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1. Xiao L, Qiong L, Yan Z, Zheng Z, Luxi S, Li X, Ying T, Yizhi L, Quan P: Experimental and clinical characteristics in myelodysplastic syndrome patients with or without HLA-DR15 allele. Hematol Oncol; 2010 Jun;28(2):98-103
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  • [Title] Experimental and clinical characteristics in myelodysplastic syndrome patients with or without HLA-DR15 allele.
  • We studied the effects of the presence of the HLA-DR15 allele on the experimental and clinical features of myelodysplastic syndrome (MDS) by assessing the clinical data of 136 patients with MDS.
  • We observed that the frequency of HLA-DR15 expression in MDS patients (38.7%) was significantly higher than that in the healthy controls (p < 0.01).
  • We noted the following observations with regard to disease progression: None of the 46 HLA-DR15 positive patients with international prognostic scoring system (IPSS) scores <or=1 developed acute myeloid leukaemia (AML) during the follow-up period, while six of the 63 DR15-negative patients with the same IPSS score developed AML within a shorter follow-up period (p = 0.039).
  • In addition, we also recorded the following observations with regard to bone marrow (BM) failure: The bicytopenia/pancytopenia ratio in the DR15-positive patients was higher than that in the DR15-negative patients (92.4 vs. 78.3%; p = 0.029).
  • We concluded that the presence of the HLA-DR15 allele is indicative of a genetic susceptibility to MDS and, the presence of the HLA-DR15 allele showed less association with disease progression and greater association with BM failure.
  • [MeSH-major] Genes, MHC Class II. HLA-DR Antigens / genetics. Myelodysplastic Syndromes / immunology

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  • [Copyright] (c) 2009 John Wiley & Sons, Ltd.
  • (PMID = 19593744.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-DR Antigens; 0 / HLA-DR Serological Subtypes; 0 / HLA-DR15 antigen; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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2. 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


3. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML. Leukemia; 2005 Feb;19(2):197-200
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  • [Title] Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.
  • Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%).
  • The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics


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4. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.
  • The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • Given the general paucity of economic modelling work in MDS and the limitations of the submitted industry model there is an evident need for an independent cost-effectiveness analysis of aza in MDS.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


5. Bhatia S, Krailo MD, Chen Z, Burden L, Askin FB, Dickman PS, Grier HE, Link MP, Meyers PA, Perlman EJ, Rausen AR, Robison LL, Vietti TJ, Miser JS: Therapy-related myelodysplasia and acute myeloid leukemia after Ewing sarcoma and primitive neuroectodermal tumor of bone: A report from the Children's Oncology Group. Blood; 2007 Jan 1;109(1):46-51
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  • [Title] Therapy-related myelodysplasia and acute myeloid leukemia after Ewing sarcoma and primitive neuroectodermal tumor of bone: A report from the Children's Oncology Group.
  • This study describes the magnitude of risk of therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) in 578 individuals diagnosed with Ewing sarcoma and enrolled on Children's Oncology Group therapeutic protocol, INT-0091.
  • Eleven patients developed t-MDS/AML, resulting in a cumulative incidence of 2% at 5 years.
  • While patients treated on regimens A and B were at a low risk for development of t-MDS/AML (cumulative incidence: 0.4% and 0.9% at 5 years, respectively), patients treated on regimen C were at a 16-fold increased risk of developing t-MDS/AML (cumulative incidence: 11% at 5 years), when compared with those treated on regimen A.
  • Increasing exposure to ifosfamide from 90 to 140 g/m2, cyclophosphamide from 9.6 to 17.6 g/m2, and doxorubicin from 375 to 450 mg/m2 increased the risk of t-MDS/AML significantly.


6. Zebisch A, Czernilofsky AP, Keri G, Smigelskaite J, Sill H, Troppmair J: Signaling through RAS-RAF-MEK-ERK: from basics to bedside. Curr Med Chem; 2007;14(5):601-23
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  • This review provides an understanding of this signaling cascade as revealed by genetic and biochemical approaches and discusses the existing or arising possibilities to interfere with unphysiological activation in cancer.
  • Signaling aberrations and signal transduction therapies will be discussed exemplary for two types of hematological neoplasia, acute myeloid leukemia (AML) and the myelodysplastic syndromes (MDS).

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  • (PMID = 17346150.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / W 1101
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 2.7.11.1 / raf Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 3.6.1.- / GTP-Binding Proteins
  • [Number-of-references] 202
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7. 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


8. Zhang Y, Zhang M, Yang L, Xiao Z: NPM1 mutations in myelodysplastic syndromes and acute myeloid leukemia with normal karyotype. Leuk Res; 2007 Jan;31(1):109-11
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  • [Title] NPM1 mutations in myelodysplastic syndromes and acute myeloid leukemia with normal karyotype.
  • Mutations at exon 12 of the nucleophosmin (NPM1) gene are the most frequent acquired molecular abnormalities in adult and pediatric acute myeloid leukaemia (AML) with normal karyotype.
  • We screened 28 patients with new diagnosed primary AML with normal karyotype, 38 patients with myelodysplastic symdromes (MDS) and 19 healthy volunteer for mutations at exon 12 of NPM1 gene.
  • NPM1 mutations were identified in four AML patients and two MDS patients, including one novel sequence variant.
  • As far as we know, this is the first report of NPM1 mutation in patients with MDS in the English literature until now, and our primary data support that NPM1 mutations may be also involved in the pathogenesis of MDS.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics


9. Evers C, Beier M, Poelitz A, Hildebrandt B, Servan K, Drechsler M, Germing U, Royer HD, Royer-Pokora B: Molecular definition of chromosome arm 5q deletion end points and detection of hidden aberrations in patients with myelodysplastic syndromes and isolated del(5q) using oligonucleotide array CGH. Genes Chromosomes Cancer; 2007 Dec;46(12):1119-28
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  • [Title] Molecular definition of chromosome arm 5q deletion end points and detection of hidden aberrations in patients with myelodysplastic syndromes and isolated del(5q) using oligonucleotide array CGH.
  • Isolated deletions of the long arm of chromosome 5, del(5q), are observed in 10% of myelodysplastic syndromes (MDS) and are associated with a more favorable prognosis, although the clinical course varies considerably.
  • To assess the frequency of hidden abnormalities in cases with an isolated cytogenetic del(5q), we have performed a genome wide high resolution 44 K 60mer oligonucleotide array comparative genomic hybridization (aCGH) study using DNA from bone marrow cells of 12 MDS and one AML patient.
  • In addition, the high sensitivity of this method enables the study of whole bone marrow cells from MDS patients, a disease with a low blast count.
  • [MeSH-major] Chromosome Aberrations. Chromosome Deletion. Chromosomes, Human, Pair 5. Genome, Human. Myelodysplastic Syndromes / genetics. Oligonucleotide Array Sequence Analysis / methods


10. Barnard DR, Woods WG: Treatment-related myelodysplastic syndrome/acute myeloid leukemia in survivors of childhood cancer--an update. Leuk Lymphoma; 2005 May;46(5):651-63
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  • [Title] Treatment-related myelodysplastic syndrome/acute myeloid leukemia in survivors of childhood cancer--an update.
  • Treatment-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/t-AML) is a devastating complication of treatment for childhood cancer.
  • The understanding of the presentation, incidence, predisposing risk factors and pathobiology of t-MDS/t-AML is increasing.
  • This increased understanding has not yet been translated into improved outcomes of therapy for t-MDS/t-AML.
  • [MeSH-major] Leukemia, Myeloid / etiology. Myelodysplastic Syndromes / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Child. Female. Humans. Male. Neoplasms / therapy. Survivors


11. Yoneda K, Morii T, Nieda M, Tsukaguchi N, Amano I, Tanaka H, Yagi H, Narita N, Kimura H: The peripheral blood Valpha24+ NKT cell numbers decrease in patients with haematopoietic malignancy. Leuk Res; 2005 Feb;29(2):147-52
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  • In this study, we assessed the Valpha24+ NKT cell numbers in peripheral blood (PB) from 30 healthy donors and 70 patients with haematopoietic malignancy including chronic myelogenous leukemia (CML), malignant lymphoma (ML), acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).

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  • (PMID = 15607362.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Receptors, Antigen, T-Cell, alpha-beta
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12. Piekarz RL, Bates SE: Epigenetic modifiers: basic understanding and clinical development. Clin Cancer Res; 2009 Jun 15;15(12):3918-26
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  • DNA methyltransferase (DNMT) inhibitors such as 5-aza-2'-deoxycytidine or 5-azacytidine have been approved in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML), whereas the histone deacetylase inhibitors (HDIs) including vorinostat, romidepsin, panobinostat, belinostat, and entinostat have been shown to be active in cutaneous and peripheral T-cell lymphoma.

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  • (PMID = 19509169.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; EC 2.1.1.- / Methyltransferases; EC 3.5.1.98 / Histone Deacetylases
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13. Chen HM, Yuan HY, Fan X, He HY, Chen B, Shi JY, Zhu YM: [Application of multiplex rt-PCR assay for screening rare or cryptic chromosome translocations in de novo patients with acute myeloid leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1138-42
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  • [Title] [Application of multiplex rt-PCR assay for screening rare or cryptic chromosome translocations in de novo patients with acute myeloid leukemia].
  • This study was aimed to investigate the clinical feasibility of using multiplex PT-PCR assay for screening rare/cryptic chromosome translocations in patients with de novo acute myeloid leukemia.
  • For 126 patients with de novo AML-M4/M5 without common chromosome translocations including t(15;17), t(8;21) and t(16;16), 3 parallel multiplex RT-PCR assays were set up to detect 6 mll-related gene rearrangements (mll/af10, mll/af17, mll/ell, mll/af9, mll/af6 and mll/enl) with low detection rate and 4 rare fusion genes (dek/can, tls/erg, aml1/mds (evi1) and npm/mlf1).
  • Among them, 10 cases were AML-M5 (16.67%), 1 cases AML-M4 (1.51%).


14. 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


15. 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 01;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


16. Yeh CH, Tseng R, Hannah A, Estrov Z, Estey E, Kantarjian H, Albitar M: Clinical correlation of circulating heat shock protein 70 in acute leukemia. Leuk Res; 2010 May;34(5):605-9
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  • [Title] Clinical correlation of circulating heat shock protein 70 in acute leukemia.
  • Using electrochemiluminescence protein detection immunoassay, we measured the cHSP70 levels in the plasma of patients with acute myeloid leukemia (AML) (n=96), myelodysplastic syndrome (MDS) (n=28), and acute lymphoblastic leukemia (ALL) (n=40) and compared with those in normal individuals (n=99).
  • cHSP70 levels were significantly higher in AML (median: 10.71 ng/mL, range: 1.93-79.0 ng/mL) and ALL (median: 27.59 ng/mL, range: 5.09-129.6 ng/mL) as compared to those in MDS (median: 4.54 ng/mL, range: 1.35-58.3 ng/mL) or healthy controls (median: 4.13 ng/mL, range: 1.75-13.6 ng/mL).
  • Levels of cHSP70 showed significant positive correlation with lactate dehydrogenase (LDH) and white blood cells (WBC) in AML and ALL patients, which may reflect overall tumor load.
  • Furthermore, patients with higher levels of cHSP70 had significantly shorter survival in AML (P=0.04) and ALL (P=0.05), suggesting that in these two acute diseases, cHSP70 is an indicator for poor prognosis.
  • [MeSH-major] Biomarkers, Tumor / blood. HSP70 Heat-Shock Proteins / blood. Leukemia, Myeloid, Acute / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
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  • (PMID = 19800118.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA100632
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HSP70 Heat-Shock Proteins
  • [Other-IDs] NLM/ NIHMS593249; NLM/ PMC4127889
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17. Estey E, de Lima M, Tibes R, Pierce S, Kantarjian H, Champlin R, Giralt S: Prospective feasibility analysis of reduced-intensity conditioning (RIC) regimens for hematopoietic stem cell transplantation (HSCT) in elderly patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS). Blood; 2007 Feb 15;109(4):1395-400
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  • [Title] Prospective feasibility analysis of reduced-intensity conditioning (RIC) regimens for hematopoietic stem cell transplantation (HSCT) in elderly patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS).
  • To prospectively assess the applicability of reduced-intensity conditioning hematopoietic stem cell transplantation (RIC-HSCT), we wrote a protocol in which all untreated patients 50 years or older with acute myeloid leukemia (AML) and unfavorable cytogenetics would be evaluated during induction for a possible RIC-HSCT in first complete remission (CR1).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Aged. Antineoplastic Agents / therapeutic use. Feasibility Studies. Humans. Middle Aged. Patient Selection. Prospective Studies. Survival Analysis. Tissue Donors


18. 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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19. Morita Y, Kanamaru A, Miyazaki Y, Imanishi D, Yagasaki F, Tanimoto M, Kuriyama K, Kobayashi T, Imoto S, Ohnishi K, Naoe T, Ohno R: Comparative analysis of remission induction therapy for high-risk MDS and AML progressed from MDS in the MDS200 study of Japan Adult Leukemia Study Group. Int J Hematol; 2010 Jan;91(1):97-103
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  • [Title] Comparative analysis of remission induction therapy for high-risk MDS and AML progressed from MDS in the MDS200 study of Japan Adult Leukemia Study Group.
  • A total of 120 patients with high-risk myelodysplastic syndrome (MDS) and AML progressed from MDS (MDS-AML) were registered in a randomized controlled study of the Japan Adult Leukemia Study Group (JALSG).
  • Untreated adult patients with high-risk MDS and MDS-AML were randomly assigned to receive either idarubicin and cytosine arabinoside (IDR/Ara-C) (Group A) or low-dose cytosine arabinoside and aclarubicin (CA) (Group B).
  • In conclusion, it is necessary to introduce the first line therapy excluding the chemotherapy that can prolong survival in patients with high-risk MDS and MDS-AML.
  • [MeSH-major] Aclarubicin / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / administration & dosage. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 74KXF8I502 / Aclarubicin; ZRP63D75JW / Idarubicin
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20. Natelson EA, Pyatt D: Temozolomide-induced myelodysplasia. Adv Hematol; 2010;2010:760402
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  • A patient who had received temozolomide (TMZ) as a single agent in treatment of malignant glioma developed therapy-induced myelodysplasia (T-MDS).
  • Observations on this patient, and on similarly treated others, suggest that the cumulative dose threshold (CDT) for TMZ that predisposes to T-MDS and which may potentially lead to acute myeloid leukemia (T-AML) is around 18000 to 20000 mg/sq m.
  • Although the incidence of T-MDS and the predisposing CDT of TMZ may differ from that of other potentially leukemogenic compounds currently and formerly used as chemotherapeutic agents, all alkylating agents, including TMZ, should be considered potentially leukemogenic when administered long term.

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  • (PMID = 20224797.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2833319
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21. Asou H, Matsui H, Ozaki Y, Nagamachi A, Nakamura M, Aki D, Inaba T: Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome. Biochem Biophys Res Commun; 2009 May 29;383(2):245-51
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  • [Title] Identification of a common microdeletion cluster in 7q21.3 subband among patients with myeloid leukemia and myelodysplastic syndrome.
  • Monosomy 7 and interstitial deletions in the long arm of chromosome 7 (-7/7q-) is a common nonrandom chromosomal abnormality found frequently in myeloid disorders including acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), and juvenile myelomonocytic leukemia (JMML).
  • Gene copy number assessment of three genes by real-time PCR revealed heterozygous deletion of these three genes in adult patients with AML and MDS at high frequency, in addition to JMML patients.
  • The three genes located to 7q21.3 would be candidates for myeloid tumor-suppressor genes on 7q.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 7 / genetics. Genes, Tumor Suppressor. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Sequence Deletion


22. Wang SA, Jabbar K, Lu G, Chen SS, Galili N, Vega F, Jones D, Raza A, Kantarjian H, Garcia-Manero G, McDonnell TJ, Medeiros LJ: Trisomy 11 in myelodysplastic syndromes defines a unique group of disease with aggressive clinicopathologic features. Leukemia; 2010 Apr;24(4):740-7
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  • [Title] Trisomy 11 in myelodysplastic syndromes defines a unique group of disease with aggressive clinicopathologic features.
  • Trisomy 11 in myelodysplastic syndromes (MDS) is rare, with undefined clinical significance and is currently assigned to the International Prognostic Scoring System (IPSS) intermediate-risk group.
  • Over a 15-year period, we identified 17 MDS patients with trisomy 11 either as a sole abnormality (n=10) or associated with one or two additional alterations (n=7), comprising 0.3% of all MDS cases reviewed.
  • Of 16 patients with Bone Marrow material available for review, 14 (88%) patients presented with excess blasts, 69% patients evolved to acute myeloid leukemia (AML) in a 5-month median interval and the median survival was 14 months.
  • For comparison, we studied 19 AML patients with trisomy 11 in a noncomplex karyotype, of which, a substantial subset of patients had morphologic dysplasia, and/or preexisting cytopenia(s)/MDS.
  • Genomic DNA PCR showed MLL partial tandem duplication in 5 of 10 MDS and 7 of 11 AML patients.
  • A review of literature identified 17 additional cases of MDS with trisomy 11, showing similar clinicopathologic features to our patients.
  • Compared with our historical data comprising 1165 MDS patients, MDS patients with trisomy 11 had a significantly inferior survival to patients in the IPSS intermediate-risk cytogenetic group (P=0.0002), but comparable to the poor-risk group (P=0.97).
  • We conclude that trisomy 11 in MDS correlates with clinical aggressiveness, may suggest an early/evolving AML with myelodysplasia-related changes and is best considered a high-risk cytogenetic abnormality in MDS prognostication.
  • [MeSH-major] Chromosome Disorders / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Trisomy / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Southern. DNA, Neoplasm / genetics. Female. Gene Duplication. Genes, ras / genetics. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Mutation / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Prognosis. Proto-Oncogene Proteins / genetics. Retrospective Studies. Survival Rate. fms-Like Tyrosine Kinase 3 / genetics. ras Proteins / genetics


23. Kröger N, Shimoni A, Zabelina T, Schieder H, Panse J, Ayuk F, Wolschke C, Renges H, Dahlke J, Atanackovic D, Nagler A, Zander A: Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS). Bone Marrow Transplant; 2006 Feb;37(4):339-44
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  • [Title] Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS).
  • We investigated a dose-reduced conditioning regimen consisting of treosulfan and fludarabine followed by allogeneic stem cell transplantation (SCT) in 26 patients with secondary AML or MDS.
  • Acute graft-versus-host disease (GvHD) grade II-IV was seen in 23% and severe grade III GvHD in 12% of the patients.
  • No patients experienced grade IV acute GvHD.
  • The relapse rate was higher in patients beyond CR1 or with intermediate two or high risk MDS (P = 0.02).
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Disease-Free Survival. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. HLA Antigens / analysis. Humans. Male. Middle Aged. Prospective Studies. Recurrence. Siblings. Survival Rate. Transplantation, Homologous. Treatment Outcome


24. Harada H, Harada Y, Kimura A: Implications of somatic mutations in the AML1/RUNX1 gene in myelodysplastic syndrome (MDS): future molecular therapeutic directions for MDS. Curr Cancer Drug Targets; 2006 Sep;6(6):553-65
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  • [Title] Implications of somatic mutations in the AML1/RUNX1 gene in myelodysplastic syndrome (MDS): future molecular therapeutic directions for MDS.
  • Myelodysplastic syndrome (MDS) is a clonal disorder of hematopoietic stem cells characterized by ineffective and inadequate hematopoiesis.
  • MDS is also a susceptibility to acute myeloid leukemia (AML) and shown to be extremely resistant to current therapeutic strategies.
  • MDS in a subset of 10-20% of patients arise after previous chemotherapy or radiation exposure for other malignancies.
  • Because MDS is a heterogeneous disorder, specific gene abnormalities playing a role in the myelodysplastic process have been difficult to identify.
  • Cytogenetic abnormalities are seen in half of MDS patients, and generally consist of partial or complete chromosome deletion or addition, whereas balanced translocations are rare.
  • Genes more frequently implicated in the pathogenesis of MDS remain unknown.
  • Although point mutations of critical genes have been demonstrated to contribute to the development MDS, there was no strong correlation between these mutations and clinical features.
  • Recently, we reported the high incidence of somatic mutations in the AML1/RUNX1 gene, which is a critical regulator of definitive hematopoiesis and the most frequent target for translocation of AML, in MDS, especially refractory anemia with excess blasts (RAEB), RAEB in transformation (RAEBt) and AML following MDS (defined here as MDS/AML).
  • The MDS/AML patients with AML1 mutations had a significantly worse prognosis than those without AML1 mutations.
  • Most of AML1/RUNX1 mutants lose trans-activation potential, which leads to a loss of AML1 function indicating that AML1/RUNX1 dysfunction is one of the major pathogenesis of MDS/AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genetic Therapy / trends. Mutation. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / therapy


25. Niimi H, Harada H, Harada Y, Ding Y, Imagawa J, Inaba T, Kyo T, Kimura A: Hyperactivation of the RAS signaling pathway in myelodysplastic syndrome with AML1/RUNX1 point mutations. Leukemia; 2006 Apr;20(4):635-44
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  • [Title] Hyperactivation of the RAS signaling pathway in myelodysplastic syndrome with AML1/RUNX1 point mutations.
  • AML1/RUNX1 mutations have been reported frequently in myelodysplastic syndrome (MDS) patients, especially those diagnosed with refractory anemia with excess blast (RAEB), RAEB in transformation (RAEBt), or AML following MDS (these categories are defined as MDS/AML).
  • Although AML1 mutations are suspected to play a pivotal role in the development of MDS/AML, acquisition of additional genetic alterations is also necessary.
  • We analyzed gene alterations in MDS/AML patients with AML1 mutations, comparing them to alterations in those without an AML1 mutation.
  • AML1 mutations were significantly associated with -7/7q-, whereas MDS/AML patients without AML1 mutations showed a high frequency of -5/5q- and a complex karyotype.
  • Patients with AML1 mutations showed more mutations of their FLT3, N-RAS, PTPN11, and NF1 genes, resulting in a significantly higher mutation frequency for receptor tyrosine kinase (RTK)-RAS signaling pathways in AML1-mutated MDS/AML patients compared to AML1-wild-type MDS/AML patients (38% versus 6.3%, P < 0.0001).
  • Furthermore, blast cells of the AML1-mutated patients expressing surface c-KIT, and SHP-2 mutants contributed to prolonged and enhanced extracellular signal-regulated kinase activation following stem cell factor stimulation.
  • Our results suggest that MDS/AML arising from AML1/RUNX1 mutations has a significant association with -7/7q- alteration, and frequently involves RTK-RAS signaling pathway activation.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Genes, ras. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Point Mutation. Signal Transduction


26. Kobayashi H, Matsuyama T, Ueda M, Suzuki T, Ozaki K, Mori M, Nagai T, Muroi K, Ozawa K: Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome. Intern Med; 2009;48(18):1629-33
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  • [Title] Predictive factors of response and survival following chemotherapy treatment in acute myeloid leukemia progression from myelodysplastic syndrome.
  • OBJECTIVE: The progression of myelodysplastic syndrome to acute myeloid leukemia (MDS/AML) is generally incurable and its prognosis is extremely poor.
  • METHODS: Twenty-nine patients who had been diagnosed of MDS/AML and had undergone chemotherapy between April 2001 and March 2008 were retrospectively analyzed.
  • Twenty-four patients were administered a low-dose AraC containing regimen and 5 received an AML-like regimen as the initial chemotherapy.
  • CONCLUSION: In MDS/AML, patients with a normal karyotype tended to have a better response to chemotherapy.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


27. Brakensiek K, Länger F, Schlegelberger B, Kreipe H, Lehmann U: Hypermethylation of the suppressor of cytokine signalling-1 (SOCS-1) in myelodysplastic syndrome. Br J Haematol; 2005 Jul;130(2):209-17
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  • [Title] Hypermethylation of the suppressor of cytokine signalling-1 (SOCS-1) in myelodysplastic syndrome.
  • In contrast to acute myeloid leukaemia (AML), comparably little is known about aberrant methylation in myelodysplastic syndrome (MDS), a heterogeneous clonal stem cell disorder with a risk of transformation into secondary AML of up to 30%.
  • Employing a newly developed quantitative real-time polymerase chain reaction-based methylation assay we analysed, for the first time, SOCS-1 methylation in MDS and found disease-specific hypermethylation in 27 of 86 MDS patients (31%).
  • Demethylation experiments provided direct evidence that aberrant methylation of SOCS-1 induces transcriptional silencing in myeloid cells.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Myelodysplastic Syndromes / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Acute Disease. Cell Differentiation. DNA Methylation. Down-Regulation. Granulocytes / metabolism. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Neoplasm Proteins / metabolism. Polymerase Chain Reaction / methods. Protein-Tyrosine Kinases / metabolism. Signal Transduction. Suppressor of Cytokine Signaling Proteins. Tumor Cells, Cultured

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  • (PMID = 16029449.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Repressor Proteins; 0 / SOCS1 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases
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28. Maslak P, Chanel S, Camacho LH, Soignet S, Pandolfi PP, Guernah I, Warrell R, Nimer S: Pilot study of combination transcriptional modulation therapy with sodium phenylbutyrate and 5-azacytidine in patients with acute myeloid leukemia or myelodysplastic syndrome. Leukemia; 2006 Feb;20(2):212-7
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  • [Title] Pilot study of combination transcriptional modulation therapy with sodium phenylbutyrate and 5-azacytidine in patients with acute myeloid leukemia or myelodysplastic syndrome.
  • We designed a pilot study to target DNA methylation and histone deacetylation through the sequential administration of 5-azacytidine followed by sodium phenylbutyrate (PB) in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • Ten evaluable patients (eight AML, two MDS) were treated with seven consecutive daily subcutaneous injections of 5-azacytidine at 75 mg/m2 followed by 5 days of sodium PB given intravenously at a dose of 200 mg/kg.
  • One patient with MDS proceeded to allogeneic stem cell transplantation and is alive without evidence of disease 39 months later.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Phenylbutyrates / therapeutic use. Transcription, Genetic / drug effects
  • [MeSH-minor] Acetylation / drug effects. Acute Disease. Adult. Aged. Antimetabolites, Antineoplastic / therapeutic use. DNA Methylation. Drug Administration Schedule. Drug Therapy, Combination. Female. Histones / drug effects. Histones / metabolism. Humans. Male. Middle Aged. Pilot Projects. Treatment Outcome


29. 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


30. Valcárcel D, Martino R, Caballero D, Martin J, Ferra C, Nieto JB, Sampol A, Bernal MT, Piñana JL, Vazquez L, Ribera JM, Besalduch J, Moraleda JM, Carrera D, Brunet MS, Perez-Simón JA, Sierra J: Sustained remissions of high-risk acute myeloid leukemia and myelodysplastic syndrome after reduced-intensity conditioning allogeneic hematopoietic transplantation: chronic graft-versus-host disease is the strongest factor improving survival. J Clin Oncol; 2008 Feb 1;26(4):577-84
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  • [Title] Sustained remissions of high-risk acute myeloid leukemia and myelodysplastic syndrome after reduced-intensity conditioning allogeneic hematopoietic transplantation: chronic graft-versus-host disease is the strongest factor improving survival.
  • This reduction makes it possible for patients who are ineligible for high-dose myeloablative conditioning allo-SCT to benefit from graft-versus-leukemia reaction.
  • In this multicenter, prospective study of patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS), we investigated the efficacy of RIC allo-SCT from a human leukocyte antigen-identical sibling by using a regimen that uses fludarabine and busulfan.
  • PATIENTS AND METHODS: Ninety-three patients with AML (n = 59) and MDS (n = 34) were included, and the median age was of 53 years.
  • The 1- and 4-year relapse cumulative incidences were 23% and 37%, respectively, and leukemia recurrence was the main cause of death.
  • [MeSH-major] Graft vs Host Disease / prevention & control. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Transplantation Conditioning


31. Frampton JE, Scott LJ: Posaconazole : a review of its use in the prophylaxis of invasive fungal infections. Drugs; 2008;68(7):993-1016
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  • Posaconazole provided effective prophylaxis against invasive fungal infections and was generally well tolerated in two large, well designed trials in HSCT recipients with GVHD, or patients receiving induction-remission chemotherapy for acute myeloid leukaemia (AML) or myelodysplastic syndrome (MDS) that was expected to result in prolonged neutropenia.

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  • (PMID = 18457464.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
  • [Number-of-references] 122
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32. Follo MY, Finelli C, Mongiorgi S, Clissa C, Bosi C, Testoni N, Chiarini F, Ramazzotti G, Baccarani M, Martelli AM, Manzoli L, Martinelli G, Cocco L: Reduction of phosphoinositide-phospholipase C beta1 methylation predicts the responsiveness to azacitidine in high-risk MDS. Proc Natl Acad Sci U S A; 2009 Sep 29;106(39):16811-6
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  • [Title] Reduction of phosphoinositide-phospholipase C beta1 methylation predicts the responsiveness to azacitidine in high-risk MDS.
  • Lipid signaling pathways are involved in cell growth, differentiation, and apoptosis, and could have a role in the progression of myelodysplastic syndromes (MDS) into acute myeloid leukemia (AML).
  • Indeed, recent studies showed that phosphoinositide-phospholipase (PI-PL)Cbeta1 mono-allelic deletion correlates with a higher risk of AML evolution.
  • Also, a single patient treated with azacitidine, a DNA methyltransferase inhibitor currently used in MDS, displayed a direct correlation between PI-PLCbeta1 gene expression and drug responsiveness.
  • First, we analyzed the structure of PI-PLCbeta1 gene promoter, then quantified the degree of PI-PLCbeta1 promoter methylation and gene expression in MDS patients at baseline and during azacitidine administration.
  • Our results demonstrate not only that PI-PLCbeta1 promoter is hypermethylated in high-risk MDS patients, but also that the amount of PI-PLCbeta1 mRNA could predict the clinical response to azacitidine, therefore indicating a promising new therapeutic approach.
  • [MeSH-major] Azacitidine / pharmacology. Enzyme Inhibitors / pharmacology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / enzymology. Phosphoinositide Phospholipase C / metabolism. Phospholipase C beta / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Middle Aged. Promoter Regions, Genetic. RNA, Messenger / metabolism


33. Christiansen DH, Andersen MK, Desta F, Pedersen-Bjergaard J: Mutations of genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal transduction pathway in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia; 2005 Dec;19(12):2232-40
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  • [Title] Mutations of genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal transduction pathway in therapy-related myelodysplasia and acute myeloid leukemia.
  • Mutations of the FLT3, c-KIT, c-FMS, KRAS, NRAS, BRAF and CEBPA genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal-transduction pathway are frequent in acute myeloid leukemia (AML).
  • We examined 140 patients with therapy-related myelodysplasia or AML (t-MDS/t-AML) for point mutations of these seven genes.
  • All but one patient with a FLT3 mutation presented with t-AML (P=0.0002).
  • Furthermore, FLT3 mutations were significantly associated with previous radiotherapy without chemotherapy (P=0.03), and with a normal karyotype (P=0.004), but inversely associated with previous therapy with alkylating agents (P=0.003) and with -7/7q- (P=0.001).
  • RAS mutations were associated with AML1 point mutations (P=0.046) and with progression from t-MDS to t-AML (P=0.008).
  • Noteworthy, all three patients with BRAF mutations presented as t-AML of M5 subtype with t(9;11)(p22;q23) and MLL-rearrangement (P=0.01).
  • In t-AML RAS/BRAF mutations were significantly associated with a very short survival (P=0.017).
  • [MeSH-major] Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Point Mutation. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. CCAAT-Enhancer-Binding Protein-alpha / genetics. Child. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Proto-Oncogene Proteins B-raf / genetics. Receptor, Macrophage Colony-Stimulating Factor / genetics. Signal Transduction. fms-Like Tyrosine Kinase 3. ras Proteins / genetics


34. 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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35. Göhring G, Giagounidis A, Büsche G, Kreipe HH, Zimmermann M, Hellström-Lindberg E, Aul C, Schlegelberger B: Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression. Ann Hematol; 2010 Apr;89(4):365-74
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  • [Title] Patients with del(5q) MDS who fail to achieve sustained erythroid or cytogenetic remission after treatment with lenalidomide have an increased risk for clonal evolution and AML progression.
  • Lenalidomide consistently induces transfusion independence and complete cytogenetic response in patients with myelodysplastic syndromes with 5q deletion.
  • We performed a long-term follow-up analysis of 42 patients with low or intermediate risk myelodysplastic syndromes and 5q deletion treated with lenalidomide.
  • Thirty-six percent of patients progressed into acute myeloid leukaemia.
  • However, erythroid and cytogenetic responders had a significantly decreased risk of progression to acute myeloid leukaemia (p = 0.001 and p = 0.009, respectively) compared to non-responders.
  • Three and 5 years after study entry, the cumulative incidence of acute myeloid leukaemia for patients with a cytogenetic response was 10% and 21%, respectively, and for patients without cytogenetic response, it was 46% and 60%.
  • Patients with del(5q) myelodysplastic syndromes without erythroid or cytogenetic remission after treatment with lenalidomide have a high risk for clonal evolution and acute myeloid leukaemia progression.
  • Regular follow-up investigations of del(5q) myelodysplastic syndrome patients treated with lenalidomide may help to identify patients requiring alternative treatment strategies.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Erythroid Cells / drug effects. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / pathology. Thalidomide / analogs & derivatives


36. 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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37. Konrad TA, Karger A, Hackl H, Schwarzinger I, Herbacek I, Wieser R: Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes. J Leukoc Biol; 2009 Oct;86(4):813-22
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  • [Title] Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes.
  • The oncogene EVI1 has been implicated in the etiology of AML and MDS.
  • Although AML cells are characterized by accelerated proliferation and differentiation arrest, MDS cells hyperproliferate when immature but fail to differentiate later and die instead.
  • In agreement with its roles in AML and in immature MDS cells, EVI1 was found to stimulate cell proliferation and inhibit differentiation in several experimental systems.
  • In the present study, we expressed EVI1 and MDS1/EVI1 in a tetracycline-regulable manner in the human myeloid cell line U937.
  • In summary, these data show that inducible expression of EVI1 in U937 cells causes phenotypes that may be relevant for its role in MDS and provides a basis for further investigation of its contribution to this fatal disease.
  • [MeSH-major] Cell Differentiation. DNA-Binding Proteins / biosynthesis. G1 Phase. Myelodysplastic Syndromes / metabolism. Myeloid Cells / metabolism. Resting Phase, Cell Cycle. Transcription Factors / biosynthesis
  • [MeSH-minor] Apoptosis. DNA Fragmentation. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / mortality. Phosphatidylserines / genetics. Phosphatidylserines / metabolism. Proto-Oncogenes / genetics. U937 Cells

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  • (PMID = 19605700.001).
  • [ISSN] 1938-3673
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / P 17896; Austria / Austrian Science Fund FWF / / P 19795; Austria / Austrian Science Fund FWF / / P 20920
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Phosphatidylserines; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2777892
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38. Babicka L, Ransdorfova S, Brezinova J, Zemanova Z, Sindelarova L, Siskova M, Maaloufova J, Cermak J, Michalova K: Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH. Leuk Res; 2007 Jan;31(1):39-47
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  • [Title] Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH.
  • We analyzed complex chromosomal aberrations in 37 adult patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) using classical cytogenetic method, FISH with locus-specific probes, multicolor FISH (mFISH) and multicolor banding (mBAND).
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Gene Rearrangement / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


39. Makishima H, Cazzolli H, Szpurka H, Dunbar A, Tiu R, Huh J, Muramatsu H, O'Keefe C, Hsi E, Paquette RL, Kojima S, List AF, Sekeres MA, McDevitt MA, Maciejewski JP: Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies. J Clin Oncol; 2009 Dec 20;27(36):6109-16
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  • [Title] Mutations of e3 ubiquitin ligase cbl family members constitute a novel common pathogenic lesion in myeloid malignancies.
  • PURPOSE: Acquired somatic uniparental disomy (UPD) is commonly observed in myelodysplastic syndromes (MDS), myelodysplastic/myeloproliferative neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes harboring mutations.
  • METHODS: We applied high-density SNP-A karyotyping to identify loss of heterozygosity of 11q in 442 patients with MDS, MDS/MPN, MPN, sAML evolved from these conditions, and primary AML.
  • RESULTS: We identified c-Cbl mutations in 5% and 9% of patients with chronic myelomonocytic leukemia (CMML) and sAML, and also in CML blast crisis and juvenile myelomonocytic leukemia (JMML).
  • CONCLUSION: Mutations in the Cbl family RING finger domain or linker sequence constitute important pathogenic lesions associated with not only preleukemic CMML, JMML, and other MPN, but also progression to AML, suggesting that impairment of degradation of activated tyrosine kinases constitutes an important cancer mechanism.

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  • (PMID = 19901108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K24 HL077522; United States / NHLBI NIH HHS / HL / R01 HL082983; United States / NCRR NIH HHS / RR / U54 RR019391; United States / NHLBI NIH HHS / HL / K24 HL-077522; United States / NHLBI NIH HHS / HL / R01HL-082983; United States / NCRR NIH HHS / RR / S10 RR019391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
  • [Other-IDs] NLM/ PMC3040009
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40. Schmid C, Schleuning M, Hentrich M, Markl GE, Gerbitz A, Tischer J, Ledderose G, Oruzio D, Hiddemann W, Kolb HJ: High antileukemic efficacy of an intermediate intensity conditioning regimen for allogeneic stem cell transplantation in patients with high-risk acute myeloid leukemia in first complete remission. Bone Marrow Transplant; 2008 Apr;41(8):721-7
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  • [Title] High antileukemic efficacy of an intermediate intensity conditioning regimen for allogeneic stem cell transplantation in patients with high-risk acute myeloid leukemia in first complete remission.
  • The goal of this analysis was to define the role of the moderate-intensity fludarabin Ara-C amsacrin (FLAMSA)-reduced intensity conditioning (RIC) regimen for patients with high-risk AML undergoing allogeneic SCT (alloSCT) in first CR1.
  • High-risk was defined by (1) AML secondary to MDS or radio/chemotherapy, (2) unfavorable cytogenetics or (3) delayed response to induction chemotherapy.
  • A total of 23 of 44 AML patients referred to the University of Munich for alloSCT in CR1 between 1999 and 2006 fulfilled these criteria and received FLAMSA chemotherapy, followed by RIC (4 Gy TBI/cyclophosphamide/ATG) for alloSCT.
  • Four-year overall and leukemia-free survival was 72.7% (median follow-up among survivors: 35 months).
  • The results of this high-risk cohort were compared to the outcome of 21 consecutive standard-risk patients <55 years, who had received standard, myeloablative sibling SCT in CR1 AML within the same center and time period.
  • In conclusion, the FLAMSA-RIC regimen produces long-term remission in a high proportion of patients with high-risk AML transplanted in CR1.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods


41. Larsson N, Billström R, Lilljebjörn H, Lassen C, Richter J, Ekblom M, Fioretos T: Genetic analysis of dasatinib-treated chronic myeloid leukemia rapidly developing into acute myeloid leukemia with monosomy 7 in Philadelphia-negative cells. Cancer Genet Cytogenet; 2010 Jun;199(2):89-95
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  • [Title] Genetic analysis of dasatinib-treated chronic myeloid leukemia rapidly developing into acute myeloid leukemia with monosomy 7 in Philadelphia-negative cells.
  • Despite the recent success of tyrosine kinase inhibitors (TKIs) in the treatment of chronic myeloid leukemia (CML), approximately 2-17% of patients develop clonal cytogenetic changes in the Philadelphia-negative (Ph(-)) cell population.
  • A fraction of these patients, in particular those displaying trisomy 8 or monosomy 7, are at risk of developing a myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).
  • At 20 months after dasatinib initiation, the patient developed MDS, which rapidly progressed into AML.
  • Given the strong association between monosomy 7 and mutation of genes involved in the RAS pathway in juvenile myelomonocytic leukemia, we also screened for pathogenetic variants in KRAS, NRAS, and PTPN11, but did not detect any changes.
  • [MeSH-major] Chromosomes, Human, Pair 7 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Chronic, Atypical, BCR-ABL Negative / genetics. Monosomy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Dasatinib. Female. Genes, ras / genetics. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Middle Aged. Mutation / genetics. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Oligonucleotide Array Sequence Analysis. Polymorphism, Single Nucleotide. Prognosis. Protein Kinase Inhibitors / therapeutic use. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics. Proto-Oncogene Proteins / genetics. ras Proteins / genetics


42. Koenecke C, Hofmann M, Bolte O, Gielow P, Dammann E, Stadler M, Franzke A, Boerner AR, Eder M, Ganser A, Knapp W, Hertenstein B: Radioimmunotherapy with [188Re]-labelled anti-CD66 antibody in the conditioning for allogeneic stem cell transplantation for high-risk acute myeloid leukemia. Int J Hematol; 2008 May;87(4):414-21
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  • [Title] Radioimmunotherapy with [188Re]-labelled anti-CD66 antibody in the conditioning for allogeneic stem cell transplantation for high-risk acute myeloid leukemia.
  • Between July 2000 and June 2003 a total of 21 patients with high-risk acute myeloid leukemia (AML; n = 14), AML after myelodysplastic syndrome (MDS; n = 6) or advanced MDS (n = 1) were treated with an 188-Re labelled anti-CD66 antibody in the conditioning regimen for allogeneic stem cell transplantation.
  • The combination of RIT with chemotherapeutic conditioning seems to be a therapy with an acceptable risk of treatment related morbidity and mortality as well as occurrence of severe acute GvHD.
  • [MeSH-major] Antibodies / therapeutic use. Antigens, CD / immunology. Cell Adhesion Molecules / immunology. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / radiotherapy. Radioimmunotherapy. Rhenium. Stem Cell Transplantation

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  • (PMID = 18415659.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD; 0 / CD66 antigens; 0 / Cell Adhesion Molecules; 0 / Radioisotopes; 7440-15-5 / Rhenium
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43. Giles F, Rizzieri D, Karp J, Vey N, Ravandi F, Faderl S, Khan KD, Verhoef G, Wijermans P, Advani A, Roboz G, Kantarjian H, Bilgrami SF, Ferrant A, Daenen SM, Karsten V, Cahill A, Albitar M, Mufti G, O'Brien S: Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia. J Clin Oncol; 2007 Jan 1;25(1):25-31
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  • [Title] Cloretazine (VNP40101M), a novel sulfonylhydrazine alkylating agent, in patients age 60 years or older with previously untreated acute myeloid leukemia.
  • A multicenter phase II study of cloretazine was conducted in patients 60 years of age or older with previously untreated acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS).
  • Patients were stratified by age, performance score, cytogenetic risk category, type of AML, and comorbidity.
  • Response rates in 44 de novo AML patients, 45 secondary AML patients, and 15 high-risk MDS patients were 50%, 11%, and 40%, respectively.
  • CONCLUSION: Cloretazine has significant activity and modest extramedullary toxicity in elderly patients with AML or high-risk MDS.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Hydrazines / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Sulfonamides / therapeutic use


44. de Vos D, van Overveld W: Decitabine: a historical review of the development of an epigenetic drug. Ann Hematol; 2005 Dec;84 Suppl 1:3-8
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  • The use of decitabine in MDS, AML, CML, stem cell transplant, sickle cell anemia and thalassemia looks promising.
  • [MeSH-minor] Anemia, Sickle Cell / drug therapy. Drug Design. History, 20th Century. History, 21st Century. Humans. Myelodysplastic Syndromes / drug therapy. Transplantation Conditioning / methods

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  • [ErratumIn] Ann Hematol. 2006 Aug;85(8):557
  • (PMID = 16220311.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 776B62CQ27 / decitabine; EC 2.1.1.- / DNA Modification Methylases; M801H13NRU / Azacitidine
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45. Barouk-Simonet E, Soenen-Cornu V, Roumier C, Cosson A, Laï JL, Fenaux P, Preudhomme C: Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases. Cancer Genet Cytogenet; 2005 Mar;157(2):118-26
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  • [Title] Role of multiplex FISH in identifying chromosome involvement in myelodysplastic syndromes and acute myeloid leukemias with complex karyotypes: a report on 28 cases.
  • Chromosomal abnormalities are found by conventional cytogenetic (CC) analysis in about 50% of myelodysplastic syndromes (MDS) and 70% of acute myeloid leukemias (AML).
  • We studied by M-FISH 28 cases of MDS and AML with complex chromosomal abnormalities, 10 of them were therapy-related.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Humans. Karyotyping. Male. Middle Aged


46. Galbraith D, Gross SA, Paustenbach D: Benzene and human health: A historical review and appraisal of associations with various diseases. Crit Rev Toxicol; 2010 Nov;40 Suppl 2:1-46
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  • Over the last century, benzene has been a well-studied chemical, with some acute and chronic exposures being directly associated with observed hematologic effects in humans and animals.
  • Chronic heavy exposures to benzene have also been associated with acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) in humans.
  • We also review the available scientific and medical evidence relating to benzene and the risk of developing various disorders following specific levels of exposure.
  • Our evaluation indicates that the only malignant hematopoietic disease that has been clearly linked to benzene exposure is AML.
  • [MeSH-minor] Female. History, 20th Century. History, 21st Century. Humans. Leukemia, Myeloid, Acute / epidemiology. Lymphoma, Non-Hodgkin / epidemiology. Male. Multiple Myeloma / epidemiology. Myelodysplastic Syndromes / epidemiology. Workplace

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  • (PMID = 20939751.001).
  • [ISSN] 1547-6898
  • [Journal-full-title] Critical reviews in toxicology
  • [ISO-abbreviation] Crit. Rev. Toxicol.
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] J64922108F / Benzene
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47. Dicker F, Haferlach C, Kern W, Haferlach T, Schnittger S: Trisomy 13 is strongly associated with AML1/RUNX1 mutations and increased FLT3 expression in acute myeloid leukemia. Blood; 2007 Aug 15;110(4):1308-16
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  • [Title] Trisomy 13 is strongly associated with AML1/RUNX1 mutations and increased FLT3 expression in acute myeloid leukemia.
  • Somatic mutations in RUNX1 are preferentially detected in acute myeloid leukemia (AML) M0, myeloid malignancies with acquired trisomy 21, and certain myelodysplastic syndrome (MDS) cases.
  • By correlating the presence of RUNX1 mutations with cytogenetic and molecular aberration in a large cohort of AML M0 (N = 90) at diagnosis, we detected RUNX1 mutations in 46% of cases, with all trisomy 13 cases (n = 18) being affected.
  • Quantitation of FLT3 transcript levels revealed a highly significant (P < .001) about 5-fold increase in AML with RUNX1 mutations and trisomy 13 compared with samples without trisomy 13.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid / genetics. Mutation / genetics. Trisomy. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. DNA, Neoplasm. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged

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  • (PMID = 17485549.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA, Neoplasm; 0 / RUNX1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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48. Slape C, Lin YW, Hartung H, Zhang Z, Wolff L, Aplan PD: NUP98-HOX translocations lead to myelodysplastic syndrome in mice and men. J Natl Cancer Inst Monogr; 2008;(39):64-8
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  • [Title] NUP98-HOX translocations lead to myelodysplastic syndrome in mice and men.
  • The myelodysplastic syndromes (MDS) are a group of clonal hematopoietic stem cell disorders characterized by ineffective hematopoiesis, peripheral blood cytopenias, dysplasia, and a propensity for transformation to acute myeloid leukemia (AML).
  • A wide spectrum of genetic aberrations has been associated with MDS, including chromosomal translocations involving the NUP98 gene, most commonly leading to fusions of NUP98 with abd-b group HOX genes, including HOXD13.
  • NHD13 transgenic mice faithfully recapitulate all the key features of MDS, including peripheral blood cytopenias, bone marrow dysplasia and apoptosis, and transformation to acute leukemia.
  • The MDS that develops in NHD13 transgenic mice is highly lethal; within 14 months, 90% of the mice died of either leukemic transformation or severe anemia and leukopenia due to progressive MDS.
  • These mice provide a preclinical model that can be used for the evaluation of MDS therapy and biology.
  • [MeSH-major] Homeodomain Proteins / genetics. Myelodysplastic Syndromes / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics. Translocation, Genetic


49. 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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50. Cashen AF, Shah AK, Todt L, Fisher N, DiPersio J: Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). Cancer Chemother Pharmacol; 2008 Apr;61(5):759-66
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  • [Title] Pharmacokinetics of decitabine administered as a 3-h infusion to patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • PURPOSE: In this study, pharmacokinetics (PK) of decitabine administered as a 3-h intravenous infusion of 15 mg/m2 every 8 h for 3 days (cycles repeated every 6 weeks) was evaluated in patients with MDS or AML.
  • METHODS: The PK of this dosing regimen was evaluated in sixteen patients with MDS or AML.
  • CONCLUSIONS: Decitabine dosed at 15 mg/m2 iv every 8 h for 3 days resulted in a predictable and manageable toxicity profile in patients with MDS/AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacokinetics. Azacitidine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


51. Hofmann WK, Koeffler HP: Myelodysplastic syndrome. Annu Rev Med; 2005;56:1-16
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  • [Title] Myelodysplastic syndrome.
  • During the past 15 years, important progress has been made in the understanding of the biology and prognosis of myelodysplastic syndrome (MDS).
  • MDS is a clonal disorder characterized by ineffective hematopoiesis, which can lead to either fatal cytopenias or acute myelogenous leukemia (AML).
  • Risk-adapted treatment strategies were established because of the high median age (60-75 years) of the MDS patients and the individual history of the disease (number of cytopenias, cytogenetic changes, transfusion requirements).
  • Allogeneic bone marrow transplantation currently offers the only potentially curative treatment, but this form of therapy is not available for the typical MDS patient, who is >60 years of age.
  • Innovative uses of immunomodulatory agents and the optimizing of cytotoxic treatment should continue to help in the treatment of MDS.
  • [MeSH-major] Myelodysplastic Syndromes / complications
  • [MeSH-minor] Aged. Bone Marrow Transplantation. Cause of Death. Erythropoietin / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Middle Aged. Pancytopenia / diagnosis. Pancytopenia / etiology. Pancytopenia / mortality. Pancytopenia / therapy. Prognosis. Survival Rate


52. Owen C, Barnett M, Fitzgibbon J: Familial myelodysplasia and acute myeloid leukaemia--a review. Br J Haematol; 2008 Jan;140(2):123-32
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  • [Title] Familial myelodysplasia and acute myeloid leukaemia--a review.
  • Familial occurrence of myelodysplasia (MDS) and/or acute myeloid leukaemia (AML) is rare but can provide a useful resource for the investigation of predisposing mutations in these myeloid malignancies.
  • To date, examination of families with MDS/AML has lead to the detection of two culprit genes, RUNX1 and CEBPA.
  • Germline mutations in RUNX1 result in familial platelet disorder with propensity to myeloid malignancy and inherited mutations of CEBPA predispose to AML.
  • Further insight into the molecular mechanisms of familial MDS/AML will require awareness by clinicians of new patients with relevant family histories.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Neoplastic Syndromes, Hereditary / genetics


53. Sakajiri S, O'kelly J, Yin D, Miller CW, Hofmann WK, Oshimi K, Shih LY, Kim KH, Sul HS, Jensen CH, Teisner B, Kawamata N, Koeffler HP: Dlk1 in normal and abnormal hematopoiesis. Leukemia; 2005 Aug;19(8):1404-10
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  • We have found by real-time RT-PCR that Dlk1 mRNA levels were high in CD34(+) cells in 10 of 12 MDS samples compared with CD34(+) cells from 11 normals.
  • Also, Dlk1 mRNA was elevated in mononuclear, low density bone marrow cells from 11/38 MDS patients, 5/11 AML M6 and 2/4 AML M7 samples.
  • Furthermore, 5/6 erythroleukemia and 2/2 megakaryocytic leukemia cell lines highly expressed Dlk1 mRNA.
  • In summary, Dlk1 is overexpressed in selected samples of MDS (especially RA and RAEB) and AML (particularly M6, M7), and it appears to be associated with normal development of megakaryocytes and B cells.
  • [MeSH-minor] Animals. Antigens, CD34. Case-Control Studies. Cell Differentiation. Cell Proliferation. Clone Cells / pathology. Gene Expression Regulation. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / pathology. Humans. Leukemia / genetics. Leukemia / pathology. Mice. Mice, Knockout. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction


54. Georgiou G, Karali V, Zouvelou C, Kyriakou E, Dimou M, Chrisochoou S, Greka P, Dufexis D, Vervesou E, Dimitriadou E, Efthymiou A, Petrikkos L, Dima K, Lilakos K, Panayiotidis P: Serial determination of FLT3 mutations in myelodysplastic syndrome patients at diagnosis, follow up or acute myeloid leukaemia transformation: incidence and their prognostic significance. Br J Haematol; 2006 Aug;134(3):302-6
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  • [Title] Serial determination of FLT3 mutations in myelodysplastic syndrome patients at diagnosis, follow up or acute myeloid leukaemia transformation: incidence and their prognostic significance.
  • The incidence of FLT3 mutations (internal tandem duplication and Asp835) was investigated in bone marrow samples from 97 patients with myelodysplastic syndrome [(MDS); excluding cases with refractory anaemia with excess blasts in transformation] at the time of diagnosis and several time points thereafter.
  • Forty-two patients progressed to acute myeloid leukaemia (AML), including the three patients with FLT3 mutations at MDS diagnosis.
  • Three additional patients acquired FLT3 mutations and progressed to AML in 1 month.
  • FLT3 mutations seem to be a critical additional genetic event that transforms a minority of MDS patients to AML.
  • [MeSH-major] Mutation. Myelodysplastic Syndromes / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. DNA Mutational Analysis. Disease Progression. Female. Humans. Leukemia, Myeloid / genetics. Male. Middle Aged. Prognosis. Proportional Hazards Models. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Survival Rate


55. 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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56. Rosenberg PS, Zeidler C, Bolyard AA, Alter BP, Bonilla MA, Boxer LA, Dror Y, Kinsey S, Link DC, Newburger PE, Shimamura A, Welte K, Dale DC: Stable long-term risk of leukaemia in patients with severe congenital neutropenia maintained on G-CSF therapy. Br J Haematol; 2010 Jul;150(2):196-9
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  • In severe congenital neutropenia (SCN), long-term therapy with granulocyte colony-stimulating factor (G-CSF) has reduced mortality from sepsis, revealing an underlying predisposition to myelodysplastic syndrome and acute myeloid leukaemia (MDS/AML).
  • We have reported the early pattern of evolution to MDS/AML, but the long-term risk remains uncertain.
  • Long-term, the annual risk of MDS/AML attained a plateau (2.3%/year after 10 years).
  • This risk now appears similar to, rather than higher than, the risk of AML in Fanconi anaemia and dyskeratosis congenita.

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  • (PMID = 20456363.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL079582; United States / NIAID NIH HHS / AI / R24 AI049393; United States / Intramural NIH HHS / / Z99 CA999999; United States / NIAID NIH HHS / AI / 2R24AI049393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS216450; NLM/ PMC2906693
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57. Öztürk A, Akyol Erikci A, Sayan Ö: Results of treatment of acute myeloid leukemia and myelodysplastic syndrome with etoposide, thioguanine, cytarabine (ETC) in elderly patients. Turk J Haematol; 2006 Dec 5;23(4):193-6
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  • [Title] Results of treatment of acute myeloid leukemia and myelodysplastic syndrome with etoposide, thioguanine, cytarabine (ETC) in elderly patients.
  • [Transliterated title] Yaşlı akut myeloid lösemili ve myelodisplastik sendromlu hastalarda etoposid, thioguanin, sitarabin tedavisinin sonuçları.
  • Treatment in elderly patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) remains controversial, and results have been poor with most regimens.
  • Eight patients had MDS (one transformed to AML) and six had AML.

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  • (PMID = 27265661.001).
  • [ISSN] 1300-7777
  • [Journal-full-title] Turkish journal of haematology : official journal of Turkish Society of Haematology
  • [ISO-abbreviation] Turk J Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
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58. Shimoni A, Hardan I, Shem-Tov N, Yerushalmi R, Nagler A: Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: long-term follow-up. Leukemia; 2010 May;24(5):1050-2
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  • [Title] Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: long-term follow-up.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myeloablative Agonists / therapeutic use. Myelodysplastic Syndromes / therapy. Transplantation Conditioning


59. Alter BP, Giri N, Savage SA, Peters JA, Loud JT, Leathwood L, Carr AG, Greene MH, Rosenberg PS: Malignancies and survival patterns in the National Cancer Institute inherited bone marrow failure syndromes cohort study. Br J Haematol; 2010 Jul;150(2):179-88
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  • Fanconi anaemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anaemia (DBA), and Shwachman-Diamond syndrome (SDS) comprise major inherited bone marrow failure syndromes (IBMFS).
  • Adverse events include severe bone marrow failure (BMF), myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML), and solid tumours (ST).
  • Most patients in each syndrome survived to young adulthood.
  • While FA and DC patients had markedly increased risks of cancer, AML and MDS, there were no cases of leukaemia in DBA or SDS patients.
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Anemia, Diamond-Blackfan / complications. Anemia, Diamond-Blackfan / genetics. Child. Child, Preschool. Dyskeratosis Congenita / complications. Dyskeratosis Congenita / genetics. Epidemiologic Methods. Fanconi Anemia / complications. Fanconi Anemia / genetics. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Prognosis. Syndrome. Young Adult


60. Economopoulou P, Pappa V, Kontsioti F, Papageorgiou S, Foukas P, Liakata E, Economopoulou C, Vassilatou D, Ioannidou ED, Chondropoulos S, Tsirigotis P, Papageorgiou E, Dervenoulas J, Economopoulos T: Expression analysis of proteins involved in the non homologous end joining DNA repair mechanism, in the bone marrow of adult de novo myelodysplastic syndromes. Ann Hematol; 2010 Mar;89(3):233-9
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  • [Title] Expression analysis of proteins involved in the non homologous end joining DNA repair mechanism, in the bone marrow of adult de novo myelodysplastic syndromes.
  • Myelodysplastic syndromes (MDS) are characterized by genetic instability which is associated with abnormal DNA repair mechanisms.
  • The aim of the present study was the analysis of expression of proteins required for NHEJ in bone marrow cells of adult de novo MDS and their association with clinical characteristics and prognosis.
  • Our analysis included 48 cases of MDS; 19 RA, 5 RARS, 19 RAEB, 3 RAEB-T, 1 CMML, 1 transformation to AML according to FAB classification.
  • The mean Ligase IV expression value was significantly lower in MDS patients compared to normal controls (0.53 vs. 0.78, p = 0.03).
  • Our findings suppor-t a potential role of NHEJ enzyme Ligase IV in the pathogenesis of MDS.
  • [MeSH-major] DNA Ligases / genetics. DNA Repair / genetics. Gene Expression Profiling. Myelodysplastic Syndromes / genetics. Proteins / genetics

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  • (PMID = 19727724.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / DNA-Binding Proteins; 0 / Ku autoantigen; 0 / Nuclear Proteins; 0 / Proteins; 0 / XRCC4 protein, human; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / PRKDC protein, human; EC 6.5.1.- / DNA Ligases; EC 6.5.1.1 / DNA ligase (ATP)
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61. Lu Y, Chen ZM, Xu WL, Mu QT, Jin J: [Clinical analysis of 24 cases of acute myeloid leukemia with 3q abnormalities]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2010 May;39(3):241-5
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  • [Title] [Clinical analysis of 24 cases of acute myeloid leukemia with 3q abnormalities].
  • OBJECTIVE: To investigate the clinical characteristics of acute myeloid leukemia patients with 3q abnormalities.
  • METHODS: Conventional cytogenetic analysis of R-banding was used to detect the abnormalities of 3q in 657 patients with acute myeloid leukemia (AML).
  • RESULT: Twenty-four (3.7%) out of 657 patients had abnormalities of 3q, of which 3q21 or 3q26 were involved in 18 cases (75.0%); 3q21q26 abnormalities were harbored in 11 patients (45.8%), including 9 of t (3;3) and 2 cases of inv (3), of which 3 cases progressed from MDS.
  • CONCLUSION: 3q21q26 anomaly is the most common karyotype in acute myeloid patients with 3q abnormalities.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. Leukemia, Myeloid, Acute / genetics


62. Pilatrino C, Cilloni D, Messa E, Morotti A, Giugliano E, Pautasso M, Familiari U, Cappia S, Pelicci PG, Lo Coco F, Saglio G, Guerrasio A: Increase in platelet count in older, poor-risk patients with acute myeloid leukemia or myelodysplastic syndrome treated with valproic acid and all-trans retinoic acid. Cancer; 2005 Jul 1;104(1):101-9
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  • [Title] Increase in platelet count in older, poor-risk patients with acute myeloid leukemia or myelodysplastic syndrome treated with valproic acid and all-trans retinoic acid.
  • BACKGROUND: The authors investigated the efficacy and safety of the histone deacetylase inhibitors valproic acid (VPA) and all-trans retinoic acid (ATRA) as differentiation agents in a cohort of older, poor-risk patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • METHODS: Twenty older patients with recurrent or refractory AML or MDS were treated in a Phase II protocol with sequential VPA and ATRA therapy.
  • CONCLUSIONS: Differentiation therapy with VPA was of clinical benefit in approximately 30% of elderly patients with AML and MDS of the refractory anemia with excess of blast type with unfavorable prognostic features.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Platelet Count. Tretinoin / therapeutic use. Valproic Acid / therapeutic use
  • [MeSH-minor] Acute Disease. Aged. Female. Humans. Male. Middle Aged. Risk


63. Desta F, Christiansen DH, Andersen MK, Pedersen-Bjergaard J: Activating mutations of JAK2V617F are uncommon in t-MDS and t-AML and are only observed in atypic cases. Leukemia; 2006 Mar;20(3):547-8
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  • [Title] Activating mutations of JAK2V617F are uncommon in t-MDS and t-AML and are only observed in atypic cases.
  • [MeSH-major] Leukemia, Myeloid / genetics. Mutation. Myelodysplastic Syndromes / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Acute Disease. Humans. Janus Kinase 2. Karyotyping

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  • (PMID = 16424876.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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64. Alyea EP, Kim HT, Ho V, Cutler C, DeAngelo DJ, Stone R, Ritz J, Antin JH, Soiffer RJ: Impact of conditioning regimen intensity on outcome of allogeneic hematopoietic cell transplantation for advanced acute myelogenous leukemia and myelodysplastic syndrome. Biol Blood Marrow Transplant; 2006 Oct;12(10):1047-55
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  • [Title] Impact of conditioning regimen intensity on outcome of allogeneic hematopoietic cell transplantation for advanced acute myelogenous leukemia and myelodysplastic syndrome.
  • We reviewed 136 patients with advanced acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) undergoing allogeneic transplantation to assess the impact of conditioning regimen intensity on outcome.
  • Patients receiving NST were at high risk for treatment-related complications given that they were older, 57 vs 43 years (P < .001), and more likely had received previous or myeloablative transplantation (54% vs 2%; P < .0001).
  • Despite the high-risk features of patients with advanced AML or MDS undergoing NST, OS and PFS in these patients was similar to those in patients receiving myeloablative transplantation.
  • These results suggest that NST is a reasonable alternative for patients with advanced AML and MDS at high risk for complications after myeloablative transplantation.
  • [MeSH-major] Bone Marrow Transplantation. Busulfan / administration & dosage. Cyclophosphamide / administration & dosage. Leukemia, Myeloid / surgery. Myelodysplastic Syndromes / surgery. Peripheral Blood Stem Cell Transplantation. Transplantation Conditioning. Vidarabine / analogs & derivatives. Whole-Body Irradiation
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Graft Survival. Graft vs Host Disease / epidemiology. Graft vs Host Disease / etiology. Humans. Incidence. Kaplan-Meier Estimate. Male. Middle Aged. Recurrence. Reoperation. Retrospective Studies. Tissue Donors. Transplantation, Homologous / mortality. Treatment Outcome


65. 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


66. Naito K, Ohnishi K: [Current and new therapeutic strategies in acute myeloid leukemia]. Gan To Kagaku Ryoho; 2005 Mar;32(3):292-6
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  • [Title] [Current and new therapeutic strategies in acute myeloid leukemia].
  • Seventy to 80% of patients with acute myeloid leukemia (AML) achieve complete remission (CR) by chemotherapy, but more than 50% of them then relapse.
  • Phase III clinical trials in the treatment of patients with previously untreated AML and acute promyelocytic leukemia (APL) are ongoing in Japan (JALSG AML 201, APL 204).
  • We discussed six topics in the treatment of AML. (1) To determine whether adding the MDR-1 modulator to chemotherapy provided clinical benefits to patients with AML and high-risk myelodysplastic syndrome (MDS), a phase III randomized study was performed using PSC 833.
  • In a randomized phase III trial, patients with high-risk MDS or patients with AML were randomized to receive 2 induction courses consisting of Ara-C and G-CSF during and after chemotherapy with or without fludarabine (FLAG versus AG).
  • In combined phase II studies of 277 patients with CD 33-positive AML in their first relapse, the overall response rate was 26%. (5) Arsenic trioxide (ATO) has been established as a highly effective therapy for patients with APL, even for those with disease refractory to ATRA.
  • ATO was recently approved in Japan. (6) There has been great interest in developing FLT 3 inhibitors because of the high frequency and poor prognosis of AML patients with mutant FLT 3.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Aminoglycosides / administration & dosage. Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Carbazoles / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Indoles / administration & dosage. Mice. Middle Aged. Mitoxantrone / administration & dosage. Piperazines / administration & dosage. Prognosis. Proto-Oncogene Proteins / antagonists & inhibitors. Quinazolines / administration & dosage. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. fms-Like Tyrosine Kinase 3

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  • (PMID = 15791811.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Carbazoles; 0 / Indoles; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; DO989GC5D1 / lestaurtinib; E1IO3ICJ9A / tandutinib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; MAV protocol
  • [Number-of-references] 8
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67. 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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68. Zhao MQ, Zhao HG: [Serum level of angiogenesis-related cytokins in patients with myelodysplastic syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):519-22
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  • [Title] [Serum level of angiogenesis-related cytokins in patients with myelodysplastic syndrome].
  • To study the serum levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in patients with myelodysplastic syndrome (MDS), serum from 43 MDS patients was examined by enzyme linked immunosorbent assay (ELISA).
  • The results showed that serum levels of VEGF, bFGF in MDS patients were significantly elevated compared with normal control.
  • No significant difference of serum levels of VEGF and bFGF was found between RAEBT patients and acute myeloid leukemia (AML) patients.
  • It is concluded that the secretion of VEGF and bFGF in MDS patients is elevated and the serum levels of VEGF and bFGF are related to the classification and prognosis in MDS.


69. 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


70. Niu Y, Chen SC, Jiang B, Li DG, Ge CW, Li RS: [Erythroleukemia - a subtype of myelodysplastic syndrome?]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Apr;15(2):219-23
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  • [Title] [Erythroleukemia - a subtype of myelodysplastic syndrome?].
  • In order to study whether erythroleukemia was really a subtype of acute leukemia, the clinical laboratory characteristics and development of disease in 21 cases of erythroleukemia were analyzed.
  • The median percentage of erythro-lineage, myeloblast of NEC and displasia were (58.3 +/- 8.0)%, (58.0 +/- 18.4)% and 66.7% respectively, that is different from typical AML.
  • 52.4% of M(6) patients transferred to RAEB/RAEB-T and AML-M(2) subtype in the disease progression.
  • The median survival length of M(6) and MDS-->M(6) from time of diagnosis were 13.0 +/- 13.2 and 2.3 +/- 1.3 months respectively.
  • It is concluded that there are differences between M(6) and typical AML.
  • Most of M(6) patients would rather be classified MDS RAEB and RAEB-t with over-hyperplasia of erythron lineage than a subtype of AML.


71. Bessho F, Imashuku S, Hibi S, Tsuchida M, Nakahata T, Miyazaki S, Kojima S, Tsukimoto I, Hamajima N, Pediatric AA Follow-up Study Group in Japan: Serial morphologic observation of bone marrow in aplastic anemia in children. Int J Hematol; 2005 Jun;81(5):400-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent reports of myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) developing after treatment with immunosuppressants and granulocyte colony-stimulating factor (G-CSF) has raised the question of whether previously unrecognized myelodysplastic features had been present or whether actual transformation had occurred.
  • In each case, bone marrow specimens were tested at study entry and every 6 months for 3 years to detect t-MDS/AML as defined by morphologic and molecular/cytogenetic criteria.
  • The patients in 4 of these cases had clonal cytogenetic abnormalities and received MDS diagnoses.
  • An elucidation of the role of mast cells may provide information about the differences between aplastic anemia and MDS or about the transition of aplastic anemia to MDS.
  • [MeSH-minor] Bone Marrow Examination. Child. Chromosome Aberrations. Disease Progression. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / adverse effects. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / diagnosis. Mast Cells / pathology. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / diagnosis

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  • [Cites] Hum Pathol. 1979 Mar;10(2):242-3 [422194.001]
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  • (PMID = 16158820.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 143011-72-7 / Granulocyte Colony-Stimulating Factor
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72. de Lima M, Giralt S: Allogeneic transplantation for the elderly patient with acute myelogenous leukemia or myelodysplastic syndrome. Semin Hematol; 2006 Apr;43(2):107-17
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  • [Title] Allogeneic transplantation for the elderly patient with acute myelogenous leukemia or myelodysplastic syndrome.
  • Acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) are diseases of the elderly.
  • Major obstacles to extending this form of treatment to older patients are lack of promptly available donors, graft-versus-host disease (GVHD), delayed immune recovery, and the high prevalence of refractory and relapsed disease intrinsic to the natural history of these myeloid malignancies.
  • Here we review current results of allogeneic blood and marrow transplantation for AML and MDS in the elderly.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


73. Szotkowski T, Rohon P, Zapletalova L, Sicova K, Hubacek J, Indrak K: Secondary acute myeloid leukemia - a single center experience. Neoplasma; 2010;57(2):170-8
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  • [Title] Secondary acute myeloid leukemia - a single center experience.
  • Secondary acute myeloid leukemia (sAML) may arise from the previous clonal disorder of hematopoiesis, usually from myelodysplastic syndrome (MDS) or from chronic myeloproliferative neoplasia (cMPN) or after exposure to a leukemogenic agent (previous chemotherapy or radiotherapy, some immunosuppressive drugs or environmental leukemogenic agents).
  • Secondary origin of AML is associated with unfavorable prognosis and it is not considered to be conventionally curable (with the exception of secondary acute promyelocytic leukemia).
  • Over that period of time, a total 574 patients with AML were diagnosed.
  • Of those, 430 patients were diagnosed as having primary AML; in 86 patients, sAML transformed from myelodysplastic syndrome and 58 patients were followed or treated for various malignancies or were treated with potentially leukemogenic agents because of non-malignant disorders.
  • Patients with secondary AML are older and less commonly treated with curative intention than those with primary AML.
  • With the exception of secondary acute promyelocytic leukemia, the prognosis of which does not differ from very good prognosis of the primary forms, secondary AML is not considered a conventionally curable disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Neoplasm Recurrence, Local / etiology. Neoplasms, Second Primary / etiology


74. Swolin B, Rödjer S, Westin J: Therapy-related patterns of cytogenetic abnormalities in acute myeloid leukemia and myelodysplastic syndrome post polycythemia vera: single center experience and review of literature. Ann Hematol; 2008 Jun;87(6):467-74
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  • [Title] Therapy-related patterns of cytogenetic abnormalities in acute myeloid leukemia and myelodysplastic syndrome post polycythemia vera: single center experience and review of literature.
  • A minor fraction of patients with polycythemia vera (PV) develop a terminal acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).
  • Analysis of the cytogenetic abnormalities during AML or MDS may help in understanding if this development is part of the natural course of the disease or induced by myelosuppressive therapy.
  • Thirty-six cases with AML or MDS post PV, collected in a single Swedish institution during a 33-year period, are described with special regard to time to development of AML or MDS, therapy given during active PV, and cytogenetic findings during AML or MDS.
  • A further 118 cases of AML or MDS post PV, in whom type of therapy during active PV and cytogenetic findings during AML or MDS were reported, were collected from the literature.
  • AML or MDS developed in our own series after 1-30 years with a fairly constant rate (two cases per year).
  • The type of therapy given during active PV influences the type of chromosome abnormalities present during terminal AML or MDS and can also be instrumental in the development of leukemia.
  • [MeSH-major] Abnormalities, Drug-Induced / genetics. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Polycythemia Vera / complications


75. Park TS, Choi JR, Yoon SH, Song J, Kim J, Kim SJ, Kwon O, Min YH: Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript. Cancer Genet Cytogenet; 2008 Dec;187(2):61-73
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  • [Title] Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript.
  • Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (AML) that is characterized by peculiar clinical and biologic features, including severe hemorrhagic diathesis, specific recurrent chromosomal aberration, and distinct morphologic features with predominant pathologic promyelocytes.
  • A reciprocal translocation involving chromosomes 15 and 17, t(15;17)(q22;q21), is a characteristic feature of APL that represents approximately 5-8% of AML.
  • In contrast to other AML subtypes, APL is particularly sensitive to treatment with all trans-retinoic acid (ATRA) combined with chemotherapy, converting this once fatal leukemia to a highly curable disease.
  • Nonetheless, therapy-related myelodysplastic syndrome-acute myelogenous leukemia (t-MDS/AML) has been reported as a rare complication of chemotherapy in APL.
  • Of 30 APL cases described as t-MDS/AML in the literature, only 1 case relapsed as acute leukemia with t(3;21)(q26;q22).
  • Here we describe a rare case of APL relapsing as secondary AML with t(3;21)(q26;q22) and clinically characterize this patient using the RUNX1 (previously AML1)-MDS1-EVI1 fusion transcript (with follow-up for 55 months), and review the relevant literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic


76. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
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  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology


77. Nimer SD: MDS: a stem cell disorder--but what exactly is wrong with the primitive hematopoietic cells in this disease? Hematology Am Soc Hematol Educ Program; 2008;:43-51
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  • [Title] MDS: a stem cell disorder--but what exactly is wrong with the primitive hematopoietic cells in this disease?
  • Despite the various abnormalities identified in the immune system or the bone marrow microenvironment in patients with myelodysplastic syndrome (MDS), most of the investigation of this disorder has centered on the hematopoietic stem/progenitor compartment.
  • It is generally written that MDS is a stem cell disorder, and there is certainly evidence supporting this view.
  • However, whether it occurs in a cell with only myeloid multipotentiality (i.e., that involves megakaryocytic, erythroid and granulocytic/monocytic lineages) or occurs in a true stem cell is open to debate.
  • Clearly, the common cytogenetic and genetic abnormalities found in MDS are most indicative of a clonal myeloid disease similar to AML, rather than a lymphoid disease, and the often tri-lineage ineffective hematopoiesis and dysplasia are generally not found within the lymphoid compartment.

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  • (PMID = 19074057.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / R01 DK52208; United States / NIDDK NIH HHS / DK / R01 DK52621
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, Thy-1
  • [Number-of-references] 62
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78. Neukirchen J, Blum S, Kuendgen A, Strupp C, Aivado M, Haas R, Aul C, Gattermann N, Germing U: Platelet counts and haemorrhagic diathesis in patients with myelodysplastic syndromes. Eur J Haematol; 2009 Nov;83(5):477-82
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  • [Title] Platelet counts and haemorrhagic diathesis in patients with myelodysplastic syndromes.
  • OBJECTIVES: Most patients with myelodysplastic syndromes (MDS) present with single or multiple lineage cytopenias in peripheral blood despite a hypercellular bone marrow.
  • However, there are hardly any studies on the clinical relevance of low platelet counts in MDS.
  • METHODS: We retrospectively analysed data from 2900 patients in the Duesseldorf MDS Registry who were diagnosed at our laboratory between 1982 and 2007.
  • Platelets were lower than 20 000/microL in 7% of the patients, especially in those with advanced stages of MDS, who showed a higher frequency of thrombocytopenia and platelet transfusion dependency.
  • Platelets lower than 100 000/microL were associated with significantly shortened survival (P < 0.00005), because of an increased risk of progression to acute myeloid leukaemia (AML) (30% vs. 21%) (P < 0.02) and bleeding (16% vs. 8%) (P = 0.0005).
  • [MeSH-major] Hemorrhagic Disorders / blood. Hemorrhagic Disorders / mortality. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / mortality. Platelet Count
  • [MeSH-minor] Disease-Free Survival. Female. Humans. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Platelet Transfusion. Predictive Value of Tests. Registries. Retrospective Studies. Survival Rate. Thrombocytopenia / blood. Thrombocytopenia / complications. Thrombocytopenia / mortality. Thrombocytopenia / therapy


79. 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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80. Aggerholm A, Holm MS, Guldberg P, Olesen LH, Hokland P: Promoter hypermethylation of p15INK4B, HIC1, CDH1, and ER is frequent in myelodysplastic syndrome and predicts poor prognosis in early-stage patients. Eur J Haematol; 2006 Jan;76(1):23-32
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  • [Title] Promoter hypermethylation of p15INK4B, HIC1, CDH1, and ER is frequent in myelodysplastic syndrome and predicts poor prognosis in early-stage patients.
  • The propensity of myelodysplastic syndrome (MDS) to transform into acute myeloid leukemia (AML) suggests the existence of common pathogenic components for these malignancies.
  • Here, four genes implicated in the development of AML were examined for promoter CpG island hypermethylation in cells from 37 patients with different stages of MDS.
  • Concurrent hypermethylation of > or = 3 genes was more frequent in advanced compared with early-stage MDS (P < or = 0.05), and hypermethylation of p15INK4B was associated with leukemic transformation in early MDS (P < or = 0.05).
  • Specifically, promoter hypermethylation identified a subgroup of early MDS with a particularly poor prognosis (median overall survival 20 months vs. 102 months; P = 0.004).
  • These data suggest that hypermethylation of p15INK4B, HIC1, CDH1, and ER contribute to the development and outcome of MDS.
  • [MeSH-major] Cadherins / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. DNA Methylation. DNA-Binding Proteins / genetics. Myelodysplastic Syndromes / genetics. Promoter Regions, Genetic / genetics. Receptors, Estrogen / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Disease-Free Survival. Female. Humans. Kruppel-Like Transcription Factors. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Multivariate Analysis. Polymerase Chain Reaction. Predictive Value of Tests. Prognosis. Risk Factors


81. Saba HI, Wijermans PW: Decitabine in myelodysplastic syndromes. Semin Hematol; 2005 Jul;42(3 Suppl 2):S23-31
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  • [Title] Decitabine in myelodysplastic syndromes.
  • Myelodysplastic syndromes (MDS) are a heterogenous group of hematopoietic stem cell disorders that are multifactorial in their etiology.
  • Aberrant DNA hypermethylation is now thought to be involved in MDS, as numerous tumor-suppressor genes have been identified that are silenced in these patients.
  • Several phase I/II studies have been conducted using a low-dose schedule of decitabine in MDS patients.
  • Recent results of a phase III study also confirmed that patients treated with decitabine compared to standard supportive care had higher overall response rates and longer time to AML transformation.
  • Decitabine appears to be a promising new therapy for the treatment of MDS; however, defining the optimal dosing schedule and exploring the possible use in combination with other agents such as the histone deacetylase inhibitors need further evaluation.
  • [MeSH-major] Azacitidine / analogs & derivatives. Myelodysplastic Syndromes / drug therapy


82. Breccia M, Mengarelli A, Mancini M, Biondo F, Gentilini F, Latagliata R, Mandelli F, Alimena G: Myelodysplastic syndromes in patients under 50 years old: a single institution experience. Leuk Res; 2005 Jul;29(7):749-54
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  • [Title] Myelodysplastic syndromes in patients under 50 years old: a single institution experience.
  • We report on our experience relating to 62 patients with myelodysplastic syndrome (MDS) aged less than 50 years, seen at our Institution and conservatively treated from July 1983 to December 2000.
  • Patients demographics and clinical features at diagnosis were analysed for their prognostic value on survival and on risk of transformation to acute leukaemia.
  • At a median follow-up of 15 months 19 patients (31%) progressed to acute myeloid leukaemia (AML).
  • From univariate analysis we identified some features, which appeared to be predictive of outcome and risk of transformation to AML.
  • Age above 40 years (p = 0.002) and high risk according to IPSS score (p = 0.002) were found to be predictive for a shorter survival; FAB grouping (p = 0.0001), percentage > 5% of blasts in the bone marrow (p = 0.001) and high risk by IPSS score (p = 0.0003) were found to be predictive for a higher risk of transformation to AML.
  • Presenting features in young MDS patients may identify subjects at higher risk of unfavourable outcome.
  • [MeSH-major] Myelodysplastic Syndromes / physiopathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia, Sideroblastic / etiology. Cell Transformation, Neoplastic. Female. Humans. Leukemia / etiology. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis


83. Heilig CE, Löffler H, Mahlknecht U, Janssen JW, Ho AD, Jauch A, Krämer A: Chromosomal instability correlates with poor outcome in patients with myelodysplastic syndromes irrespectively of the cytogenetic risk group. J Cell Mol Med; 2010 Apr;14(4):895-902
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  • [Title] Chromosomal instability correlates with poor outcome in patients with myelodysplastic syndromes irrespectively of the cytogenetic risk group.
  • Thereby, CIN was measured in 65 patients with myelodysplastic syndromes (MDS), acute myeloid leukaemia (AML) and control subjects.
  • Among MDS patients, a subgroup with elevated levels of CIN was identified.
  • At a median follow-up of 17.2 months, all patients within this 'high CIN' subgroup had died or progressed to AML, while 80% of MDS patients with normal CIN levels had stable disease (P < 0.001).
  • Notably, there was no statistically significant difference between 'normal CIN' and 'high CIN' MDS patients regarding established risk factors.
  • Furthermore, in all three MDS patients for whom serial measurements were available, development of AML was preceded by increasing CIN levels.
  • In conclusion, elevated CIN levels may be valuable as an early indicator of poor prognosis in MDS, hence corroborating the concept of CIN as a driving force in tumour progression.
  • [MeSH-major] Chromosomal Instability / genetics. Cytogenetic Analysis. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Humans. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Risk Factors. Treatment Outcome. Tumor Cells, Cultured


84. 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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85. Wang ZM, Cong YQ, Ma LN, Hu XJ: [Expression of cysteine rich 61 and vascular endothelial growth factor genes in patients with myelodysplastic syndromes and their relationship.]. Zhonghua Xue Ye Xue Za Zhi; 2009 Nov;30(11):745-8
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  • [Title] [Expression of cysteine rich 61 and vascular endothelial growth factor genes in patients with myelodysplastic syndromes and their relationship.].
  • OBJECTIVE: To explore the expression of Cysleine-rich 61(Cyr61) gene in the different subtypes of myelodysplastic syndromes (MDS), and the significance of Cyr61 in the genesis progression, and transformation of MDS and the relationship between Cyr61 and vascular endothelial grown factor (VEGF).
  • METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemical S-P were used to detect mRNA and protein expressions of Cyr61 and VEGF in bone marrow mononuclear cells (BMMNC) from 28 MDS, 12 acute myeloid leukemia (AML) patients, and 10 normal volunteers.
  • RESULTS: Expressions of Cyr61 and VEGF were higher in MDS and AML patients than in controls (P < 0.05).
  • The expressions of Cyr61 and VEGF were significantly higher in high risk group (0.3998 +/- 0.2647, 0.4775 +/- 0.1342) than that in low risk MDS group (0.2213 +/- 0.1465, 0.2872 +/- 0.2341) (P < 0.05), but no significant difference between high risk MDS and AML patients.
  • Expressions of Cyr61 and VEGF protein were higher in MDS patients than in normal controls (P < 0.05), and were significantly higher in high risk MDS group \[(38.7 +/- 2.9)%, (43.2 +/- 2.7)%\] than in low risk group \[(31.4 +/- 3.1)%, (33.5 +/- 3.4)%\] (P < 0.05).
  • CONCLUSION: Cyr61 and VEGF may play a role in the angiogenesis and pathogenesis of MDS.
  • [MeSH-major] Myelodysplastic Syndromes. Vascular Endothelial Growth Factor A
  • [MeSH-minor] Bone Marrow Cells / metabolism. Cysteine. Humans. Leukemia, Myeloid, Acute


86. Braun T, Carvalho G, Coquelle A, Vozenin MC, Lepelley P, Hirsch F, Kiladjian JJ, Ribrag V, Fenaux P, Kroemer G: NF-kappaB constitutes a potential therapeutic target in high-risk myelodysplastic syndrome. Blood; 2006 Feb 1;107(3):1156-65
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  • [Title] NF-kappaB constitutes a potential therapeutic target in high-risk myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS) is a preneoplastic condition that frequently develops into overt acute myeloid leukemia (AML).
  • The P39 MDS/AML cell line manifested constitutive NF-kappaB activation.
  • Bone marrow cells from high-risk MDS patients also exhibited constitutive NF-kappaB activation similar to bone marrow samples from MDS/AML patients.
  • Purified hematopoietic stem cells (CD34+) and immature myeloid cells (CD33+) from high-risk MDS patients demonstrated the nuclear translocation of the p65 NF-kappaB subunit.
  • NF-kappaB activation was confined to those cells that carried MDS-associated cytogenetic alterations.
  • Since NF-kappaB inhibition induced rapid apoptosis of bone marrow cells from high-risk MDS patients, we postulate that NF-kappaB activation is responsible for the progressive suppression of apoptosis affecting differentiating MDS cells and thus contributes to malignant transformation.
  • NF-kappaB inhibition may constitute a novel therapeutic strategy if apoptosis induction of MDS stem cells is the goal.
  • [MeSH-major] Apoptosis / drug effects. Cell Nucleus / metabolism. Myelodysplastic Syndromes / metabolism. Myeloid Progenitor Cells / metabolism. RNA, Small Interfering / pharmacology. Transcription Factor RelA / antagonists & inhibitors


87. Tsimberidou AM, Estey E, Wen S, Pierce S, Kantarjian H, Albitar M, Kurzrock R: The prognostic significance of cytokine levels in newly diagnosed acute myeloid leukemia and high-risk myelodysplastic syndromes. Cancer; 2008 Oct 1;113(7):1605-13
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  • [Title] The prognostic significance of cytokine levels in newly diagnosed acute myeloid leukemia and high-risk myelodysplastic syndromes.
  • BACKGROUND: Tumor necrosis factor (TNF)-alpha and other cytokines are involved in the pathogenesis of acute myeloid leukemia (AML) and high-risk myelodysplastic syndromes (MDS), but their prognostic significance in these diseases is unknown.
  • In the current study, the authors assessed the association between serum levels of various cytokines and clinical outcomes in patients with untreated AML or high-risk MDS.
  • METHODS: Serum levels of TNF-alpha, interleukin (IL)-1 receptor antagonist, IL-6, IL-10, and endostatin were measured in patients with AML or high-risk MDS who presented for treatment at The University of Texas M. D.
  • RESULTS: Higher TNF-alpha levels were found to correlate with poorer performance status; higher leukocyte counts; higher levels of beta2-microglobulin, creatinine, uric acid, and alkaline phosphatase; lower levels of creatinine clearance and albumin; baseline infection; and M4-M5 AML subtypes.
  • CONCLUSIONS: High serum TNF-alpha level is an adverse prognostic factor for survival and EFS in patients with untreated AML or high-risk MDS.
  • [MeSH-major] Cytokines / blood. Leukemia, Myeloid, Acute / blood. Myelodysplastic Syndromes / blood. Tumor Necrosis Factor-alpha / blood


88. van Besien K, Kunavakkam R, Rondon G, De Lima M, Artz A, Oran B, Giralt S: Fludarabine-melphalan conditioning for AML and MDS: alemtuzumab reduces acute and chronic GVHD without affecting long-term outcomes. Biol Blood Marrow Transplant; 2009 May;15(5):610-7
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  • [Title] Fludarabine-melphalan conditioning for AML and MDS: alemtuzumab reduces acute and chronic GVHD without affecting long-term outcomes.
  • The purpose of this study was to determine the effect of alemtuzumab on treatment-related mortality (TRM), relapse, overall survival (OS), and disease-free survival (DSF) in patients with acute myelogenous leukemia (AML) and myelodysplastic syndromes (MDS) undergoing reduced intensity conditioning (RIC).
  • The incidence of acute graft-versus-host disease (aGVHD) grade II-IV (relative risk [RR] 5.5, P < .01) and chronic GVHD (cGVHD) (RR 6.6, P < .01) were significantly lower in patients receiving alemtuzumab.
  • The addition of alemtuzumab to an RIC regimen dramatically reduces the incidence of aGVHD and cGVHD in patients with AML and MDS undergoing allogeneic transplantation.

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  • (PMID = 19361753.001).
  • [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 / K24 CA116471; United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / R21 CA101337; United States / NCI NIH HHS / CA / 1-R21 CA 101337-01
  • [Publication-type] Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate; 3A189DH42V / alemtuzumab; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS589065; NLM/ PMC4348112
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89. Bonati A, Rizzoli V, Lunghi P: Arsenic trioxide in hematological malignancies: the new discovery of an ancient drug. Curr Pharm Biotechnol; 2006 Dec;7(6):397-405
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  • Currently, Arsenic Trioxide (ATO) is considered the treatment of choice for patients with relapsed acute promyelocytic leukemia (APL).
  • The results of clinical trials of ATO administration as single agent in multiple myeloma (MM) and myelodisplastic syndromes (MDS) were encouraging and showed clinical effects but they were not close to APL success.
  • On the contrary, results of clinical trials to treat non-APL acute myeloid leukemia (AML) were disappointing.
  • We suggest that a combination therapy with drugs targeting specific pro-survival molecules or capable to enhance pro-apoptotic pathways may lead to an improvement of ATO efficacy against hematological malignancies, in particular AML.
  • Our pre-clinical studies showed that ATO is capable to induce cell death in acute leukemia cells but the apoptotic function is limited since it can induce also a mechanism of cell defense by activating pro-survival molecules such as MEK-ERK, Bcl-xL, Bcl-2.
  • Our results provide an experimental basis for combined or sequential treatment with MEK inhibitors and ATO in AML.


90. Spanaki A, Perdikogianni C, Linardakis E, Kalmanti M: Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia. Leuk Res; 2007 May;31(5):639-42
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  • [Title] Quantitative assessment of PRAME expression in diagnosis of childhood acute leukemia.
  • The purpose of this study was to investigate PRAME expression levels in children with acute leukemia with real-time PCR analysis.
  • Seventeen children with newly diagnosed or relapsed acute leukemia (11 ALL, 4 AML, 1 acute myeloblastic leukemia secondary to MDS, 1 ALL at relapse) and a control group of seven children were studied.
  • Overexpression of PRAME was found in 52.9% (3 AML, 6 ALL) of the patients studied.
  • The above findings indicate that PRAME expression in acute leukemia does not seem to be of prognostic significance, whereas it might represent a candidate marker for the monitoring of minimal residual disease.
  • [MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Leukemia, Myeloid / genetics. Neoplasm, Residual / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Humans. Prognosis. RNA, Messenger. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16860864.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger
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91. Fabre C, Carvalho G, Tasdemir E, Braun T, Adès L, Grosjean J, Boehrer S, Métivier D, Souquère S, Pierron G, Fenaux P, Kroemer G: NF-kappaB inhibition sensitizes to starvation-induced cell death in high-risk myelodysplastic syndrome and acute myeloid leukemia. Oncogene; 2007 Jun 14;26(28):4071-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-kappaB inhibition sensitizes to starvation-induced cell death in high-risk myelodysplastic syndrome and acute myeloid leukemia.
  • CD34(+) bone marrow blasts from high-risk myelodysplastic syndrome (MDS) patients as well as MDS patient-derived cell lines (P39 and MOLM13) constitutively activate the nuclear factor-kappaB (NF-kappaB) pathway and undergo apoptosis when NF-kappaB is inhibited.
  • In contrast, BAY11-7082 (which targets the NF-kappaB-activating I-kappaB kinase (IKK) complex) or knockdown of essential components of the NF-kappaB system (such as the IKK1 and IKK2 subunits of the IKK complex and the p65 subunit of NF-kappaB), by small interfering RNAs sensitized MDS cell lines to starvation-induced apoptosis.
  • The combination of BAY11-7082 and nutrient depletion synergistically killed the acute myeloid leukemia (AML) cell line U937 as well as primary CD34(+) bone marrow blasts from AML and high-risk MDS patients.
  • These results suggest that in MDS cells, NF-kappaB inhibition can precipitate a bioenergetic crisis that leads to an autophagic stress response followed by apoptotic cell death.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Death. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. NF-kappa B / antagonists & inhibitors. Nitriles / therapeutic use. Sulfones / therapeutic use
  • [MeSH-minor] Acute Disease. Fluorescent Antibody Technique. Humans


92. 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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93. Parker TM, Klaassen RJ, Johnston DL: Spontaneous remission of myelodysplastic syndrome with monosomy 7 in a young boy. Cancer Genet Cytogenet; 2008 Apr 15;182(2):122-5
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  • [Title] Spontaneous remission of myelodysplastic syndrome with monosomy 7 in a young boy.
  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder that often results in progression to acute myeloid leukemia (AML), particularly when additional genetic abnormalities are present, such as monosomy 7.
  • In the present case, a previously healthy 3-year-old boy diagnosed with MDS and monosomy 7 achieved spontaneous remission without intervention 30 months after initial diagnosis.
  • [MeSH-major] Chromosomes, Human, Pair 7 / genetics. Monosomy / genetics. Myelodysplastic Syndromes / genetics


94. Stauder R, Wimazal F, Nösslinger T, Krieger O, Sperr WR, Sill H, Pfeilstöcker M, Valent P: [Individualized management and therapy of myelodysplastic syndromes]. Wien Klin Wochenschr; 2008;120(17-18):523-37
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  • [Title] [Individualized management and therapy of myelodysplastic syndromes].
  • Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis and a tendency to transition to acute myeloid leukemia.
  • Due to the increasing number of older patients in Austria and the high frequency of therapy-associated MDS following successful chemo- and/or radiotherapy of a primary tumor, the frequency and relevance of MDS are continuously increasing.
  • While therapeutic options were until recently limited to best supportive care, AML-like induction chemotherapy and hematopoietic stem cell transplantation (HSCT) in younger patients, in recent years new therapeutic options have become available.
  • In addition, immune-modulating drugs (IMiDs) like lenalidomide or epigenetically effective agents like the cytosine analogues or histone deacetylase (HDAC) inhibitors have become available and are highly effective in distinct subgroups of MDS patients.
  • The development of state-of-the art recommendations is one of the major aims of the MDS Platform of the Austrian Society of Hematology and Oncology.
  • This manuscript reviews recent developments in clinical scoring and targeted and individualized MDS therapy and discusses their relevance in and potential applicability to daily practice.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Immunologic Factors / therapeutic use. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation / trends


95. Germing U, Strupp C, Kuendgen A, Isa S, Knipp S, Hildebrandt B, Giagounidis A, Aul C, Gattermann N, Haas R: Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes. Haematologica; 2006 Dec;91(12):1596-604
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  • [Title] Prospective validation of the WHO proposals for the classification of myelodysplastic syndromes.
  • BACKGROUND AND OBJECTIVES: The aim of this study was a prospective validation of the World Health Organization (WHO) proposals for the classification of myelodysplastic syndromes (MDS) with respect to their prognostic relevance.
  • DESIGN AND METHODS: We classified 1095 patients with MDS diagnosed at our institution between November 1999 and December 2004 according to French-American-British (FAB) and WHO criteria by central morphologic review.
  • Patients were followed for survival and disease evolution to acute myeloid leukemia (AML) through December 31th, 2005.
  • RESULTS: According to the WHO classification, there were 89 cases of refractory anemia (RA), 293 of refractory cytopenias with multilineage dysplasia (RCMD), 31 RA with ringed sideroblasts (RARS), 139 RCMD with ringed sideroblasts (RCMD-RS), 142 RA with excess blasts (RAEB) I and 149 RAEB II and 52 patients with 5q- syndrome.
  • The cumulative risk of AML evolution 2 years after diagnosis was 0% in RA and RARS, 8% in 5q-, 9% in RCMD, 12% in RCMD-RS, 13% in RAEB I and 40% in RAEB II.
  • [MeSH-major] Myelodysplastic Syndromes / classification. World Health Organization


96. Miesner M, Haferlach C, Bacher U, Weiss T, Macijewski K, Kohlmann A, Klein HU, Dugas M, Kern W, Schnittger S, Haferlach T: Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC). Blood; 2010 Oct 14;116(15):2742-51
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  • [Title] Multilineage dysplasia (MLD) in acute myeloid leukemia (AML) correlates with MDS-related cytogenetic abnormalities and a prior history of MDS or MDS/MPN but has no independent prognostic relevance: a comparison of 408 cases classified as "AML not otherwise specified" (AML-NOS) or "AML with myelodysplasia-related changes" (AML-MRC).
  • The World Health Organization classification of acute myeloid leukemia (AML) is hierarchically structured and integrates genetics, data on patients' history, and multilineage dysplasia (MLD).
  • The category "AML with myelodysplastic syndrome (MDS)-related changes" (AML-MRC) is separated from "AML not otherwise specified" (AML-NOS) by presence of MLD, MDS-related cytogenetics, or history of MDS or MDS/myeloproliferative neoplasm (MPN).
  • We analyzed 408 adult patients categorized as AML-MRC or AML-NOS.
  • However, MLD correlated with preexisting MDS (P < .001) and MDS-related cytogenetics (P = .035).
  • Patients with MLD as sole AML-MRC criterion (AML-MLD-sole; n = 90) had less frequently FLT3 internal tandem duplication (P = .032) and lower median age than AML-NOS (n = 232).
  • Contrarily, patients with AML-NOS combined with AML-MLD-sole (n = 323) had better 3-year EFS (16.9 vs 10.7 months; P = .005) and 3-year OS (55.8% vs 32.5%; P = .001) than patients with history of MDS or MDS/MPN or MDS-related cytogenetics (n = 85).
  • Gene expression analysis showed distinct clusters for AML-MLD-sole combined with AML-NOS versus AML with MDS-related cytogenetics or MDS history.
  • Thus, MLD alone showed no independent clinical effect, whereas cytogenetics and MDS history were prognostically relevant.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


97. Li X, Wu LY, Ying SX, Chang CK, He Q, Song LQ, Pu Q: [Preliminary study of biological characteristics of myelodysplastic syndromes clonal cells]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):478-83
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  • [Title] [Preliminary study of biological characteristics of myelodysp