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1. Kobayashi H, Matsuyama T, Ueda M, Suzuki T, Ozaki K, Mori M, Nagai T, Muroi K, Ozawa K: Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome. Intern Med; 2009;48(18):1629-33
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  • [Title] Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome.
  • OBJECTIVE: The progression of myelodysplastic syndrome to acute myeloid leukemia (MDS/AML) is generally incurable and its prognosis is extremely poor.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


2. Gore SD, Hermes-DeSantis ER: Enhancing survival outcomes in the management of patients with higher-risk myelodysplastic syndromes. Cancer Control; 2009 Oct;16 Suppl:2-10
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  • The myelodysplastic syndromes (MDS) are a collection of clonal myeloid neoplasms characterized by bone marrow failure and cytopenias.
  • The most significant treatment goals in these patients involve prolonging the time to acute myeloid leukemia progression and extending overall survival.


3. Kim HG, Kojima K, Swindle CS, Cotta CV, Huo Y, Reddy V, Klug CA: FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia. Blood; 2008 Feb 01;111(3):1567-74
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  • [Title] FLT3-ITD cooperates with inv(16) to promote progression to acute myeloid leukemia.
  • The inversion of chromosome 16 in the inv(16)(p13q22) is one of the most frequent cytogenetic abnormalities observed in acute myeloid leukemia (AML).
  • Compared with animals transplanted with only CBFbeta-SMMHC-expressing cells, FLT3-ITD further restricted early myeloid differentiation and promoted peripheralization of primitive myeloblasts as early as 2.5 weeks after transplantation.
  • FLT3-ITD also accelerated disease progression in all CBFbeta-SMMHC/FLT3-ITD-reconstituted animals, which died of a highly aggressive and transplantable AML within 3 to 5 months.
  • [MeSH-major] Chromosome Inversion / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Oncogene Proteins, Fusion / metabolism. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Animals. Core Binding Factor beta Subunit / genetics. Core Binding Factor beta Subunit / metabolism. Disease Progression. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Lymphopoiesis. Mice. Mutation / genetics. Myelopoiesis. Smooth Muscle Myosins / genetics. Smooth Muscle Myosins / metabolism. Survival Rate

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  • (PMID = 17967943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK067186; United States / NCI NIH HHS / CA / R01 CA096798; United States / NIAID NIH HHS / AI / T32 AI007051; United States / NCI NIH HHS / CA / R01CA96798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor beta Subunit; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / Smooth Muscle Myosins
  • [Other-IDs] NLM/ PMC2214774
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4. Konieczna I, Horvath E, Wang H, Lindsey S, Saberwal G, Bei L, Huang W, Platanias L, Eklund EA: Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia. J Clin Invest; 2008 Mar;118(3):853-67
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  • [Title] Constitutive activation of SHP2 in mice cooperates with ICSBP deficiency to accelerate progression to acute myeloid leukemia.
  • Development of a block in myeloid differentiation is associated with progression of MPD to acute myeloid leukemia (AML) and portends poor prognosis.
  • Interferon consensus sequence binding protein (ICSBP, also known as IRF8) is an interferon-regulatory transcription factor that functions as a leukemia tumor suppressor.
  • Since activity of ICSBP is influenced by tyrosine phosphorylation state, we hypothesized that mutations in molecular pathways that regulate this process might synergize with ICSBP deficiency for progression to AML.
  • Consistent with this, we found that constitutive activation of SHP2 protein tyrosine phosphatase synergized with ICSBP haploinsufficiency to facilitate cytokine-induced myeloproliferation, apoptosis resistance, and rapid progression to AML in a murine bone marrow transplantation model.
  • Constitutive SHP2 activation cooperated with ICSBP deficiency to increase the number of progenitors in the bone marrow and myeloid blasts in circulation, indicating a block in differentiation.
  • Since SHP2 activation and ICSBP deficiency may coexist in human myeloid malignancies, our studies have identified a molecular mechanism potentially involved in disease progression in such diseases.

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  • (PMID = 18246201.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA095266; United States / NCI NIH HHS / CA / R01-CA095266
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-8; 42HK56048U / Tyrosine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2214847
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5. Tamura H, Dan K, Tamada K, Nakamura K, Shioi Y, Hyodo H, Wang SD, Dong H, Chen L, Ogata K: Expression of functional B7-H2 and B7.2 costimulatory molecules and their prognostic implications in de novo acute myeloid leukemia. Clin Cancer Res; 2005 Aug 15;11(16):5708-17
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  • [Title] Expression of functional B7-H2 and B7.2 costimulatory molecules and their prognostic implications in de novo acute myeloid leukemia.
  • Their roles in the progression of human cancers, however, are not well established.
  • The aim of this study was to examine whether leukemic cells of acute myeloid leukemia express functional B7 family molecules and, if so, whether such expression has any clinical significance.
  • EXPERIMENTAL DESIGN: The expression of four B7 family molecules, B7.1, B7.2, B7-H1, and B7-H2, on leukemic cells from acute myeloid leukemia patients was analyzed by flow cytometry.
  • RESULTS: Although B7.1 and B7-H1 expressions were rare, the cells from a substantial number of acute myeloid leukemia cases expressed B7.2 and B7-H2 molecules [mean percentages of B7.2- and B7-H2-positive cells were 28.9% (n = 58) and 15.3% (n = 59), respectively].
  • Consistent with this finding, acute myeloid leukemia cells expressing B7.2 and B7-H2 induced allogeneic CD4+ T cells to proliferate and secrete interleukin-4 and interleukin-10 in vitro, effects that were partially blocked by antibodies against B7.2 and B7-H2.
  • CONCLUSIONS: Our results indicate the expression of functional B7.2 and B7-H2 molecules, and these molecules may facilitate progression of acute myeloid leukemia.
  • [MeSH-major] Antigens, CD86 / genetics. Leukemia, Myeloid / pathology. Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Analysis of Variance. Antigens, CD. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. CD4-Positive T-Lymphocytes / cytology. CD4-Positive T-Lymphocytes / metabolism. Cell Line, Tumor. Cell Proliferation. Coculture Techniques. Culture Media, Conditioned / chemistry. Culture Media, Conditioned / metabolism. Female. Flow Cytometry. Gene Expression Regulation, Neoplastic. HL-60 Cells. Humans. Inducible T-Cell Co-Stimulator Ligand. Interferon-gamma / metabolism. Interleukin-10 / metabolism. Interleukin-2 / metabolism. Interleukin-4 / metabolism. Jurkat Cells. K562 Cells. Male. Middle Aged. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. U937 Cells

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  • (PMID = 16115907.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD86; 0 / CD86 protein, human; 0 / Culture Media, Conditioned; 0 / ICOSLG protein, human; 0 / Inducible T-Cell Co-Stimulator Ligand; 0 / Interleukin-2; 0 / Proteins; 0 / RNA, Messenger; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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6. 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.
  • The fusion protein induced abnormal myeloid progenitors (AMPs) with limited proliferative potential but leukemic predisposition similar to that of HSCs in transplanted mice.
  • 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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7. Plass C, Oakes C, Blum W, Marcucci G: Epigenetics in acute myeloid leukemia. Semin Oncol; 2008 Aug;35(4):378-87
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  • [Title] Epigenetics in acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a disease characterized by uncontrolled proliferation of clonal neoplastic hematopoietic precursor cells.
  • Major breakthroughs in the past have contributed to our understanding of the genetic failures and the changed biology in AML cells that underlie the initiation and progression of the disease.

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  • (PMID = 18692688.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 93548; United States / NCI NIH HHS / CA / R01 CA102031; United States / NCI NIH HHS / CA / P01 CA101956; United States / NCI NIH HHS / CA / R01 CA093548; United States / NCI NIH HHS / CA / CA 101956; United States / NCI NIH HHS / CA / CA 102031; United States / NCI NIH HHS / CA / P30 CA 16058; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / R01 CA093548-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / RNA, Untranslated
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS66042; NLM/ PMC3463865
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8. Loaiza-Bonilla A, Gore SD, Carraway HE: Novel approaches for myelodysplastic syndromes: beyond hypomethylating agents. Curr Opin Hematol; 2010 Mar;17(2):104-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DNA methyltransferase inhibitors are well tolerated in outpatient settings, with azacitidine prolonging survival and decreasing time to acute myeloid leukemia progression in patients with high-risk myelodysplastic syndromes.

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  • (PMID = 20178141.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / L30 CA111124
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoates; 0 / Enzyme Inhibitors; 0 / Hydrazines; 0 / Pyrazoles; 0 / eltrombopag; 4Z8R6ORS6L / Thalidomide; EC 2.1.1.- / Methyltransferases; F0P408N6V4 / lenalidomide
  • [Number-of-references] 48
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9. Suemitsu R, Fukuyama S, Ondo K, Ueda H: Resection of mediastinal granulocytic sarcoma triggered the rapid progression of acute myeloid leukemia. Ann Thorac Cardiovasc Surg; 2008 Jun;14(3):181-3
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  • [Title] Resection of mediastinal granulocytic sarcoma triggered the rapid progression of acute myeloid leukemia.
  • We experienced a case of acute myeloid leukemia (AML) that took a rapid turn for the worse after the resection of a mediastinal GS.
  • The immunohistological findings showed the features of leukemia, and GS was diagnosed.
  • Despite chemotherapy, the patient died on POD 28 as a result of rapid disease progression.
  • [MeSH-major] Diagnostic Errors. Leukemia, Myeloid, Acute / pathology. Mediastinal Neoplasms / pathology. Sarcoma, Myeloid / pathology. Thymectomy / adverse effects. Thymoma / pathology. Thymus Neoplasms / pathology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Sternum / surgery. Tomography, X-Ray Computed

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  • (PMID = 18577899.001).
  • [ISSN] 1341-1098
  • [Journal-full-title] Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia
  • [ISO-abbreviation] Ann Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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10. Nakamura S, Hirano I, Okinaka K, Takemura T, Yokota D, Ono T, Shigeno K, Shibata K, Fujisawa S, Ohnishi K: The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia. Carcinogenesis; 2010 Nov;31(11):2012-21
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  • [Title] The FOXM1 transcriptional factor promotes the proliferation of leukemia cells through modulation of cell cycle progression in acute myeloid leukemia.
  • However, it is not clearly understood how FOXM1 contributes to acute myeloid leukemia (AML) cell proliferation.
  • In summary, we found that FOXM1B mRNA is predominantly expressed in AML cells and that aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.
  • [MeSH-major] Cell Cycle. Cell Cycle Proteins / metabolism. Cell Proliferation. Forkhead Transcription Factors / physiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adult. Aged. Aldehyde Dehydrogenase / genetics. Aldehyde Dehydrogenase / metabolism. Apoptosis. Aurora Kinase B. Aurora Kinases. Blotting, Western. Cells, Cultured. Cyclin B1 / genetics. Cyclin B1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Disease Progression. Fluorescent Antibody Technique. Humans. Inhibitor of Apoptosis Proteins. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocytes / metabolism. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Middle Aged. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. RNA, Messenger / genetics. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. S-Phase Kinase-Associated Proteins / genetics. S-Phase Kinase-Associated Proteins / metabolism

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  • (PMID = 20823107.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / CCNB1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Inhibitor of Apoptosis Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule-Associated Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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11. Hentschel N, Krusch M, Kiener PA, Kolb HJ, Salih HR, Schmetzer HM: Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma. Eur J Haematol; 2006 Aug;77(2):91-101
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  • [Title] Serum levels of sCD137 (4-1BB) ligand are prognostic factors for progression in acute myeloid leukemia but not in non-Hodgkin's lymphoma.
  • Recently, we demonstrated that low levels of soluble (s) CD137L and high levels of sCD178 correlate significantly with a long progression free survival in patients with myelodysplastic syndrome (MDS).
  • In this study, we correlated sCD137L and sCD178 levels in sera of 42 samples of patients with acute myeloid leukemia (AML) and 46 samples of patients with non-Hodgkin's lymphoma (NHL) with stages, subtypes, and the clinical course of the diseases and determined cut-off values with maximum probability for significant differentiation between cases with higher/lower probability for progress free survival.
  • Furthermore, in AML patients sCD137L levels correlate significantly with the probabilities to achieve complete remission (CR), stay in CR or with progress of the disease.
  • [MeSH-major] Biomarkers, Tumor / blood. Leukemia, Myeloid / blood. Lymphoma, Non-Hodgkin / blood. Membrane Glycoproteins / blood. Neoplasm Proteins / blood. Tumor Necrosis Factors / blood
  • [MeSH-minor] 4-1BB Ligand. Acute Disease. Adult. Aged. Aged, 80 and over. Blast Crisis / blood. Child, Preschool. Disease Progression. Disease-Free Survival. Fas Ligand Protein. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Lymphoma, B-Cell / blood. Lymphoma, T-Cell / blood. Male. Middle Aged. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Prognosis. Retrospective Studies. Solubility. Survival Analysis

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  • (PMID = 16800841.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / 4-1BB Ligand; 0 / Biomarkers, Tumor; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / TNFSF9 protein, human; 0 / Tumor Necrosis Factors
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12. Cocco L, Manzoli L, Palka G, Martelli AM: Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia. Adv Enzyme Regul; 2005;45:126-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia.
  • PLC beta1 is a well-known example, given that it has been shown that only the enzyme located in the nucleus targets the cyclin D3/cdk4 complex, playing, in turn, a key role in the control of normal progression through the G1 phase of the cell cycle.
  • Moreover, non-specific alterations in chromosome 20 have been found in patients affected by MDS and acute myeloid leukemia AML.
  • The availability of a highly specific probe gave an opportunity to perform in patients affected with MDS/AML, associated with normal karyotype, painting and FISH analysis aimed to check the PLC beta1 gene, given that this signaling molecule is a key player in the control of some checkpoints of the normal progression through the cell cycle.
  • The reported data strengthen the contention of a key role played by PLC beta1 in the nucleus, suggest a possible involvement of PLC beta1 in the progression of MDS to AML and pave the way for a larger investigation aimed at identifying a possible high risk group among MDS patients with a normal karyotype.
  • [MeSH-major] Cell Cycle / physiology. Cell Nucleus / enzymology. Isoenzymes / physiology. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology. Type C Phospholipases / physiology
  • [MeSH-minor] Acute Disease. Gene Deletion. Humans. Phospholipase C beta. Signal Transduction / physiology


13. van Luijn MM, van den Ancker W, Chamuleau ME, Ossenkoppele GJ, van Ham SM, van de Loosdrecht AA: Impaired antigen presentation in neoplasia: basic mechanisms and implications for acute myeloid leukemia. Immunotherapy; 2010 Jan;2(1):85-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired antigen presentation in neoplasia: basic mechanisms and implications for acute myeloid leukemia.
  • During onset, treatment and progression of acute myeloid leukemia (AML), inadequate immune responses against certain myeloid leukemic blasts might be associated with the occurrence of minimal residual disease and subsequent relapse.
  • In tumor cells that can express HLA class II molecules, such as myeloid leukemic blasts, abnormalities in the processing pathways of endogenous antigens could also result in impaired HLA class II-restricted tumor-associated antigen presentation to CD4(+) T helper cells.
  • More insight into impaired tumor-associated antigen presentation by myeloid leukemic blasts could explain their escape from immune recognition and might be crucial for selecting appropriate strategies to improve whole-cell or dendritic cell-based tumor vaccine efficacy in the treatment of AML patients.
  • [MeSH-major] Antigen Presentation / immunology. Leukemia, Myeloid / immunology. Neoplasm, Residual / immunology. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Acute Disease. Cancer Vaccines / immunology. Dendritic Cells / immunology. Humans. Immunotherapy / methods. Neoplasms / immunology. Neoplasms / therapy

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  • (PMID = 20635891.001).
  • [ISSN] 1750-7448
  • [Journal-full-title] Immunotherapy
  • [ISO-abbreviation] Immunotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cancer Vaccines
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14. Lonetti A, Iacobucci I, Ferrari A, Messina M, Cilloni D, Soverini S, Papayannidis C, Baccarani M, Foà R, Martinelli G: Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients. J Clin Oncol; 2009 May 20;27(15_suppl):7049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients.
  • : 7049 Since the activation-induced cytidine deaminase (AID) enzyme can target non-immunoglobulin (Ig) genes and may even act as a genome-wide mutator, we investigated AID expression in BCR-ABL1-positive ALL and in chronic myeloid leukemia (CML) at the time of progression to blast crisis.
  • On the 61 de novo adult BCR-ABL1-positive ALL patients (pts), AID mRNA and protein were detected in 36 (59%); their expression correlated with BCR-ABL1 transcript levels and disappeared after treatment with tyrosine kinase inhibitors at the time of remission.
  • AID expression was also found in lymphoid blast crisis CML (50%), but not in myeloid lineage or in chronic phase CML.
  • Our findings show that BCR-ABL1-positive ALL cells aberrantly express different isoforms of AID that can act as mutator outside the Ig gene loci in promoting genetic instability in leukemia cells.

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  • (PMID = 27961429.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Plunkett W, Thomas DA, O'Brien SM, Federl S, Giles FJ, Nicol SJ, Gill J, Zhao L, Ravandi F, Kantarjian H: Phase I study of pemetrexed in patients with relapsed or refractory acute leukemia or lymphoid blast phase chronic myelogenous leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of pemetrexed in patients with relapsed or refractory acute leukemia or lymphoid blast phase chronic myelogenous leukemia.
  • The purpose of this phase I trial was to define the dose-limiting toxicity (DLT), maximum tolerated dose (MTD), and recommended phase II dose (RP2D) of pemetrexed given with vitamin supplementation to patients with relapsed or refractory leukemia.
  • METHODS: Patients ≥15 years of age were enrolled with relapsed or refractory leukemia, Eastern Cooperative Oncology Group performance status ≤2, adequate renal and hepatic function, and life expectancy of ≥6 weeks.
  • RESULTS: Twenty-two patients entered the trial; median age was 50 years (range: 18-75); 15 patients had acute myeloid leukemia and 7 patients had acute lymphocytic leukemia (ALL).
  • Two patients died during the study due to disease progression and 1 patient discontinued due to a subdural hematoma of unknown cause.

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  • (PMID = 27961463.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Naik SG, Negrin R, Laport G, Miklos D, Shizuru J, Arai S, Blume K, Wong R, Lowsky R, Johnston L: Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies.
  • : 7033 Patients (pts) with high risk (HR) or advanced myeloid malignancies have limited effective treatment options.
  • Disease status at transplantation was induction failure (IF) acute myeloid leukemia (AML) (n = 10), HR AML in 1st complete remission (CR1) n = 11, in CR2 (n = 5), in CR3 (n = 2), relapsed refractory (RR) AML (n = 14), chronic myeloid leukemia (CML) in second chronic phase (n = 6), blast crisis (n = 2), myelofibrosis (n = 6), myeloproliferative disorders (n = 2), and MDS (n = 38).
  • With a median follow up of 5.6 yrs (1.6-14.6 yrs) actuarial 5-year overall survival (OS) was 32% (95% CI 22-42%) and 5-year probability for freedom from progression (FFP) was 64% (95% CI 52%-76%).
  • Cumulative incidence of acute (grade 3-4) and chronic GVHD was 28% (95% CI 19%-37%) and 38% (95% CI 24%-52%), respectively.
  • These results confirm that pts with high-risk or advanced myeloid malignancies can achieve long-term survival following myeloablative allogeneic HCT with aggressive conditioning.
  • Relapse and acute GVHD remain significant causes of mortality.

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  • (PMID = 27961395.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Pigazzi M, Manara E, Baron E, Beghin A, Basso G: The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e22045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia.
  • CREB was previously demonstrated to be overexpressed in acute leukemia, whereas ICER was found rapidly degradated being unable to control gene transcription.
  • ICER exogenous expression was demonstrated to repress CREB targets preventing leukemia progression.
  • RESULTS: We revealed that ICER was able to control gene expression in leukemia, principally of genes involved in cell death and survival.

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  • (PMID = 27963227.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Medeiros BC, Gotlib JR, Coutre SE, Jones C, Khan SA, Rajwanshi R, Rajwanshi R, Zehnder J, Zehnder J: Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia.
  • : 7052 Background: High treatment-related mortality and low response rates often discourage elderly patients with acute myeloid leukemia from receiving treatment.
  • De novo AML was diagnosed in eight patients and five patients had s-AML.
  • Seven patients have died from disease progression, while two patients died of neutropenic sepsis (early deaths).

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  • (PMID = 27961417.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Iliopoulou EG, Kountourakis P, Karamouzis MV, Doufexis D, Ardavanis A, Baxevanis CN, Rigatos G, Papamichail M, Perez SA: A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):3001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3001 Background: HLA-mismatched NK cells have been found effective in acute myeloid leukemia pts.
  • RESULTS: Between 11/2007 and 11/2008 16 pts (performance status 0-1) were enrolled; 1 pt had rapid disease progression before treatment.

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  • (PMID = 27962051.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Ayan I, Kebudi R, Ozger H, Yaman Agaoglu F, Gorgun O, Bilgic B, Eralp L, Dizdar Y, Darendeliler E: Childhood osteosarcoma: Evaluation of 94 cases. A single institution study. J Clin Oncol; 2009 May 20;27(15_suppl):10040

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 26 patients died; 20 of disease, 5 of toxicity, and 1 of second malignancy (acute myeloid leukemia).
  • A total of 33 patients experienced relapse and/or progression at a median of 9 months (range 0-40 months).

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  • (PMID = 27962466.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Göhring G, Giagounidis A, Büsche G, Kreipe HH, Zimmermann M, Hellström-Lindberg E, Aul C, Schlegelberger B: Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression. Ann Hematol; 2010 Apr;89(4):365-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression.
  • Thirty-six percent of patients progressed into acute myeloid leukaemia.
  • However, erythroid and cytogenetic responders had a significantly decreased risk of progression to acute myeloid leukaemia (p = 0.001 and p = 0.009, respectively) compared to non-responders.
  • Three and 5 years after study entry, the cumulative incidence of acute myeloid leukaemia for patients with a cytogenetic response was 10% and 21%, respectively, and for patients without cytogenetic response, it was 46% and 60%.
  • Patients with del(5q) myelodysplastic syndromes without erythroid or cytogenetic remission after treatment with lenalidomide have a high risk for clonal evolution and acute myeloid leukaemia progression.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Erythroid Cells / drug effects. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Thalidomide / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Follow-Up Studies. Humans. Karyotyping. Male. Middle Aged. Remission Induction. Risk Factors. Treatment Failure

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  • (PMID = 19855965.001).
  • [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] 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
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22. Knoche E, McLeod HL, Graubert TA: Pharmacogenetics of alkylator-associated acute myeloid leukemia. Pharmacogenomics; 2006 Jul;7(5):719-29
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  • [Title] Pharmacogenetics of alkylator-associated acute myeloid leukemia.
  • Therapy-related acute myeloid leukemia (t-AML) is a lethal late complication of alkylator chemotherapy.
  • Both t-AML and de novo AML are complex genetic diseases, requiring cooperating mutations in interacting pathways for disease initiation and progression.
  • Germline variants of these 'leukemia pathway' genes may cooperate with somatic mutations to induce both de novo and therapy-related AML.
  • Several cancer susceptibility syndromes have been identified that cause an inherited predisposition to de novo and t-AML.
  • [MeSH-major] Alkylating Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16886897.001).
  • [ISSN] 1462-2416
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents
  • [Number-of-references] 98
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23. Kiyoi H, Naoe T: FLT3 mutations in acute myeloid leukemia. Methods Mol Med; 2006;125:189-97
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  • [Title] FLT3 mutations in acute myeloid leukemia.
  • The prevalence of an internal tandem duplication (ITD) of the juxtamembrane domain-coding sequence and a missense mutation of D835 within the kinase domain of the FLT3 gene is 15-35% and 5-10% of adults with acute myeloid leukemia (AML), respectively.
  • Several large-scale studies in well-documented patients published to date have demonstrated that FLT3 mutations are strongly associated with a poor prognosis and a high leukemia cell count in patients with AML, suggesting that FLT3 mutations are involved in disease progression.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adult. DNA Mutational Analysis / methods. Gene Duplication. Humans. Mutation, Missense. Point Mutation. Sequence Deletion

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  • (PMID = 16502586.001).
  • [ISSN] 1543-1894
  • [Journal-full-title] Methods in molecular medicine
  • [ISO-abbreviation] Methods Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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24. Vélez-Ruelas MA, Martínez-Jaramillo G, Arana-Trejo RM, Mayani H: Hematopoietic changes during progression from Fanconi anemia into acute myeloid leukemia: case report and brief review of the literature. Hematology; 2006 Oct;11(5):331-4
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  • [Title] Hematopoietic changes during progression from Fanconi anemia into acute myeloid leukemia: case report and brief review of the literature.
  • Around 9% of FA patients develop acute myeloid leukemia (AML), which makes FA a good genetic model to study leukemogenesis.
  • Interestingly, no significant changes in the karyotype of marrow cells were observed, indicating that progression from FA into AML may proceed without major chromosomal alterations (i.e. translocations and/or deletions).
  • [MeSH-major] Fanconi Anemia / pathology. Hematopoietic Stem Cells / pathology. Leukemia, Myeloid / pathology
  • [MeSH-minor] Bone Marrow Cells / pathology. Child. Disease Progression. Humans. Karyotyping. Male

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  • (PMID = 17607582.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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25. Ko RM, Kim HG, Wolff L, Klug CA: Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia. Leuk Res; 2008 Jul;32(7):1101-11
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  • [Title] Roles of p15Ink4b and p16Ink4a in myeloid differentiation and RUNX1-ETO-associated acute myeloid leukemia.
  • Inactivation of p15(Ink4b) expression by promoter hypermethylation occurs in up to 80% of acute myeloid leukemia (AML) cases and is particularly common in the FAB-M2 subtype of AML, which is characterized by the presence of the RUNX1-ETO translocation in 40% of cases.
  • To establish whether the loss of p15(Ink4b) contributes to AML progression in association with RUNX1-ETO, we have expressed the RUNX1-ETO fusion protein from a retroviral vector in hematopoietic progenitor cells isolated from wild-type, p15(Ink4b) or p16(Ink4a) knockout bone marrow.
  • Analysis of lethally irradiated recipient mice reconstituted with RUNX1-ETO-expressing cells showed that neither p15(Ink4b) or p16(Ink4a) loss significantly accelerated disease progression over the time period of one year post-transplantation.
  • Loss of p15(Ink4b) alone resulted in increased myeloid progenitor cell frequencies in bone marrow by 10-month post-transplant and a 19-fold increase in the frequency of Lin(-)c-Kit(+)Sca-1(+) (LKS) cells that was not associated with expansion of long-term reconstituting HSC.

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  • (PMID = 18037485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096798; United States / NCI NIH HHS / CA / R01 CA087549; United States / NCI NIH HHS / CA / R01CA087549; United States / NCI NIH HHS / CA / CA096798-05; United States / NCI NIH HHS / CA / R01 CA096798-05; United States / NCI NIH HHS / CA / R01CA096798
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ NIHMS49471; NLM/ PMC2430055
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26. Mao G, Yuan F, Absher K, Jennings CD, Howard DS, Jordan CT, Gu L: Preferential loss of mismatch repair function in refractory and relapsed acute myeloid leukemia: potential contribution to AML progression. Cell Res; 2008 Feb;18(2):281-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preferential loss of mismatch repair function in refractory and relapsed acute myeloid leukemia: potential contribution to AML progression.
  • Acute myeloid leukemia (AML) is an aggressive hematological cancer.
  • To explore whether loss of DNA mismatch repair (MMR) function is involved in AML, we screened two key MMR genes, MSH2 and MLH1, for mutations and promoter hypermethylation in leukemia specimens from 53 AML patients and blood from 17 non-cancer controls.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. DNA Methylation. DNA Mismatch Repair. Leukemia, Myeloid, Acute / genetics. MutS Homolog 2 Protein / genetics. Mutation. Neoplasm Proteins / genetics. Nuclear Proteins / genetics

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  • (PMID = 18227862.001).
  • [ISSN] 1748-7838
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA104333
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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27. Moreau-Gachelin F: Lessons from models of murine erythroleukemia to acute myeloid leukemia (AML): proof-of-principle of co-operativity in AML. Haematologica; 2006 Dec;91(12):1644-52
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  • [Title] Lessons from models of murine erythroleukemia to acute myeloid leukemia (AML): proof-of-principle of co-operativity in AML.
  • The models of acute erythroleukemia caused in mice by the Friend retrovirus SFFV (spleen focus forming virus) and the Spi-1/PU.1 transgenesis provide considerable information to help to understand the molecular mechanisms underlying the multi-stage nature of leukemia.
  • Leukemogenesis in these murine models is initiated from an acute hyperplasia of erythroid progenitor cells followed later on by a blastic crisis.
  • This review highlights recent findings demonstrating the key roles of the co-operation of two mutations occurring during leukemic progression, a mutation interfering with differentiation and a mutation conferring a proliferative advantage to cells.
  • Through their multi-step evolution, these mouse erythroleukemia models resemble the two phases of human acute myeloid leukemia (AML).
  • The findings we discuss provide evidence for similar molecular mechanisms involved in the evolution of leukemia in mice and men.
  • [MeSH-major] Disease Models, Animal. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Animals. Friend murine leukemia virus / genetics. Humans. Mice. Mice, Transgenic


28. Khalid S, Adil SN, Khurshid M: Waldenstrom's macroglobulinemia terminating in acute myeloid leukemia. J Pak Med Assoc; 2006 Jun;56(6):291-2
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  • [Title] Waldenstrom's macroglobulinemia terminating in acute myeloid leukemia.
  • The most common causes of death in these patients are progression of the malignant lymphoproliferative process, infection and cardiac failure.
  • Acute leukemia is a rare event in the clinical course of WM.
  • A number of case reports have documented the development of terminal acute leukemia in patients with WM following prolonged chemotherapy.
  • Four years later, he developed acute leukemia.
  • [MeSH-major] Cyclophosphamide / adverse effects. Leukemia, Myeloid, Acute / etiology. Waldenstrom Macroglobulinemia / diagnosis. Waldenstrom Macroglobulinemia / drug therapy

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  • (PMID = 16827257.001).
  • [ISSN] 0030-9982
  • [Journal-full-title] JPMA. The Journal of the Pakistan Medical Association
  • [ISO-abbreviation] J Pak Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Pakistan
  • [Chemical-registry-number] 18D0SL7309 / Chlorambucil; 8N3DW7272P / Cyclophosphamide
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29. Barabé F, Kennedy JA, Hope KJ, Dick JE: Modeling the initiation and progression of human acute leukemia in mice. Science; 2007 Apr 27;316(5824):600-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modeling the initiation and progression of human acute leukemia in mice.
  • Our understanding of leukemia development and progression has been hampered by the lack of in vivo models in which disease is initiated from primary human hematopoietic cells.
  • We showed that upon transplantation into immunodeficient mice, primitive human hematopoietic cells expressing a mixed-lineage leukemia (MLL) fusion gene generated myeloid or lymphoid acute leukemias, with features that recapitulated human diseases.
  • Analysis of serially transplanted mice revealed that the disease is sustained by leukemia-initiating cells (L-ICs) that have evolved over time from a primitive cell type with a germline immunoglobulin heavy chain (IgH) gene configuration to a cell type containing rearranged IgH genes.
  • The L-ICs retained both myeloid and lymphoid lineage potential and remained responsive to microenvironmental cues.
  • [MeSH-major] Disease Models, Animal. Leukemia, Lymphoid. Leukemia, Myeloid. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Animals. Bone Marrow Transplantation. Cell Transformation, Neoplastic. Disease Progression. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Genes, Immunoglobulin. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Immunoglobulin Heavy Chains / genetics. Mice. Transduction, Genetic. Tumor Cells, Cultured

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  • (PMID = 17463288.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / MLL-AF9 fusion protein, human; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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30. Lu L, Zhang L, Xiao Z, Lu S, Yang R, Han ZC: Neuropilin-1 in acute myeloid leukemia: expression and role in proliferation and migration of leukemia cells. Leuk Lymphoma; 2008 Feb;49(2):331-8
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  • [Title] Neuropilin-1 in acute myeloid leukemia: expression and role in proliferation and migration of leukemia cells.
  • The role of NRP-1 in the growth and progression of leukemia is unknown.
  • Our results showed that NRP-1 mRNA was expressed in six of seven leukemic cell lines and primary leukemias derived from all 24 patients with acute myeloid leukemia (AML).
  • Reduced NRP-1 expression by RNA interference led to a decrease of VEGF-mediated mitogenic and migration responses in acute myeloid leukemic cell line HEL.
  • [MeSH-major] Cell Movement. Cell Proliferation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / pathology. Neuropilin-1 / analysis. Vascular Endothelial Growth Factor A / physiology

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  • (PMID = 18231921.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 144713-63-3 / Neuropilin-1
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31. Pedersen-Bjergaard J, Andersen MK, Andersen MT, Christiansen DH: Genetics of therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2008 Feb;22(2):240-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetics of therapy-related myelodysplasia and acute myeloid leukemia.
  • Myelodysplasia (MDS) and acute myeloid leukemia (AML) are heterogeneous, closely associated diseases arising de novo or following chemotherapy with alkylating agents, topoisomerase II inhibitors, or after radiotherapy.
  • Whereas de novo MDS and AML are almost always subclassified according to cytogenetic characteristics, therapy-related MDS (t-MDS) and therapy-related AML (t-AML) are often considered as separate entities and are not subdivided.
  • An increasing number of gene mutations are now observed to cluster differently in these pathways with an identical pattern in de novo and in t-MDS and t-AML.
  • Point mutations of AML1 and RAS seem to cooperate and predispose to progression from t-MDS to t-AML.
  • As de novo and t-MDS and t-AML are biologically identical diseases, they ought to be subclassified and treated similarly.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics


32. Mayani H, Flores-Figueroa E, Chávez-González A: In vitro biology of human myeloid leukemia. Leuk Res; 2009 May;33(5):624-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro biology of human myeloid leukemia.
  • For about 40 years, the biology of human myeloid leukemia (ML) has been studied in different in vitro systems.
  • Throughout this time, semisolid colony assays, Dexter-type long-term cultures and liquid suspension cultures have contributed to our understanding of the mechanisms involved in the origin and progression of this hematological disorder.
  • By using such systems, it has been possible to identify the cells in which leukemia originates; to recognize a functional hierarchy within the hematopoietic system of leukemia patients; to identify factors, soluble and cell-associated, that regulate leukemic growth; and to study the effects of different antineoplastic drugs.
  • Still, many questions and problems remain unsolved regarding the biology of myeloid leukemia in vitro.
  • This article presents a comprehensive review on the behavior of leukemic stem and progenitor cells, both from acute and chronic myeloid leukemia, in the different culture systems mentioned above.
  • [MeSH-major] Leukemia, Myeloid / pathology

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  • (PMID = 19108888.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 199
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33. Suzuki T, Kiyoi H, Ozeki K, Tomita A, Yamaji S, Suzuki R, Kodera Y, Miyawaki S, Asou N, Kuriyama K, Yagasaki F, Shimazaki C, Akiyama H, Nishimura M, Motoji T, Shinagawa K, Takeshita A, Ueda R, Kinoshita T, Emi N, Naoe T: Clinical characteristics and prognostic implications of NPM1 mutations in acute myeloid leukemia. Blood; 2005 Oct 15;106(8):2854-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characteristics and prognostic implications of NPM1 mutations in acute myeloid leukemia.
  • Recently, somatic mutations of the nucleophosmin gene (NPM1), which alter the subcellular localization of the product, have been reported in acute myeloid leukemia (AML).
  • In 190 patients without the M3 French-American-British (FAB) subtype who were treated with the protocol of the Japan Adult Leukemia Study Group, multivariate analyses showed that the NPM1 mutation was a favorable factor for achieving complete remission but was associated with a high relapse rate.
  • These results suggest that the NPM1 mutation is not necessarily an early event during leukemogenesis or that leukemia clones with NPM1 mutations are sensitive to chemotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Disease Progression. Exons / genetics. Female. Genotype. Humans. Male. Middle Aged. Molecular Sequence Data. Prognosis. Survival Rate

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  • (PMID = 15994285.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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34. Kirstetter P, Schuster MB, Bereshchenko O, Moore S, Dvinge H, Kurz E, Theilgaard-Mönch K, Månsson R, Pedersen TA, Pabst T, Schrock E, Porse BT, Jacobsen SE, Bertone P, Tenen DG, Nerlov C: Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells. Cancer Cell; 2008 Apr;13(4):299-310
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells.
  • Mutations in the CEBPA gene are present in 7%-10% of human patients with acute myeloid leukemia (AML).
  • However, p42 was required for control of myeloid progenitor proliferation, and p42-deficient mice developed AML with complete penetrance. p42-deficient leukemia could be transferred by a Mac1+c-Kit+ population that gave rise only to myeloid cells in recipient mice.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / pathology. Models, Biological. Mutant Proteins / metabolism. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Differentiation. Disease Progression. Gene Expression Profiling. Granulocytes / cytology. Macrophage-1 Antigen / metabolism. Mice. Mice, Knockout. Myeloid Progenitor Cells / pathology. Neoplasm Transplantation. Phenotype. Protein Isoforms / metabolism. Proto-Oncogene Proteins c-kit / metabolism

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  • [CommentIn] Cancer Cell. 2008 Apr;13(4):289-91 [18394549.001]
  • (PMID = 18394553.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501838; United States / NHLBI NIH HHS / HL / R01 HL112719
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Macrophage-1 Antigen; 0 / Mutant Proteins; 0 / Protein Isoforms; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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35. Kuo MC, Liang DC, Huang CF, Shih YS, Wu JH, Lin TL, Shih LY: RUNX1 mutations are frequent in chronic myelomonocytic leukemia and mutations at the C-terminal region might predict acute myeloid leukemia transformation. Leukemia; 2009 Aug;23(8):1426-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RUNX1 mutations are frequent in chronic myelomonocytic leukemia and mutations at the C-terminal region might predict acute myeloid leukemia transformation.
  • RUNX1 mutations have rarely been reported in chronic myelomonocytic leukemia (CMML).
  • There was no difference in overall survival between patients with and without RUNX1 mutations, but a trend of higher risk of acute myeloid leukemia (AML) progression was observed in mutation-positive patients (16/30 vs 17/51, P=0.102), especially in patients with C-terminal mutations (P=0.023).
  • The median time to AML progression was 6.8 months in patients with C-terminal mutations compared with 28.3 months in those without mutations (P=0.022).
  • [MeSH-major] Blast Crisis / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Mutation. Neoplasm Proteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Female. Genes, ras. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Protein Structure, Tertiary. fms-Like Tyrosine Kinase 3 / genetics


36. Kroeger H, Jelinek J, Estécio MR, He R, Kondo K, Chung W, Zhang L, Shen L, Kantarjian HM, Bueso-Ramos CE, Issa JP: Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse. Blood; 2008 Aug 15;112(4):1366-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant CpG island methylation in acute myeloid leukemia is accentuated at relapse.
  • DNA methylation of CpG islands around gene transcription start sites results in gene silencing and plays a role in leukemia pathophysiology.
  • Its impact in leukemia progression is not fully understood.
  • We performed genomewide screening for methylated CpG islands and identified 8 genes frequently methylated in leukemia cell lines and in patients with acute myeloid leukemia (AML): NOR1, CDH13, p15, NPM2, OLIG2, PGR, HIN1, and SLC26A4.
  • Our data suggest that DNA methylation is involved in AML progression and provide a rationale for the use of epigenetic agents in remission maintenance.

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  • (PMID = 18523155.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / 5P01CA108631-03; United States / NCI NIH HHS / CA / 5P50CA100632-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2515110
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37. Sun Q, So CC, Yip SF, Wan TS, Ma SK, Chan LC: Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia. Leuk Res; 2008 Sep;32(9):1374-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional alterations of Lin-CD34+CD38+ cells in chronic myelomonocytic leukemia and on progression to acute leukemia.
  • The functional behavior of hematopoietic stem cell (HSC) and progenitors in chronic myelomonocytic leukemia (CMML) and on disease progression is little known.
  • We performed cell proliferation, apoptosis, hematopoietic colony forming/replating and differentiation potential studies in the purified subpopulations of Lin(-)CD34(+)CD38(-) and Lin(-)CD34(+)CD38(+) cells from 16 CMML with 6 cases after acute myeloid leukemia transformation (AML-t).
  • The Lin(-)CD34(+)CD38(+) cells in AML-t displayed high proliferative activity, resistance to apoptosis, enhanced myeloid colony formation/replating ability and a complete dendritic cell (DC) differentiation block.
  • Our findings suggest Lin(-)CD34(+)CD38(+) cells instead of Lin(-)CD34(+)CD38(-) cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML, which have implications for the further study of the biology of leukemic transformation and the design of new strategies for the effective treatment of CMML.
  • [MeSH-major] Antigens, CD34 / metabolism. Antigens, CD38 / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myelomonocytic, Chronic / metabolism. Membrane Glycoproteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis / physiology. Cell Cycle / physiology. Cell Proliferation. Cell Transformation, Neoplastic. Colony-Forming Units Assay. Dendritic Cells / metabolism. Disease Progression. Flow Cytometry. Granulocyte Colony-Stimulating Factor / administration & dosage. Hematopoietic Stem Cells. Humans. Middle Aged. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 18372040.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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38. van der Heiden PL, Jedema I, Willemze R, Barge RM: Efficacy and toxicity of gemtuzumab ozogamicin in patients with acute myeloid leukemia. Eur J Haematol; 2006 May;76(5):409-13
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  • [Title] Efficacy and toxicity of gemtuzumab ozogamicin in patients with acute myeloid leukemia.
  • Patients with acute myeloid leukemia (AML) at diagnosis and relapsed AML were treated with 6 and 9 mg/m(2) GO.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal, Humanized. Antigens, CD / biosynthesis. Antigens, Differentiation, Myelomonocytic / biosynthesis. Disease Progression. Female. Humans. Kinetics. Leukocyte Count. Male. Middle Aged. Prognosis. Recurrence. Remission Induction. Retrospective Studies. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome

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  • (PMID = 16480432.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [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 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab
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39. Bies J, Sramko M, Fares J, Rosu-Myles M, Zhang S, Koller R, Wolff L: Myeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia. Blood; 2010 Aug 12;116(6):979-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myeloid-specific inactivation of p15Ink4b results in monocytosis and predisposition to myeloid leukemia.
  • Inactivation of p15INK4b, an inhibitor of cyclin-dependent kinases, through DNA methylation is one of the most common epigenetic abnormalities in myeloid leukemia.
  • Although this suggests a key role for this protein in myeloid disease suppression, experimental evidence to support this has not been reported.
  • To address whether this event is critical for premalignant myeloid disorders and leukemia development, mice were generated that have loss of p15Ink4b specifically in myeloid cells.
  • The p15Ink4b(fl/fl)-LysMcre mice develop nonreactive monocytosis in the peripheral blood accompanied by increased numbers of myeloid and monocytic cells in the bone marrow resembling the myeloproliferative form of chronic myelomonocytic leukemia.
  • Spontaneous progression from chronic disease to acute leukemia was not observed.
  • Nevertheless, MOL4070LTR retrovirus integrations provided cooperative genetic mutations resulting in a high frequency of myeloid leukemia in knockout mice.
  • Two common retrovirus insertion sites near c-myb and Sox4 genes were identified, and their transcript up-regulated in leukemia, suggesting a collaborative role of their protein products with p15Ink4b-deficiency in promoting malignant disease.
  • This new animal model demonstrates experimentally that p15Ink4b is a tumor suppressor for myeloid leukemia, and its loss may play an active role in the establishment of preleukemic conditions.

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  • (PMID = 20457873.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn2b protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / SOXC Transcription Factors; 0 / Sox4 protein, mouse
  • [Other-IDs] NLM/ PMC2924230
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40. Lal D, Park JA, Demock K, Marinaro J, Perez AM, Lin MH, Tian L, Mashtare TJ, Murphy M, Prey J, Wetzler M, Fetterly GJ, Wang ES: Aflibercept exerts antivascular effects and enhances levels of anthracycline chemotherapy in vivo in human acute myeloid leukemia models. Mol Cancer Ther; 2010 Oct;9(10):2737-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aflibercept exerts antivascular effects and enhances levels of anthracycline chemotherapy in vivo in human acute myeloid leukemia models.
  • The efficacy of aflibercept alone and in combination with doxorubicin was evaluated in human VEGF-expressing acute myeloid leukemia (AML) cell lines and primary cells xenotransplanted into immunodeficient mice.
  • Aflibercept therapy slowed disease progression in two systemic human AML xenograft models and reduced peripheral leukemia disease in a primary relapsed AML model in NOD/SCID/IL2Rγnull mice.
  • These data suggest that inefficient drug delivery by leukemia-associated vasculature may mediate chemoresistance and support further clinical evaluation of combination aflibercept and anthracycline therapy in refractory/relapsed AML patients.
  • [MeSH-major] Anthracyclines / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Recombinant Fusion Proteins / pharmacology

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  • (PMID = 20924124.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA016156
  • [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 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Recombinant Fusion Proteins; 15C2VL427D / aflibercept; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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41. Palmisano M, Grafone T, Ottaviani E, Testoni N, Baccarani M, Martinelli G: NPM1 mutations are more stable than FLT3 mutations during the course of disease in patients with acute myeloid leukemia. Haematologica; 2007 Sep;92(9):1268-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1 mutations are more stable than FLT3 mutations during the course of disease in patients with acute myeloid leukemia.
  • NPM1 mutations have been reported to be the most frequent mutations in acute myeloid leukemia (AML).
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation / genetics. Neoplasm, Residual / genetics. Nuclear Proteins / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. DNA Mutational Analysis. Disease Progression. Humans. Phosphoproteins / genetics

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  • (PMID = 17768124.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Phosphoproteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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42. Ayala F, Dewar R, Kieran M, Kalluri R: Contribution of bone microenvironment to leukemogenesis and leukemia progression. Leukemia; 2009 Dec;23(12):2233-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Contribution of bone microenvironment to leukemogenesis and leukemia progression.
  • Tumor microenvironment has a major role in cancer progression and resistance to treatment.
  • The bone marrow (BM) is a dynamic network of growth factors, cytokines and stromal cells, providing a permissive environment for leukemogenesis and progression.
  • Both BM stroma and leukemic blasts promote angiogenesis, which is increased in acute lymphoblastic leukemia and acute myeloid leukemia.
  • Growth factors like vascular endothelial growth factor (VEGF), basic fibroblast growth factor and angiopoietins are the main proangiogenic mediators in acute leukemia.
  • Interactions of stromal cells and extracellular matrix with leukemic blasts can also generate antiapoptotic signals that contribute to neoplastic progression and persistence of treatment-resistant minimal residual disease.
  • High expression of CXC chemokine ligand 4 (CXCR4) by leukemic blasts and activation of the CXCR4-CXCL12 axis is involved in leukemia progression and disruption of normal hematopoiesis.
  • Leukemia-associated bone microenvironment markers could be used as prognostic or predictive indicators of disease progression and/or treatment outcome.
  • Studies related to bone microenvironment would likely provide a better understanding of the treatment resistance associated with leukemia therapy and design of new treatments.

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  • (PMID = 19727127.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK61688; United States / NIDDK NIH HHS / DK / DK55001; United States / NIAAA NIH HHS / AA / R01 AA013913; United States / NIDDK NIH HHS / DK / R01 DK061688; United States / NIDDK NIH HHS / DK / R01 DK062987; United States / NCI NIH HHS / CA / R01 CA125550; United States / NCI NIH HHS / CA / CA125550; United States / NIDDK NIH HHS / DK / R01 DK055001; United States / NIDDK NIH HHS / DK / DK62987; United States / NIAAA NIH HHS / AA / AA13913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS590537; NLM/ PMC4313556
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43. Gyurkocza B, Storb R, Storer BE, Chauncey TR, Lange T, Shizuru JA, Langston AA, Pulsipher MA, Bredeson CN, Maziarz RT, Bruno B, Petersen FB, Maris MB, Agura E, Yeager A, Bethge W, Sahebi F, Appelbaum FR, Maloney DG, Sandmaier BM: Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia. J Clin Oncol; 2010 Jun 10;28(17):2859-67
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  • [Title] Nonmyeloablative allogeneic hematopoietic cell transplantation in patients with acute myeloid leukemia.
  • PURPOSE: Allogeneic hematopoietic cell transplantation (HCT) after high-dose conditioning regimens imposes prohibitively high risks of morbidity and mortality for patients with high-risk acute myeloid leukemia (AML) who are older or have comorbid conditions.
  • PATIENTS AND METHODS: Two hundred seventy-four patients (median age, 60 years) with de novo or secondary AML underwent allogeneic HCT from related (n = 118) or unrelated donors (n = 156) after conditioning with 2 Gy of total-body irradiation (TBI) with or without fludarabine.
  • The estimated 5-year relapse/progression and nonrelapse mortality rates were 42% and 26%, respectively.
  • The cumulative incidences of grades 2, 3, and 4 acute graft-versus-host disease (GVHD) were 38%, 9%, and 5%, respectively.
  • CONCLUSION: Allogeneic HCT from related or unrelated donors after conditioning with low-dose TBI and fludarabine, relying almost exclusively on graft-versus-leukemia effects, can result in long-term remissions in older or medically infirm patients with AML.

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  • (PMID = 20439626.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA78902; United States / NCI NIH HHS / CA / R21 CA106177; United States / NCI NIH HHS / CA / CA15704; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / CA106177; United States / NCI NIH HHS / CA / P01 CA078902
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2903320
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44. Lerch E, Espeli V, Zucca E, Leoncini L, Scali G, Mora O, Bordoni A, Cavalli F, Ghielmini M: Prognosis of acute myeloid leukemia in the general population: data from southern Switzerland. Tumori; 2009 May-Jun;95(3):303-10
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  • [Title] Prognosis of acute myeloid leukemia in the general population: data from southern Switzerland.
  • AIMS AND BACKGROUND: To evaluate the outcome of adult patients with de novo acute myeloid leukemia in the Italian-speaking part of Switzerland and to identify prognostic factors, time to progression and overall survival.
  • METHODS AND STUDY DESIGN: Data of all adult patients diagnosed with acute myeloid leukemia from January 1984 to December 2003 were collected retrospectively.
  • Univariate and multivariate analysis for time to progression and overall survival were performed.
  • RESULTS: The incidence of acute myeloid leukemia in the adult population in southern Switzerland is 2.6/100,000 per year.
  • Median time to progression was 3 months.
  • In multivariate analysis (not including cytogenetic data), only age (P = 0.005), performance status > 1 (P = 0.001) and treatment given before/after 1993 (P = 0.044) were found to be independent prognostic factors for both overall survival and time to progression.
  • CONCLUSIONS: Most patients with acute myeloid leukemia are older than 60 years, and their outcome is still disappointing.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Analysis of Variance. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Comorbidity. Cytarabine / administration & dosage. Disease Progression. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Multivariate Analysis. Odds Ratio. Palliative Care. Prognosis. Retrospective Studies. Switzerland / epidemiology

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  • (PMID = 19688968.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
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45. Pedersen-Bjergaard J, Christiansen DH, Desta F, Andersen MK: Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2006 Nov;20(11):1943-9
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  • [Title] Alternative genetic pathways and cooperating genetic abnormalities in the pathogenesis of therapy-related myelodysplasia and acute myeloid leukemia.
  • Alternative genetic pathways were previously outlined in the pathogenesis of therapy-related myelodysplasia (t-MDS) and acute myeloid leukemia (t-AML) based on cytogenetic characteristics.
  • In addition, there is a significant association between class I and class II mutations possibly indicating cooperation in leukemogenesis, and between mutations of AML1 and RAS related to subsequent progression from t-MDS to t-AML.
  • Therapy-related and de novo myelodysplasia and acute myeloid leukemia seem to share genetic pathways, and surprisingly gene mutations were in general not more frequent in patients with t-MDS or t-AML as compared to similar cases of de novo MDS and AML studied previously.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Chromosome Aberrations. Humans. Mutation


46. Falini B, Tiacci E, Martelli MP, Ascani S, Pileri SA: New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues. Discov Med; 2010 Oct;10(53):281-92
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  • [Title] New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues.
  • Here, we focus on changes that, as compared to the 2001 edition, were introduced into the 2008 WHO classification of acute myeloid leukemia (AML) and related precursor neoplasms.
  • Finally, we describe the unique characteristics of myeloid proliferations associated with Down syndrome and blastic plasmacytoid dendritic cell neoplasm.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / pathology. Lymphoproliferative Disorders / classification. Lymphoproliferative Disorders / pathology. Medical Oncology / trends. Neoplasms / classification. Neoplasms / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Down Syndrome / complications. Down Syndrome / pathology. Humans. Precancerous Conditions / classification. Precancerous Conditions / genetics. Precancerous Conditions / pathology. World Health Organization

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  • (PMID = 21034669.001).
  • [ISSN] 1944-7930
  • [Journal-full-title] Discovery medicine
  • [ISO-abbreviation] Discov Med
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] United States
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47. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics
  • [MeSH-minor] Chromosomes, Human, Pair 8. Clone Cells. Disease Progression. Humans. Male. Mutation. Neoplasms, Second Primary. Trisomy

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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48. Palmqvist L, Argiropoulos B, Pineault N, Abramovich C, Sly LM, Krystal G, Wan A, Humphries RK: The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia. Blood; 2006 Aug 1;108(3):1030-6

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  • [Title] The Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions in acute myeloid leukemia.
  • Here, we demonstrate that overexpression of the wild-type (wt) Flt3 receptor tyrosine kinase collaborates with NUP98-HOX fusions (NUP98-HOXA10 and NUP98-HOXD13) to induce aggressive acute myeloid leukemia (AML).
  • We used a mouse transplantation model to show their synergism in cotransduced bone marrow cells as well as in a cellular model of leukemic progression.
  • Furthermore, our data support the finding that Meis1 overexpression leads to marked elevation in Flt3 transcription and extend it to the context of NUP98-HOX-induced leukemia.
  • Together, these results support a multistep model where the synergism between NUP98-HOX and wt-Flt3 is the result of the ability of Flt3 to increase proliferation of myeloid progenitors blocked in differentiation by NUP98-HOX fusions and reveal a direct role for wt-Flt3 in the pathobiology of AML.
  • Given the similarities in the leukemogenic role of native HOX and NUP98-fused HOX genes, our results underscore the clinical significance of the recurrent co-overexpression of wt-FLT3 and HOX in human leukemia and suggest that specific FLT3 inhibitors could be useful in treatment of HOX-induced AML or acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia, Myeloid / etiology. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion
  • [MeSH-minor] Acute Disease. Animals. Bone Marrow Cells. Bone Marrow Transplantation. Cell Differentiation. Cell Line. Cell Proliferation. Gene Expression Regulation, Neoplastic. Mice. Transcription Factors. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16861351.001).
  • [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 / Homeodomain Proteins; 0 / Hoxd13 protein, mouse; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 140441-81-2 / HOXA10 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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49. Kim DH, Sohn SK, Kim JG, Lee NY, Sung WJ, Baek JH, Suh JS, Lee KS, Lee KB: Parameters for predicting allogeneic PBSCT outcome of acute myeloid leukemia: cytogenetics at presentation versus disease status at transplantation. Ann Hematol; 2005 Jan;84(1):25-32
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  • [Title] Parameters for predicting allogeneic PBSCT outcome of acute myeloid leukemia: cytogenetics at presentation versus disease status at transplantation.
  • As such, the current study examined various parameters, including the cytogenetics at presentation and clinical disease status at transplantation, regarding their effect on the transplant outcomes of acute myeloid leukemia (AML) patients in an allogeneic peripheral blood stem cell transplantation (PBSCT) setting.
  • Multivariate analysis revealed that higher CD34+ cell doses, favorable cytogenetics at presentation, and a lower marrow blast percentage at transplantation were all strongly associated with favorable transplant outcomes, including overall survival (OS), progression-free survival (PFS), and the probability of progression.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / therapy. Peripheral Blood Stem Cell Transplantation / methods. Predictive Value of Tests
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Cytogenetic Analysis. Disease Progression. Female. Humans. Male. Middle Aged. Multivariate Analysis. Prognosis. Remission Induction. Survival Analysis. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 15349754.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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50. Jiang Y, Dunbar A, Gondek LP, Mohan S, Rataul M, O'Keefe C, Sekeres M, Saunthararajah Y, Maciejewski JP: Aberrant DNA methylation is a dominant mechanism in MDS progression to AML. Blood; 2009 Feb 5;113(6):1315-25
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  • [Title] Aberrant DNA methylation is a dominant mechanism in MDS progression to AML.
  • Myelodysplastic syndromes (MDSs) are clonal hematologic disorders that frequently represent an intermediate disease stage before progression to acute myeloid leukemia (AML).
  • In 184 patients with MDS and AML, DNA methylation microarray and high-density single nucleotide polymorphism array (SNP-A) karyotyping were used to assess the relative contributions of aberrant DNA methylation and chromosomal deletions to tumor-suppressor gene (TSG) silencing during disease progression.
  • However, the ubiquity, extent, and correlation with disease progression suggest that aberrant DNA methylation is the dominant mechanism for TSG silencing and clonal variation in MDS evolution to AML.

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  • [Cites] Am J Hum Genet. 2007 Jul;81(1):114-26 [17564968.001]
  • [Cites] Science. 2007 Nov 16;318(5853):1108-13 [17932254.001]
  • (PMID = 18832655.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / S10 RR019391; United States / NCRR NIH HHS / RR / U54 RR019391
  • [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 / FZD3 protein, human; 0 / Frizzled Receptors; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2637194
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51. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Amare P, Arora B, Banavali SD, Nair CN: Clinico-hematological profile in biphenotypic acute leukemia. Indian J Cancer; 2009 Apr-Jun;46(2):160-8
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  • [Title] Clinico-hematological profile in biphenotypic acute leukemia.
  • BACKGROUND: We present a clinico-hematological profile and treatment outcome of Biphenotypic Acute Leukemia (BAL).
  • We included those cases, which fulfilled the European Group for the Immunological Characterization of Acute Leukemia's (EGIL's) scoring system criteria for the diagnosis of BAL, as per recommendation of the WHO classification.
  • B-Myeloid (14 cases) followed by T-Myeloid BAL (13 cases) were the commonest subtypes.
  • Polymorphous population of blasts (16 cases) was commonly associated with T-Myeloid BAL (10 cases).
  • BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic myeloid leukemia (CML) in blast crisis with biphenotypic expression and treated accordingly.
  • [MeSH-major] Immunophenotyping. Leukemia, Biphenotypic, Acute / blood. Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Disease Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged. Phenotype. Retrospective Studies. Young Adult

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  • (PMID = 19346652.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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52. Tabori U, Revach G, Nathan PC, Strahm B, Rachlis A, Shago M, Grant R, Doyle J, Malkin D: Toxicity and outcome of children with treatment related acute myeloid leukemia. Pediatr Blood Cancer; 2008 Jan;50(1):17-23
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  • [Title] Toxicity and outcome of children with treatment related acute myeloid leukemia.
  • BACKGROUND: The aim of this study was to evaluate the clinical course and outcome of children with treatment related acute myeloid leukemia (tAML) and compare them to children with primary AML (pAML).
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Child. Disease Progression. Female. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Male. Survival Analysis. Survival Rate


53. Weiss JR, Baer MR, Ambrosone CB, Blanco JG, Hutson A, Ford LA, Moysich KB: Concordance of pharmacogenetic polymorphisms in tumor and germ line DNA in adult patients with acute myeloid leukemia. Cancer Epidemiol Biomarkers Prev; 2007 May;16(5):1038-41
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  • [Title] Concordance of pharmacogenetic polymorphisms in tumor and germ line DNA in adult patients with acute myeloid leukemia.
  • However, genotypes determined in tumor and somatic tissues may differ due to cytogenetic and molecular changes associated with malignant transformation and progression.
  • Discordance between germ line and tumor genotypes may be particularly relevant in leukemia because cytogenetic abnormalities are frequent.
  • We compared genotypes determined in DNA extracted from paired pretreatment bone marrow and buccal samples from 80 adult patients with acute myeloid leukemia (AML).
  • [MeSH-major] Bone Marrow Cells / pathology. DNA, Neoplasm / analysis. Leukemia, Myeloid, Acute / genetics. Mouth Mucosa / cytology. Pharmacogenetics. Polymorphism, Genetic


54. Chou WC, Tang JL, Lin LI, Yao M, Tsay W, Chen CY, Wu SJ, Huang CF, Chiou RJ, Tseng MH, Lin DT, Lin KH, Chen YC, Tien HF: Nucleophosmin mutations in de novo acute myeloid leukemia: the age-dependent incidences and the stability during disease evolution. Cancer Res; 2006 Mar 15;66(6):3310-6
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  • [Title] Nucleophosmin mutations in de novo acute myeloid leukemia: the age-dependent incidences and the stability during disease evolution.
  • Nucleophosmin (NPM) mutations have been found in a significant proportion of adults with de novo acute myeloid leukemia (AML), especially in those of a normal karyotype.
  • In this study, NPM mutations were analyzed in 173 Chinese patients of de novo AML, including adults and children.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Amino Acid Sequence. Base Sequence. Child. Child, Preschool. Disease Progression. Exons. Female. Humans. Immunophenotyping. Infant. Male. Middle Aged. Molecular Sequence Data

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  • (PMID = 16540685.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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55. Iwai M, Kiyoi H, Ozeki K, Kinoshita T, Emi N, Ohno R, Naoe T: Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome. Leukemia; 2005 Aug;19(8):1367-75
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  • [Title] Expression and methylation status of the FHIT gene in acute myeloid leukemia and myelodysplastic syndrome.
  • To clarify the role of fragile histidine triad (FHIT) in hematological malignancies, we examined the methylation status and the expression level of the FHIT gene in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) cells in comparison with the methylation of the p15(INK4B) gene.
  • These results suggested that FHIT methylation was accumulated through the disease progression of MDS and AML, and the role of the FHIT gene as a tumor suppressor seemed different in AML and MDS.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Bone Marrow / pathology. Cell Cycle Proteins / genetics. Cyclin-Dependent Kinase Inhibitor p15. Genes, Tumor Suppressor. Humans. RNA, Messenger / analysis. Recurrence. Tumor Suppressor Proteins / genetics

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  • [Copyright] Leukemia (2005) 19, 1367-1375.
  • (PMID = 15902282.001).
  • [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 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 0 / fragile histidine triad protein; 776B62CQ27 / decitabine; EC 3.6.- / Acid Anhydride Hydrolases; M801H13NRU / Azacitidine
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56. Licht JD, Sternberg DW: The molecular pathology of acute myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2005;:137-42
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  • [Title] The molecular pathology of acute myeloid leukemia.
  • The pathogenesis of acute myelogenous leukemia (AML) involves an array of molecular alterations that disrupt almost every facet of cell transformation.
  • This overview describes some of the critical molecular alterations and implicates the rogue leukemogenic proteins in the onset and progression of AML.

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  • (PMID = 16304371.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA82261; United States / NCI NIH HHS / CA / R01 CA59936
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Transcription Factors
  • [Number-of-references] 40
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57. Zhang SJ, Ma LY, Huang QH, Li G, Gu BW, Gao XD, Shi JY, Wang YY, Gao L, Cai X, Ren RB, Zhu J, Chen Z, Chen SJ: Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia. Proc Natl Acad Sci U S A; 2008 Feb 12;105(6):2076-81
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  • [Title] Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia.
  • Acquisition of additional genetic and/or epigenetic abnormalities other than the BCR/ABL fusion gene is believed to cause disease progression in chronic myeloid leukemia (CML) from chronic phase to blast crisis (BC).
  • To gain insights into the underlying mechanisms of progression to BC, we screened DNA samples from CML patients during blast transformation for mutations in a number of transcription factor genes that are critical for myeloid-lymphoid development.
  • A L359V substitution within zinc finger domain (ZF) 2 of GATA-2 was found in eight cases with myelomonoblastic features, whereas an in-frame deletion of 6 aa (delta341-346) spanning the C-terminal border of ZF1 was detected in one patient at myeloid BC with eosinophilia.
  • These data strongly suggest that GATA-2 mutations may play a role in acute myeloid transformation in a subset of CML patients.


58. Cilloni D, Gottardi E, Saglio G: WT1 overexpression in acute myeloid leukemia and myelodysplastic syndromes. Methods Mol Med; 2006;125:199-211
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  • [Title] WT1 overexpression in acute myeloid leukemia and myelodysplastic syndromes.
  • Several years ago, it was demonstrated that it is also overexpressed in acute and chronic leukemias.
  • WT1 quantitative assessment may therefore represent a useful tool for the diagnosis and follow up of leukemia patients.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Myelodysplastic Syndromes / genetics. WT1 Proteins / genetics
  • [MeSH-minor] Acute Disease. Base Sequence. Codon / genetics. DNA Primers. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Disease Progression. Humans. Polymerase Chain Reaction / methods. Tandem Repeat Sequences / genetics


59. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
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  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


60. Loges S, Tinnefeld H, Metzner A, Jücker M, Butzal M, Bruweleit M, Fischer U, Draab E, Schuch G, O'-Farrel AM, Hossfeld DK, Bokemeyer C, Fiedler W: Downregulation of VEGF-A, STAT5 and AKT in acute myeloid leukemia blasts of patients treated with SU5416. Leuk Lymphoma; 2006 Dec;47(12):2601-9
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  • [Title] Downregulation of VEGF-A, STAT5 and AKT in acute myeloid leukemia blasts of patients treated with SU5416.
  • In acute myeloid leukemia (AML), autocrine or paracrine activation of receptor tyrosine kinases such as c-kit and FLT3 contributes to proliferation and apoptosis resistance of leukemic blasts.
  • Additionally, protein expression of STAT5 and AKT was assessed by western blotting in these patient samples, as well as in the leukemia cell line, M-07e, treated in vitro with SU5416 as a model system.
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Cell Line, Tumor. Cell Separation. DNA Primers / chemistry. Disease Progression. Flow Cytometry. Humans. Protein Kinase Inhibitors / pharmacology. Signal Transduction. Treatment Outcome

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  • (PMID = 17169805.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / DNA Primers; 0 / Indoles; 0 / Protein Kinase Inhibitors; 0 / Pyrroles; 0 / STAT5 Transcription Factor; 0 / Vascular Endothelial Growth Factor A; 71IA9S35AJ / Semaxinib; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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61. Wang H, Lindsey S, Konieczna I, Bei L, Horvath E, Huang W, Saberwal G, Eklund EA: Constitutively active SHP2 cooperates with HoxA10 overexpression to induce acute myeloid leukemia. J Biol Chem; 2009 Jan 23;284(4):2549-67
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  • [Title] Constitutively active SHP2 cooperates with HoxA10 overexpression to induce acute myeloid leukemia.
  • The homeodomain transcription factor HoxA10 is maximally expressed in myeloid progenitor cells.
  • Sustained HoxA10 expression during differentiation has been described in poor prognosis human acute myeloid leukemia (AML).
  • In myeloid progenitor cells, HoxA10 represses transcription of genes that encode phagocyte effector proteins such as gp91PHOX and p67PHOX.
  • In immature myeloid cells, HoxA10 also activates transcription of the DUSP4 gene that encodes Mkp2, an anti-apoptotic protein.
  • Therefore, both myeloid-specific gene repression and DUSP4 activation by HoxA10 decrease during myelopoiesis.
  • HoxA10 is de-phosphorylated by SHP2 protein-tyrosine phosphatase in myeloid progenitors.
  • This mechanism maintains HoxA10 in a nonphosphorylated state in immature, but not differentiating, myeloid cells.
  • In this study, we hypothesize that constitutive SHP2 activation synergizes with HoxA10 overexpression to accelerate progression to AML.
  • Because both HoxA10 overexpression and constitutive SHP2 activation are found in poor prognosis human AML, these studies contribute to understanding biochemical aspects of disease progression in myeloid malignancy.

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  • (PMID = 19022774.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / 01 HL87717
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Homeodomain Proteins; 140441-81-2 / HOXA10 protein, human; 42HK56048U / Tyrosine; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • [Other-IDs] NLM/ PMC2629090
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62. Raza A, Mehdi M, Mumtaz M, Ali F, Lascher S, Galili N: Combination of 5-azacytidine and thalidomide for the treatment of myelodysplastic syndromes and acute myeloid leukemia. Cancer; 2008 Oct 1;113(7):1596-604
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  • [Title] Combination of 5-azacytidine and thalidomide for the treatment of myelodysplastic syndromes and acute myeloid leukemia.
  • Eventually, 30% of patients with MDS will progress and develop acute myeloid leukemia (AML).
  • Six patients had refractory anemia (RA), 2 patients had RA with ringed sideroblasts, 10 patients had RA with excess blasts (RAEB), 1 patient had RAEB in transformation, 4 patients had chronic myelomonocytic leukemia, 1 patient had chronic idiopathic myelofibrosis, and 16 patients had AML.
  • RESULTS: A hematologic improvement (HI) was observed in 15 of 36 patients (42%), stable disease was observed in 5 of 36 patients (14%), and 10 of 36 patients (28%) had disease progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Azacitidine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Thalidomide / administration & dosage


63. Kharas MG, Lengner CJ, Al-Shahrour F, Bullinger L, Ball B, Zaidi S, Morgan K, Tam W, Paktinat M, Okabe R, Gozo M, Einhorn W, Lane SW, Scholl C, Fröhling S, Fleming M, Ebert BL, Gilliland DG, Jaenisch R, Daley GQ: Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia. Nat Med; 2010 Aug;16(8):903-8
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  • [Title] Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia.
  • Overexpression of human MSI2 in a mouse model increases HSC cell cycle progression and cooperates with the chronic myeloid leukemia-associated BCR-ABL1 oncoprotein to induce an aggressive leukemia.
  • MSI2 is overexpressed in human myeloid leukemia cell lines, and its depletion leads to decreased proliferation and increased apoptosis.
  • Expression levels in human myeloid leukemia directly correlate with decreased survival in patients with the disease, thereby defining MSI2 expression as a new prognostic marker and as a new target for therapy in acute myeloid leukemia (AML).


64. Pulikkan JA, Dengler V, Peramangalam PS, Peer Zada AA, Müller-Tidow C, Bohlander SK, Tenen DG, Behre G: Cell-cycle regulator E2F1 and microRNA-223 comprise an autoregulatory negative feedback loop in acute myeloid leukemia. Blood; 2010 Mar 4;115(9):1768-78
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  • [Title] Cell-cycle regulator E2F1 and microRNA-223 comprise an autoregulatory negative feedback loop in acute myeloid leukemia.
  • Transcription factor CCAAT enhancer binding protein alpha (C/EBPalpha) is essential for granulopoiesis and its function is deregulated in leukemia.
  • Inhibition of E2F1, the master regulator of cell-cycle progression, by C/EBPalpha is pivotal for granulopoiesis.
  • We show that miR-223 blocks cell-cycle progression in myeloid cells. miR-223 is down-regulated in different subtypes of acute myeloid leukemia (AML).

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  • (PMID = 20029046.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / R01 CA118316; United States / NHLBI NIH HHS / HL / R01 HL056745
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / DNA Primers; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / E2f1 protein, mouse; 0 / MIRN223 microRNA, human; 0 / MIRN223 microRNA, mouse; 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2832809
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65. van Besien K, Artz A, Smith S, Cao D, Rich S, Godley L, Jones D, Del Cerro P, Bennett D, Casey B, Odenike O, Thirman M, Daugherty C, Wickrema A, Zimmerman T, Larson RA, Stock W: Fludarabine, melphalan, and alemtuzumab conditioning in adults with standard-risk advanced acute myeloid leukemia and myelodysplastic syndrome. J Clin Oncol; 2005 Aug 20;23(24):5728-38
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  • [Title] Fludarabine, melphalan, and alemtuzumab conditioning in adults with standard-risk advanced acute myeloid leukemia and myelodysplastic syndrome.
  • PURPOSE: This prospective phase II study evaluated toxicity, relapse rate, progression-free survival, and overall survival after allogeneic transplantation and conditioning with fludarabine, melphalan, and alemtuzumab in patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • RESULTS: After a median follow-up of 18 months (range, 2 to 34 months), 1-year survival was 48% (95% CI, 34% to 61%), progression-free survival was 38% (95% CI, 25% to 52%), relapse rate was 27% (95% CI, 15% to 40%), and treatment-related mortality was 33% (95% CI, 20% to 46%).
  • Patients with standard-risk leukemia (first or second complete remission) or MDS (< 5% blasts) had excellent outcomes despite unfavorable disease characteristics.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Disease-Free Survival. Female. Graft vs Host Disease / prevention & control. Humans. Male. Melphalan / administration & dosage. Middle Aged. Proportional Hazards Models. Prospective Studies. Remission Induction. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 16009946.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 101337
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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66. Sanada M, Uike N, Ohyashiki K, Ozawa K, Lili W, Hangaishi A, Kanda Y, Chiba S, Kurokawa M, Omine M, Mitani K, Ogawa S: Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms. Leukemia; 2007 May;21(5):992-7
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  • [Title] Unbalanced translocation der(1;7)(q10;p10) defines a unique clinicopathological subgroup of myeloid neoplasms.
  • The unbalanced translocation, der(1;7)(q10;p10), is one of the characteristic cytogenetic abnormalities found in myelodysplastic syndromes (MDS) and other myeloid neoplasms.
  • In contrast with other -7/7q- cases, where the abnormality tends to be found in one or more partial karyotypes, der(1;7)(q10;p10) represents the abnormality common to all the abnormal clones and usually appears as a sole chromosomal abnormality during the entire clinical courses, or if not, is accompanied only by a limited number and variety of additional abnormalities, mostly trisomy 8 and/or loss of 20q. der(1;7)(q10;p10)-positive MDS cases showed lower blast counts (P<0.0001) and higher hemoglobin concentrations (P<0.0075) at diagnosis and slower progression to acute myeloid leukemia (P=0.0043) than other -7/7q- cases. der(1;7)(q10;p10) cases showed significantly better clinical outcome than other -7/7q cases (P<0.0001).
  • In conclusion, der(1;7)(q10;p10) defines a discrete entity among myeloid neoplasms, showing unique clinical and cytogenetic characteristics.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Translocation, Genetic


67. Mehta PA, Harris RE, Davies SM, Kim MO, Mueller R, Lampkin B, Mo J, Myers K, Smolarek TA: Numerical chromosomal changes and risk of development of myelodysplastic syndrome--acute myeloid leukemia in patients with Fanconi anemia. Cancer Genet Cytogenet; 2010 Dec;203(2):180-6
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  • [Title] Numerical chromosomal changes and risk of development of myelodysplastic syndrome--acute myeloid leukemia in patients with Fanconi anemia.
  • Fanconi Anemia (FA) is an inherited bone marrow failure syndrome characterized by congenital abnormalities, progressive marrow failure and predisposition to myelodysplastic syndrome (MDS), acute myeloid leukemia (AML), and solid tumors.
  • A few reports also suggest that gains of 3q are associated with progression to MDS-AML and overall poor prognosis.
  • In conclusion, children with FA should be followed closely with FISH analyses, because some of the clonal chromosomal abnormalities may be early indicators of progression toward MDS-AML and thus also of the need for hematopoietic stem cell transplantation.
  • [MeSH-major] Chromosome Deletion. Chromosome Mapping. Fanconi Anemia / complications. Fanconi Anemia / genetics. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / genetics


68. Shih LY, Huang CF, Lin TL, Wu JH, Wang PN, Dunn P, Kuo MC, Tang TC: Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia. Clin Cancer Res; 2005 Mar 1;11(5):1821-6
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  • [Title] Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia.
  • PURPOSE: We aimed to assess the role of CEBPalpha mutations in the progression of myelodysplastic syndrome (MDS) to acute myelogenous leukemia (AML) and their cooperating mutations.
  • RESULTS: CEBPalpha mutations were identified in four patients at diagnosis of MDS, including one with refractory anemia with excess blasts and three with chronic myelomonocytic leukemia.
  • CEBPalpha mutations had no influence on the time to AML progression or overall survival.
  • CONCLUSIONS: Our results show that CEBPalpha mutations play a role in a subset of patients with MDS, especially in chronic myelomonocytic leukemia.
  • The mutation status was heterogeneous, exhibiting identical clone, clonal change, or clonal evolution during the progression to AML.
  • [MeSH-major] CCAAT-Enhancer-Binding Protein-alpha / genetics. Cell Transformation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Adult. Aged. Alleles. DNA Mutational Analysis. Disease Progression. Female. Humans. Leucine Zippers. Male. Middle Aged


69. Fu J, Fu J, Chen X, Zhang Y, Gu H, Bai Y: CD147 and VEGF co-expression predicts prognosis in patients with acute myeloid leukemia. Jpn J Clin Oncol; 2010 Nov;40(11):1046-52
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  • [Title] CD147 and VEGF co-expression predicts prognosis in patients with acute myeloid leukemia.
  • OBJECTIVE: To investigate the possible role of CD147 and vascular endothelial growth factor in progression and prognosis of acute myeloid leukemia.
  • METHODS: Immunohistochemical staining was performed to detect the expression of CD147 and vascular endothelial growth factor in paraffin-embedded sections from 62 bone marrow biopsies obtained from an equal number of patients with newly diagnosed acute myeloid leukemia.
  • RESULTS: CD147 and vascular endothelial growth factor expression in the bone marrow of acute myeloid leukemia patients were significantly higher than those in normal controls (both P < 0.001).
  • In addition, higher levels of CD147 and vascular endothelial growth factor were also found in acute myeloid leukemia patients with an unfavorable karyotype compared with those with intermediate and favorable karyotypes (both P = 0.01).
  • Furthermore, the co-expression of CD147 and vascular endothelial growth factor in the bone marrow indicated a poor prognosis in acute myeloid leukemia and was an independent prognostic factor for overall survival by multivariate analysis.
  • CONCLUSIONS: Our data show for the first time that the co-expression of CD147 and vascular endothelial growth factor may indicate a poor prognosis in acute myeloid leukemia and may be a highly sensitive marker for predicting the clinical outcome of patients.
  • [MeSH-major] Antigens, CD147 / metabolism. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. Neovascularization, Pathologic / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 20558462.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BSG protein, human; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 136894-56-9 / Antigens, CD147
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70. Rassool FV, Gaymes TJ, Omidvar N, Brady N, Beurlet S, Pla M, Reboul M, Lea N, Chomienne C, Thomas NS, Mufti GJ, Padua RA: Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia? Cancer Res; 2007 Sep 15;67(18):8762-71
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  • [Title] Reactive oxygen species, DNA damage, and error-prone repair: a model for genomic instability with progression in myeloid leukemia?
  • Myelodysplastic syndromes (MDS) comprise a heterogeneous group of disorders characterized by ineffective hematopoiesis, with an increased propensity to develop acute myelogenous leukemia (AML).
  • The molecular basis for MDS progression is unknown, but a key element in MDS disease progression is loss of chromosomal material (genomic instability).
  • Using our two-step mouse model for myeloid leukemic disease progression involving overexpression of human mutant NRAS and BCL2 genes, we show that there is a stepwise increase in the frequency of DNA damage leading to an increased frequency of error-prone repair of double-strand breaks (DSB) by nonhomologous end-joining.
  • There is a concomitant increase in reactive oxygen species (ROS) in these transgenic mice with disease progression.
  • Our data link gene abnormalities to constitutive DNA damage and increased DSB repair errors in vivo and provide a mechanism for an increase in the error rate of DNA repair with MDS disease progression.
  • [MeSH-major] DNA Damage. DNA Repair. Genomic Instability. Leukemia, Myeloid / genetics. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Animals. Disease Models, Animal. Disease Progression. Genes, bcl-2. Genes, ras. Mice. Mice, Transgenic


71. Li GC, Li N, Zhang YH, Li X, Wang YG, Liu XY, Qian WB, Liu XC: Mannose-exposing myeloid leukemia cells detected by the sCAR-PPA fusion protein. Int J Hematol; 2009 Jun;89(5):611-7
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  • [Title] Mannose-exposing myeloid leukemia cells detected by the sCAR-PPA fusion protein.
  • Altered glycosylation may be a hallmark of malignant transformation and cancer progression.
  • The adenoviral transduction of acute myeloid leukemia (AML) cell lines Kasumi-1 and HL-60 was increased by sCAR-PPA, indicating that a fraction of AML cells exposing mannose residues was detected by PPA.
  • Furthermore, the infectious efficiency of Ad-EGFP in chronic myeloid leukemia cell line K562 was significantly increased by sCAR-PPA as well.
  • We, herein, report that PPA recognized a fraction of myeloid leukemia cells showing mannose-exposing phenotype.
  • The sCAR-PPA fusion protein combined with the adenoviral vector system may provide a useful tool for investigating myeloid leukemia cells exposing mannose residues and further elucidating the role of these cells in the leukemia development.
  • [MeSH-major] Agglutinins. Leukemia, Myeloid / pathology. Mannose / metabolism. Mannose-Binding Lectin

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  • (PMID = 19377843.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Agglutinins; 0 / CLMP protein, human; 0 / Coxsackie and Adenovirus Receptor-Like Membrane Protein; 0 / Mannose-Binding Lectin; 0 / Receptors, Virus; 0 / Recombinant Fusion Proteins; PHA4727WTP / Mannose
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72. Thepot S, Itzykson R, Seegers V, Raffoux E, Quesnel B, Chait Y, Sorin L, Dreyfus F, Cluzeau T, Delaunay J, Sanhes L, Eclache V, Dartigeas C, Turlure P, Harel S, Salanoubat C, Kiladjian JJ, Fenaux P, Adès L, Groupe Francophone des Myelodysplasies (GFM): Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM). Blood; 2010 Nov 11;116(19):3735-42
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  • [Title] Treatment of progression of Philadelphia-negative myeloproliferative neoplasms to myelodysplastic syndrome or acute myeloid leukemia by azacitidine: a report on 54 cases on the behalf of the Groupe Francophone des Myelodysplasies (GFM).
  • Transformation of Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs) to myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) is associated with poor response to chemotherapy and short survival.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / etiology. Myeloproliferative Disorders / complications. Myeloproliferative Disorders / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. France / epidemiology. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Philadelphia Chromosome. Prognosis. Treatment Outcome


73. Yang HP, Dai M, Zhou HS, Huang L, Zhang DH: [Detection of SOCS-1 mRNA expression by RT-PCR in the patients with myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):677-80
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  • [Title] [Detection of SOCS-1 mRNA expression by RT-PCR in the patients with myeloid leukemia].
  • In order to investigate the suppressor of cytokine signaling-1 (SOCS-1) expression in peripheral blood mononuclear cells (PBMNC) of patients with acute and chronic myeloid leukemia and analyze its clinical significance, RT-PCR method was used for detecting SOCS-1 mRNA expression in PBMNC of 50 newly diagnosed patients.
  • In CML group, 2 out of 12 cases with non-progression (chronic phase), 9 of 13 cases with progression showed the positive expression, the difference between two subgroups was statistically significant.
  • It is concluded that the SOCS-1 mRNA can be detected in the PBMNC of the patients with acute and chronic myeloid leukemia.

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  • (PMID = 16928298.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / SOCS1 protein, human; 0 / Suppressor of Cytokine Signaling Proteins
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74. Tadmor T, Vadazs Z, Dar H, Laor R, Attias D: Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-. J Pediatr Hematol Oncol; 2006 Aug;28(8):544-6
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  • [Title] Hemophagocytic syndrome preceding acute myeloid leukemia with der t [7:17][q12; q11], monosomy, 17 and 5p-.
  • Hemophagocytic syndrome (HS) is a severe and acute proliferative process of histiocytes, often associated with infection or malignancy.
  • We report a case of a child presented with HS, who progressed later to acute myeloid leukemia (AML)-M4, associated with a clonal evolution, from normal to a complex karyotype consisting of t [7:17] and deletions in chromosomes 7, 17, and 5.
  • Additional studies are required to establish the association reported here, between HS with progression to AML and chromosome rearrangements that involve chromosome 7q.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid / genetics. Lymphohistiocytosis, Hemophagocytic / genetics
  • [MeSH-minor] Acute Disease. Child, Preschool. Fatal Outcome. Humans. Male. Remission Induction. Treatment Outcome

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  • (PMID = 16912598.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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75. Panani AD: Gain of an isochromosome 5p: a rare recurrent abnormality in acute myeloid leukemia. In Vivo; 2006 May-Jun;20(3):359-60
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  • [Title] Gain of an isochromosome 5p: a rare recurrent abnormality in acute myeloid leukemia.
  • Chromosomal abnormalities characterize the biological behavior of acute myeloid leukemia (AML), also facilitating the identification of genes responsible for its development and/or progression.
  • [MeSH-major] Chromosome Disorders / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 8 / genetics. Isochromosomes / genetics. Leukemia, Myeloid, Acute / genetics


76. Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H: High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder. Blood; 2009 May 28;113(22):5583-7
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  • [Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
  • Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).
  • So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.
  • Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.
  • [MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics


77. Gupta V, Daly A, Lipton JH, Hasegawa W, Chun K, Kamel-Reid S, Tsang R, Yi QL, Minden M, Messner H, Kiss T: Nonmyeloablative stem cell transplantation for myelodysplastic syndrome or acute myeloid leukemia in patients 60 years or older. Biol Blood Marrow Transplant; 2005 Oct;11(10):764-72
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  • [Title] Nonmyeloablative stem cell transplantation for myelodysplastic syndrome or acute myeloid leukemia in patients 60 years or older.
  • We analyzed the outcomes of 24 consecutive patients aged >or=60 years with poor-prognosis myelodysplastic syndrome or acute myeloid leukemia undergoing transplantation with nonmyeloablative conditioning using fludarabine (125 mg/m2) and low-dose total body irradiation (2 Gy) followed by allogeneic peripheral blood stem cell grafts from HLA-identical sibling donors.
  • The probabilities of 2-year overall and progression-free survival were 52% and 44%, respectively.
  • The cumulative probabilities of relapse and of acute and chronic GVHD were 27%, 45%, and 74%, respectively.
  • These data suggest that nonmyeloablative stem cell transplantation is a feasible treatment option in patients aged >or=60 years with poor-prognosis myelodysplastic syndrome or acute myeloid leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Aged. Female. Graft Survival. Graft vs Host Disease. Histocompatibility Testing. Humans. Male. Middle Aged. Opportunistic Infections. Siblings. Survival Analysis. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation


78. Hartmann U, Brümmendorf TH, Balabanov S, Thiede C, Illme T, Schaich M: Telomere length and hTERT expression in patients with acute myeloid leukemia correlates with chromosomal abnormalities. Haematologica; 2005 Mar;90(3):307-16
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  • [Title] Telomere length and hTERT expression in patients with acute myeloid leukemia correlates with chromosomal abnormalities.
  • BACKGROUND AND OBJECTIVES: Acute myeloid leukemia (AML) is a malignant, genetically heterogenous disorder characterized by uncontrolled growth of immature myeloid cells.
  • It is assumed that critical telomere shortening in AML blasts could lead to telomerase activation and therefore prevent blasts from replicative senescence, one possible mechanism for clonal selection and disease progression.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / genetics. Telomerase / genetics. Telomere / ultrastructure
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Case-Control Studies. Gene Expression Regulation, Neoplastic. Humans. Middle Aged

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  • [CommentIn] Haematologica. 2005 Mar;90(3):289B [15749652.001]
  • (PMID = 15749662.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
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79. Cimino G, Lo-Coco F, Fenu S, Travaglini L, Finolezzi E, Mancini M, Nanni M, Careddu A, Fazi F, Padula F, Fiorini R, Spiriti MA, Petti MC, Venditti A, Amadori S, Mandelli F, Pelicci PG, Nervi C: Sequential valproic acid/all-trans retinoic acid treatment reprograms differentiation in refractory and high-risk acute myeloid leukemia. Cancer Res; 2006 Sep 1;66(17):8903-11
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  • [Title] Sequential valproic acid/all-trans retinoic acid treatment reprograms differentiation in refractory and high-risk acute myeloid leukemia.
  • Epigenetic alterations of chromatin due to aberrant histone deacetylase (HDAC) activity and transcriptional silencing of all-trans retinoic acid (ATRA) pathway are events linked to the pathogenesis of acute myeloid leukemia (AML) that can be targeted by specific treatments.
  • Stable disease and disease progression were observed in five and one cases, respectively.
  • Further studies are needed to evaluate whether VPA-ATRA treatment by reprogramming differentiation of the leukemic clone might improve the response to chemotherapy in leukemia patients.
  • [MeSH-major] Cell Differentiation / drug effects. Leukemia, Myeloid, Acute / drug therapy. Tretinoin / therapeutic use. Valproic Acid / therapeutic use

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  • (PMID = 16951208.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 5688UTC01R / Tretinoin; 614OI1Z5WI / Valproic Acid
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80. Flotho C, Claus R, Batz C, Schneider M, Sandrock I, Ihde S, Plass C, Niemeyer CM, Lübbert M: The DNA methyltransferase inhibitors azacitidine, decitabine and zebularine exert differential effects on cancer gene expression in acute myeloid leukemia cells. Leukemia; 2009 Jun;23(6):1019-28
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  • [Title] The DNA methyltransferase inhibitors azacitidine, decitabine and zebularine exert differential effects on cancer gene expression in acute myeloid leukemia cells.
  • The three DNA methyltransferase (DNMT)-inhibiting cytosine nucleoside analogues, azacitidine, decitabine and zebularine, which are currently studied as nonintensive therapy for myelodysplastic syndromes and acute myeloid leukemia (AML), differ in structure and metabolism, suggesting that they may have differential molecular activity.
  • Under in vitro conditions mimicking those used in clinical trials, the DNMT inhibitors inhibited proliferation and triggered apoptosis but did not induce myeloid differentiation.
  • The DNMT inhibitors showed no interference with cell-cycle progression whereas cytarabine treatment resulted in an S-phase arrest.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Cytidine / analogs & derivatives. DNA Modification Methylases / antagonists & inhibitors. Gene Expression Regulation, Neoplastic / drug effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 19194470.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 3690-10-6 / pyrimidin-2-one beta-ribofuranoside; 5CSZ8459RP / Cytidine; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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81. Chen S, Xue Y, Zhu X, Wu Y, Pan J: Minimally differentiated acute myeloid leukemia with t(12;22)(p13;q11) translocation showing primary multidrug resistance and expressing multiple multidrug-resistant proteins. Acta Haematol; 2007;118(1):38-41
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  • [Title] Minimally differentiated acute myeloid leukemia with t(12;22)(p13;q11) translocation showing primary multidrug resistance and expressing multiple multidrug-resistant proteins.
  • Here we report a rare chromosomal translocation, t(12;22)(p13;q11), which was detected in a 53-year-old female patient diagnosed as having minimally differentiated acute myeloid leukemia (AML-M0) according to the French-American-British classification criteria.
  • [MeSH-major] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Proto-Oncogene Proteins / analysis. Translocation, Genetic
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 22. Disease Progression. Fatal Outcome. Female. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17476096.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins
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82. Chandra P, Luthra R, Zuo Z, Yao H, Ravandi F, Reddy N, Garcia-Manero G, Kantarjian H, Jones D: Acute myeloid leukemia with t(9;11)(p21-22;q23): common properties of dysregulated ras pathway signaling and genomic progression characterize de novo and therapy-related cases. Am J Clin Pathol; 2010 May;133(5):686-93
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  • [Title] Acute myeloid leukemia with t(9;11)(p21-22;q23): common properties of dysregulated ras pathway signaling and genomic progression characterize de novo and therapy-related cases.
  • We compared pathogenetic features of 32 de novo and 29 therapy-related (t) t(9;11)(p21-22;q23)/MLLT3-MLL acute myeloid leukemia (AML) cases to identify progression factors and to assess whether distinction between these manifestations is warranted.
  • Ras point mutations were common in both groups (overall, 18/50 [36%]) and associated with monocytic phenotype and aneuploid progression.
  • Ras activation seems to complement the MLLT3-MLL oncogene in transformation with features of de novo and t-AML with MLLT3-MLL being similar.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Leukemia, Myelomonocytic, Acute / genetics. Translocation, Genetic. ras Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Disease Progression. Female. Gene Expression Profiling. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Male. MicroRNAs / genetics. MicroRNAs / metabolism. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Point Mutation. Signal Transduction. Survival Rate. Texas / epidemiology. Young Adult

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  • (PMID = 20395514.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT3 protein, human; 0 / MicroRNAs; 0 / Nuclear Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.6.5.2 / ras Proteins
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83. Kujawski L, Talpaz M: Strategies for overcoming imatinib resistance in chronic myeloid leukemia. Leuk Lymphoma; 2007 Dec;48(12):2310-22
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  • [Title] Strategies for overcoming imatinib resistance in chronic myeloid leukemia.
  • Imatinib was the first treatment for chronic myeloid leukemia (CML) that specifically targeted the causative BCR-ABL oncoprotein, and represented a major therapeutic advance in this disease; however, some patients develop resistance or intolerance.
  • Resistance can be classified as BCR-ABL-dependent (e.g., mutation in the BCR-ABL gene) or BCR-ABL-independent (alternative pathways of disease progression, e.g., SRC-family tyrosine kinases).
  • Dasatinib is active across all phases of CML and Philadelphia chromosome-positive acute lymphoblastic leukemia, and demonstrates activity in almost all imatinib-resistant mutations.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 18067005.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Number-of-references] 104
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84. Keller G, Brassat U, Braig M, Heim D, Wege H, Brümmendorf TH: Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy. Hematol Oncol; 2009 Sep;27(3):123-9
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  • [Title] Telomeres and telomerase in chronic myeloid leukaemia: impact for pathogenesis, disease progression and targeted therapy.
  • However, elevated telomerase activity has also been reported in the majority of solid tumours as well as in acute and chronic leukaemia.
  • Chronic myeloid leukaemia (CML) serves as a model disease to study telomere biology in clonal myeloproliferative disorders.
  • In addition, telomerase activity (TA) is already increased in CP CML and further upregulated with disease progression to accelerated phase and blast crisis (BC).
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Telomere / pathology
  • [MeSH-minor] Animals. Disease Progression. Humans

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  • (PMID = 19569255.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  • [Number-of-references] 67
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85. Martelli AM, Nyåkern M, Tabellini G, Bortul R, Tazzari PL, Evangelisti C, Cocco L: Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia. Leukemia; 2006 Jun;20(6):911-28
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  • [Title] Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.
  • The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is crucial to many aspects of cell growth, survival and apoptosis, and its constitutive activation has been implicated in the both the pathogenesis and the progression of a wide variety of neoplasias.
  • Recent studies showed that PI3K/Akt signaling is frequently activated in acute myeloid leukemia (AML) patient blasts and strongly contributes to proliferation, survival and drug resistance of these cells.
  • [MeSH-major] Leukemia, Myeloid / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Acute Disease. Humans. Models, Biological. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use

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  • (PMID = 16642045.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Number-of-references] 250
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86. Popat U, Heslop HE, Durett A, May R, Krance RA, Brenner MK, Carrum G: Outcome of reduced-intensity allogeneic hematopoietic stem cell transplantation (RISCT) using antilymphocyte antibodies in patients with high-risk acute myeloid leukemia (AML). Bone Marrow Transplant; 2006 Mar;37(6):547-52
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  • [Title] Outcome of reduced-intensity allogeneic hematopoietic stem cell transplantation (RISCT) using antilymphocyte antibodies in patients with high-risk acute myeloid leukemia (AML).
  • It is therefore particularly unsuited to older individuals, who are most at risk of developing acute myeloid leukemia (AML).
  • Both progression-free survival and overall survival are 40% (95% CI, 17-64%).
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid / therapy. Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Follow-Up Studies. Graft vs Host Disease / epidemiology. Humans. Infection / epidemiology. Major Histocompatibility Complex. Male. Middle Aged. Time Factors. Transplantation Chimera. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16462757.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents
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87. Walter MJ, Park JS, Ries RE, Lau SK, McLellan M, Jaeger S, Wilson RK, Mardis ER, Ley TJ: Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha. Proc Natl Acad Sci U S A; 2005 Aug 30;102(35):12513-8
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  • [Title] Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha.
  • Recently, haploinsufficiency for PU.1 has been shown to cause a shift in myelomonocytic progenitor fate toward the myeloid lineage.
  • We have previously shown that transgenic mice expressing PML-RARalpha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a large (>20 Mb) interstitial deletion of chromosome 2 that includes PU.1.
  • To directly assess the relevance of levels of expression of PU.1 for leukemia progression, we bred hCG-PR mice with PU.1+/- mice and assessed their phenotype.
  • Young, nonleukemic hCG-PR x PU.1+/- mice developed splenomegaly because of the abnormal expansion of myeloid cells in their spleens. hCG-PR x PU.1+/- mice developed a typical APL syndrome after a long latent period, but the penetrance of disease was 84%, compared with 7% in hCG-PR x PU.1+/+ mice (P < 0.0001).
  • However, PR expression in U937 myelomonocytic cells and primary murine myeloid bone marrow cells caused a reduction in PU.1 mRNA levels.
  • Therefore, the loss of one copy of PU.1 through a deletional mechanism, plus down-regulation of the residual allele caused by PR expression, may synergize to expand the pool of myeloid progenitors that are susceptible to transformation, increasing the penetrance of APL.

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  • (PMID = 16113082.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA101937; United States / NCI NIH HHS / CA / R01 CA083962; United States / NCI NIH HHS / CA / CA101937; United States / NCI NIH HHS / CA / CA83962
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Trans-Activators; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 0 / proto-oncogene protein Spi-1
  • [Other-IDs] NLM/ PMC1188022
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88. El-Zawahry HM, Zeeneldin AA, Samra MA, Mattar MM, El-Gammal MM, Abd El-Samee A, Darwish T: Cost and outcome of treatment of adults with acute myeloid leukemia at the National Cancer Institute-Egypt. J Egypt Natl Canc Inst; 2007 Jun;19(2):106-13
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  • [Title] Cost and outcome of treatment of adults with acute myeloid leukemia at the National Cancer Institute-Egypt.
  • BACKGROUND: Despite important advances in the therapy of acute myeloid leukemia (AML), the majority of patients die of their disease, unless bone marrow transplantation (BMT) is done.
  • Progress in therapy and supportive care has led to gradual improvement in the overall results, but further improvements are still needed.
  • Infections were the major mortality cause, followed by disease progression then bleeding (65% , 28% and 7% respectively).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / economics

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  • (PMID = 19034340.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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89. Perz JB, Khorashad JS, Marin D, Apperley JF, Olavarria E: Imatinib preceding allogeneic stem cell transplantation in chronic myeloid leukemia. Haematologica; 2006 Aug;91(8):1145-6
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  • [Title] Imatinib preceding allogeneic stem cell transplantation in chronic myeloid leukemia.
  • In 37 adults with chronic myeloid leukemia undergoing allogeneic stem cell transplantation imatinib prior to transplant had no discernible negative impact on 100-day mortality (13%) and severe acute (22%) or extensive chronic graft-versus- host disease (31%).
  • After a median of 203 days (range: 18-1419) overall and progression-free survival rates are 62% and 54%, respectively.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation / methods
  • [MeSH-minor] Acute Disease. Adult. Benzamides. Chronic Disease. Combined Modality Therapy. Disease-Free Survival. Drug Administration Schedule. Graft vs Host Disease / epidemiology. Humans. Imatinib Mesylate. Incidence. Retrospective Studies. Time Factors. Transplantation, Homologous


90. Kakihana K, Kubo F, Wakabayashi S, Kurosu T, Miki T, Murakami N, Miura O: A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia. Cancer Genet Cytogenet; 2008 Jul 15;184(2):109-12
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  • [Title] A novel variant form of MLL-ELL fusion transcript with t(11;19)(q23;p13.1) in chronic myelomonocytic leukemia transforming to acute myeloid leukemia.
  • MLL located at 11q23 is fused with a variety of partner genes by recurrent chromosomal translocations in acute leukemias.
  • Here we report a case of chronic myelomonocytic leukemia (CMML) with a 46,XY,t(11;19)(q23;p13.1) karyotype that transformed to acute myeloid leukemia (AML) without showing any karyotypic evolution.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Leukemia, Myeloid, Acute / genetics. Leukemia, Myelomonocytic, Chronic / genetics. Leukemia, Myelomonocytic, Chronic / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Aged. Base Sequence. Disease Progression. Humans. Male


91. Maitta RW, Cannizzaro LA, Ramesh KH: Association of MLL amplification with poor outcome in acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):40-3
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  • [Title] Association of MLL amplification with poor outcome in acute myeloid leukemia.
  • Chromosomal rearrangements and amplification of the MLL gene at 11q23 are common abnormalities found in patients with severe myelodysplastic disorders and lymphoid and acute myeloid leukemias.
  • We report the clinical, cytogenetic and histologic findings of a patient who presented with a de novo diagnosis of AML-M4 and who fits the profile of patients presenting with MLL alterations, such as old age at presentation, rapid progression, therapeutic refractoriness, and poor outcome.
  • [MeSH-major] Gene Amplification / physiology. Leukemia, Myeloid, Acute / diagnosis. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19480936.001).
  • [ISSN] 1873-4456
  • [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] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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92. Janus A, Linke A, Cebula B, Robak T, Smolewski P: Rapamycin, the mTOR kinase inhibitor, sensitizes acute myeloid leukemia cells, HL-60 cells, to the cytotoxic effect of arabinozide cytarabine. Anticancer Drugs; 2009 Sep;20(8):693-701
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  • [Title] Rapamycin, the mTOR kinase inhibitor, sensitizes acute myeloid leukemia cells, HL-60 cells, to the cytotoxic effect of arabinozide cytarabine.
  • Overexpression of the mTOR signaling pathway has been described in several tumor cells, including the majority of acute myeloid leukemia (AML) cases.
  • The study showed that RAPA in concentrations of 1-10 nmol/l arrested the cell cycle progression of Hl-60 cells in the G1 phase, without evident cytotoxic effect.
  • In conclusion, these data indicate that RAPA might be effective in the treatment of acute leukemia patients, especially in combination with Ara-C, the drug routinely used in AML treatment.

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  • (PMID = 19584709.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Cyclins; 0 / EIF4EBP1 protein, human; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Phosphoproteins; 04079A1RDZ / Cytarabine; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 3.4.22.- / Caspase 3; W36ZG6FT64 / Sirolimus
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93. Weinberg OK, Seetharam M, Ren L, Seo K, Ma L, Merker JD, Gotlib J, Zehnder JL, Arber DA: Clinical characterization of acute myeloid leukemia with myelodysplasia-related changes as defined by the 2008 WHO classification system. Blood; 2009 Feb 26;113(9):1906-8
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  • [Title] Clinical characterization of acute myeloid leukemia with myelodysplasia-related changes as defined by the 2008 WHO classification system.
  • Although some studies have validated the 2001 World Health Organization (WHO) classification of acute myeloid leukemia (AML), including the importance of multilineage dysplasia, others have suggested that multilineage dysplasia correlates with unfavorable cytogenetics but has no independent impact on prognosis.
  • Multivariate analysis indicated that patients with AML-MRC had a significantly worse overall survival, progression-free survival, and complete response compared with AML-not otherwise specified (all P< .001).
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Myelodysplastic Syndromes / classification. World Health Organization

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  • (PMID = 19131546.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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94. Karajannis MA, Vincent L, Direnzo R, Shmelkov SV, Zhang F, Feldman EJ, Bohlen P, Zhu Z, Sun H, Kussie P, Rafii S: Activation of FGFR1beta signaling pathway promotes survival, migration and resistance to chemotherapy in acute myeloid leukemia cells. Leukemia; 2006 Jun;20(6):979-86
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  • [Title] Activation of FGFR1beta signaling pathway promotes survival, migration and resistance to chemotherapy in acute myeloid leukemia cells.
  • Recent evidence suggests that FGF signaling through FGF receptors (FGFRs) may play a role in the proliferation of subsets of acute myeloid leukemias (AMLs).
  • These data suggest that activation of FGF-2/FGFR1beta supports progression and chemoresistance in subsets of AML.
  • [MeSH-major] Cell Movement. Drug Resistance, Neoplasm. Leukemia, Myeloid / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism. Signal Transduction
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Agouti-Related Protein. Animals. Antibodies / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Fibroblast Growth Factor 2 / pharmacology. Humans. Intercellular Signaling Peptides and Proteins / metabolism. Male. Mice. Mice, SCID. Phosphorylation. Protein Subunits / drug effects. Protein Subunits / metabolism. RNA, Messenger / genetics. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 16598308.001).
  • [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 / Agouti-Related Protein; 0 / Antibodies; 0 / Intercellular Signaling Peptides and Proteins; 0 / Protein Subunits; 0 / RNA, Messenger; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1
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95. Follo MY, Finelli C, Clissa C, Mongiorgi S, Bosi C, Martinelli G, Baccarani M, Manzoli L, Martelli AM, Cocco L: Phosphoinositide-phospholipase C beta1 mono-allelic deletion is associated with myelodysplastic syndromes evolution into acute myeloid leukemia. J Clin Oncol; 2009 Feb 10;27(5):782-90
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  • [Title] Phosphoinositide-phospholipase C beta1 mono-allelic deletion is associated with myelodysplastic syndromes evolution into acute myeloid leukemia.
  • Kaplan-Meier analysis revealed a significant association (P < .0001) between the PI-PLCbeta1 mono-allelic deletion and a higher risk of evolution into acute myeloid leukemia (AML), since 23 of 35 MDS patients (65.7%) bearing the PI-PLCbeta1 mono-allelic deletion evolved into AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / genetics. Phospholipase C beta / genetics. Phospholipase C gamma / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Deletion. Gene Expression. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction


96. Preiss BS, Bergmann OJ, Friis LS, Sørensen AG, Frederiksen M, Gadeberg OV, Mourits-Andersen T, Oestergaard B, Kerndrup GB, AML Study Group of Southern Denmark: Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML. Cancer Genet Cytogenet; 2010 Oct 15;202(2):108-22
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  • [Title] Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML.
  • During a 15-year period, 161 adult patients were diagnosed with secondary acute myeloid leukemia (s-AML) in the region of Southern Denmark.
  • The frequencies of aberrations in s-AML patients were compared with an age-matched group of de novo AML patients diagnosed in the same area and period.
  • In 42 patients, we found that MDS patients with an abnormal karyotype were more likely to show cytogenetic evolution during progression to AML than MDS patients with a normal karyotype (P = 0.01).
  • We conclude that population-based cytogenetic studies of adult s-AML and age- and sex-matched de novo AML show comparable distributions of chromosome abnormalities.
  • [MeSH-major] Chromosome Aberrations. Cytogenetic Analysis. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


97. Wu L, Li X, Su J, Chang C, He Q, Zhang X, Xu L, Song L, Pu Q: Effect of low-dose cytarabine, homoharringtonine and granulocyte colony-stimulating factor priming regimen on patients with advanced myelodysplastic syndrome or acute myeloid leukemia transformed from myelodysplastic syndrome. Leuk Lymphoma; 2009 Sep;50(9):1461-7
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  • [Title] Effect of low-dose cytarabine, homoharringtonine and granulocyte colony-stimulating factor priming regimen on patients with advanced myelodysplastic syndrome or acute myeloid leukemia transformed from myelodysplastic syndrome.
  • A total of 32 patients (25 with advanced MDS and 7 with t-AML) were enrolled in this study to evaluate the efficacy and toxicity of the low-dose cytarabine and homoharringtonine in combination with granulocyte colony-stimulating factor (G-CSF) (CHG protocol) in patients with advanced myelodysplastic syndromes (MDS) or MDS-transformed acute myeloid leukemia (t-AML).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Harringtonines / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Disease Progression. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Neoadjuvant Therapy. Treatment Outcome. Young Adult


98. Oke A, Pearce D, Wilkinson RW, Crafter C, Odedra R, Cavenagh J, Fitzgibbon J, Lister AT, Joel S, Bonnet D: AZD1152 rapidly and negatively affects the growth and survival of human acute myeloid leukemia cells in vitro and in vivo. Cancer Res; 2009 May 15;69(10):4150-8
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  • [Title] AZD1152 rapidly and negatively affects the growth and survival of human acute myeloid leukemia cells in vitro and in vivo.
  • In this study, we report the in vitro and in vivo activities of AZD1152, a compound that has selectivity for aurora B kinase, in acute myeloid leukemia (AML) cell lines, primary AML samples, and cord blood cells.
  • However, concentration-dependent effects on cell growth, apoptosis, and cell cycle progression were also observed when human cord blood and primary lineage-negative stem and progenitor cells were analyzed in vitro and in vivo.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Division / drug effects. Cell Survival / drug effects. Enzyme Inhibitors / pharmacology. Hematopoietic Stem Cells / drug effects. Leukemia, Myeloid, Acute / pathology. Organophosphates / pharmacology. Quinazolines / pharmacology

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  • (PMID = 19366807.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A3589
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate; 0 / Annexin A5; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Organophosphates; 0 / Quinazolines; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Other-IDs] NLM/ PMC2684546; NLM/ UKMS4271
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99. Huang Y, Li WJ, Wei CX, Zhou Z, Nie B: [Expression of HoxA10 in acute leukemia and its significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):959-63
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  • [Title] [Expression of HoxA10 in acute leukemia and its significance].
  • To investigate the expression of HoxA(10) mRNA in acute leukemia patients and its significance, HoxA(10) level was detected by reverse transcription polymerase chain reaction (RT-PCR) in 50 patients with acute leukemias, 7 healthy volunteers and 3 patients with ITP (idiopathic thrombocytopenic purpura).
  • The regularity of the expression of HoxA(10) gene in acute leukemia and the relationship between HoxA(10) level and the prognosis of leukemia was explored.
  • The results showed that HoxA(10) was expressed in all types of acute myelogenous leukemia; HoxA(10) message was also observed in acute lymphoblastic leukemia patients and part of control groups.
  • The level of HoxA(10) mRNA of acute myelogenous leukemia patients was significantly higher than that of acute lymphoblastic leukemia patients and controls (P < 0.01).
  • HoxA(10) gene appeared to be more strongly expressed in AML-M(1) and -M(2) subtypes than in AML-M(4) and -M(5) subtypes, and the gene was notable high expressed in acute promyelocytic leukemia.
  • HoxA(10) was overexpressed in acute myelogenous leukemia.
  • It is concluded that HoxA(10) is a major transcription factor regulating hematopoiesis and a mark to differentiate lymphoid leukemia and myelogenous leukemia, but not a specific gene of cancer.
  • The level of HoxA(10) is related with load of leukemic cells and curative effect, and can affect occurrence and development of leukemia in combination with many cytokines, HoxA(10) may facilitate the leukemia progression with another cofactors.

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  • (PMID = 16403259.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 140441-81-2 / HOXA10 protein, human
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100. Szpecht D, Derwich K, Wachowiak J, Konatkowska B, Dworacki G: [Lineage switch - conversion of acute lymphoblastic leukaemia to acute myeloid leukaemia in 4 years old girl]. Med Wieku Rozwoj; 2008 Oct-Dec;12(4 Pt 2):1041-4
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  • [Title] [Lineage switch - conversion of acute lymphoblastic leukaemia to acute myeloid leukaemia in 4 years old girl].
  • We report a case of a 4-year-old girl with diagnosed proB acute lymphoblastic leukaemia with co-expression CD33 antigen, treated according to Acute Lymphoblastic Leukaemia Intercontinental - Berlin Frankfurt Münster 2002 (ALL-IC BFM 2002) protocol for standard risk group.
  • The late isolated bone marrow relapse of acute myeloid leukaemia, type 7 was noted in our patient.
  • We recognized this case as a lineage switch acute lymphoblastic leukaemia to acute myeloid leukaemia.
  • In spite of Ida Flag regimen and following Acute Myeloid Leukaemia - Berlin Frankfurt Münster 2004 (AML-BFM 2004) protocol were administered, the clinical and haematological remission was not achieved and the patient died because of disease progression (circulatory and respiratory insufficiency).
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / therapeutic use. Cell Lineage. Cell Transformation, Neoplastic. Child, Preschool. Daunorubicin / therapeutic use. Disease Progression. Fatal Outcome. Female. Humans. Prednisone / therapeutic use. Remission Induction. Vincristine / therapeutic use

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  • (PMID = 19531823.001).
  • [Journal-full-title] Medycyna wieku rozwojowego
  • [ISO-abbreviation] Med Wieku Rozwoj
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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