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1. Tong FK, Chow S, Hedley D: Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells. Cytometry B Clin Cytom; 2006 May;70(3):107-14
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  • [Title] Pharmacodynamic monitoring of BAY 43-9006 (Sorafenib) in phase I clinical trials involving solid tumor and AML/MDS patients, using flow cytometry to monitor activation of the ERK pathway in peripheral blood cells.
  • In this article, we describe its application to phase I trials of BAY 43-9006 in solid tumor and AML/MDS patients.
  • A modified whole blood fixation protocol was developed for the AML/MDS trial, using the c-kit ligand stem cell factor (SCF) to activate ERK as an alternative to PMA, and incorporating immunophenotypic markers to identify leukemic blasts.
  • A similar effect was seen in the lymphocytes of AML/MDS patients during treatment with BAY 43-9006.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukocytes, Mononuclear / drug effects. MAP Kinase Signaling System / drug effects. Myelodysplastic Syndromes / drug therapy. Neoplasms / drug therapy. Pyridines / therapeutic use


2. Andersson BS, de Lima M, Thall PF, Wang X, Couriel D, Korbling M, Roberson S, Giralt S, Pierre B, Russell JA, Shpall EJ, Jones RB, Champlin RE: Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS. Biol Blood Marrow Transplant; 2008 Jun;14(6):672-84
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  • [Title] Once daily i.v. busulfan and fludarabine (i.v. Bu-Flu) compares favorably with i.v. busulfan and cyclophosphamide (i.v. BuCy2) as pretransplant conditioning therapy in AML/MDS.
  • To account for improved supportive care and other unidentified factors that may affect outcome ("period" effects), 78 acute myelogenous leukemia (AML) patients receiving Melphalan-Flu (MF), treated in parallel during this time (1997-2004) were used to estimate the period effect.
  • These results support replacing BuCy +/- ATG with Bu-Flu +/- rabbit-antithymocyte globulin (ATG), and warrant a prospective comparison between allogeneic HSCT and conventional induction/consolidation chemotherapy for AML in CR1.

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  • (PMID = 18489993.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164-160020; United States / NCI NIH HHS / CA / 2P30CA16672-26; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS52878; NLM/ PMC4230823
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3. Finazzi G, Caruso V, Marchioli R, Capnist G, Chisesi T, Finelli C, Gugliotta L, Landolfi R, Kutti J, Gisslinger H, Marilus R, Patrono C, Pogliani EM, Randi ML, Villegas A, Tognoni G, Barbui T, ECLAP Investigators: Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study. Blood; 2005 Apr 1;105(7):2664-70
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  • [Title] Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study.
  • Progression to acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) is a possible evolution of polycythemia vera (PV), but whether some patients are at increased natural risk for this complication and how much the contribution of pharmacologic cytoreduction can affect the natural course of the disease remain uncertain.
  • AML/MDS was diagnosed in 22 patients after a median of 2.5 years from recruitment in the study and a median of 8.4 years from the diagnosis of PV.
  • Variables associated with progression to AML/MDS were assessed using different models of multivariate analysis.
  • Exposure to P32, busulphan, and pipobroman (HR, 5.46; 95% CI, 1.84-16.25; P = .0023), but not to hydroxyurea (HU) alone (HR, 0.86; 95% CI, 0.26-2.88; P = .8021), had an independent role in producing an excess risk for progression to AML/MDS compared with treatment with phlebotomy or interferon.
  • [MeSH-major] Leukemia, Myeloid / epidemiology. Polycythemia Vera / epidemiology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aspirin / therapeutic use. Databases, Factual. Disease Progression. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multivariate Analysis. Platelet Aggregation Inhibitors / therapeutic use. Prospective Studies. Risk Factors

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  • [CommentIn] Curr Hematol Rep. 2005 May;4(3):211-2 [15865873.001]
  • (PMID = 15585653.001).
  • [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 / Platelet Aggregation Inhibitors; R16CO5Y76E / Aspirin
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4. Gurkan E, Patah PA, Saliba RM, Ramos CA, Anderson BS, Champlin R, de Lima M, Lichtiger B: Efficacy of prophylactic transfusions using single donor apheresis platelets versus pooled platelet concentrates in AML/MDS patients receiving allogeneic hematopoietic stem cell transplantation. Bone Marrow Transplant; 2007 Sep;40(5):461-4
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  • [Title] Efficacy of prophylactic transfusions using single donor apheresis platelets versus pooled platelet concentrates in AML/MDS patients receiving allogeneic hematopoietic stem cell transplantation.
  • We studied all transfusions administered to 33 patients with AML/MDS during the first 100 days after busulfan-based, myeloablative HSCT.
  • In the week following any given transfusion, the median number of new transfusions was similar (n=2), as well as the need of further transfusion (16 versus 24%, P=0.2).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Platelet Transfusion / methods
  • [MeSH-minor] Acute Disease. Adult. Aged. Blood Platelets / cytology. Female. Hemorrhage / prevention & control. Humans. Male. Middle Aged. Platelet Count. Retrospective Studies. Transplantation, Homologous

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  • (PMID = 17589530.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] England
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5. Broberg K, Höglund M, Gustafsson C, Björk J, Ingvar C, Albin M, Olsson H: Genetic variant of the human homologous recombination-associated gene RMI1 (S455N) impacts the risk of AML/MDS and malignant melanoma. Cancer Lett; 2007 Dec 8;258(1):38-44
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  • [Title] Genetic variant of the human homologous recombination-associated gene RMI1 (S455N) impacts the risk of AML/MDS and malignant melanoma.
  • Mutations altering BLM function are associated with highly elevated cancer susceptibility (Bloom's syndrome).
  • We have analyzed the common polymorphism Ser455Asn in RMI1 and its association with cancer risk in acute myeloid leukemia (AML, N=93), myelodysplatic syndromes (MDS, N=74), and malignant melanoma (MM, N=166).
  • The results showed a consistent pattern, where carriers of the Asn variant had a significantly increased risk of AML/MDS.
  • The risk of AML/MDS for SerAsn+AsnAsn subjects was odds ratio (OR)=1.7, 95% confidence interval (CI) 1.1-2.5 or MM was OR=1.5, 95% CI 1.0-2.2.
  • [MeSH-major] Carrier Proteins / genetics. Genetic Variation. Leukemia, Myeloid, Acute / genetics. Melanoma / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Recombination, Genetic. Skin Neoplasms / genetics
  • [MeSH-minor] Adenosine Triphosphatases / genetics. Adult. Aged. Aged, 80 and over. Bloom Syndrome / genetics. Case-Control Studies. DNA Helicases / genetics. Female. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Genetic. RecQ Helicases

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  • (PMID = 17900800.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / RMI1 protein, human; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / Bloom syndrome protein; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / RecQ Helicases
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6. Al-Rahawan MM, Alter BP, Bryant BJ, Elghetany MT: Bone marrow cell cycle markers in inherited bone marrow failure syndromes. Leuk Res; 2008 Dec;32(12):1793-9
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  • Patients with inherited bone marrow failure syndromes (IBMFS) are at increased risk of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), possibly related to cell cycle dysregulation.
  • In a cross-sectional analysis of bone marrow from 77 IBMFS, 71 sporadic conditions (AML, MDS, acquired aplastic anemia) and 22 normal controls we found overexpression of p53 in IBMFS, AML, and MDS; of Ki-67 in IBMFS and AML; and of survivin in IBMFS compared with all other groups.
  • [MeSH-major] Bone Marrow Cells / pathology. Bone Marrow Diseases / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology

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  • (PMID = 18606449.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers; 0 / Inhibitor of Apoptosis Proteins; 0 / Ki-67 Antigen; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ NIHMS77574; NLM/ PMC2716700
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7. Reindl C, Quentmeier H, Petropoulos K, Greif PA, Benthaus T, Argiropoulos B, Mellert G, Vempati S, Duyster J, Buske C, Bohlander SK, Humphries KR, Hiddemann W, Spiekermann K: CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes. Clin Cancer Res; 2009 Apr 1;15(7):2238-47
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  • [Title] CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes.
  • In this study, we determined the frequency of CBL mutations in acute leukemias and evaluated the oncogenic potential of mutant CBL.
  • EXPERIMENTAL DESIGN: The cDNA of 300 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and acute lymphoblastic leukemia (ALL) patients and 82 human leukemic cell lines was screened for aberrations in the linker and RING finger domain of CBL.
  • RESULTS: We identified 3 of 279 AML/MDS patients expressing CBL exon 8/9 deletion mutants.
  • One of 116 sequenced AML/MDS cases carried a R420G missense mutation.
  • All AML/MDS patients with identified CBL mutants belonged to the core binding factor and 11q deletion AML subtypes.
  • CONCLUSION: CBL exon8/9 mutants occur in genetically defined AML/MDS subtypes and transform hematopoietic cells by constitutively activating the FLT3 pathway.
  • This phenotype resembles the one of mutated RTKs and suggests that CBL mutant AML patients might benefit from treatment with FLT3 PTK inhibitors.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics. fms-Like Tyrosine Kinase 3 / metabolism


8. Clausen J, Wolf D, Petzer AL, Gunsilius E, Schumacher P, Kircher B, Gastl G, Nachbaur D: Impact of natural killer cell dose and donor killer-cell immunoglobulin-like receptor (KIR) genotype on outcome following human leucocyte antigen-identical haematopoietic stem cell transplantation. Clin Exp Immunol; 2007 Jun;148(3):520-8
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  • [Title] Impact of natural killer cell dose and donor killer-cell immunoglobulin-like receptor (KIR) genotype on outcome following human leucocyte antigen-identical haematopoietic stem cell transplantation.
  • To define the role of quantitative graft composition and donor killer-cell immunoglobulin-like receptor (KIR) genotype in clinical outcome following unmanipulated peripheral blood stem cell transplantation (PBSCT) from human leucocyte antigen (HLA)-identical siblings, 43 consecutive transplants for haematological malignancies were analysed retrospectively.
  • In patients with acute myelogenous leukaemia or myelodysplastic syndrome (AML/MDS; n = 18), no relapse occurred following transplants meeting both a high (above median) natural killer (NK) cell count and missing HLA-ligand(s) to donor's KIR(s), compared to all other AML/MDS patients (0% versus 44%; P = 0.049).
  • Moreover, in AML/MDS patients, this constellation predicted superior overall survival (OS) (P = 0.046).
  • [MeSH-minor] Acute Disease. Chronic Disease. Cytomegalovirus Infections / immunology. Female. Genotype. Graft vs Host Disease / immunology. Graft vs Host Disease / therapy. Graft vs Tumor Effect / genetics. Histocompatibility Testing. Humans. Ligands. Lymphocyte Count. Male. Opportunistic Infections / immunology. Receptors, KIR. Receptors, KIR3DL2. Recurrence. Retrospective Studies. Survival Analysis. Transplantation Conditioning / methods. Treatment Outcome

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  • (PMID = 17493020.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / KIR3DL2 protein, human; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR; 0 / Receptors, KIR3DL2
  • [Other-IDs] NLM/ PMC1941931
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9. Inaba T: [Radiation-induced and therapy-related AML/MDS]. Nihon Rinsho; 2009 Oct;67(10):1880-3
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  • [Title] [Radiation-induced and therapy-related AML/MDS].
  • Radiation induced acute myeloid leukemia (AML) was recognized a century ago, soon after mankind found radiation.
  • Atomic bomb survivors developed de novo AML with relatively short latency with very high frequency.
  • By contrast, excess occurrence of myelodysplastic syndrome (MDS) as well as solid tumors was found decades late.
  • This difference may be due to etiology that many de novo AML patients harbor chimeric leukemogenic genes caused by chromosomal translocations, while MDS patients rarely carry chimeras.
  • Therapy related leukemia is mainly caused by topoisomerase II inhibitors that cause de novo AML with an 11q23 translocation or by alkyrating agents that induce MDS/AML with an AML1 point mutation and monosomy 7.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Myelodysplastic Syndromes / etiology

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  • (PMID = 19860183.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 7
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10. Zatkova A, Schoch C, Speleman F, Poppe B, Mannhalter C, Fonatsch C, Wimmer K: GAB2 is a novel target of 11q amplification in AML/MDS. Genes Chromosomes Cancer; 2006 Sep;45(9):798-807
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  • [Title] GAB2 is a novel target of 11q amplification in AML/MDS.
  • Chromosome arm 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are rare but recurrent aberrations in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Thus, the adaptor molecule GAB2 that has already been shown to enhance oncogenic signaling in other neoplasias appears as a novel target of 11q amplification in AML/MDS.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Chromosomes, Human, Pair 11. Gene Amplification / physiology. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


11. Borthakur G, Estey AE: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome. Curr Oncol Rep; 2007 Sep;9(5):373-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome.
  • Therapy-related acute myelogenous leukemia and myelodysplastic syndrome (t-AML/MDS) are increasing in prevalence with aging of the population and improved survival of patients treated with chemotherapy or radiotherapy for other malignancies.
  • Research focused on the pathogenesis of t-AML/MDS will provide insight into the pathogenesis of de novo AML/MDS.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced


12. Hake CR, Graubert TA, Fenske TS: Does autologous transplantation directly increase the risk of secondary leukemia in lymphoma patients? Bone Marrow Transplant; 2007 Jan;39(2):59-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does autologous transplantation directly increase the risk of secondary leukemia in lymphoma patients?
  • Patients who undergo autologous stem cell transplantation (ASCT) for lymphoma have a significant risk of therapy-related acute myeloid leukemia and myelodysplasia (t-AML/MDS).
  • Compared to that seen in other indications such as breast cancer, multiple myeloma or germ cell tumors, there is a substantially increased risk for t-AML/MDS following ASCT for lymphoma.
  • In many of the larger series to date, it has not been possible to directly implicate autologous transplantation itself as a risk factor for t-AML/MDS.
  • Although pre-transplant therapy is certainly an important factor in the development of t-AML/MDS, specific components of the autologous transplantation procedure itself may also contribute to the risk of t-AML/MDS.
  • Specifically, priming chemotherapy, total body irradiation, and the extensive cellular proliferation which occurs during engraftment may all play a role in the development of t-AML/MDS.
  • Furthermore, there is an increasing body of evidence that certain inherited polymorphisms in genes governing drug metabolism, DNA repair and leukemogenesis may influence susceptibility to t-AML/MDS.
  • In this paper, we review the evidence implicating the above risk factors for t-AML/MDS, present a potential mechanism for t-AML/MDS and propose interventions to reduce the rate of t-AML/MDS in lymphoma patients.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Leukemia, Myeloid / etiology. Lymphoma / surgery. Transplantation, Autologous / adverse effects
  • [MeSH-minor] Humans. Incidence. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / etiology

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  • (PMID = 17143301.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [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
  • [Number-of-references] 98
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13. Czibere A, Prall WC, Zerbini LF, Jäger M, Kobbe G, Knipp S, Libermann TA, Haas R, Aivado M: Exisulind induces apoptosis in advanced myelodysplastic syndrome (MDS) and acute myeloid leukaemia/MDS. Br J Haematol; 2006 Nov;135(3):355-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exisulind induces apoptosis in advanced myelodysplastic syndrome (MDS) and acute myeloid leukaemia/MDS.
  • The influence of Exisulind on the viability and apoptosis of CD34(+) stem cells from patients with advanced myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML)/MDS was investigated.
  • Addition of a specific JNK-inhibitor to Exisulind-treated advanced MDS and AML/MDS cells partly abrogated apoptosis.
  • We propose that Exisulind is tested in clinical phase I/II trials for the treatment of advanced MDS and AML/MDS.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, Myeloid / physiopathology. Myelodysplastic Syndromes / physiopathology. Sulindac / analogs & derivatives
  • [MeSH-minor] Acute Disease. Antigens, CD34. Cell Survival / drug effects. Cells, Cultured. Enzyme Activation. Humans. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. JNK Mitogen-Activated Protein Kinases / metabolism. Stem Cells / drug effects. Stem Cells / physiology


14. Wong AK, Fang B, Zhang L, Guo X, Lee S, Schreck R: Loss of the Y chromosome: an age-related or clonal phenomenon in acute myelogenous leukemia/myelodysplastic syndrome? Arch Pathol Lab Med; 2008 Aug;132(8):1329-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of the Y chromosome: an age-related or clonal phenomenon in acute myelogenous leukemia/myelodysplastic syndrome?
  • CONTEXT: The clinical association between loss of the Y chromosome and acute myelogenous leukemia and myelodysplastic syndrome (AML/MDS) has been debated because both phenomena are related to aging.
  • OBJECTIVE: To evaluate the relationship between loss of the Y chromosome and AML/MDS.
  • Of these, 16 patients demonstrated myeloid disease, with 2 cases of AML and 14 cases of MDS.
  • An increased incidence (P < .05) of AML/MDS was seen only in the group composed of 8 patients with complete loss of the Y chromosome in all karyotyped cells (1 case of AML and 7 cases of MDS).
  • However, in individuals in which all cells on cytogenetic analysis showed loss of the Y chromosome, there was a statistically significant increase in AML/MDS, suggesting that the absence of any normal-dividing cells in a bone marrow analysis may be indicative of AML/MDS.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Y. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • : 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.
  • METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m<sup>2</sup> AZA during their first treatment cycle.

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  • (PMID = 27961481.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Steensma D, Kantarjian H, Wijermans P: Clinical experience with different dosing schedules of decitabine in patients with myelodysplastic syndromes (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7011

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical experience with different dosing schedules of decitabine in patients with myelodysplastic syndromes (MDS).
  • : 7011 Background: Decitabine, a potent DNA hypomethylating agent, has demonstrated efficacy in MDS patients using two dosing regimens: 15 mg/m<sup>2</sup> intravenous (IV) over 3 hours (hrs) every (q) 8 hrs for 3 days q 6 weeks (wks) and 20 mg/m<sup>2</sup> IV over 1 hr once daily for 5 consecutive days q 4 wks.
  • Data from each clinical trial supporting overall improvement, duration of improvement, time to AML or death, progression-free survival (PFS), and transfusion independence was assessed.
  • RESULTS: Patients had IPSS classification scores of intermediate-2 or high-risk (D-0007, 70%; EORTC-06011, 93%; ID03-0180, 66%; DACO-020, 46%) and de novo MDS (D-0007, 87%; EORTC-06011, 88%; ID03-0180, 70%; DACO-020, 89%).
  • Comparable overall improvement (complete response [CR] + partial response [PR] + hematologic improvement [HI]), time to AML or death, and PFS was observed across all trials (Table).
  • Increasing the number of decitabine treatment cycles administered may provide additional benefit to MDS patients.

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  • (PMID = 27961372.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Spadaro P, Ingemi M, Pitini V, Arrigo C, Soto Parra H: Myelodysplastic syndromes developing after imatinib therapy for GIST. J Clin Oncol; 2009 May 20;27(15_suppl):10532

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndromes developing after imatinib therapy for GIST.
  • Previously, we had detected clonal chromosomal abnormalities in the bone marrow of GIST pts. who developed a myelodysplastic syndrome during treatment with imatinib, so we performed a systematic study in a series of male and female GIST pts. during treatment with imatinib.
  • All pathologic material was reviewed to identify pts. with MDS or AML according to the WHO classification.
  • A trisomy 8 was detectable in seven pts. even if, curiously, in four of these pts. this come and went on repeated sampling without any apparent clinical effect, three pts. developed an MDS (two refractory cytopenias with multilineage dysplasia, and one refractory cytopenia with multilineage dysplasia and ringed sideroblast).
  • One patient developed a RAEB-1 with monosomy 7 which rapidly transformed into AML.

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  • (PMID = 27963910.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Bello CM, Yu D, Zhu W, Wetzstein GA, Lancet JE: Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors. J Clin Oncol; 2009 May 20;27(15_suppl):7088

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors.
  • : 7088 Background: Secondary acute myeloid leukemia (sAML) arising from myelodysplasia (MDS) or a myeloproliferative neoplasm (MPN) has a poor prognosis.
  • METHODS: Retrospective chart review of patients with untreated AML from MDS/MPN treated with standard induction therapy from January 2004 to September 2008.
  • Age, IPSS, ECOG PS, cytogenetics, duration of MDS, and prior MDS treatment were evaluated for their impact on obtaining complete remission (CR) or CR with low platelets (CRp) and overall survival (OS).
  • RESULTS: Sixty-one patients with sAML who received induction therapy were evaluated: median age (range) = 66 (36-82) years; M = 67%, ECOG PS 0 or 1 = 86%; poor-risk (PR) cytogenetics = 33%; IPSS > 1 = 43%; prior therapy for MDS with decitabine or azacitidine (DM) or lenalidomide (L) = 41% (25 pts).
  • Multivariable analysis indicated that the same three factors were significantly negatively associated with CR/CRp as well as OS: PR cytogenetics, prior treatment with DM/L, and long transformation to AML on log scale.
  • CONCLUSIONS: Prior MDS treatment with a DM/L, PR cytogenetics and long transformation to AML are independent negative prognostic factors for response and OS in patients with sAML following induction therapy, suggesting that such patients may be better served by novel approaches, and that stratification for these risk factors should be considered in future clinical trials.

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  • (PMID = 27961482.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Batty G, Kantarjian H, Issa JJ, Garcia-Manero G, Pierce S, O'Brien S, Jabbour E, Cortes J, Ravandi F: Feasibility of hypomethylating therapy in patients with renal insufficiency. J Clin Oncol; 2009 May 20;27(15_suppl):7089

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7089 Background: Epigenetic therapy with hypomethylating agents (HA) is the standard of care in patients (pts) with myelodysplastic syndrome (MDS).
  • Moreover, there are no reports of use of these agents in pts with renal insufficiency (RI) commonly seen in pts with MDS.
  • METHODS: We investigated the outcomes of pts with RI and MDS, chronic myelomonocytic leukemia (CMML), or acute myeloid leukemia (AML) receiving therapy with HA.
  • RESULTS: Forty-two pts with sCr ≥ 1.5 mg/dL (including 17 with MDS, 16 with AML, and 9 with CMML) were treated with DAC or 5AZA alone or in combination with other agents (primarily histone deacetylase inhibitors).
  • CONCLUSIONS: The use of HA is well tolerated in pts with MDS and AML and RI who achieved comparable OR rates to those without RI.

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  • (PMID = 27961273.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • Thirteen (81%) pts had R/R AML, and 3 (19%) had R/R ALL of which 5 (31%) had diploid and 6 (38%) had adverse cytogenetics.

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Sekeres M, Kantarjian H, Fenaux P, Becker P, Boruchov A, Guerci-Bresler A, Hu K, Franklin J, Berger D: Subcutaneous or intravenous administration of romiplostim in thrombocytopenic patients with myelodysplastic syndrome (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcutaneous or intravenous administration of romiplostim in thrombocytopenic patients with myelodysplastic syndrome (MDS).
  • : 7009 Background: Thrombocytopenia is common in patients (pts) with MDS, and treatment options are currently limited to platelet (plt) transfusions.
  • Eligibility criteria included IPSS low or intermediate-1 risk MDS and a mean baseline plt count ≤50x10<sup>9</sup>/L.
  • Five pts experienced serious AEs, and there were 2 cases of disease progression to AML: one pt in the QWSC cohort who received romiplostim for 4 weeks and one in the Q2WSC cohort who received romiplostim for 20 weeks.
  • CONCLUSIONS: IV and SC romiplostim appeared well-tolerated and effective in raising plt counts and avoiding plt transfusions in low and intermediate-1 risk MDS pts.

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  • (PMID = 27961381.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Chaubey R, Sazawal S, Mahapatra M, Saxena R: Low frequency of RAS and absence of FLT3-ITD gene mutations in patients with Myelodysplastic Syndromes in India: AIIMS experience. J Clin Oncol; 2009 May 20;27(15_suppl):e22231

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low frequency of RAS and absence of FLT3-ITD gene mutations in patients with Myelodysplastic Syndromes in India: AIIMS experience.
  • : e22231 Background: Chromosomal abnormalities and molecular detection has potential importance for diagnosis and prognosis of MDS, although the mechanisms underlying the development of MDS and their progressive evolution to AML are still largely unknown.
  • Since, no studies have been reported from India on the prevalence of N-RAS, K- RAS point mutation in codon 12 and FLT3-ITD mutations in patients with MDS, we undertook this study.
  • CONCLUSIONS: Thus, it appears that the RAS and FLT3 mutations are uncommon in MDS patients in India.

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  • (PMID = 27964108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. 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).
  • Cumulative incidence of acute (grade 3-4) and chronic GVHD was 28% (95% CI 19%-37%) and 38% (95% CI 24%-52%), respectively.
  • There was no statistically significant difference in OS; 31% versus 32% (p = 0.89) or FFP 71% versus 60% (p = 0.29) for recipients of BM versus PBMC with similar results in IF and RR AML.
  • 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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24. Dutreix C, Huntsman Labed A, Roesel J, Lanza C, Wang Y: Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients. J Clin Oncol; 2009 May 20;27(15_suppl):e14540

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients.
  • : e14540 Background: Midostaurin is a multi-tyrosine-kinases inhibitor targeting class III tyrosine-protein-kinases, including Fms-like tyrosine kinase-3 (FLT3), involved in hematopoiesis and leukemia.
  • METHODS: The two studies presented here involved patients with wild-type or FLT3-mutated de novo (phase Ib) or relapsed (phase II) AML or MDS.
  • Following multiple oral daily single-agent doses, midostaurin and CGP62221 concentrations accumulated significantly in the first 3-5 days then declined by 40- 80% prior to a new steady state 2-3 weeks post-dose.
  • These results support the ongoing phase III AML study in AML FLT3-mutated patients with midostaurin given in combination with chemotherapy.

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  • (PMID = 27963644.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Hollmig K, Waheed S, Nair B, Haessler J, Petty N, Pineda-Roman M, Alsayed Y, van Rhee F, Crowley J, Barlogie B: MDS-associated cytogenetic abnormalities (MDS-CA) after total therapy (TT) regimens for newly diagnosed multiple myeloma (MM): Apparent surge after introduction of post-transplant consolidation chemotherapy (CONS) in TT2 and TT3. J Clin Oncol; 2009 May 20;27(15_suppl):8595

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MDS-associated cytogenetic abnormalities (MDS-CA) after total therapy (TT) regimens for newly diagnosed multiple myeloma (MM): Apparent surge after introduction of post-transplant consolidation chemotherapy (CONS) in TT2 and TT3.
  • : 8595 Background: We have previously reported on the variables associated with the development of MDS-CA in the context of autologous transplant-supported high-dose therapy regimens for MM (Barlogie et al, Blood 2008).
  • METHODS: Due to a perceived increase in MDS-CA frequency, our MM data base was reviewed again to determine the potential effect of CONS introduced in TT2 and retained in TT3 trials.
  • The frequency of MDS-CA post-transplant was determined, using Kaplan-Meier estimate plots, for 183 patients who received TT1, 554 enrolled in TT2 and 305 receiving TT3.
  • Persistence of MDS-CA implied their documentation on 3 successive occasions.
  • RESULTS: 3-year MDS-CA estimates were 2% for both TT1 and TT2 and 4% for TT3 (TT3 v TT2, p=0.04; TT3 v TT1, p=0.11); persistent MDS-CA were also more frequently observed in TT3 in comparison with TT2 and TT1 (2% v 0% v 0%, both p=0.01).
  • Multivariate analysis of features associated with transient and persistent MDS-CA revealed TT3 as an adverse feature (HR=2.84, p=0.043), along with incomplete platelet recovery of <165,000/uL 3mo after 1<sup>st</sup> transplant.
  • CONCLUSIONS: Despite reduced induction chemotherapy prior to and CONS after tandem melphalan (200mg/m2)-based autotransplants from 4 in TT2 to 2 in TT3, overall and persistent MDS-CA increased significantly in TT3.
  • Clinical MDS and AML were rarely observed and a full account of hematopathologic findings will be presented.

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  • (PMID = 27962291.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Chamberlain MC, Raizer J: Extended exposure to alkylator chemotherapy: Delayed appearance of myelodysplasia. J Clin Oncol; 2009 May 20;27(15_suppl):e13030

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

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  • (PMID = 27962878.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Popat UR, Saliba R, Hosing C, Khouri I, Alousi AM, Giralt SA, de Lima MJ, Qazilbash MH, Champlin R, Anderlini P: Age at diagnosis does not adversely affect outcome in patients with Hodgkin's Disease (HD) after autologous transplantation. J Clin Oncol; 2009 May 20;27(15_suppl):e19507

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cumulative incidence of secondary MDS or AML was 8%.

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  • (PMID = 27960864.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Jabbour E, Faderl S, Ravandi F, Konopleva M, Verstovsek S, Cortes J, Wierda W, Newsome WM, Yang H, Kantarjian H, Garcia-Manero G: Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML).
  • : 7004 Background: Standard induction therapy for pts with AML has not changed over the last 2 decades nor has the outcome of these pts.
  • We designed a phase II study of V with IA as front-line therapy for MDS/AML.
  • METHODS: Pts with untreated int-2/high-risk MDS or AML ages 15-65 with adequate liver and renal functions and PS, and EF ≥ 50% were eligible.
  • 3 pts with relapsed/refractory AML were treated in the run-in phase.
  • Following these, 19 pts were enrolled on the phase 2 portion.
  • CONCLUSIONS: The combination of IA and V is safe and active in AML/MDS.

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  • (PMID = 27961376.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Ritchie EK, Roboz G, Hinchcliff K, Curcio T, Scandura J, Feldman E: Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7054

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS.
  • : 7054 Background: Laromustine is a novel sulfonylhydrazine-alkylating agent with activity in acute myeloid leukemia (AML).
  • Laromustine in phase I and II trials shows activity in patients with relapsed/refractory leukemia (1) and elderly patients with new AML (2).
  • Based on this data, a phase I study to evaluate the safety and efficacy of combining escalating doses of laromustine with infusional ara-C in AML and MDS patients over 60.

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  • (PMID = 27961420.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Garcia-Manero G, Luger S, Venugopal P, Maness L, Wetzler M, Coutre S, Stock W, Borthakur G, Chiao J, Kantarjian H: A randomized phase II study of sapacitabine, an oral nucleoside analogue, in elderly patients with AML previously untreated or in first relapse or previously treated MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7021

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

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  • (PMID = 27961383.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Villano JL, Letarte N, Yu JM, Shakir AR, Bressler L: Hematologic adverse events associated with temozolomide (TMZ). J Clin Oncol; 2009 May 20;27(15_suppl):2053

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

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  • (PMID = 27964671.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Drexler HG, Dirks WG, Macleod RA: Many are called MDS cell lines: one is chosen. Leuk Res; 2009 Aug;33(8):1011-6
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  • [Title] Many are called MDS cell lines: one is chosen.
  • Myelodysplastic syndromes (MDS) comprise a heterogenous group of clonal disorders of hematopoietic progenitors, showing genetic instability and in many cases progression to acute myeloid leukemia (AML).
  • When MDS progress towards AML (AML/MDS), additional genetic lesions cause a block in differentiation and an accumulation of blast cells.
  • Hence, both pathophysiologically and clinically the MDS and AML/MDS phases are distinguishable.
  • Leukemia cell lines are key resources for modelling hematological malignancies.
  • Some 31 cell lines have been described in the literature purportedly established from patients with MDS.
  • However, a significant minority of these has proved false after DNA profiling which revealed their cross-contamination with older established leukemia cell lines.
  • Most remaining ("authentic") MDS cell lines were established during the leukemic phase of the disease progression rather than during the MDS phase.
  • Based on these data we have assigned the 31 candidate MDS cell lines to one of the three categories:.
  • (2) malignant cell lines established in the AML/MDS leukemic phase; and (3) apparently legitimate MDS cell lines established during the MDS phase.
  • While MDS and AML/MDS cell lines both provide singular resources for modelling pathology, mining oncogenically modified macromolecules, and testing druggability, we contend these groups should be considered separately.
  • [MeSH-major] Cell Line, Tumor. Hematopoietic Stem Cells. Myelodysplastic Syndromes
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Genomic Instability. Humans. Leukemia, Myeloid, Acute. Models, Biological


33. Praga C, Bergh J, Bliss J, Bonneterre J, Cesana B, Coombes RC, Fargeot P, Folin A, Fumoleau P, Giuliani R, Kerbrat P, Hery M, Nilsson J, Onida F, Piccart M, Shepherd L, Therasse P, Wils J, Rogers D: Risk of acute myeloid leukemia and myelodysplastic syndrome in trials of adjuvant epirubicin for early breast cancer: correlation with doses of epirubicin and cyclophosphamide. J Clin Oncol; 2005 Jun 20;23(18):4179-91
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  • [Title] Risk of acute myeloid leukemia and myelodysplastic syndrome in trials of adjuvant epirubicin for early breast cancer: correlation with doses of epirubicin and cyclophosphamide.
  • PURPOSE: We reviewed follow-up of patients treated in 19 randomized trials of adjuvant epirubicin in early breast cancer to determine incidence, risk, and risk factors for subsequent acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Cases of AML or MDS (AML/MDS) were reported, with disease characteristics.
  • RESULTS: In 7,110 patients treated with epirubicin-containing regimens (92% of whom also received cyclophosphamide), 8-year cumulative probability of AML/MDS was 0.55% (95% CI, 0.33% to 0.78%).
  • The risk of developing AML/MDS increased in relation to planned epirubicin dose per cycle, planned epirubicin dose-intensity, and administered cumulative doses of epirubicin and cyclophosphamide.
  • Patients with administered cumulative doses of both epirubicin and cyclophosphamide not exceeding those used in standard regimens (</= 720 mg/m(2) and </= 6,300 mg/m(2), respectively) had an 8-year cumulative probability of developing AML/MDS of 0.37% (95% CI, 0.13% to 0.61%) compared with 4.97% (95% CI, 2.06% to 7.87%) for patients administered higher cumulative doses of both epirubicin and cyclophosphamide.
  • CONCLUSION: Patients treated with standard cumulative doses of adjuvant epirubicin (</= 720 mg/m(2)) and cyclophosphamide (</= 6,300 mg/m(2)) for early breast cancer have a lower probability of secondary leukemia than patients treated with higher cumulative doses.
  • Increased risk of secondary leukemia must be considered when assessing the potential benefit to risk ratio of higher than standard doses.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cyclophosphamide / adverse effects. Epirubicin / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced


34. Basecke J, Podleschny M, Becker A, Seiffert E, Schwiers I, Schwiers R, Haase D, Glass B, Schmitz N, Trumper L, Griesinger F: Therapy-associated genetic aberrations in patients treated for non-Hodgkin lymphoma. Br J Haematol; 2008 Apr;141(1):52-9
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  • Therapy-associated myelodysplastic syndromes and acute myeloid leukaemia (t-AML/MDS) following high dose chemotherapy are significant problems, with a cumulative incidence of 20% or more in myeloablative treatment regimen.
  • Retrospective findings indicated that t-AML/MDS associated genetic aberrations can be observed directly after exposure to chemotherapy and can precede t-AML by several months.
  • None of these patients developed a t-AML/MDS during a 3-year clinical follow up period.
  • We concluded that the high incidence of genetic aberrations reflected a dose-dependent, transient therapy-induced genetic damage which is not predictive of a t-AML/MDS.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cyclophosphamide / therapeutic use. Dose-Response Relationship, Drug. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Follow-Up Studies. Humans. Leukemia, Myeloid, Acute / chemically induced. Middle Aged. Prednisolone / therapeutic use. Prognosis. Prospective Studies. Reverse Transcriptase Polymerase Chain Reaction / methods. Translocation, Genetic. Vincristine / therapeutic use

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  • (PMID = 18324966.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; CHOEP protocol
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35. Le Deley MC, Suzan F, Cutuli B, Delaloge S, Shamsaldin A, Linassier C, Clisant S, de Vathaire F, Fenaux P, Hill C: Anthracyclines, mitoxantrone, radiotherapy, and granulocyte colony-stimulating factor: risk factors for leukemia and myelodysplastic syndrome after breast cancer. J Clin Oncol; 2007 Jan 20;25(3):292-300
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anthracyclines, mitoxantrone, radiotherapy, and granulocyte colony-stimulating factor: risk factors for leukemia and myelodysplastic syndrome after breast cancer.
  • PURPOSE: To determine the risk factors for acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) after breast cancer.
  • We included 182 AML and MDS patients and 534 matched controls.
  • RESULTS: The risk of AML/MDS was increased after topoisomerase-II inhibitor-based chemotherapy (P < 10-16) and was higher for mitoxantrone-based chemotherapy than for anthracycline-based chemotherapy (relative risk [RR] = 15.6; 95% CI, 7.1 to 34.2; and RR = 2.7; 95% CI, 1.7 to 4.5, respectively).
  • After adjustment for other treatment components, the risk of AML/MDS in patients who received radiotherapy was multiplied by 3.9 (95% CI, 1.4 to 10.8) but was not increased by alkylating agents.
  • Patients receiving granulocyte colony-stimulating factor (G-CSF) support had an increased risk of AML/MDS (RR = 6.3; 95% CI, 1.9 to 21), even when controlling for chemotherapy doses.
  • Similar results were obtained when AML and MDS were considered separately.
  • CONCLUSION: This large case-control study demonstrates that the risk of AML/MDS is much higher with mitoxantrone-based chemotherapy than with anthracyclines-based chemotherapy in a population of women recently treated for breast cancer.
  • The risk of AML/MDS associated with mitoxantrone must be kept in mind when using this drug to treat diseases other than breast cancer (eg, prostate cancer or multiple sclerosis).
  • [MeSH-major] Anthracyclines / adverse effects. Antineoplastic Agents / adverse effects. Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Leukemia, Myeloid / chemically induced. Mitoxantrone / adverse effects. Myelodysplastic Syndromes / chemically induced. Neoplasms, Radiation-Induced
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. France / epidemiology. Humans. Middle Aged. Risk Factors


36. Lyman GH, Dale DC, Culakova E, Poniewierski MS, Wolff D, Kuderer NM, Lambert K, Crawford J: Acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) and overall mortality with chemotherapy (CT) and granulocyte colony-stimulating factor (G-CSF): A meta-analysis of randomized controlled trials (RCTs). J Clin Oncol; 2009 May 20;27(15_suppl):9524

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

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  • (PMID = 27964513.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Nguyen-Khac F, Lesty C, Eclache V, Couronné L, Kosmider O, Andrieux J, Collonge-Rame MA, Penther D, Lafage M, Bilhou-Nabera C, Chapiro E, Mozziconacci MJ, Mugneret F, Gachard N, Nadal N, Lippert E, Struski S, Dastugue N, Cabrol C, Bernard OA, Groupe Francophone de Cytogénétique Hématologique: Chromosomal abnormalities in transformed Ph-negative myeloproliferative neoplasms are associated to the transformation subtype and independent of JAK2 and the TET2 mutations. Genes Chromosomes Cancer; 2010 Oct;49(10):919-27
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  • Evolution to myelofibrosis (MF), acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) may occur over time in myeloproliferative neoplasms (MPN) patients most likely due to the acquisition of additional mutations.
  • The Groupe Francophone de cytogenetique hematologique (GFCH) has collected and reviewed 82 patients with transformation of MPN (66 AML/MDS and 16 MF).
  • Significantly more -7/del(7q) (P = 0.004) and -5/del(5q) (P = 0.03) were found in AML/MDS with a higher incidence of dup1q (P = 0.01) in MF.
  • In multivariate analysis, two factors were independently associated with an inferior overall survival (OS); AML/MDS transformation (P < 0.0001) and -5/del(5q) abnormality (P = 0.02).
  • Although both giving rise to loss of 7q, der(1;7) differed from other 7q deletions in terms of distribution (lower frequency of AML/MDS, P = 0.02), association with chromosomal abnormalities (absence of -5/del(5q), P = 0.003; increased del(20q), P = 0.05), and longer OS (P = 0.0007).
  • We detected 24/40 (60%) JAK2V617F and 8/25 (32%) TET2 mutations in samples following transformation, ranging from wild-type to mutated forms of both genes.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Chromosome Aberrations. DNA-Binding Proteins / genetics. Janus Kinase 2 / genetics. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Mutation / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 20629097.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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38. Paulsson K, Heidenblad M, Strömbeck B, Staaf J, Jönsson G, Borg A, Fioretos T, Johansson B: High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration. Leukemia; 2006 May;20(5):840-6
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  • [Title] High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration.
  • Although trisomy 8 as the sole chromosome aberration is the most common numerical abnormality in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), little is known about its pathogenetic effects.
  • Considering that +8 is a frequent secondary change in AML/MDS, cryptic--possibly primary--genetic aberrations may occur in cases with trisomy 8 as the apparently single anomaly.
  • We performed a high-resolution genome-wide array-based comparative genome hybridization (array CGH) analysis of 10 AML/MDS cases with isolated +8, utilizing a 32K bacterial artificial chromosome array set, providing >98% coverage of the genome with a resolution of 100 kb.
  • A 1.8 Mb deletion at 7p14.1, which had occurred prior to the +8, was identified in MDS transforming to AML.
  • The present results show that cryptic genetic abnormalities are frequent in trisomy 8-positive AML/MDS cases and that +8 as the sole cytogenetic aberration is not always the primary genetic event.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Genome. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Nucleic Acid Hybridization / methods. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged


39. Tebbi CK, London WB, Friedman D, Villaluna D, De Alarcon PA, Constine LS, Mendenhall NP, Sposto R, Chauvenet A, Schwartz CL: Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin's disease. J Clin Oncol; 2007 Feb 10;25(5):493-500
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  • [Title] Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin's disease.
  • We evaluated incidence and risk factors of acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and second malignant neoplasms (SMNs).
  • Six of eight patients developed AML/MDS, and both solid tumors (osteosarcoma and papillary thyroid carcinoma) occurred in recipients of DRZ.
  • With median 58 months' follow-up, 4-year cumulative incidence rate (CIR) for AML/MDS was 2.55% +/- 1.0% with DRZ versus 0.85% +/- 0.6% in the non-DRZ group (P = .160).
  • Among patients receiving DRZ, the standardized incidence rate (SIR) for AML/MDS was 613.6 compared with 202.4 for those not receiving DRZ (P = .0990).
  • Adding DRZ to ABVE and ABVE-PC may have increased the incidence of SMN and AML/MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chelating Agents / adverse effects. Hodgkin Disease / drug therapy. Leukemia, Myeloid / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Razoxane / adverse effects
  • [MeSH-minor] Acute Disease. Adolescent. Cohort Studies. Enzyme Inhibitors / adverse effects. Female. Follow-Up Studies. Heart Diseases / chemically induced. Heart Diseases / prevention & control. Humans. Incidence. Lung Diseases / chemically induced. Lung Diseases / prevention & control. Male. Neoplasm Staging. Osteosarcoma / chemically induced. Risk Assessment. Risk Factors. Thyroid Neoplasms / chemically induced. Time Factors. Topoisomerase II Inhibitors


40. Leleu X, Terriou L, Duhamel A, Moreau AS, Andrieux J, Dupire S, Coiteux V, Berthon C, Micol JB, Guieze R, Facon T, Bauters F: Long-term outcome in acquired aplastic anemia treated with an intensified dose schedule of horse antilymphocyte globulin in combination with androgens. Ann Hematol; 2006 Oct;85(10):711-6
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  • ALG has been incriminated in the emergence of 10 to 20% therapy-related AML/MDS (t-AML/MDS) with the usual doses.
  • Questions remain whether higher doses of ALG could improve the response and OS rates and whether the combination with androgens is able to protect patients from t-AML/MDS.
  • The incidence of t-AML/MDS was 2.3% with an estimated 10-year cumulative incidence of 3.1.
  • Our results show that higher doses of ALG combined to androgens are feasible and give results close to those recently describe with the immunosuppressive treatments including ALG associated to cyclosporine, with a low SMD/AML incidence rate.

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  • (PMID = 16830141.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgens; 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents
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41. Duhoux F, Libouton J, Bahloula K, Ameye G, Poirel HA: Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):11037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies.
  • It has been shown to be involved in the reciprocal translocation t(1;3)(p36;q21) and more rarely the t(1;21)(p36;q22) which both occur in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML).
  • This overexpression might play an important role in the pathogenesis of MDS and AML in blocking myeloid differentiation.
  • METHODS: We studied 35 myeloid malignancies, 12 lymphoid malignancies and 3 undifferentiated acute leukemias with 1p36 abnormalities by fluorescent in situ hybridization (FISH) with a bacterial artificial chromosomes (BAC) contig containing 50 BAC probes on 1p36.
  • RESULTS: In addition to the known t(1;3)(p36;q21) (11 cases) and t(1;21)(p36;q22) (1 case) involving RPN1 andAML1/RUNX1 respectively in myeloid malignancies, we specifically found PRDM16 to be rearranged in 4 additional translocations : a t(1;12)(p36;p13) in an AML-M4, a t(1;7)(p36;p12) in a MDS, an add(1)(p36) in an AML-M2 and a t(1;2)(p36;p12) in a relapsed AML-M4.
  • CONCLUSIONS: In our series of 50 cases of hematological malignancies with 1p36 abnormalities, PRDM16 was involved in about 45% of myeloid malignancies, and was never involved in lymphoid malignancies.
  • Interestingly, the shortest isoform of MDS/EVI-1, lacking the PR domain, is supposed to have an oncogenic effect due to its translocation-induced upregulation in AML.
  • Further characterization of these new partner genes and functional studies should give us more insight into the pathogenesis of AML and MDS mediated by PRDM16, and the role of its partner genes.

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  • (PMID = 27964015.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Padmanabhan A, Baker JA, Zirpoli G, Sait SN, Ford LA, Moysich KB, Baer MR: Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members. Leuk Res; 2008 Dec;32(12):1820-3
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  • [Title] Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members.
  • Adjuvant chemotherapy and radiation therapy for breast cancer are associated with therapy-related acute myeloid leukemia (AML)/myelodysplastic syndromes (MDS), but little is known about additional risk factors.
  • Thirty-four patients with AML (n=26)/MDS (n=8) following breast cancer (cases) were compared with 2029 breast cancer patients without AML/MDS (controls).
  • Thus risk factors for AML/MDS following breast cancer include older age, other cancers and multiple first-degree relatives with cancer.
  • [MeSH-major] Breast Neoplasms / complications. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / epidemiology. Neoplasms / complications. Neoplasms, Second Primary / epidemiology


43. Lyman GH, Dale DC, Wolff DA, Culakova E, Poniewierski MS, Kuderer NM, Crawford J: Acute myeloid leukemia or myelodysplastic syndrome in randomized controlled clinical trials of cancer chemotherapy with granulocyte colony-stimulating factor: a systematic review. J Clin Oncol; 2010 Jun 10;28(17):2914-24
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  • [Title] Acute myeloid leukemia or myelodysplastic syndrome in randomized controlled clinical trials of cancer chemotherapy with granulocyte colony-stimulating factor: a systematic review.
  • PURPOSE: To evaluate the risk of acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) and overall mortality in patients receiving chemotherapy with or without granulocyte colony-stimulating factor (G-CSF), a systematic review of randomized controlled trials (RCTs) was conducted.
  • Eligibility included solid tumor or lymphoma patients randomly assigned to chemotherapy with or without G-CSF support, > or = 2 years of follow-up, and reporting AML/MDS or all second malignancies.
  • At mean and median follow-up across studies of 60 and 53 months, respectively, AML/MDS was reported in 22 control patients and 43 G-CSF-treated patients, with an estimated RR of 1.92 (95% CI, 1.19 to 3.07; P = .007) and AR increase of 0.41% (95% CI, 0.10% to 0.72%; P = .009).
  • CONCLUSION: Delivered chemotherapy dose-intensity and risk of AML/MDS are increased but all-cause mortality is decreased in patients receiving chemotherapy with G-CSF support.
  • [MeSH-major] Granulocyte Colony-Stimulating Factor / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


44. Tefferi A, Gangat N, Wolanskyj AP, Schwager S, Pardanani A, Lasho TL, Mesa R, McClure RF, Li CY, Hanson CA: 20+ yr without leukemic or fibrotic transformation in essential thrombocythemia or polycythemia vera: predictors at diagnosis. Eur J Haematol; 2008 May;80(5):386-90
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  • OBJECTIVES: The current study identified patients with either essential thrombocythemia (ET) or polycythemia vera (PV) who have survived for at least 20 yr without the development of either acute myeloid leukemia/myelodysplastic syndrome (AML/MDS) or myelofibrosis (MF) and compared their presenting features with those in whom these complications occurred in the first 10 yr of disease.
  • In both instances, three distinct groups were delineated and their presenting features compared; group A included patients who have remained AML/MDS/MF free after a minimum follow-up of 20 yr; groups B and C included patients who developed either AML/MDS or MF, respectively, in the first decade of their disease.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Fibrosis / pathology. Humans. Leukemia / pathology. Male. Middle Aged. Time Factors


45. Shimoni A, Hardan I, Shem-Tov N, Yeshurun M, Yerushalmi R, Avigdor A, Ben-Bassat I, Nagler A: Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: the role of dose intensity. Leukemia; 2006 Feb;20(2):322-8
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  • [Title] Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: the role of dose intensity.
  • Allogeneic stem-cell transplantation (SCT) with both myeloablative and reduced-intensity conditioning (RIC) is an effective therapy in AML/MDS.
  • To define the role of dose intensity, we analyzed SCT outcomes of 112 consecutive patients with AML/MDS.
  • Myeloablative and RIC regimens had similar outcomes when leukemia was in remission at SCT; however, patients with active disease could only be salvaged by myeloablative conditioning.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myeloablative Agonists / therapeutic use. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Transplantation, Homologous. Treatment Outcome


46. Daskalakis M, Blagitko-Dorfs N, Hackanson B: Decitabine. Recent Results Cancer Res; 2010;184:131-57
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  • Multiple clinical trials have shown the promising activity of low-dose decitabine in AML, MDS, CML, and hemoglobinopathies, whereas its efficacy in solid tumors is rather limited.Clinical responses appear to be induced by both epigenetic alterations and the induction of cell-cycle arrest and/or apoptosis.
  • [MeSH-minor] Animals. Humans. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Primary Myelofibrosis / drug therapy. Stem Cell Transplantation. Transplantation, Homologous

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  • (PMID = 20072836.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
  • [Number-of-references] 161
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47. La Starza R, Aventin A, Matteucci C, Crescenzi B, Romoli S, Testoni N, Pierini V, Ciolli S, Sambani C, Locasciulli A, Di Bona E, Lafage-Pochitaloff M, Martelli MF, Marynen P, Mecucci C: Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia. Leukemia; 2006 Jun;20(6):958-64
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  • [Title] Genomic gain at 6p21: a new cryptic molecular rearrangement in secondary myelodysplastic syndrome and acute myeloid leukemia.
  • Fluorescence in situ hybridization and comparative genomic hybridization characterized 6p rearrangements in eight primary and in 10 secondary myeloid disorders (including one patient with Fanconi anemia) and found different molecular lesions in each group.
  • In the 10 patients with secondary acute myeloid leukemia/myelodysplastic syndrome (AML/MDS), the short arm of chromosome 6 was involved in unbalanced translocations in 7.
  • Consequently, in secondary AML/MDS, we hypothesize that 6p gains are major pathogenetic events arising from acquired and/or congenital genomic instability.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Sensitivity and Specificity


48. Andersson BS, de Lima M, Thall PF, Madden T, Russell JA, Champlin RE: Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia. Curr Opin Oncol; 2009 Jun;21 Suppl 1:S11-5
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  • [Title] Reduced-toxicity conditioning therapy with allogeneic stem cell transplantation for acute leukemia.
  • We hypothesized that standardized systemic drug delivery would improve treatment safety and provide better leukemia control.
  • We used a Bayesian method to compare the outcomes of 67 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) patients who received intravenous busulfan-cyclophosphamide (BuCy2) with 148 subsequent AML/MDS patients who received busulfan-fludarabine (Bu-Flu).
  • Overall, the data support replacing BuCy2 with or without antithymocyte globulin (ATG) with Bu-Flu with or without rabbit-ATG for AML or MDS.
  • The extremely low one-year treatment-related mortality as well as high overall and event-free survival of patients in the Bu-Flu group indicate that it is time to revisit the value of alloSCT compared with conventional maintenance chemotherapy for patients in first complete remission of AML/MDS.

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  • (PMID = 19561406.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS588342; NLM/ PMC4037323
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49. Lee HJ, Oran B, Saliba RM, Couriel DM, Shin K, Massey P, Neumann J, de Lima M, Champlin R, Giralt S: Steroid myopathy in patients with acute graft-versus-host disease treated with high-dose steroid therapy. Bone Marrow Transplant; 2006 Aug;38(4):299-303
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  • [Title] Steroid myopathy in patients with acute graft-versus-host disease treated with high-dose steroid therapy.
  • High-dose steroids are the first line of treatment for acute graft-versus-host disease (aGVHD).
  • To determine the frequency and severity of steroid myopathy and other steroid related complications in patients with acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) who developed grade >or=2 aGVHD after allogeneic hematopoietic stem cell transplantation (HSCT), we performed a retrospective analysis.
  • Patients were included in the analysis if they had a diagnosis of AML/MDS, underwent an allogeneic HSCT between January 1996 and December 2001 and developed grade >or=2 aGVHD that was treated with 2 mg/kg of methylprednisolone and survived at least 100 days post transplant.
  • We concluded that steroid myopathy is a common complication of high-dose steroid therapy after allogeneic HSCT in AML/MDS.
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Hematopoietic Stem Cell Transplantation / adverse effects. Humans. Leukemia, Myeloid / complications. Leukemia, Myeloid / therapy. Male. Methylprednisolone / administration & dosage. Methylprednisolone / toxicity. Middle Aged. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / therapy. Retrospective Studies

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  • (PMID = 16819437.001).
  • [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 / Steroids; X4W7ZR7023 / Methylprednisolone
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50. Ciurea SO, Saliba R, Rondon G, Pesoa S, Cano P, Fernandez-Vina M, Qureshi S, Worth LL, McMannis J, Kebriaei P, Jones RB, Korbling M, Qazilbash M, Shpall EJ, Giralt S, de Lima M, Champlin RE, Gajewski J: Reduced-intensity conditioning using fludarabine, melphalan and thiotepa for adult patients undergoing haploidentical SCT. Bone Marrow Transplant; 2010 Mar;45(3):429-36
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  • A total of 21 out of 22 patients with AML/myelodysplastic syndrome (MDS) achieved remission after transplant (16 with relapsed/refractory AML).
  • Five out of the 12 patients (42%) with AML/MDS with <15% BM blasts survived long term as compared with none with more advanced disease (P=0.03).
  • HaploSCT with this fludarabine, melphalan and thiotepa and ATG RIC is an effective, well-tolerated conditioning regimen for patients with AML/MDS with low disease burden at the time of transplant and allowed a high rate of engraftment in patients without DSA.
  • [MeSH-minor] Adolescent. Adult. Antilymphocyte Serum / administration & dosage. Child. Female. Hematologic Neoplasms / therapy. Humans. Infection / etiology. Leukemia, Myeloid, Acute / therapy. Male. Melphalan / administration & dosage. Middle Aged. Myelodysplastic Syndromes / therapy. Survival Rate. T-Lymphocytes / immunology. Thiotepa / administration & dosage. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult

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  • (PMID = 19668237.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Myeloablative Agonists; 905Z5W3GKH / Thiotepa; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS598753; NLM/ PMC4080627
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51. Lessard M, Hélias C, Struski S, Perrusson N, Uettwiller F, Mozziconacci MJ, Lafage-Pochitaloff M, Dastugue N, Terré C, Brizard F, Cornillet-Lefebvre P, Mugneret F, Barin C, Herry A, Luquet I, Desangles F, Michaux L, Verellen-Dumoulin C, Perrot C, Van den Akker J, Lespinasse J, Eclache V, Berger R, Groupe Francophone de Cytogénétique Hématologique: Fluorescence in situ hybridization analysis of 110 hematopoietic disorders with chromosome 5 abnormalities: do de novo and therapy-related myelodysplastic syndrome-acute myeloid leukemia actually differ? Cancer Genet Cytogenet; 2007 Jul 1;176(1):1-21
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  • [Title] Fluorescence in situ hybridization analysis of 110 hematopoietic disorders with chromosome 5 abnormalities: do de novo and therapy-related myelodysplastic syndrome-acute myeloid leukemia actually differ?
  • A retrospective cytogenetic study of acute myeloid leukemias (AML) and myelodysplastic syndromes (MDS) was conducted by the Groupe Francophone de Cytogénétique Hématologique (GFCH) to evaluate the structural abnormalities of chromosome 5 associated with other chromosomal abnormalities, in particular of chromosome 7, in these pathologies.
  • In all, 110 cases of AML/MDS were recruited based on the presence of chromosome 5 abnormalities under conventional cytogenetics and supplemented by a systematic fluorescence in situ hybridization study of chromosomes 5 and 7.
  • Among 82 patients with de novo AML/MDS, 63 were older than 60 years.
  • Systematic investigation of the exposure to mutagens and oncogenes is thus essential to specify the factors potentially involved in MDS/AML with 5q abnormalities.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5. Chromosomes, Human, Pair 7. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Chromosome Deletion. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasms, Radiation-Induced. Translocation, Genetic


52. Joslin JM, Fernald AA, Tennant TR, Davis EM, Kogan SC, Anastasi J, Crispino JD, Le Beau MM: Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders. Blood; 2007 Jul 15;110(2):719-26
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  • [Title] Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders.
  • Loss of a whole chromosome 5 or a deletion of the long arm, del(5q), is a recurring abnormality in myelodysplastic syndromes (MDSs) and acute myeloid leukemia (AML).
  • To identify a leukemia-related gene on chromosome 5, we previously delineated a 970-kb segment of 5q31 that is deleted in all patients examined, and prepared a transcript map of this region.
  • To test the hypothesis that loss of function of Egr1 is an initiating event in the pathogenesis of AML/MDS, Egr1-deficient mice were treated with a potent DNA alkylating agent, N-ethyl-nitrosourea (ENU), to induce secondary cooperating mutations.
  • Our data suggest that haploinsufficiency for Egr1 plays a role in murine leukemogenesis, and in the development of AML/MDS characterized by abnormalities of chromosome 5.

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  • (PMID = 17420284.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-06; United States / NCI NIH HHS / CA / CA101774-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse
  • [Other-IDs] NLM/ PMC1924479
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53. Kremser A, Dressig J, Grabrucker C, Liepert A, Kroell T, Scholl N, Schmid C, Tischer J, Kufner S, Salih H, Kolb HJ, Schmetzer H: Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods. J Immunother; 2010 Feb-Mar;33(2):185-99
The Lens. Cited by Patents in .

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  • [Title] Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods.
  • Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
  • We studied the capability of 6 serum-free DC culture methods, chosen according to different mechanisms, to induce DC differentiation in 137 cases of AML and 52 cases of MDS.
  • Comparing these methods on average 15% to 32% DC, depending on methods used, could be obtained from blast-containing mononuclear cells (MNC) in AML/MDS cases with a DC viability of more than 60%.
  • Average results of all culture methods tested were comparable, however not every given case of AML could be differentiated to DC with 1 selected method.
  • [MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology

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  • (PMID = 20139775.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil
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54. Meyers CA, Albitar M, Estey E: Cognitive impairment, fatigue, and cytokine levels in patients with acute myelogenous leukemia or myelodysplastic syndrome. Cancer; 2005 Aug 15;104(4):788-93
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  • [Title] Cognitive impairment, fatigue, and cytokine levels in patients with acute myelogenous leukemia or myelodysplastic syndrome.
  • BACKGROUND: The objective of the current study was to assess the correlations between cognitive function, fatigue, quality of life, and circulating cytokine levels in patients with acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).
  • METHODS: Fifty-four patients with AML/MDS were seen for pretreatment evaluation of their cognitive function and symptoms.
  • CONCLUSIONS: Patients with AML/MDS are highly symptomatic and experience cognitive impairment and fatigue before the initiation of their treatment.
  • [MeSH-major] Cognition Disorders / etiology. Cytokines / blood. Fatigue / etiology. Leukemia, Myeloid, Acute / complications. Myelodysplastic Syndromes / complications


55. Stam WB, O'Sullivan AK, Rijnders B, Lugtenburg E, Span LF, Janssen JJ, Jansen JP: Economic evaluation of posaconazole vs. standard azole prophylaxis in high risk neutropenic patients in the Netherlands. Eur J Haematol; 2008 Dec;81(6):467-74
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  • BACKGROUND: Acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients experience prolonged neutropenia after treatment with intensive chemotherapy, leading to a high risk of invasive fungal infections (IFI).
  • METHODS: A decision-tree model was developed using data from a randomized trial that compared posaconazole and standard azole (fluconazole or itraconazole) prophylaxis in neutropenic patients receiving remission-induction chemotherapy for AML/MDS (Cornely et al., N Engl J Med 2007;356:348-359).
  • Following initiation of prophylaxis, clinical events are modeled with chance nodes reflecting probabilities of IFIs, IFI-related death, and death from other causes.
  • CONCLUSION: Given the underlying data and assumptions, the economic evaluation demonstrated that posaconazole prophylaxis is expected to be cost-effective compared with fluconazole/itraconazole in neutropenic AML/MDS patients after intensive chemotherapy.
  • [MeSH-major] Antifungal Agents / economics. Fluconazole / economics. Itraconazole / economics. Leukemia, Myeloid, Acute / economics. Mycoses / economics. Myelodysplastic Syndromes / economics. Neutropenia / economics. Triazoles / economics

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  • (PMID = 18754857.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 304NUG5GF4 / Itraconazole; 6TK1G07BHZ / posaconazole; 8VZV102JFY / Fluconazole
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56. Zatkova A, Merk S, Wendehack M, Bilban M, Muzik EM, Muradyan A, Haferlach C, Haferlach T, Wimmer K, Fonatsch C, Ullmann R: AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes. Genes Chromosomes Cancer; 2009 Jun;48(6):510-20
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  • [Title] AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes.
  • AML/MDS patients carrying 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are characterized by a complex aberrant karyotype (CAK) frequently including deletions within 5q, 17p, and 7q, older age and fast progression of the disease with extremely poor prognosis.
  • In this study, we investigated 19 patients with AML/MDS and MLL gain/amplification.
  • Furthermore, we demonstrate that the gene expression signature can be used to discriminate AML/MDS with MLL amplification from several other types of AML.
  • [MeSH-major] Gene Dosage. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19306356.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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57. Storb R: Reduced-intensity conditioning transplantation in myeloid malignancies. Curr Opin Oncol; 2009 Jun;21 Suppl 1:S3-5
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  • [Title] Reduced-intensity conditioning transplantation in myeloid malignancies.
  • The development of non-myeloablative and reduced-intensity conditioning regimens has enabled older or medically infirm patients with myeloid malignancies to be treated with allogeneic hematopoietic cell transplantation (HCT).
  • The regimens are sufficiently immunosuppressive to allow engraftment of allogeneic cells and they rely largely on graft-versus-leukemia effects rather than high-dose cytotoxic therapy to eliminate malignant cells.
  • Overall 2-5-year survivals after allogeneic HCT in older patients with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS) have ranged from 25% to 64%.
  • Despite still existing problems, early results in elderly patients with AML/MDS have been encouraging.

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  • (PMID = 19561410.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA015704; United States / NHLBI NIH HHS / HL / HL036444; United States / NCI NIH HHS / CA / CA078902; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA018029; United States / NCI NIH HHS / CA / P01 CA018029-36; United States / NCI NIH HHS / CA / P01 CA078902-13; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / P01 CA078902; United States / NHLBI NIH HHS / HL / P01 HL036444-30; United States / NCI NIH HHS / CA / P30 CA015704-37; United States / NCI NIH HHS / CA / CA078902-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 9
  • [Other-IDs] NLM/ NIHMS211792; NLM/ PMC2895692
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58. Bacher U, Haferlach C, Schnittger S, Kohlmann A, Kern W, Haferlach T: Mutations of the TET2 and CBL genes: novel molecular markers in myeloid malignancies. Ann Hematol; 2010 Jul;89(7):643-52
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  • [Title] Mutations of the TET2 and CBL genes: novel molecular markers in myeloid malignancies.
  • Despite recent progress in molecular research in myeloid malignancies, in subsets of patients with myelodysplastic syndrome (MDS) so far no underlying mutation was identified.
  • In acute myeloid leukemia (AML), clinical variability exists within distinct subgroups.
  • Sequencing studies revealed heterogeneous mutations in 10-25% of patients with acute myeloid leukemia (AML), MDS, and MPNs, while the frequency might be higher in chronic myelomonocytic leukemia (CMML).
  • In rare cases of human AML (<2%), CBL mutants were identified, with a higher frequency in core binding factor leukemias.
  • These novel mutations deepened insights in the mechanisms of leukemogenesis, might contribute to the identification of new therapeutic targets, and improve diagnostics in the myeloid malignancies.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromosomes, Human, Pair 4 / metabolism. DNA-Binding Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism. Mutation. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-cbl / metabolism
  • [MeSH-minor] Humans. Myelodysplastic Syndromes

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  • (PMID = 20195608.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Number-of-references] 57
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59. Braun T, Fenaux P: Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia. Br J Haematol; 2008 May;141(5):576-86
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  • [Title] Farnesyltransferase inhibitors and their potential role in therapy for myelodysplastic syndromes and acute myeloid leukaemia.
  • Novel strategies are required for treatment of acute myeloid leukaemia (AML) and higher risk myelodysplastic syndrome (MDS) patients who are not eligible for intensive chemotherapy and/or allogenic stem cell transplantation.
  • Clinical phase II studies with the oral FTIs tipifarnib and lonafarnib in previously untreated AML, MDS and chronic myelomonocytic leukaemia yielded rather encouraging results while results in relapsed and/or refractory AML were disappointing.
  • Results of a phase III trial in untreated AML in the elderly with tipifarnib were also disappointing.
  • The combination of existing FTIs with other treatments, such as chemotherapy (in AML) and hypomethylating agents (in MDS and AML), is under investigation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Farnesyltranstransferase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


60. Nemoto N, Suzukawa K, Shimizu S, Shinagawa A, Takei N, Taki T, Hayashi Y, Kojima H, Kawakami Y, Nagasawa T: Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23). Genes Chromosomes Cancer; 2007 Sep;46(9):813-9
SciCrunch. OMIM: Data: Gene Annotation .

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  • [Title] Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23).
  • We have identified a novel fusion partner of MLL, namely the mastermind like 2 (MAML2 gene), in secondary acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with inv(11)(q21q23).
  • RT-PCR and sequencing revealed that exon 7 of MLL was fused to exon 2 of MAML2 in the AML and MDS cells.
  • MLL-MAML2 in secondary AML/MDS and MECT1-MAML2 in mucoepithelioid carcinoma, benign Wartin's tumor, and clear cell hidradenoma consist of the same COOH-terminal part of MAML2.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics


61. Beyer V, Mühlematter D, Parlier V, Cabrol C, Bougeon-Mamin S, Solenthaler M, Tobler A, Pugin P, Gregor M, Hitz F, Hess U, Chapuis B, Laurencet F, Schanz U, Schmidt PM, van Melle G, Jotterand M: Polysomy 8 defines a clinico-cytogenetic entity representing a subset of myeloid hematologic malignancies associated with a poor prognosis: report on a cohort of 12 patients and review of 105 published cases. Cancer Genet Cytogenet; 2005 Jul 15;160(2):97-119
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  • [Title] Polysomy 8 defines a clinico-cytogenetic entity representing a subset of myeloid hematologic malignancies associated with a poor prognosis: report on a cohort of 12 patients and review of 105 published cases.
  • Here we report on a series of 12 patients with acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), or myeloproliferative disorder (MPD) associated with polysomy 8 as detected by conventional cytogenetics and fluorescence in situ hybridization (FISH).
  • Our study demonstrates the existence of a polysomy 8 syndrome, which represents a subtype of AML, MDS, and MPD characterized by a high incidence of secondary diseases, myelomonocytic or monocytic involvement in AML and poor overall survival (6 months).
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Prognosis. Survival Rate

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  • (PMID = 15993266.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 140
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62. Ye Y, McDevitt MA, Guo M, Zhang W, Galm O, Gore SD, Karp JE, Maciejewski JP, Kowalski J, Tsai HL, Gondek LP, Tsai HC, Wang X, Hooker C, Smith BD, Carraway HE, Herman JG: Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies. Cancer Res; 2009 Nov 1;69(21):8482-90
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  • [Title] Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies.
  • Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).
  • This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in AML and MDS.
  • In 146 AML cases, methylation of CTNNA1 was frequent, and more common in AML patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed.
  • In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (>or=RAEB2), but not in low-risk MDS (<RAEB2), indicating that CTNNA1 methylation might be important in the transformation of MDS to AML.
  • CTNNA1 expression was lowest in AML/MDS patients with CTNNA1 methylation, although reduced expression was found in some patients without promoter methylation.
  • Repressive chromatin marks (H3K27me3) at the promoter were identified in CTNNA1-repressed AML cell lines and primary leukemias, with the most repressive state correlating with DNA methylation.
  • These results suggest progressive, acquired epigenetic inactivation at CTNNA1, including histone modifications and promoter CpG methylation, as a component of leukemia progression in patients with both 5q- and non-5q- myeloid malignancies.

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  • (PMID = 19826047.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA058184-090013; United States / NCI NIH HHS / CA / P50 CA058184; United States / NCI NIH HHS / CA / P50 CA058184-090013
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNA1 protein, human; 0 / Chromatin; 0 / RNA, Messenger; 0 / alpha Catenin; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ NIHMS142652; NLM/ PMC3081599
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63. Pulliam-Leath AC, Ciccone SL, Nalepa G, Li X, Si Y, Miravalle L, Smith D, Yuan J, Li J, Anur P, Orazi A, Vance GH, Yang FC, Hanenberg H, Bagby GC, Clapp DW: Genetic disruption of both Fancc and Fancg in mice recapitulates the hematopoietic manifestations of Fanconi anemia. Blood; 2010 Oct 21;116(16):2915-20
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  • Fanconi anemia (FA) is an inherited chromosomal instability syndrome characterized by bone marrow failure, myelodysplasia (MDS), and acute myeloid leukemia (AML).
  • Here we show that double-mutant Fancc(-/-);Fancg(-/-) mice develop spontaneous hematologic sequelae including bone marrow failure, AML, MDS and complex random chromosomal abnormalities that the single-mutant mice do not.
  • Importantly, this model closely recapitulates the phenotypes found in FA patients and may be useful as a preclinical platform to evaluate the molecular pathogenesis of spontaneous bone marrow failure, MDS and AML in FA.


64. Lübbert M, Müller-Tidow C, Hofmann WK, Koeffler HP: Advances in the treatment of acute myeloid leukemia: from chromosomal aberrations to biologically targeted therapy. J Cell Biochem; 2008 Aug 15;104(6):2059-70
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  • [Title] Advances in the treatment of acute myeloid leukemia: from chromosomal aberrations to biologically targeted therapy.
  • We describe several recent advances in our understanding and treatment of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) including the use of cytogenetics to classify these diseases and to identify therapies that are specific for the abnormalities.
  • The two clear successes include the use of retinoic acid for acute promyelocytic leukemia and tyrosine kinase inhibitors (e.g., imatinib) for chronic myelogenous leukemia.
  • Very recent results suggest a particular activity of lenalidomide, an analogue of thalidomide, in MDS patients with deletions of the long arm of chromosome 5 (so-called 5q minus syndrome), and notable activity of azanucleoside DNA demethylating agents in MDS with loss of chromosome 7.
  • However, for the vast majority of cytogenetic abnormalities found in AML/MDS, no specific therapies have been identified.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 18613031.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA109295; United States / NCI NIH HHS / CA / 5R01CA026038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 90
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65. Bunin N, Aplenc R, Leahey A, Magira E, Grupp S, Pierson G, Monos D: Outcomes of transplantation with partial T-cell depletion of matched or mismatched unrelated or partially matched related donor bone marrow in children and adolescents with leukemias. Bone Marrow Transplant; 2005 Jan;35(2):151-8
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  • Relapse occurred in 6% of ALL patients, and 22.8% of AML/MDS patients.
  • [MeSH-major] Bone Marrow Transplantation / methods. Histocompatibility. Leukemia / therapy. Lymphocyte Depletion / methods


66. Davidsson J, Paulsson K, Johansson B: Multicolor fluorescence in situ hybridization characterization of cytogenetically polyclonal hematologic malignancies. Cancer Genet Cytogenet; 2005 Dec;163(2):180-3
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  • Occasionally, however, clones with unrelated karyotypic anomalies are found, as, for example, in approximately 2% of acute myeloid leukemias (AML), myelodysplastic syndromes (MDS), and chronic myeloproliferative disorders (CMD).
  • Fourteen AML, MDS, and CMD cases were investigated.
  • In none of these was a cryptic aberration found, common to all subclones, although the karyotypes were revised in two AMLs and one MDS.

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  • (PMID = 16337865.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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67. Verma D, O'Brien S, Thomas D, Faderl S, Koller C, Pierce S, Kebriaei P, Garcia-Manero G, Cortes J, Kantarjian H, Ravandi F: Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens. Cancer; 2009 Jan 1;115(1):101-6
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  • [Title] Therapy-related acute myelogenous leukemia and myelodysplastic syndrome in patients with acute lymphoblastic leukemia treated with the hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone regimens.
  • BACKGROUND: Secondary malignancies including myeloid neoplasms occur infrequently in acute lymphoblastic leukemia (ALL) and to the authors' knowledge have not been as well documented in adults as in children.
  • RESULTS: Sixteen patients (2.49%) developed secondary acute myelogenous leukemia (AML) (6 patients) or myelodysplastic syndrome (MDS) (10 patients).
  • Karyotype at time of AML/MDS diagnosis was -5, -7 in 9 patients, normal in 1 patient, complex in 1 patient, inv(11) in 1 patient, t(4;11) in 1 patient, del(20) in 1 patient, and unavailable in 2 patients.
  • Secondary AML/MDS developed at a median of 32 months after ALL diagnosis.
  • Cytarabine plus anthracycline-based treatment was given to 12 patients with AML and high-risk MDS.
  • One patient with MDS received arsenic trioxide, 1 received clofarabine, and 2 received decitabine.
  • Eight patients (1 with AML and 7 with MDS) underwent allogeneic stem cell transplantation, and all but 2 died at a median of 3 months (range, 0.5-11 months) after transplantation.
  • The median overall survival after a diagnosis of secondary AML and MDS was 9.25 months (range, 1+ to 26+ months).
  • CONCLUSIONS: Secondary AML and MDS occur infrequently in adult patients with de novo ALL treated with the hyper-CVAD regimens, and response to therapy is poor.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


68. Mackinnon RN, Selan C, Wall M, Baker E, Nandurkar H, Campbell LJ: The paradox of 20q11.21 amplification in a subset of cases of myeloid malignancy with chromosome 20 deletion. Genes Chromosomes Cancer; 2010 Nov;49(11):998-1013
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  • [Title] The paradox of 20q11.21 amplification in a subset of cases of myeloid malignancy with chromosome 20 deletion.
  • Deletion of the long arm of one chromosome 20 (del(20q)) is a well-recognized abnormality in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) and is presumed to cause loss of a tumor suppressor gene at 20q12.
  • In a previously published series of MDS and AML cases, which had lost this region via unbalanced translocation, around 40% of cases were shown to have additional copies of the chromosome 20 abnormalities, with resulting gain or amplification of the retained parts of chromosome 20, most often 20q11.2.
  • Localized and high level amplification of the common 250 kb region is evidence for activation of an oncogene in this region in these MDS and AML cases.
  • Cases with 20q11.21 amplification tended to have a high proportion of erythroblasts in the marrow, with two cases diagnosed as erythroleukemia (AML-M6).
  • Chromosome sub-band 20q11.21 amplification may therefore prove to be a marker of a specific subset of AML/MDS with a significant erythroid component.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 20. Myelodysplastic Syndromes / genetics

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20645416.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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69. Liu YQ, Qiu HX, Li JY, Xu W, Xu J, Lü X, Wu HX: [Secondary acute myeloid leukemia complicated after treatment of non-Hodgkin's lymphoma]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):756-9
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  • [Title] [Secondary acute myeloid leukemia complicated after treatment of non-Hodgkin's lymphoma].
  • The aim of this study was to investigate the mechanism, susceptibility, (18)F-FDG positron emission computerized tomography ((18)F-FDG PET/CT) features and the treatment of therapy-related acute myeloid leukemia.
  • One patient with NHL was affected with t-MDS after treatment and then progressed to t-AML.
  • The interval time from the chemotherapy of NHL to the occurrence of t-MDS was 105 months and t-MDS progressed to AML-M(2) in 2 months.
  • Karyotype analysis results of t-MDS and t-AML were normal. (18)F-FDG PET indicated that the FDG uptake in the bone raised diffusely.
  • In conclusion, the occurrence of t-AML/MDS may be associated with the application of the cytotoxic chemotherapeutics. (18)F-FDG PET may be an indicator predicting the transformation of t-MDS to t-AML.


70. Nakamura S, Okinaka K, Hirano I, Ono T, Sugimoto Y, Shigeno K, Fujisawa S, Shinjo K, Ohnishi K: KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells. Leuk Res; 2008 Sep;32(9):1358-65
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  • [Title] KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.
  • We showed that KIS protein directly interacted with p27(Kip1) protein, and reduction of KIS inhibited the S10 phosphorylation of p27(Kip1) in leukemia cells.
  • We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.
  • Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).
  • This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells.
  • [MeSH-major] Cell Cycle / physiology. Cell Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Intracellular Signaling Peptides and Proteins / physiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein-Serine-Threonine Kinases / physiology

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  • (PMID = 18384876.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human
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71. Lim ZY, Pearce L, Ho AY, Barber L, Ingram W, Usai M, Tobal K, Devereux S, Pagliuca A, Mufti GJ: Delayed attainment of full donor chimaerism following alemtuzumab-based reduced-intensity conditioning haematopoeitic stem cell transplantation for acute myeloid leukaemia and myelodysplastic syndromes is associated with improved outcomes. Br J Haematol; 2007 Aug;138(4):517-26
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  • [Title] Delayed attainment of full donor chimaerism following alemtuzumab-based reduced-intensity conditioning haematopoeitic stem cell transplantation for acute myeloid leukaemia and myelodysplastic syndromes is associated with improved outcomes.
  • This prospective study evaluated the kinetics of lymphoid (CD3) engraftment in 110 patients with acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) after allogeneic transplantation and conditioning with fludarabine, busulphan and alemtuzumab, using ciclosporin for post-transplant immunosuppression.
  • In patients with AML/MDS undergoing alemetuzumab based-RIC HSCT, prolonged MDC beyond day+100 is associated with an improved OS.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods


72. Staber P, Langner S, Dornbusch HJ, Neumeister P: Antifungal management in cancer patients. Wien Med Wochenschr; 2007;157(19-20):503-10
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  • Established risk factors are previous fungal infection, neutropenia exceeding 10 days, older age, active cancer, corticosteroid therapy, administration of broad spectrum antibiotics, allogeneic HSCT, central venous catheter and organ dysfunction.
  • Benefit of antifungal prophylaxis has been proven for fluconazole (400 mg/d) in allogeneic transplant recipients, and for posaconazole (600 mg/d) in patients during AML/MDS induction chemotherapy as well as in patients with GvHD.

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  • (PMID = 18030555.001).
  • [ISSN] 0043-5341
  • [Journal-full-title] Wiener medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Wien Med Wochenschr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Antifungal Agents
  • [Number-of-references] 61
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73. Shimoni A, Hardan I, Shem-Tov N, Rand A, Yerushalmi R, Nagler A: Fludarabine and treosulfan: a novel modified myeloablative regimen for allogeneic hematopoietic stem-cell transplantation with effective antileukemia activity in patients with acute myeloid leukemia and myelodysplastic syndromes. Leuk Lymphoma; 2007 Dec;48(12):2352-9
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  • [Title] Fludarabine and treosulfan: a novel modified myeloablative regimen for allogeneic hematopoietic stem-cell transplantation with effective antileukemia activity in patients with acute myeloid leukemia and myelodysplastic syndromes.
  • Allogeneic stem-cell transplantation (SCT) is potentially curative treatment for AML and MDS.
  • Treosulfan is an alkylating agent with in vitro cytotoxicity against leukemia as well as myeloablative and immunosuppressive properties when used in escalated doses.
  • We explored a regimen of fludarabine (30 mg/m(2) x 5) and treosulfan (12 gr/m(2) x 3) in 24 patients, median age 55 years (range, 30-69), with AML (n = 19) or MDS (n = 5), not eligible for standard myeloablation.
  • The incidence of acute and chronic GVHD was 15% and 47%, respectively.
  • The fludarabine/treosulfan regimen can be considered a fully intensive, modified myeloablative regimen with effective antileukemia activity and acceptable toxicity in patients with AML/MDS not eligible for standard myeloablation, and merits further study in larger scale studies.
  • [MeSH-major] Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives


74. Rund D, Krichevsky S, Bar-Cohen S, Goldschmidt N, Kedmi M, Malik E, Gural A, Shafran-Tikva S, Ben-Neriah S, Ben-Yehuda D: Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients. Leukemia; 2005 Nov;19(11):1919-28
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  • [Title] Therapy-related leukemia: clinical characteristics and analysis of new molecular risk factors in 96 adult patients.
  • Therapy-related leukemia or myelodysplasia (t-leuk/MDS) is a serious problem that is increasing in frequency.
  • We studied the clinical characteristics of 96 patients (pts) with a mean age of 48 years, and analyzed the molecular parameters that could predispose to t-leuk/MDS.
  • The mean latency until the development of t-AML was 45.5 months.
  • Analysis of drug metabolism and disposition genes showed a protective effect of the CYP3A4 1*B genotype against the development of t-leuk/MDS, whereas the CC genotype of MDR1 C3435T and the NAD(P)H:quinone oxidoreductase1 codon 187 polymorphism were both noncontributory.
  • In conclusion, genetic predisposition as well as epigenetic events contribute to the etiology of t-AML/MDS.
  • [MeSH-major] Genetic Predisposition to Disease. Leukemia / chemically induced. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / genetics

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  • (PMID = 16167058.001).
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 2.7.11.1 / RPS6KA4 protein, human; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 90-kDa
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75. Nelson RP Jr, Yu M, Schwartz JE, Robertson MJ, Hromas R, Fausel CA, Vance GH, Dlouhy SR, Baute JA, Cox EA, Wood LL, Srivastava S, Robertson KA, Haut PR, Farag SS, Abonour R, Cornetta K, Cripe LD: Long-term disease-free survival after nonmyeloablative cyclophosphamide/fludarabine conditioning and related/unrelated allotransplantation for acute myeloid leukemia/myelodysplasia. Bone Marrow Transplant; 2010 Aug;45(8):1300-8
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  • [Title] Long-term disease-free survival after nonmyeloablative cyclophosphamide/fludarabine conditioning and related/unrelated allotransplantation for acute myeloid leukemia/myelodysplasia.
  • A total of 50 consecutive patients (median age, 57.5 years) with AML (n=30) or myelodysplasia (MDS, n=20) underwent HLA matched related donor (MRD, n=27) or unrelated donor (MUD, n=23) peripheral blood hematopoietic cell transplantation after nonmyeloablative CY/fludarabine (Flu) conditioning.
  • Overall grade 3/4 acute GVHD (aGVHD) occurred in 26% in the absence of antecedent mucositis and was associated with chronic GVHD (cGVHD) and poor OS.
  • This study provides further evidence for prolonged DFS after CY/Flu MRD allotransplantation for AML/MDS, and extends the findings to older patients and those with unrelated donors.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods


76. Deschler B, de Witte T, Mertelsmann R, Lübbert M: Treatment decision-making for older patients with high-risk myelodysplastic syndrome or acute myeloid leukemia: problems and approaches. Haematologica; 2006 Nov;91(11):1513-22
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  • [Title] Treatment decision-making for older patients with high-risk myelodysplastic syndrome or acute myeloid leukemia: problems and approaches.
  • BACKGROUND AND OBJECTIVES: High-risk myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are mainly diseases of patients over the age of 60 years.
  • RESULTS: In 36 AML studies involving a total of 12,370 patients (median age 70 years) median overall survival approached 30 weeks for intensively treated patients.
  • In 18 large studies approximately 50% of AML patients received induction therapy, 30% non-intensive chemotherapy and 20% supportive care only.
  • INTERPRETATION AND CONCLUSIONS: Due to the scarcity of randomized AML/MDS trials in which older patients are assigned to either induction or less intense therapy, predictors to identify older patients most likely to benefit from intensive therapy and novel tools to optimize (or even standardize) recommendations are needed.
  • [MeSH-major] Decision Making. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Problem Solving


77. Garcia-Manero G, Yang H, Bueso-Ramos C, Ferrajoli A, Cortes J, Wierda WG, Faderl S, Koller C, Morris G, Rosner G, Loboda A, Fantin VR, Randolph SS, Hardwick JS, Reilly JF, Chen C, Ricker JL, Secrist JP, Richon VM, Frankel SR, Kantarjian HM: Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes. Blood; 2008 Feb 1;111(3):1060-6
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  • [Title] Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes.
  • Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinically in cutaneous T-cell lymphoma and preclinically in leukemia.
  • Patients with relapsed or refractory leukemias or myelodysplastic syndromes (MDS) and untreated patients who were not candidates for chemotherapy were eligible.
  • Of 41 patients, 31 had acute myeloid leukemia (AML), 4 chronic lymphocytic leukemia, 3 MDS, 2 acute lymphoblastic leukemia, and 1 chronic myelocytic leukemia.
  • There were no drug-related deaths; 7 patients had hematologic improvement response, including 2 complete responses and 2 complete responses with incomplete blood count recovery (all with AML treated at/below MTD).
  • Further evaluation of vorinostat in AML/MDS is warranted.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Histone Deacetylase Inhibitors. Hydroxamic Acids / therapeutic use. Leukemia / drug therapy. Leukemia / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology


78. Caramazza D, Hussein K, Siragusa S, Pardanani A, Knudson RA, Ketterling RP, Tefferi A: Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations. Eur J Haematol; 2010 Mar;84(3):191-200
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  • [Title] Chromosome 1 abnormalities in myeloid malignancies: a literature survey and karyotype-phenotype associations.
  • The current review is focused on myeloid malignancies where we summarize the relevant published literature and discuss specific karyotype-phenotype associations.
  • Although occasionally seen in chronic phase MPN, unbalanced 1;7 translocations, e.g. der(1;7)(q10;p10), are usually seen in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and post-MPN AML/MDS.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 1. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics

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  • (PMID = 20002154.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 50
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79. Davis BH, Schwartz M: ZAP-70 expression is low in normal precursor B cells or hematogones. Cytometry B Clin Cytom; 2006 Jul 15;70(4):315-9
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  • BACKGROUND: Zeta-associated protein (ZAP-70) expression has been associated with a less favorable prognosis in chronic lymphocytic leukemia (CLL).
  • In our sample set, the hematogone expression ranged from 2 to 18% of total leukocytes and occurred in a variety of conditions, including CLL, NHL, AML, MDS, Hodgkins Disease, and Multiple Myeloma.
  • [MeSH-major] Hematopoietic Stem Cells / metabolism. Hodgkin Disease / immunology. Leukemia / immunology. Multiple Myeloma / immunology. Myelodysplastic Syndromes / immunology. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / biosynthesis

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  • [Copyright] (c) 2006 International Society for Analytical Cytology.
  • (PMID = 16906572.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38
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80. Klimek VM, Fircanis S, Maslak P, Guernah I, Baum M, Wu N, Panageas K, Wright JJ, Pandolfi PP, Nimer SD: Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes. Clin Cancer Res; 2008 Feb 1;14(3):826-32
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  • [Title] Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes.
  • PURPOSE: Epigenetic modulation of gene expression plays an important role in cancer, including leukemia.
  • The purpose of this study was to evaluate the toxicity, pharmacokinetic profile, and selected pharmacodynamic properties of the histone deacetylase inhibitor depsipeptide in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • EXPERIMENTAL DESIGN: Depsipeptide was administered to MDS or AML patients at a (solid tumor) phase I dose of 18 mg/m(2) i.v. on days 1 and 5 every 3 weeks.
  • RESULTS: Twelve patients (nine with AML, three with MDS) received one to five cycles of depsipeptide.
  • The best response of 11 assessed patients was one complete remission in a patient with AML, stable disease in six patients, and progression of disease in four patients.
  • Exploratory laboratory studies showed modest but rapid increases in apoptosis and changes in myeloid maturation marker expression.
  • Depsipeptide monotherapy has limited clinical activity in unselected AML/MDS patients.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Depsipeptides / pharmacokinetics. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


81. Büchner T, Berdel WE, Schoch C, Haferlach T, Serve HL, Kienast J, Schnittger S, Kern W, Tchinda J, Reichle A, Lengfelder E, Staib P, Ludwig WD, Aul C, Eimermacher H, Balleisen L, Sauerland MC, Heinecke A, Wörmann B, Hiddemann W: Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia. J Clin Oncol; 2006 Jun 1;24(16):2480-9
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  • [Title] Double induction containing either two courses or one course of high-dose cytarabine plus mitoxantrone and postremission therapy by either autologous stem-cell transplantation or by prolonged maintenance for acute myeloid leukemia.
  • PURPOSE: Intensification by high-dose cytarabine in postremission or induction therapy and prolonged maintenance are established strategies to improve the outcome in patients with acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: A total of 1,770 patients (age 16 to 85 years) with de novo or secondary AML or high-risk myelodysplastic syndrome (MDS) were randomly assigned upfront for induction therapy containing one course with standard dose and one course with high-dose cytarabine, or two courses with high-dose cytarabine, and in the same step received postremission prolonged maintenance or busulfan/cyclophosphamide chemotherapy with autologous stem-cell transplantation.
  • There was no significant difference in any prognostic subgroup according to secondary AML/MDS, cytogenetics, WBC, lactate dehydrogenase, and early blast clearance.
  • CONCLUSION: The regimen of one course with standard-dose cytarabine and one course with high-dose cytarabine for induction, and prolonged maintenance for postremission chemotherapy in patients with AML is not improved by additional escalation in cytotoxic treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cytarabine / administration & dosage. Drug Administration Schedule. Female. Humans. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Mitoxantrone / administration & dosage. Multivariate Analysis. Prognosis. Prospective Studies. Remission Induction. Risk Factors. Transplantation, Autologous. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2006 Dec 1;24(34):5471-2; author reply 5472-3 [17135654.001]
  • [ErratumIn] J Clin Oncol. 2011 Jul 1;29(19):2739
  • (PMID = 16735702.001).
  • [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; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; EC 1.1.1.27 / L-Lactate Dehydrogenase
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82. Klisovic RB, Stock W, Cataland S, Klisovic MI, Liu S, Blum W, Green M, Odenike O, Godley L, Burgt JV, Van Laar E, Cullen M, Macleod AR, Besterman JM, Reid GK, Byrd JC, Marcucci G: A phase I biological study of MG98, an oligodeoxynucleotide antisense to DNA methyltransferase 1, in patients with high-risk myelodysplasia and acute myeloid leukemia. Clin Cancer Res; 2008 Apr 15;14(8):2444-9
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  • [Title] A phase I biological study of MG98, an oligodeoxynucleotide antisense to DNA methyltransferase 1, in patients with high-risk myelodysplasia and acute myeloid leukemia.
  • PURPOSE: Epigenetic silencing via aberrant promoter DNA hypermethylation of normal genes has been described as a leukemogenic mechanism in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML).
  • This phase I study was conducted to determine a biologically effective dose and describe the safety of MG98 in MDS/AML.
  • EXPERIMENTAL DESIGN: Twenty-three patients with MDS (n = 11) and AML (n = 12) were enrolled.
  • Despite this, pursuing DNMT1 down-regulation remains a sound approach for targeting aberrant epigenetics in AML/MDS.
  • [MeSH-major] DNA (Cytosine-5-)-Methyltransferase / antagonists & inhibitors. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Oligodeoxyribonucleotides / therapeutic use. Thionucleotides / therapeutic use

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  • (PMID = 18413836.001).
  • [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] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MG 98 phosphorothioate antisense oligodeoxynucleotide; 0 / Oligodeoxyribonucleotides; 0 / RNA, Messenger; 0 / Thionucleotides; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1
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83. Kurata M, Hasegawa M, Nakagawa Y, Abe S, Yamamoto K, Suzuki K, Kitagawa M: Expression dynamics of drug resistance genes, multidrug resistance 1 (MDR1) and lung resistance protein (LRP) during the evolution of overt leukemia in myelodysplastic syndromes. Exp Mol Pathol; 2006 Dec;81(3):249-54
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  • [Title] Expression dynamics of drug resistance genes, multidrug resistance 1 (MDR1) and lung resistance protein (LRP) during the evolution of overt leukemia in myelodysplastic syndromes.
  • It is well-known that leukemic cells of overt leukemia (OL) that have transformed from myelodysplastic syndromes (MDS) are more resistant to chemotherapy as compared with de novo AML cells.
  • Thus, to examine the expression levels of drug-resistant genes and their alterations with the development of OL in MDS, the expression of mRNA for MDR1 and LRP was determined in bone marrow samples from control, de novo AML, MDS, MDS at the time of OL transformation (MDS --> OL), and after transformation (OL) by quantitative real-time RT-PCR.
  • The expression of MDR1 in MDS bone marrow at the time of initial diagnosis was as low as that for control subjects.
  • However, the expression level was significantly elevated at the time of the development of OL (MDS --> OL) compared with the initial MDS subjects (P < 0.05), while expression was relatively reduced after OL development (OL).
  • The expression of LRP was significantly higher in MDS and MDS --> OL samples than control subjects.
  • However, the high expression of LRP in MDS --> OL was significantly reduced after OL development (OL).
  • The expression levels of drug-resistant genes in MDS --> OL or OL were not significantly higher than those of de novo AML samples, although LRP expression in MDS or MDS --> OL was relatively higher than that of de novo AML.
  • Detecting increases in the expression of MDR1 would be useful for predicting OL development in MDS patients.
  • [MeSH-major] Biological Evolution. Gene Expression Regulation, Neoplastic. Leukemia / genetics. Myelodysplastic Syndromes / genetics. P-Glycoprotein / genetics. Vault Ribonucleoprotein Particles / genetics


84. Storlazzi CT, Fioretos T, Surace C, Lonoce A, Mastrorilli A, Strömbeck B, D'Addabbo P, Iacovelli F, Minervini C, Aventin A, Dastugue N, Fonatsch C, Hagemeijer A, Jotterand M, Mühlematter D, Lafage-Pochitaloff M, Nguyen-Khac F, Schoch C, Slovak ML, Smith A, Solè F, Van Roy N, Johansson B, Rocchi M: MYC-containing double minutes in hematologic malignancies: evidence in favor of the episome model and exclusion of MYC as the target gene. Hum Mol Genet; 2006 Mar 15;15(6):933-42
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  • In acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), dmin are observed in approximately 1% of the cases.
  • We have characterized in detail the genomic organization of 32 AML and two MDS cases with MYC-containing dmin.
  • The TRIB1 gene was found over-expressed in only a subset of the AML/MDS cases, whereas MYC, contrary to expectations, was always silent.
  • [MeSH-major] Chromosome Breakage. Gene Targeting. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Plasmids / genetics. Proto-Oncogene Proteins c-myc / genetics

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  • (PMID = 16452126.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA32102
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / TRIB1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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85. Wilking N, Lidbrink E, Wiklund T, Erikstein B, Lindman H, Malmström P, Kellokumpu-Lehtinen P, Bengtsson NO, Söderlund G, Anker G, Wist E, Ottosson S, Salminen E, Ljungman P, Holte H, Nilsson J, Blomqvist C, Bergh J: Long-term follow-up of the SBG 9401 study comparing tailored FEC-based therapy versus marrow-supported high-dose therapy. Ann Oncol; 2007 Apr;18(4):694-700
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  • Ten patients in the tailored FEC regimen developed acute myeloid leukaemia (AML)/myelodysplasia (MDS).
  • CONCLUSION: The update of this study shows an improved outcome linked to the tailored FEC treatment in relation to breast cancer relapse, but also an increased incidence of AML/MDS.

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  • (PMID = 17301072.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
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86. Greiner RA, Meier Y, Papadopoulos G, O'Sullivan AK, Imhof A: Cost-effectiveness of posaconazole compared with standard azole therapy for prevention of invasive fungal infections in patients at high risk in Switzerland. Oncology; 2010;78(3-4):172-80
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  • METHODS: Decision tree models based on the results of two registration trials and subsequent Markov models over patient lifetimes were developed for patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) with neutropenia and for hematopoietic stem cell transplant recipients with graft-versus-host disease (GVHD).
  • RESULTS: By reducing IFIs in AML/MDS patients with posaconazole prophylaxis, the contained IFI-related treatment costs more than compensated for the incremental cost of posaconazole, resulting in savings of CHF 1,118 per patient.
  • [MeSH-minor] Cost-Benefit Analysis. Decision Support Techniques. Graft vs Host Disease / therapy. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Markov Chains. Models, Theoretical. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Neutropenia / complications. Neutropenia / drug therapy. Risk. Switzerland. Treatment Outcome

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20414005.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Triazoles; 6TK1G07BHZ / posaconazole
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87. Chun SM, Kim YL, Choi HB, Oh YT, Kim YJ, Lee S, Kim TG, Yang EG, Park YK, Kim DW, Han BD: Identification of leukemia-specific fusion gene transcripts with a novel oligonucleotide array. Mol Diagn Ther; 2007;11(1):21-8
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  • [Title] Identification of leukemia-specific fusion gene transcripts with a novel oligonucleotide array.
  • BACKGROUND: Identification of specific chromosomal translocations is essential for the diagnosis and prognosis of leukemia.
  • In this study, we employ DNA microarray technology to detect chromosomal aberrations in patients with chronic myeloid leukemia (CML) and acute myeloid leukemia (AML), as well as in leukemic cell lines.
  • A total of 23 sets of oligomers were fabricated on glass slides for the detection of normal and fusion genes, as follows: BCR/ABL, AML/EAP, AML/ETO, AML/MDS, PML/RARA, NUMA1/RARA, PLZF/RARA, and CBFB/MYH.
  • RESULTS: Gene translocation in leukemia was effectively identified with the SOA containing various leukemia-specific fusion and normal control sequences.
  • CONCLUSIONS: Probe sets on SOA can effectively discriminate between leukemia-specific fusion and normal sequences with a chip hybridization procedure.
  • [MeSH-major] Gene Fusion. Leukemia / genetics. Oligonucleotide Array Sequence Analysis. Transcription, Genetic

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  • (PMID = 17286448.001).
  • [ISSN] 1177-1062
  • [Journal-full-title] Molecular diagnosis & therapy
  • [ISO-abbreviation] Mol Diagn Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / DNA, Single-Stranded; 0 / RNA, Neoplasm
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88. Diehl V, Behringer K: Could BEACOPP be the new standard for the treatment of advanced Hodgkin's lymphoma? Cancer Invest; 2006 Jun-Jul;24(4):461-5
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  • These superior BEACOPP results are obtained inspite of a higher rate of secondary AML/MDS in the escalated BEACOPP arm.
  • To reduce acute and long-term toxicity, the GHSG started in the consecutive studies HD12 and HD15 for advanced stage HL to de-escalate BEACOPP by reducing the number of escalated BEACOPP cycles and by applying the baseline dose BEACOPP, a time dense regimen, called BEACOPP-14.

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  • (PMID = 16777701.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; BEACOPP protocol
  • [Number-of-references] 12
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89. Kwon WK, Lee JY, Mun YC, Seong CM, Chung WS, Huh J: Clinical utility of FISH analysis in addition to G-banded karyotype in hematologic malignancies and proposal of a practical approach. Korean J Hematol; 2010 Sep;45(3):171-6
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  • METHODS: Bone marrow aspirates were obtained from 135 patients at diagnosis (56 AML, 32 MDS, 20 ALL, and 27 MM) between 2005 and 2010.
  • Interphase FISH was performed using the following probes: BCR/ABL1, AML1/ETO, PML/RARA, CBFB, MLL, EGR1, CEP8, and D7S486 for AML; CEP8, D20S108, EGR1, and D7S486 for MDS; BCR/ABL1, MLL, CDKN2A (p16), ETV6, and 6q21/c-myc for ALL; IgH, TP53, D13S25, IgH/CCND1, IgH/MAF, IgH/FGFR3, and 1q21/8p21 for MM.
  • RESULTS: Additional genetic aberrations detected by FISH (which were not identified by G-banded karyotype) were 4%, 9%, 50%, and 67% in AML, MDS, ALL, and MM, respectively.
  • CONCLUSION: These results suggest that performing FISH in addition to G-banded karyotype may contribute little additional genetic information in AML and MDS, whereas routine FISH analysis appears to be an efficient screening method in ALL and MM.

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  • [Cites] Leukemia. 2001 Dec;15(12):1841-7 [11753603.001]
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  • (PMID = 21120205.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983032
  • [Keywords] NOTNLM ; Acute lymphoblastic leukemia / Acute myeloid leukemia / FISH / Karyotype / Multiple myeloma / Myelodysplastic syndrome
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90. de Lima M, Giralt S, Thall PF, de Padua Silva L, Jones RB, Komanduri K, Braun TM, Nguyen HQ, Champlin R, Garcia-Manero G: Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study. Cancer; 2010 Dec 1;116(23):5420-31
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  • [Title] Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study.
  • BACKGROUND: Recurrence is a major cause of treatment failure after allogeneic transplantation for acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS), and treatment options are very limited.
  • Azacitidine is a DNA methyltransferase inhibitor with activity in myeloid disease.
  • CONCLUSIONS: Azacitidine at 32 mg/m2 given for 5 days is safe and can be administered after allogeneic transplant for at least 4 cycles to heavily pretreated AML/MDS patients.
  • [MeSH-major] Azacitidine / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery


91. Broberg K, Huynh E, Schläwicke Engström K, Björk J, Albin M, Ingvar C, Olsson H, Höglund M: Association between polymorphisms in RMI1, TOP3A, and BLM and risk of cancer, a case-control study. BMC Cancer; 2009;9:140
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  • BACKGROUND: Mutations altering BLM function are associated with highly elevated cancer susceptibility (Bloom syndrome).
  • METHODS: In this study we have studied 26 tagged single nucleotide polymorphisms (tagSNPs) in RMI1, TOP3A, and BLM and their associations with cancer risk in acute myeloid leukemia/myelodysplatic syndromes (AML/MDS; N = 152), malignant melanoma (N = 170), and bladder cancer (N = 61).

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  • (PMID = 19432957.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / RMI1 protein, human; EC 3.6.1.- / Bloom syndrome protein; EC 3.6.4.12 / RecQ Helicases; EC 5.99.1.2 / DNA Topoisomerases, Type I; EC 5.99.1.2 / DNA topoisomerase III
  • [Other-IDs] NLM/ PMC2685436
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92. Hu J, Shekhter-Levin S, Shaw PH, Bay C, Kochmar S, Surti U: A case of myelodysplastic syndrome with acquired monosomy 7 in a child with a constitutional t(1;19) and a mosaicism for trisomy 21. Cancer Genet Cytogenet; 2005 Jan 1;156(1):62-7
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  • [Title] A case of myelodysplastic syndrome with acquired monosomy 7 in a child with a constitutional t(1;19) and a mosaicism for trisomy 21.
  • A bone marrow aspirate revealed a myelodysplastic syndrome (MDS).
  • It is also possible that the t(1;19) played some role in the development of the MDS.
  • Because acute myelogenous leukemia (AML) and MDS with Down syndrome (DS) have distinct biologic and clinical features, the identification of DS patients with a mild or normal phenotype in the AML/MDS population is of fundamental importance for clinical diagnosis and management.
  • [MeSH-major] Down Syndrome / complications. Monosomy. Mosaicism. Myelodysplastic Syndromes / genetics. Translocation, Genetic


93. Marks R, Potthoff K, Hahn J, Ihorst G, Bertz H, Spyridonidis A, Holler E, Finke JM: Reduced-toxicity conditioning with fludarabine, BCNU, and melphalan in allogeneic hematopoietic cell transplantation: particular activity against advanced hematologic malignancies. Blood; 2008 Jul 15;112(2):415-25
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  • We report on the treatment of 133 patients (median age: 55.6 years [23-73 years]) with acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS; n = 81), myeloproliferative syndromes (MPS; n = 20), and lymphoid malignancies (n = 32) using conditioning with FBM: fludarabine (5 x 30 mg/m(2)), 1,3-bis(2-chloroethyl)-1-nitrosourea (or carmustine, BCNU; 2 x 200 mg/m(2)), and melphalan (140 mg/m(2)).
  • Among patients with AML/MDS, advanced cases (n = 64, including 61 with active disease) showed an OS of 44.6% and 42.4% after 3 and 5 years, respectively.

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  • (PMID = 18451310.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan; U68WG3173Y / Carmustine
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94. Peinert S, Tam CS, Prince HM, Scarlett J, Wolf MM, Januszewicz EH, Westerman D, Seymour JF: Fludarabine based combinations are highly effective as first-line or salvage treatment in patients with Waldenström macroglobulinemia. Leuk Lymphoma; 2010 Dec;51(12):2188-97
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  • Three heavily pretreated patients subsequently developed AML/MDS (one fatal) at 56, 61, and 91 months post F-based treatment.
  • However, a possible contribution to the cumulative risk of treatment-related MDS/AML requires ongoing monitoring.

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  • [CommentIn] Leuk Lymphoma. 2010 Dec;51(12):2152-3 [21067441.001]
  • (PMID = 20939696.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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95. Diehl V, Behringer K: Could BEACOPP be the new standard for the treatment of advanced Hodgkin's lymphoma (HL)? Cancer Invest; 2006 Nov;24(7):713-7
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  • These superior BEACOPP results are obtained inspite of a higher rate of secondary AML/MDS in the esc.
  • The reduce acute and longterm toxicity, the GHSG started in the consecutive studies HD12 and HD15 for advanced stage HL to de-escalate BEACOPP by reducing the number of escalated BEACOPP cycles and by applying the baseline-dose BEACOPP, a time-dense regimen, called BEACOPP-14.

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  • (PMID = 17118782.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; BEACOPP protocol
  • [Number-of-references] 10
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96. Schulte CM, Beelen DW: Low pretransplant bone-mineral density and rapid bone loss do not increase risk for avascular osteonecrosis after allogeneic hematopoietic stem cell transplantation. Transplantation; 2005 Jun 27;79(12):1748-55
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  • METHODS: In a single-center prospective cohort study, 255 patients undergoing allogeneic SCT for CML, AML, MDS, and ALL were followed for at least 5 years.
  • [MeSH-major] Bone Density. Bone Diseases / epidemiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Stem Cell Transplantation


97. van der Straaten HM, van Biezen A, Brand R, Schattenberg AV, Egeler RM, Barge RM, Cornelissen JJ, Schouten HC, Ossenkoppele GJ, Verdonck LF, Netherlands Stem Cell Transplant Registry "TYPHON": Allogeneic stem cell transplantation for patients with acute myeloid leukemia or myelodysplastic syndrome who have chromosome 5 and/or 7 abnormalities. Haematologica; 2005 Oct;90(10):1339-45
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  • [Title] Allogeneic stem cell transplantation for patients with acute myeloid leukemia or myelodysplastic syndrome who have chromosome 5 and/or 7 abnormalities.
  • BACKGROUND AND OBJECTIVES: Chromosome 5 and/or 7 abnormalities are cytogenetic findings indicative of a poor prognosis in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • As data on allogeneic SCT in this context are limited we did a retrospective study of allogeneic SCT in patients with AML or MDS who had chromosome 5 and/or 7 abnormalities.
  • DESIGN AND METHODS: This was a retrospective study of 65 patients (16 children, 49 adults) with AML (n=33) or MDS (n=32) who had chromosome 5 and/or 7 abnormalities and who underwent allogeneic SCT in six Dutch Centers between 1983 and 2001.
  • The development of acute graft-versus-host disease (GVHD) grades II-IV was independently associated with significantly higher transplant-related mortality (TRM).
  • These patients with poor-risk chromosome 5 and/or 7 abnormalities were compared with a group of patients with a secondary AML/MDS and normal cytogenetics and were found to have significantly more relapses and significantly worse survival but a similar TRM.
  • INTERPRETATION AND CONCLUSIONS: We conclude that patients with AML or MDS with chromosome 5 and/or 7 abnormalities do rather poorly after allogeneic SCT, mainly because of the very high relapse rate.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Stem Cell Transplantation


98. Sampat KR, Garcia-Gutierrez V, Rossi A, Pierce S, Cortes J, Kantarjian H, Garcia-Manero G: Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7067

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  • [Title] Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia.
  • : 7067 Background: Little is known regarding the prevalence and natural history of pericardial disease in patients with leukemia.
  • To study this issue, we retrospectively analyzed a large cohort of patients with leukemia, who were evaluated at MD Anderson Cancer Center (MDACC), to determine the prevalence, timing, and characteristics of PEf in leukemia.
  • METHODS: We reviewed 3,327 patients with acute myeloid leukemia (AML, N = 1,809, 54%), acute lymphocytic leukemia (ALL, N = 494, 15%), or myelodysplastic syndrome (MDS, N =1,024, 31%), who were seen at MDACC from August 2003 to July 2008.
  • RESULTS: The overall prevalence of PEf was 21.7%, 21.1%, and 19.9% (p = 0.72) in patients with AML, ALL, and MDS, respectively.
  • CONCLUSIONS: PEf are relatively common in patients with leukemia at initial presentation and are usually asymptomatic.
  • Their incidence increases with therapy administration although it appears that this is not a process related to specific classes of treatment or type of leukemia.

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  • (PMID = 27961462.001).
  • [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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99. Majhail NS, Brunstein CG, Tomblyn M, Thomas AJ, Miller JS, Arora M, Kaufman DS, Burns LJ, Slungaard A, McGlave PB, Wagner JE, Weisdorf DJ: Reduced-intensity allogeneic transplant in patients older than 55 years: unrelated umbilical cord blood is safe and effective for patients without a matched related donor. Biol Blood Marrow Transplant; 2008 Mar;14(3):282-9
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  • The median age of MRD and UCB cohorts was 58 (range, 55-70) and 59 (range, 55-69) years, respectively. acute myelogenous leukemia/myelodysplastic syndrome (AML/MDS) (50%) was the most common diagnosis.
  • The cumulative incidence of grade II-IV acute graft-versus-host (aGVHD) disease (42% versus 49%, P = .20) and TRM at 180-days (23% versus 28%, P = .36) were comparable.

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  • (PMID = 18275894.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA065493-110009; United States / NCI NIH HHS / CA / P01 CA065493; United States / NCI NIH HHS / CA / P01 CA065493-120009; United States / NCI NIH HHS / CA / P01CA65493; United States / NCI NIH HHS / CA / CA065493-120009; United States / NCI NIH HHS / CA / CA065493-110009
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloablative Agonists
  • [Other-IDs] NLM/ NIHMS41246; NLM/ PMC2674378
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100. 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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  • [Title] Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia.
  • Moreover, non-specific alterations in chromosome 20 have been found in patients affected by MDS and acute myeloid leukemia AML.
  • MDS is an adult hematological disease that evolves into AML in about 30% of the cases.
  • 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.
  • FISH analysis disclosed in a small group of MDS/AML patients with normal karyotype the monoallelic deletion of the PLC beta1 gene.
  • In contrast, PLC beta4, another gene coding for a signaling molecule, located on 20pl2.3 at a distance as far as less than 1 Mb from PLC beta1, is unaffected in MDS patients with the deletion of PLC beta1 gene, hinting at an interstitial deletion.
  • The MDS patients, bearing the deletion, rapidly evolved to AML, whilst the normal karyotype MDS patients, showing non-deletion of PLC beta1 gene, are still alive at least 24 months after the diagnosis.
  • The immunocytochemical analysis using an anti PLC beta1 monoclonal antibody showed that all the AML/MDS patients who were normal at FISH analysis also had normal staining of the nucleus, which is a preferential site for PLC beta1.
  • 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






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