YL, Wang LS, Chen GQ: Hypoxia-inducible factor-1alpha-induced differentiation of myeloid leukemic cells is its transcriptional activity independent. Oncogene; 2008 Jan 17;27(4):519-27
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  • [Title] Hypoxia-inducible factor-1alpha-induced differentiation of myeloid leukemic cells is its transcriptional activity independent.
  • Hypoxia or hypoxia mimetic has been shown to induce differentiation together with the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) protein of myeloid leukemic cells and normal hematopoietic progenitors.
  • To provide direct evidence for the role of HIF-1alpha in acute myeloid leukemia (AML) cell differentiation and its mechanisms, we generated myeloid leukemic U937T transformants, in which HIF-1alpha was tightly induced by tetracycline withdrawal.
  • The results showed that the conditional HIF-1alpha induction triggered granulocytic differentiation of these transformants, while the suppression of HIF-1alpha expression by specific short hairpin RNAs (shRNAs) effectively inhibited hypoxia-induced differentiation of U937 cells, as evidenced by morphology, maturation-related antigens as well as expressions of myeloid differentiation signatures and hematopoietic cells-specific cytokine receptors.
  • The specific shRNAs-inhibited expression of HIF-1beta, an essential partner for transcription activity of HIF-1, failed, while the inhibition of hematopoietic differentiation-critical CCAAT/enhancer-binding protein-alpha (C/EBPalpha) significantly eliminated HIF-1alpha-mediated myeloid leukemic cell differentiation.
  • Collectively, this work provided several lines of direct evidence for the role of HIF-1alpha protein through its nontranscriptional activity in myeloid cell differentiation, in which C/EBPalpha elicits a role as an effector downstream to HIF-1alpha.
  • These discoveries would shed new insights for understanding mechanisms underlying leukemogenesis and designing the new therapeutic strategy for differentiation induction of AML.
  • [MeSH-major] Cell Differentiation / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Leukemia, Myeloid / pathology. Transcriptional Activation / physiology

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  • (PMID = 17637739.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Colony-Stimulating Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Small Interfering
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70. Veltroni M, Sainati L, Zecca M, Fenu S, Tridello G, Testi AM, Merlone AD, Buldini B, Leszl A, Lo Nigro L, Longoni D, Bernini G, Basso G, AIEOP-MDS Study Group: Advanced pediatric myelodysplastic syndromes: can immunophenotypic characterization of blast cells be a diagnostic and prognostic tool? Pediatr Blood Cancer; 2009 Mar;52(3):357-63
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  • BACKGROUND: The diagnosis of myelodysplastic syndromes (MDS) is mainly based on morphology and cytogenetic analysis.
  • These studies have focused on the identification of abnormalities in the maturation pathway of antigen expression of myelo-monocytic cells, and characterization of blast populations.
  • PROCEDURE: We evaluated by multiparameter flow cytometry 26 MDS pediatric patients with more than 2% of blast cells at bone marrow morphological examination (17 de novo MDS and 9 secondary MDS) and 145 pediatric de novo acute myeloid leukemia (AML) cases (M3 excluded).
  • As control group, 12 healthy age-matched donors for allogenic bone marrow transplantation (BMD) and 6 regenerating bone marrow samples, collected from children with acute lymphoblastic leukemia (ALL) in remission after induction chemotherapy, were studied.
  • [MeSH-major] Blast Crisis / diagnosis. Myelodysplastic Syndromes / diagnosis


71. 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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72. 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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73. Caprodossi S, Pedinotti M, Amantini C, Santoni G, Minucci S, Pelicci PG, Fanelli M: Differentiation response of acute promyelocytic leukemia cells and PML/RARa leukemogenic activity studies by real-time RT-PCR. Mol Biotechnol; 2005 Jul;30(3):231-8
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  • [Title] Differentiation response of acute promyelocytic leukemia cells and PML/RARa leukemogenic activity studies by real-time RT-PCR.
  • Acute promyelocytic leukemia (APL) is a human cancer generated by a chromosomal translocation t(15;17) involving the promyelocytic leukemia (PML) and retinoic acid receptor alpha (RARalpha) genes.
  • Although PML/RARalpha interferes with the normal maturation of myeloid precursors to granulocytes, pharmacological doses of retinoic acid are sufficient to restore the differentiation processes.
  • Amplifying CD11b, CD11c, and CD14 mRNAs, as specific markers of differentiation, by the real-time RT-PCR assay we could detect both retinoic acid (RA) and vitamin D3 and human transforming growth factor beta1 (VitD3/TGFbeta1) induced cellular maturation more precociously than the canonical flow-cytofluorimetric assay.
  • Moreover, by amplifying CD14 mRNA it was possible to monitor the ability of PML/RARalpha oncoprotein to block VitD3/TGFbeta1 induced differentiation in U937-PR9 promonocytic inducible model systems.The proposed real-time quantitative RT-PCR approach is a reproducible and highly sensitive assay and can be considered a valid method to study both cellular maturation state and differentiation response.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Receptors, Retinoic Acid / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transcription Factors / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Cholecalciferol / pharmacology. Humans. Promyelocytic Leukemia Protein. Proteins / pharmacology. Retinoic Acid Receptor alpha. Tretinoin / pharmacology

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  • [Cites] N Engl J Med. 1993 Jul 15;329(3):177-89 [8515790.001]
  • [Cites] Blood. 1991 Mar 1;77(5):1080-6 [1995093.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Blood. 1994 Jan 1;83(1):10-25 [8274729.001]
  • [Cites] Blood. 1998 Oct 1 ;92 (7):2244-51 [9746761.001]
  • [Cites] EMBO J. 1996 Sep 16;15(18):4949-58 [8890168.001]
  • [Cites] J Immunol. 1993 Mar 15;150(6):2418-30 [8383719.001]
  • [Cites] FASEB J. 1996 Jul;10(9):1025-30 [8801163.001]
  • [Cites] Cell. 1991 Aug 23;66(4):663-74 [1652368.001]
  • [Cites] Biotechnology (N Y). 1992 Apr;10(4):413-7 [1368485.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1977-81 [1848017.001]
  • [Cites] Cell. 1993 Aug 13;74(3):423-31 [8394219.001]
  • [Cites] Science. 1991 Nov 29;254(5036):1371-4 [1720570.001]
  • [Cites] Blood. 1999 Mar 1;93(5):1477-81 [10029573.001]
  • [Cites] Nature. 1998 Feb 19;391(6669):815-8 [9486655.001]
  • (PMID = 15988048.001).
  • [ISSN] 1073-6085
  • [Journal-full-title] Molecular biotechnology
  • [ISO-abbreviation] Mol. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Promyelocytic Leukemia Protein; 0 / Proteins; 0 / RARA protein, human; 0 / Receptors, Retinoic Acid; 0 / Retinoic Acid Receptor alpha; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 143220-95-5 / PML protein, human; 1C6V77QF41 / Cholecalciferol; 5688UTC01R / Tretinoin
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74. 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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75. Sekeres MA: The myelodysplastic syndromes. Expert Opin Biol Ther; 2007 Mar;7(3):369-77
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  • The myelodysplastic syndrome(s) (MDS), bone marrow stem cell malignancies that share pathogenetic overlap with acute myeloid leukemia, are characterized by peripheral blood cytopenias and, in more advanced subtypes, varied degrees of maturation arrest.


76. Kuo YH, Landrette SF, Heilman SA, Perrat PN, Garrett L, Liu PP, Le Beau MM, Kogan SC, Castilla LH: Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia. Cancer Cell; 2006 Jan;9(1):57-68
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  • [Title] Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia.
  • The acute myeloid leukemia (AML)-associated CBF beta-SMMHC fusion protein impairs hematopoietic differentiation and predisposes to leukemic transformation.
  • The mechanism of leukemia progression, however, is poorly understood.
  • In this study, we report a conditional Cbfb-MYH11 knockin mouse model that develops AML with a median latency of 5 months.
  • The fusion protein induced abnormal myeloid progenitors (AMPs) with limited proliferative potential but leukemic predisposition similar to that of HSCs in transplanted mice.
  • In addition, Cbf beta-SMMHC blocked megakaryocytic maturation at the CFU-Meg to megakaryocyte transition.
  • These data show that a leukemia oncoprotein can inhibit differentiation and proliferation while not affecting the maintenance of long-term HSCs.
  • [MeSH-major] Leukemia, Myeloid / pathology. Myeloid Progenitor Cells / pathology. Oncogene Proteins, Fusion / metabolism. Preleukemia / pathology
  • [MeSH-minor] Acute Disease. Animals. B-Lymphocytes / pathology. Blood Platelets / pathology. Cell Proliferation. Hematopoiesis. Megakaryocytes / metabolism. Megakaryocytes / pathology. Mice. Mice, Inbred C57BL. Mice, Mutant Strains

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  • (PMID = 16413472.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA84221; United States / NCI NIH HHS / CA / F32CA101571; United States / NCI NIH HHS / CA / R01-CA096983
  • [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 / CBFbeta-MYH11 fusion protein; 0 / Oncogene Proteins, Fusion
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77. Katsumoto T, Aikawa Y, Iwama A, Ueda S, Ichikawa H, Ochiya T, Kitabayashi I: MOZ is essential for maintenance of hematopoietic stem cells. Genes Dev; 2006 May 15;20(10):1321-30
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  • Monocytic leukemia zinc-finger protein (MOZ), a MYST family histone acetyltransferase, is involved in the chromosome translocations associated with acute myeloid leukemia.
  • On the other hand, arrest of erythroid maturation and elevated myeloid lineage populations were observed.
  • These results show that MOZ is required for maintenance of hematopoietic stem cells, and that it plays a role in differentiation of erythroid and myeloid cells.
  • [MeSH-minor] Animals. B-Lymphocytes / cytology. Cell Differentiation / genetics. Down-Regulation. Embryonic Development / genetics. Genes, Lethal. Homeodomain Proteins / genetics. Leukemia / genetics. Liver / cytology. Liver / growth & development. Mice. Mice, Mutant Strains. Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-kit / genetics. Receptors, Cytokine / genetics. Receptors, Thrombopoietin. Trans-Activators / metabolism. Transcriptional Activation


78. 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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79. Olwill SA, McGlynn H, Gilmore WS, Alexander HD: All-trans retinoic acid-induced downregulation of annexin II expression in myeloid leukaemia cell lines is not confined to acute promyelocytic leukaemia. Br J Haematol; 2005 Oct;131(2):258-64
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  • [Title] All-trans retinoic acid-induced downregulation of annexin II expression in myeloid leukaemia cell lines is not confined to acute promyelocytic leukaemia.
  • Most acute promyelocytic leukaemia (APL) patients suffer from disordered haemostasis.
  • APL can be treated successfully in most instances by all-trans retinoic acid (ATRA) therapy, which induces endpoint maturation of the leukaemic promyelocytes with the characteristic t(15;17).
  • Our group has shown previously that high levels of AnII are expressed on other acute myeloid leukaemia subtypes that are sometimes associated with disordered haemostasis, albeit less frequently than APL.
  • This study examined the effects of ATRA on AnII expression and cell differentiation, on myeloid leukaemia cell lines to determine whether a regulatory influence on AnII may contribute to the return of haemostatic stability in APL following treatment.
  • The results confirmed that AnII expression in the APL cell line (NB4) was significantly downregulated in response to ATRA (P < 0.01), with associated morphological and immunophenotypical evidence of myeloid differentiation.
  • ATRA also downregulated AnII expression on other myeloid cell lines, albeit to a lesser extent than observed on NB4 cells.
  • [MeSH-major] Annexin A2 / metabolism. Leukemia, Myeloid / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Analysis of Variance. Cell Differentiation. Cell Line, Tumor. Down-Regulation. Fibrinolysis / drug effects. Flow Cytometry. Hemostasis. Humans. Leukemia, Promyelocytic, Acute / drug therapy. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • [ErratumIn] Br J Haematol. 2006 Jan;132(1):119
  • (PMID = 16197459.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A2; 0 / RNA, Messenger; 5688UTC01R / Tretinoin
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80. Béné MC: Immunophenotyping of acute leukaemias. Immunol Lett; 2005 Apr 15;98(1):9-21
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  • [Title] Immunophenotyping of acute leukaemias.
  • Progress in the management and understanding of acute leukaemia can only be obtained if these diseases are thoroughly investigated, both clinically and with a series of biological tools.
  • Among the variety of approaches of acute leukaemia definition, immunophenotyping has taken over the past 25 years a predominant and now well-defined place, although room is left for further improvement.
  • In this review, the current state-of-the-art of immunophenotyping of acute leukaemias will be replaced in the context of physiological leukocyte maturation.
  • [MeSH-major] Immunophenotyping. Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Animals. Antigens, Differentiation, B-Lymphocyte / immunology. Antigens, Differentiation, T-Lymphocyte / immunology. B-Lymphocytes / immunology. B-Lymphocytes / pathology. Cell Lineage / immunology. Humans. Myeloid Cells / immunology. Myeloid Cells / pathology. T-Lymphocytes / immunology. T-Lymphocytes / pathology

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  • (PMID = 15790504.001).
  • [ISSN] 0165-2478
  • [Journal-full-title] Immunology letters
  • [ISO-abbreviation] Immunol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Antigens, Differentiation, T-Lymphocyte
  • [Number-of-references] 62
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81. Wei J, Chen Y: [New advance of research on prognostic factors in myelodysplastic syndrome--review]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Dec;16(6):1465-72
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  • Myelodysplastic syndrome (MDS) represents a heterogeneous group of myeloid malignancies characterized by abnormal differentiation and maturation of myeloid cells, bone marrow failure, and a genetic instability with enhanced risk to transform to acute myeloid leukemia.


82. 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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83. 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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84. Vrbanus L, Sucić M, Marković-Glamocak M, Ries S, Gjadrov-Kuvezdić K, Fabijanić I, Antulov J, Petrik J, Labar B: Apoptosis of leukemic cells: a case report. Coll Antropol; 2010 Jun;34(2):705-11
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  • Transformation of leukemic cells is associated with delay in maturation and in apoptosis, and to altered responsiveness to growth factors.
  • However, some studies have revealed that Fas (CD95/APO1) which mediates apoptotic signal and decrease of anti-apoptotic Bcl-2 are frequently observed in acute myeloid leukemia (AML) M4/M5 leukemic cells.
  • The aim of the study was to compare cytomorphology and cytochemistry of bone marrow (BM) apoptotic leukemic cells to preserved peripheral blood (PB) leukemic cells in our patient, a 76-year-old man with AML-M5b treated at Zagreb University Hospital Center.
  • BM and PB of the AL patient were analyzed after Pappenheim and cytochemical stainings, and leukemic cells were classified according to FAB and WHO classification.
  • On the basis of these findings, AML-M5b was diagnosed in our patient.
  • There are many possible explanations for our observation of BM leukemic cell apoptosis in a patient with AML-M5.
  • [MeSH-major] Apoptosis. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 20698159.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antigens, CD95
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85. 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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86. 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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  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12350-5 [10535925.001]
  • [Cites] Mol Cell Biol. 1997 Dec;17(12):7353-61 [9372966.001]
  • [Cites] Cell. 2001 Oct 19;107(2):247-58 [11672531.001]
  • [Cites] Mol Cell. 2001 Oct;8(4):817-28 [11684017.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):26293-9 [11978795.001]
  • [Cites] Biochem J. 2002 Aug 1;365(Pt 3):561-75 [12006103.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38037-44 [12161447.001]
  • [Cites] J Biol Chem. 2003 Mar 14;278(11):9134-41 [12511558.001]
  • [Cites] Mol Cell. 2003 Apr;11(4):1043-54 [12718889.001]
  • [Cites] EMBO J. 2003 May 1;22(9):2047-59 [12727872.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):675-86 [14701740.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):611-7 [14992729.001]
  • [Cites] Genes Dev. 2004 Apr 15;18(8):912-25 [15107404.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 5;101(40):14373-8 [15388847.001]
  • [Cites] Genes Dev. 1992 Mar;6(3):439-53 [1547942.001]
  • [Cites] Science. 1995 Aug 25;269(5227):1108-12 [7652557.001]
  • [Cites] Genes Dev. 1996 Apr 1;10(7):804-15 [8846917.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):3736-41 [9108047.001]
  • [Cites] Blood. 1997 Jul 15;90(2):489-519 [9226149.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):28545-8 [9786841.001]
  • [Cites] J Biol Chem. 1998 Nov 13;273(46):30057-60 [9804754.001]
  • [Cites] J Biol Chem. 1998 Nov 20;273(47):30843-6 [9812973.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):2936-45 [10082561.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(4):1325-38 [15684384.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(7):2688-97 [15767674.001]
  • [Cites] Curr Opin Hematol. 2006 Jan;13(1):7-14 [16319681.001]
  • [Cites] Dev Cell. 2005 Dec;9(6):769-79 [16326389.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]
  • [Cites] BMC Mol Biol. 2006;7:14 [16600022.001]
  • [Cites] J Biol Chem. 2006 Aug 4;281(31):21629-39 [16735515.001]
  • [Cites] Biochim Biophys Acta. 2006 Aug;1766(1):88-103 [16616425.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3560-3 [16873674.001]
  • [Cites] Trends Biochem Sci. 2007 Jun;32(6):286-95 [17499995.001]
  • [Cites] Folia Biol (Praha). 2007;53(3):97-108 [17580000.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3301-9 [17671234.001]
  • [Cites] Leukemia. 2001 Apr;15(4):688-9 [11368383.001]
  • (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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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. 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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89. Ohnishi H, Yoshino H, Yoneyama R, Ishii M, Watanabe T, Bessho F: Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation. Pediatr Hematol Oncol; 2008 Apr-May;25(3):165-70
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  • [Title] Faggot formation in mature neutrophils and metamyelocytes in acute myeloid leukemia without maturation.
  • The authors report a rare case of acute myeloid leukemia (AML) M1 with faggot formation in mature neutrophils and metamyelocytes.
  • Although Auer rods in mature neutrophils are occasionally experienced, they are usually found in AML M2, M3, or M4 cases, but not in M1 cases.
  • In addition, faggot formation in mature neutrophils, as seen in this case, is considered to be particularly unusual because most previously reported cases tended to show simple Auer rods except for AML M3 cases.
  • [MeSH-major] Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology. Neutrophils / pathology. Trisomy / pathology

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  • (PMID = 18432498.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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90. 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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  • [Cites] Hematol J. 2004;5(1):84-9 [14745436.001]
  • [Cites] J Clin Oncol. 1997 Feb;15(2):466-75 [9053467.001]
  • [Cites] Cancer. 1981 Sep 15;48(6):1426-37 [7023656.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2480-9 [16735702.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3767-75 [10577848.001]
  • [Cites] Neurosurgery. 1997 Jun;40(6):1283-7 [9179903.001]
  • [Cites] Blood. 2002 May 15;99(10):3517-23 [11986202.001]
  • [Cites] N Engl J Med. 1998 Apr 2;338(14):969 [9521985.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1643-8 [9269784.001]
  • [Cites] Int J Hematol. 2005 Oct;82(3):210-4 [16207593.001]
  • [Cites] J Clin Oncol. 1993 Apr;11(4):690-7 [8478662.001]
  • [Cites] Bone Marrow Transplant. 2005 Apr;35(8):767-73 [15735660.001]
  • [Cites] Arch Pathol Lab Med. 2006 Jun;130(6):862-6 [16740041.001]
  • [Cites] J Korean Med Sci. 2006 Aug;21(4):745-8 [16891824.001]
  • [Cites] Clin Neurol Neurosurg. 1991;93(4):341-4 [1665771.001]
  • (PMID = 19585093.001).
  • [ISSN] 1432-1289
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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91. 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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92. Anand M, Ghara N, Kumar R, Singh S, Sengar M, Panikar N, Raina V, Sharma A: Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia. Ann Hematol; 2005 Nov;84(12):767-70
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  • [Title] Myeloperoxidase cytochemical negativity: an unexpected but intrinsic property of blasts of all phases of chronic myeloid leukemia.
  • Myeloperoxidase (MPO) cytochemical activity, recognized as a very important hallmark of myeloblasts, is generally negative in chronic myeloid leukemia (CML) blast crisis (BC).
  • Myeloperoxidase cytochemistry of peripheral blood blasts in 161 cases of CML, including 103 in chronic phase (CP) and 29 each in accelerated phase (AP) and BC, was assessed and compared with that of 30 cases of acute myeloid leukemia, AML-M2.
  • Compared with the strong MPO positivity, both in terms of intensity and proportion, in the AML-M2 cases, the positivity in the CML cases was generally weak and was seen in a small number of blasts (5-15%), except in one case of BC with 20% positive blasts.
  • This also explains why MPO cytochemistry, despite its high reputation as a myeloid-lineage marker, generally does not help in CML BC.
  • CML BC should therefore be considered as a possible diagnosis along with acute lymphoblastic leukemia, AML-M0, AML-M7, etc., in the setting of MPO-negative blasts.
  • Similarity between MPO expression pattern in CML, i.e., negative in blasts and positive in the more mature cells, and that during maturation of normal myeloid series of cells shows the deranged myelopoiesis of CML to be undisturbed at least with respect to MPO expression.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Neoplasm Proteins / biosynthesis. Peroxidase / biosynthesis
  • [MeSH-minor] Female. Gene Expression Regulation, Enzymologic. Histocytochemistry. Humans. Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Leukocytes / enzymology. Leukocytes / pathology. Male. Predictive Value of Tests


93. Lulli V, Romania P, Riccioni R, Boe A, Lo-Coco F, Testa U, Marziali G: Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation. Haematologica; 2010 Oct;95(10):1633-41
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  • [Title] Transcriptional silencing of the ETS1 oncogene contributes to human granulocytic differentiation.
  • This study focuses on the role of Ets-1 during granulocytic differentiation of NB4 promyelocytic and HL60 myeloblastic leukemia cell lines induced by all-trans retinoic acid.
  • Expression of Ets-1 was also reduced during dimethylsulfoxide-induced differentiation and during granulocytic differentiation of human CD34(+) hematopoietic progenitor cells but not in NB4.R2 and HL60R cells resistant to all-trans retinoic acid.
  • In line with these observations, transduction of a transdominant negative molecule of Ets-1, which inhibited DNA binding and transcriptional activity of the wild-type Ets-1, significantly increased chemical-induced differentiation.
  • Interestingly, p51 Ets-1 over-expression was frequently observed in CD34(+) hematopoietic progenitor cells derived from patients with acute myeloid leukemia, as compared to its expression in normal CD34(+) cells.
  • CONCLUSIONS: Our results indicated that a decreased expression of Ets-1 protein generalizes to granulocytic differentiation and may represent a crucial event for granulocytic maturation.
  • [MeSH-minor] Cell Line, Tumor. HL-60 Cells. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Leukemia / pathology. Leukemia, Promyelocytic, Acute. RNA, Small Interfering / pharmacology


94. 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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  • [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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95. 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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  • [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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96. Martino V, Tonelli R, Montemurro L, Franzoni M, Marino F, Fazzina R, Pession A: Down-regulation of MLL-AF9, MLL and MYC expression is not obligatory for monocyte-macrophage maturation in AML-M5 cell lines carrying t(9;11)(p22;q23). Oncol Rep; 2006 Jan;15(1):207-11
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  • [Title] Down-regulation of MLL-AF9, MLL and MYC expression is not obligatory for monocyte-macrophage maturation in AML-M5 cell lines carrying t(9;11)(p22;q23).
  • The MLL-AF9 oncogene originates from the translocation t(9;11)(p22;q23), which is mainly associated with monocytic acute myeloid leukaemia (AML-M5; FAB-classification).
  • In AML-M5 THP-1 cells carrying t(9;11) (p22;q23) and expressing MLL-AF9, we previously showed that MLL-AF9 expression is down-regulated during monocyte-macrophage maturation.
  • MLL fusion proteins (including MLL-AF9) deregulate MYC transactivation activity, and both presence and absence of MYC down-regulation have been reported during monocyte-macrophage maturation in THP-1 cells.
  • In the present study, we analyze the expression patterns of MLL-AF9, MLL wild-type and MYC after induction of monocyte-macrophage terminal differentiation in the AML-M5 cell lines, THP-1, THP-1-R, Mono-Mac-6 (MM6) and MOLM-13, all of which carry t(9;11)(p22;q23) and express MLL-AF9.
  • [MeSH-major] Leukemia, Monocytic, Acute / genetics. Macrophages / cytology. Monocytes / cytology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-myc / genetics

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  • (PMID = 16328057.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-AF9 fusion protein, human; 0 / MYC protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-myc; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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97. 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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  • [Cites] Blood. 2003 Jan 1;101(1):270-7 [12393465.001]
  • [Cites] Cell. 1996 Jan 26;84(2):321-30 [8565077.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4284-96 [15156185.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2108-15 [10979955.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1454-63 [14551142.001]
  • [Cites] Nat Med. 2004 Mar;10(3):299-304 [14966519.001]
  • [Cites] Blood. 2002 Jan 1;99(1):15-23 [11756147.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8443-8 [15155899.001]
  • [Cites] J Exp Med. 2003 Jul 7;198(1):51-61 [12835475.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):166-75 [10508512.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4016-21 [15731354.001]
  • [Cites] Cell. 2002 Nov 27;111(5):621-33 [12464175.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 3:294-6 [9209370.001]
  • [Cites] J Clin Invest. 2004 Sep;114(5):713-9 [15343390.001]
  • [Cites] Oncogene. 2002 Apr 18;21(17):2695-703 [11965542.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(15):5506-17 [12101243.001]
  • [Cites] Mol Cell Biol. 1996 Apr;16(4):1349-55 [8657108.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1760-5 [10677531.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):63-74 [12086889.001]
  • [Cites] J Immunol. 2001 Nov 1;167(9):4957-65 [11673502.001]
  • [Cites] Oncogene. 2002 May 9;21(20):3232-40 [12082639.001]
  • [Cites] Oncogene. 2002 Sep 26;21(43):6703-12 [12242670.001]
  • [Cites] Cancer Res. 2002 Aug 15;62(16):4599-604 [12183414.001]
  • [Cites] Gene. 2000 Mar 21;245(2):223-35 [10717473.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2392-402 [9694803.001]
  • [Cites] Leuk Res. 2004 Jan;28(1):35-42 [14630078.001]
  • [Cites] J Biol Chem. 1994 Sep 30;269(39):24020-6 [7929053.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1364-72 [11830488.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4028-37 [9596646.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15184-9 [15477599.001]
  • [Cites] EMBO J. 1998 Jun 1;17(11):2994-3004 [9606182.001]
  • [Cites] Immunity. 2002 May;16(5):661-72 [12049718.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):3904-8 [12124316.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):723-33 [11179217.001]
  • [Cites] Genes Dev. 1997 Mar 1;11(5):640-53 [9119228.001]
  • [Cites] Nat Struct Mol Biol. 2004 Sep;11(9):901-6 [15322525.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2147-55 [15914564.001]
  • [Cites] Gene. 2000 Jan 11;241(2):287-95 [10675041.001]
  • [Cites] J Biol Chem. 2001 Jul 13;276(28):25834-40 [11328817.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Sep 17;322(2):623-30 [15325275.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1755-62 [12200691.001]
  • [Cites] J Immunol. 2000 Dec 15;165(12):6816-24 [11120804.001]
  • [Cites] Nat Genet. 1997 Mar;15(3):303-6 [9054947.001]
  • [Cites] Blood. 2000 Oct 1;96(7):2557-61 [11001911.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1949-54 [9050885.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4917-21 [7761424.001]
  • [Cites] Blood. 2001 May 1;97(9):2815-22 [11313276.001]
  • [Cites] Oncogene. 1996 Feb 15;12(4):883-92 [8632911.001]
  • [Cites] Science. 2004 Aug 27;305(5688):1286-9 [15333839.001]
  • [Cites] Blood. 2000 Jul 1;96(1):288-96 [10891464.001]
  • [Cites] EMBO J. 1999 May 4;18(9):2551-62 [10228168.001]
  • [Cites] Oncogene. 2003 Aug 28;22(36):5646-57 [12944913.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10398-403 [11526243.001]
  • [Cites] Blood. 2003 Feb 1;101(3):837-45 [12393383.001]
  • [Cites] Blood. 2004 Mar 15;103(6):2316-24 [14615365.001]
  • [Cites] Leuk Res. 2002 Mar;26(3):221-8 [11792409.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4220-4 [15156176.001]
  • [Cites] Mol Cell Biol. 1999 Oct;19(10):6566-74 [10490596.001]
  • [Cites] J Biol Chem. 2005 Jan 7;280(1):428-36 [15519999.001]
  • [Cites] Mol Cell Biol. 1995 May;15(5):2383-92 [7739522.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1817-24 [10068652.001]
  • [Cites] Blood. 1998 May 1;91(9):3134-43 [9558367.001]
  • [Cites] Nature. 1998 Jul 2;394(6688):92-6 [9665135.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1642-7 [8643684.001]
  • [Cites] Oncogene. 2004 May 24;23(24):4209-10 [15156174.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Oct 15;130(2):93-104 [11675129.001]
  • [Cites] Cancer Res. 2004 Jul 1;64(13):4547-54 [15231665.001]
  • [Cites] EMBO J. 1993 Jul;12(7):2715-21 [8334990.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17186-91 [15569932.001]
  • [Cites] Cell. 1996 Nov 15;87(4):697-708 [8929538.001]
  • [Cites] EMBO J. 2005 Jun 1;24(11):1976-87 [15889140.001]
  • [Cites] Gene. 2003 Jan 16;303:1-10 [12559562.001]
  • [Cites] Mol Cell Biol. 1998 Feb;18(2):846-58 [9447981.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):7176-84 [9819404.001]
  • [Cites] EMBO J. 1994 Feb 1;13(3):504-10 [8313895.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6470-83 [11533236.001]
  • [Cites] Immunity. 2000 Oct;13(4):423-31 [11070161.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Dec;31(12):1367-71 [10641791.001]
  • [Cites] Blood. 1998 Mar 1;91(5):1688-99 [9473235.001]
  • (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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98. 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


99. 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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100. Bontkes HJ, Ruizendaal JJ, Kramer D, Santegoets SJ, Scheper RJ, de Gruijl TD, Meijer CJ, Hooijberg E: Constitutively active STAT5b induces cytokine-independent growth of the acute myeloid leukemia-derived MUTZ-3 cell line and accelerates its differentiation into mature dendritic cells. J Immunother; 2006 Mar-Apr;29(2):188-200
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  • [Title] Constitutively active STAT5b induces cytokine-independent growth of the acute myeloid leukemia-derived MUTZ-3 cell line and accelerates its differentiation into mature dendritic cells.
  • The CD34(+) human acute myeloid leukemia-derived cell line MUTZ-3 is dependent on hematopoietic growth factors for its proliferation and is able to differentiate into dendritic cells (DCs) in response to the combination of granulocyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor-alpha.
  • Both DC types expressed DC maturation markers and were equally effective in inducing primary T-cell responses.
  • [MeSH-major] Cell Differentiation / immunology. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. STAT5 Transcription Factor / immunology

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  • (PMID = 16531819.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cancer Vaccines; 0 / Cytokines; 0 / STAT5 Transcription Factor; 0 / STAT5B protein, human
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