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1. Full Text Recurrent DNMT3A mutations in patients with myelodysplastic syndromes
by Walter, M.J and Ding, L and Shen, D and Shao, J and Grillot, M and McLellan, M and Fulton, R and Schmidt, H and Kalicki-Veizer, J and O'Laughlin, M and Kandoth, C and Baty, J and Westervelt, P and Dipersio, J.F and Mardis, E.R and Wilson, R.K and Ley, T.J and Graubert, T.A
Leukemia, ISSN 0887-6924, 07/2011, Volume 25, Issue 7, pp. 1153 - 1158
Alterations in DNA methylation have been implicated in the pathogenesis of myelodysplastic syndromes (MDS), although the underlying mechanism remains largely... 
myelodysplastic syndrome | mutation | DNMT3A | METHYLATION | METHYLTRANSFERASE GENE EZH2 | 4Q24 | TET2 | ALPHA | CANCER | ONCOLOGY | COMMON | HEMATOLOGY | MDS | NOVO DNA METHYLTRANSFERASE | Prognosis | Humans | Middle Aged | Male | Granulocyte Precursor Cells - enzymology | Myelodysplastic Syndromes - enzymology | Young Adult | Leukemia, Myeloid, Acute - enzymology | Aged, 80 and over | Adult | Female | Codon - genetics | Kaplan-Meier Estimate | Exons - genetics | DNA Methylation - genetics | Sequence Analysis, DNA | Disease Progression | Leukemia, Myeloid, Acute - mortality | DNA (Cytosine-5-)-Methyltransferases - genetics | Myelodysplastic Syndromes - mortality | CpG Islands - genetics | Aged | Myelodysplastic Syndromes - genetics | DNA, Neoplasm - genetics | Mutation | Leukemia, Myeloid, Acute - genetics | Gene mutations | DNA | Physiological aspects | Development and progression | Genetic aspects | Research | Methylation | Health aspects | Myelodysplastic syndromes | Risk factors
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2. Full Text Isocitrate dehydrogenase mutations in myeloid malignancies
by Medeiros, B.C and Fathi, A.T and DiNardo, C.D and Pollyea, D.A and Chan, S.M and Swords, R
Leukemia, ISSN 0887-6924, 02/2017, Volume 31, Issue 2, pp. 272 - 281
Alterations to genes involved in cellular metabolism and epigenetic regulation are implicated in the pathogenesis of myeloid malignancies. Recurring mutations... 
IDH2 MUTATIONS | OLDER PATIENTS | DOSE CYTARABINE | ONCOLOGY | MUTANT IDH2 | PROGNOSTIC-SIGNIFICANCE | DNMT3A MUTATIONS | ENZYME ISOFORMS | HEMATOLOGY | ONCOMETABOLITE 2-HYDROXYGLUTARATE | MYELODYSPLASTIC SYNDROMES | SOMATIC MUTATIONS | Prognosis | Isoenzymes | Gene Frequency | Humans | Leukemia, Myeloid, Acute - epidemiology | Isocitrate Dehydrogenase - genetics | Myelodysplastic Syndromes - epidemiology | Biomarkers, Tumor | Myelodysplastic Syndromes - enzymology | Leukemia, Myeloid, Acute - mortality | Leukemia, Myeloid, Acute - enzymology | Animals | DNA Mutational Analysis | Isocitrate Dehydrogenase - metabolism | Myelodysplastic Syndromes - genetics | Mutation | Leukemia, Myeloid, Acute - genetics | Care and treatment | Research | Isocitrate dehydrogenase | Myelodysplastic syndromes | Krebs cycle | Mutation (Biology) | Review
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3. Full Text Phase IIB Trial of Oral Midostaurin (PKC412), the FMS-Like Tyrosine Kinase 3 Receptor (FLT3) and Multi-Targeted Kinase Inhibitor, in Patients With Acute Myeloid Leukemia and High-Risk Myelodysplastic Syndrome With Either Wild-Type or Mutated FLT3
by Thomas Fischer and Richard M. Stone and Daniel J. DeAngelo and Ilene Galinsky and Elihu Estey and Carlo Lanza and Edward Fox and Gerhard Ehninger and Eric J. Feldman and Gary J. Schiller and Virginia M. Klimek and Stephen D. Nimer and D. Gary Gilliland and Catherine Dutreix and Alice Huntsman-Labed and Jodi Virkus and Francis J. Giles
Journal of Clinical Oncology, ISSN 0732-183X, 10/2010, Volume 28, Issue 28, pp. 4339 - 4345
Purpose Mutations leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blasts of 30% of patients with acute myeloid... 
RESPONSE CRITERIA | ONCOLOGY | CHEMOTHERAPY | INTERNATIONAL WORKING GROUP | Administration, Oral | Humans | Staurosporine - adverse effects | Male | Staurosporine - analogs & derivatives | Treatment Outcome | Antineoplastic Agents - therapeutic use | Antineoplastic Agents - administration & dosage | Myelodysplastic Syndromes - enzymology | fms-Like Tyrosine Kinase 3 - genetics | Leukemia, Myeloid, Acute - enzymology | Receptor Protein-Tyrosine Kinases - genetics | Antineoplastic Agents - adverse effects | Staurosporine - therapeutic use | Leukemia, Myeloid, Acute - drug therapy | Female | Aged | Myelodysplastic Syndromes - genetics | Mutation | Myelodysplastic Syndromes - drug therapy | Leukemia, Myeloid, Acute - genetics | Staurosporine - administration & dosage | Index Medicus | Hema7 | ORIGINAL REPORTS | Bios3
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4. Full Text Ezh2 loss promotes development of myelodysplastic syndrome but attenuates its predisposition to leukaemic transformation
by Sashida, Goro and Harada, Hironori and Matsui, Hirotaka and Oshima, Motohiko and Yui, Makiko and Harada, Yuka and Tanaka, Satomi and Mochizuki-Kashio, Makiko and Wang, Changshan and Saraya, Atsunori and Muto, Tomoya and Hayashi, Yoshihiro and Suzuki, Kotaro and Nakajima, Hiroshi and Inaba, Toshiya and Koseki, Haruhiko and Huang, Gang and Kitamura, Toshio and Iwama, Atsushi
Nature Communications, ISSN 2041-1723, 06/2014, Volume 5, Issue 1, p. 4177
Loss-of-function mutations of EZH2, a catalytic component of polycomb repressive complex 2 (PRC2), are observed in similar to 10% of patients with... 
POINT MUTATIONS | METHYLATION | MULTIDISCIPLINARY SCIENCES | HEMATOPOIETIC STEM-CELLS | METHYLTRANSFERASE GENE EZH2 | IN-VIVO | MYELOID-LEUKEMIA | PROLIFERATION | DIFFERENTIATION | EXPRESSION | SOMATIC MUTATIONS | Polycomb Repressive Complex 2 - genetics | Core Binding Factor Alpha 2 Subunit - metabolism | Bone Marrow Cells - enzymology | Leukemia, Myeloid, Acute - pathology | Homeodomain Proteins - metabolism | Humans | Mice, Inbred C57BL | Male | Disease Progression | Enhancer of Zeste Homolog 2 Protein | Homeodomain Proteins - genetics | Mice, Knockout | Myelodysplastic Syndromes - enzymology | Leukemia, Myeloid, Acute - enzymology | Animals | Polycomb Repressive Complex 2 - deficiency | Cell Transformation, Neoplastic | Female | Mice | Myelodysplastic Syndromes - genetics | Myelodysplastic Syndromes - pathology | Core Binding Factor Alpha 2 Subunit - genetics | Disease Models, Animal | Leukemia, Myeloid, Acute - genetics
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5. Full Text Phase 1 study of the histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid [SAHA]) in patients with advanced leukemias and myelodysplastic syndromes
by Garcia-Manero, Guillermo and Yang, Hui and Bueso-Ramos, Carlos and Ferrajoli, Alessandra and Cortes, Jorge and Wierda, William G and Faderl, Stefan and Koller, Charles and Morris, Gail and Rosner, Gary and Loboda, Andrey and Fantin, Valeria R and Randolph, Sophia S and Hardwick, James S and Reilly, John F and Chen, Cong and Ricker, Justin L and Secrist, J. Paul and Richon, Victoria M and Frankel, Stanley R and Kantarjian, Hagop M
Blood, ISSN 0006-4971, 2008, Volume 111, Issue 3, pp. 1060 - 1066
Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinically in cutaneous T-cell lymphoma and preclinically in... 
BREAST-CANCER | ADVANCED CANCER | WORKING GROUP | CHRONIC LYMPHOCYTIC-LEUKEMIA | T-CELL LYMPHOMA | VALPROIC ACID | ACUTE MYELOID-LEUKEMIA | TRANS-RETINOIC ACID | HEMATOLOGY | HEMATOLOGIC MALIGNANCIES | CLINICAL ACTIVITY | Leukemia - pathology | Humans | Hydroxamic Acids - adverse effects | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Gene Expression Profiling | Myelodysplastic Syndromes - enzymology | Dose-Response Relationship, Drug | Drug-Related Side Effects and Adverse Reactions | Aged, 80 and over | Hydroxamic Acids - administration & dosage | Adult | Female | Acetylation | Leukemia - genetics | Myelodysplastic Syndromes - drug therapy | Leukemia - enzymology | Drug Tolerance | Leukemia - drug therapy | Histone Deacetylases - metabolism | Enzyme Inhibitors - therapeutic use | Adolescent | Hydroxamic Acids - therapeutic use | Aged | Histone Deacetylase Inhibitors | Histones - metabolism | Myelodysplastic Syndromes - pathology | Neoplasm Staging | Clinical Trials, Phase I as Topic
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6. Full Text The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both "atypical" myeloproliferative disorders and myelodysplastic syndromes
by Steensma, David P and Dewald, Gordon W and Lasho, Terra L and Powell, Heather L and McClure, Rebecca F and Levine, Ross L and Gilliland, D. Gary and Tefferi, Ayalew
Blood, ISSN 0006-4971, 08/2005, Volume 106, Issue 4, pp. 1207 - 1209
A somatic mutation in the JH2 autoinhibitory domain of the Janus kinase 2 (JAK2) tyrosine kinase was recently described in polycythemia vera, essential... 
CLASSIFICATION | DISEASES | LEUKEMIA | HEMATOLOGY | CMML | IMATINIB | Myeloproliferative Disorders - enzymology | Genetic Testing | Prevalence | Humans | Middle Aged | Male | Proto-Oncogene Proteins - genetics | Mutation, Missense | Myelodysplastic Syndromes - epidemiology | Myeloproliferative Disorders - genetics | Myelodysplastic Syndromes - enzymology | Janus Kinase 2 | Protein-Tyrosine Kinases - genetics | Molecular Epidemiology | Aged, 80 and over | Myeloproliferative Disorders - epidemiology | Adult | Female | Aged | Myelodysplastic Syndromes - genetics | Bone Marrow
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7. Full Text Somatic mutations in PTPN11 in juvenile myelomonocytic leukemia, myelodysplastic syndromes and acute myeloid leukemia
by Licht, Jonathan D and Gelb, Bruce D and Jung, Andreas and Fragale, Alessandra and Song, Xiaoling and Buechner, Jochen and Niemeyer, Charlotte M and Tartaglia, Marco and Hählen, Karel and Hasle, Henrik
Nature Genetics, ISSN 1061-4036, 06/2003, Volume 34, Issue 2, pp. 148 - 150
We report here that individuals with Noonan syndrome and juvenile myelomonocytic leukemia (JMML) have germline mutations in PTPN11 and that somatic mutations... 
NOONAN-SYNDROME | TYROSINE-PHOSPHATASE SHP-2 | GENETICS & HEREDITY | Leukemia, Myelomonocytic, Acute - genetics | Protein Tyrosine Phosphatase, Non-Receptor Type 11 | Noonan Syndrome - enzymology | Leukemia, Myelomonocytic, Acute - complications | Humans | Intracellular Signaling Peptides and Proteins | Protein Tyrosine Phosphatases - metabolism | Noonan Syndrome - genetics | Myelodysplastic Syndromes - enzymology | Noonan Syndrome - complications | Leukemia, Myeloid, Acute - enzymology | Protein Tyrosine Phosphatases - genetics | Animals | Transfection | Leukemia, Myelomonocytic, Acute - enzymology | Myelodysplastic Syndromes - genetics | Mutation | COS Cells | Child | Leukemia, Myeloid, Acute - genetics | Complications and side effects | Genetic aspects | Diagnosis | Gene mutations | Risk factors | Cancer in children
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8. Full Text Activity of the oral mitogen‐activated protein kinase kinase inhibitor trametinib in RAS‐mutant relapsed or refractory myeloid malignancies
by Borthakur, Gautam and Popplewell, Leslie and Boyiadzis, Michael and Foran, James and Platzbecker, Uwe and Vey, Norbert and Walter, Roland B and Olin, Rebecca and Raza, Azra and Giagounidis, Aristoteles and Al‐Kali, Aref and Jabbour, Elias and Kadia, Tapan and Garcia‐Manero, Guillermo and Bauman, John W and Wu, Yuehui and Liu, Yuan and Schramek, Dan and Cox, Donna S and Wissel, Paul and Kantarjian, Hagop
Cancer, ISSN 0008-543X, 06/2016, Volume 122, Issue 12, pp. 1871 - 1879
BACKGROUND RAS/RAF/mitogen‐activated protein kinase activation is common in myeloid malignancies. Trametinib, a mitogen‐activated protein kinase kinase 1... 
trametinib | NRAS | KRAS | acute myeloid leukemia | myelodysplastic syndromes | chronic myelomonocytic leukemia | TRANSFORMATION | EFFICACY | FLT3 | DOSE-ESCALATION TRIAL | HEMATOPOIETIC PROGENITORS | MELANOMA | MEK INHIBITION | GENE | ONCOLOGY | MUTATIONS | Recurrence | Leukemia - blood | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Middle Aged | Myelodysplastic Syndromes - blood | Protein Kinase Inhibitors - adverse effects | Pyridones - blood | Myelodysplastic Syndromes - enzymology | Dose-Response Relationship, Drug | Young Adult | Pyridones - administration & dosage | Leukemia, Myeloid, Acute - enzymology | Aged, 80 and over | Leukemia, Myeloid, Acute - drug therapy | Adult | Myelodysplastic Syndromes - drug therapy | Leukemia - enzymology | Pyrimidinones - adverse effects | Kaplan-Meier Estimate | Leukemia - drug therapy | Leukemia, Myeloid, Acute - blood | Protein Kinase Inhibitors - blood | Protein Kinase Inhibitors - administration & dosage | MAP Kinase Signaling System - drug effects | Pyrimidinones - blood | Aged | Myelodysplastic Syndromes - genetics | Pyrimidinones - administration & dosage | Mutation | Pyridones - adverse effects | Leukemia, Myeloid, Acute - genetics | Extracellular signal-regulated kinases | Dosage and administration | Index Medicus | Abridged Index Medicus
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9. Full Text Phase I/II trial of the combination of midostaurin (PKC412) and 5‐azacytidine for patients with acute myeloid leukemia and myelodysplastic syndrome
by Strati, Paolo and Kantarjian, Hagop and Ravandi, Farhad and Nazha, Aziz and Borthakur, Gautam and Daver, Naval and Kadia, Tapan and Estrov, Zeev and Garcia‐Manero, Guillermo and Konopleva, Marina and Rajkhowa, Trivikram and Durand, Menda and Andreeff, Michael and Levis, Mark and Cortes, Jorge
American Journal of Hematology, ISSN 0361-8609, 04/2015, Volume 90, Issue 4, pp. 276 - 281
We investigated the combination of midostaurin and azacitidine (AZA) in patients with acute myeloid leukemia (AML) and high risk myelodysplastic syndrome... 
INTERNAL TANDEM DUPLICATION | ADULT PATIENTS | YOUNGER PATIENTS | WORKING GROUP | INDUCTION CHEMOTHERAPY | RESPONSE CRITERIA | FLT3 | TYROSINE KINASE INHIBITOR | SORAFENIB | HEMATOLOGY | ELDERLY-PATIENTS | fms-Like Tyrosine Kinase 3 - antagonists & inhibitors | Azacitidine - adverse effects | Antineoplastic Combined Chemotherapy Protocols - administration & dosage | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Male | Staurosporine - analogs & derivatives | Myelodysplastic Syndromes - enzymology | Dose-Response Relationship, Drug | Young Adult | fms-Like Tyrosine Kinase 3 - genetics | Leukemia, Myeloid, Acute - enzymology | Aged, 80 and over | Leukemia, Myeloid, Acute - drug therapy | Adult | Female | Myelodysplastic Syndromes - drug therapy | Azacitidine - administration & dosage | Drug Administration Schedule | Staurosporine - adverse effects | Leukemia, Myeloid, Acute - mortality | Disease-Free Survival | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Staurosporine - therapeutic use | Myelodysplastic Syndromes - mortality | Aged | Mutation | Azacitidine - therapeutic use | Staurosporine - administration & dosage | Index Medicus | AML | AZA | midostaurin | MDS
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10. Full Text Differential prognostic effect of IDH1 versus IDH2 mutations in myelodysplastic syndromes: A Mayo Clinic Study of 277 patients
by Patnaik, M.M and Hanson, C.A and Hodnefield, J.M and Lasho, T.L and Finke, C.M and Knudson, R.A and Ketterling, R.P and Pardanani, A and Tefferi, A
Leukemia, ISSN 0887-6924, 01/2012, Volume 26, Issue 1, pp. 101 - 105
Unlike the case with acute myeloid leukemia, there is limited information on the prognostic impact of isocitrate dehydrogenase (IDH) mutations in... 
myelodysplastic | prognosis | IDH1 | IDH2 | SURVIVAL | NEOPLASMS | ACUTE MYELOID-LEUKEMIA | PRIMARY MYELOFIBROSIS | IMPACT | ONCOLOGY | GENES | HEMATOLOGY | INFERIOR | Multivariate Analysis | Prognosis | Humans | Middle Aged | Isocitrate Dehydrogenase - genetics | Male | DNA Primers | Myelodysplastic Syndromes - enzymology | Base Sequence | Aged, 80 and over | Adult | Female | Aged | Myelodysplastic Syndromes - genetics | Mutation | Myelodysplastic Syndromes - pathology | Real-Time Polymerase Chain Reaction | Gene mutations | Genetic aspects | Research | Isocitrate dehydrogenase | Health aspects | Myelodysplastic syndromes | Risk factors
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11. Full Text Nuclear translocation of PKC-α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs)
by Poli, Alessandro and Ratti, Stefano and Finelli, Carlo and Mongiorgi, Sara and Clissa, Cristina and Lonetti, Annalisa and Cappellini, Alessandra and Catozzi, Alessia and Barraco, Marilena and Suh, Pann-Ghill and Manzoli, Lucia and McCubrey, James A and Cocco, Lucio and Follo, Matilde Y
FASEB Journal, ISSN 0892-6638, 02/2018, Volume 32, Issue 2, pp. 681 - 692
PI-PLC beta 1 is involved in cell proliferation, differentiation, and myelodysplastic syndrome (MDS) pathogenesis. Moreover, the increased activity of PI-PLC... 
Erythropoiesis | Nucleus | Lenalidomide | Chromosome 5q deletion | SIGNALING PATHWAYS | PI-PLC-BETA-1 | ACTIVATION | K562 CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | PHOSPHOLIPASE-C | INVOLVEMENT | nucleus | AZACITIDINE | CELL BIOLOGY | RISK MDS | chromosome 5q deletion | ACUTE LYMPHOBLASTIC-LEUKEMIA | BIOLOGY | erythropoiesis | lenalidomide | Cell Line | Protein Kinase C-alpha - metabolism | Signal Transduction | Humans | Protein Kinase C-alpha - genetics | Male | Resting Phase, Cell Cycle | Cell Nucleus - enzymology | Myelodysplastic Syndromes - enzymology | Cell Nucleus - genetics | Cell Nucleus - pathology | Aged, 80 and over | G1 Phase Cell Cycle Checkpoints | Erythroid Cells - pathology | Female | Aged | Cell Differentiation | Myelodysplastic Syndromes - genetics | Active Transport, Cell Nucleus | Erythroid Cells - enzymology | Myelodysplastic Syndromes - pathology
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12. Full Text Phase I Combination Trial of Lenalidomide and Azacitidine in Patients With Higher-Risk Myelodysplastic Syndromes
by Mikkael A. Sekeres and Alan F. List and David Cuthbertson and Ronald Paquette and Rebecca Ganetsky and Deborah Latham and Katarina Paulic and Manuel Afable and Hussain I. Saba and Thomas P. Loughran, Jr and Jaroslaw P. Maciejewski
Journal of Clinical Oncology, ISSN 0732-183X, 05/2010, Volume 28, Issue 13, pp. 2253 - 2258
Purpose Lenalidomide and azacitidine are active in patients with lower- and higher-risk myelodysplastic syndromes (MDS). These agents may complement each other... 
DECITABINE | ONCOLOGY | DELETION 5Q | CLASSIFICATION | MALIGNANCIES | UNIPARENTAL DISOMY | MUTATIONS | THALIDOMIDE | MDS | WORLD-HEALTH-ORGANIZATION | SCHEDULES | Azacitidine - adverse effects | DNA Modification Methylases - antagonists & inhibitors | United States | Humans | Middle Aged | Male | Myelodysplastic Syndromes - enzymology | Enzyme Inhibitors - administration & dosage | Precancerous Conditions - drug therapy | Thalidomide - analogs & derivatives | Time Factors | DNA Mutational Analysis | Karyotyping | Female | Drug Therapy, Combination | Myelodysplastic Syndromes - drug therapy | Azacitidine - administration & dosage | Enzyme Inhibitors - adverse effects | Thalidomide - adverse effects | Precancerous Conditions - enzymology | Drug Administration Schedule | Risk Assessment | Treatment Outcome | Thalidomide - administration & dosage | Precancerous Conditions - genetics | Chromosome Aberrations | Aged | Myelodysplastic Syndromes - genetics | Mutation | DNA Methylation - drug effects | Index Medicus | Original Reports | Hema5 | Hema6 | Hema9
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13. Full Text Combined DNA methyltransferase and histone deacetylase inhibition in the treatment of myeloid neoplasms
by Gore, Steven D and Baylin, Stephen and Sugar, Elizabeth and Carraway, Hetty and Miller, Carole B and Carducci, Michael and Grever, Michael and Galm, Oliver and Dauses, Tianna and Karp, Judith E and Rudek, Michelle A and Zhao, Ming and Smith, B. Douglas and Manning, Jasper and Jiemjit, Anchalee and Dover, George and Mays, Abbie and Zwiebel, James and Murgo, Anthony and Weng, Li-Jun and Herman, James G
Cancer Research, ISSN 0008-5472, 06/2006, Volume 66, Issue 12, pp. 6361 - 6369
Optimal reexpression of most genes silenced through promoter methylation requires the sequential application of DNA methyltransferase inhibitors followed by... 
ACUTE-LEUKEMIA | CYTIDINE DEAMINASE GENE | CPG ISLAND METHYLATION | ONCOLOGY | ARA-C SENSITIVITY | HYPOMETHYLATING AGENT | COLORECTAL-CANCER | RISK MYELODYSPLASTIC SYNDROME | LOW-DOSE 5-AZA-2'-DEOXYCYTIDINE | ORAL SODIUM PHENYLBUTYRATE | ELDERLY-PATIENTS | Azacitidine - adverse effects | Humans | Leukemia, Myeloid - genetics | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - pharmacokinetics | Phenylbutyrates - adverse effects | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Male | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Feasibility Studies | Myelodysplastic Syndromes - enzymology | Dose-Response Relationship, Drug | Phenylbutyrates - pharmacokinetics | Phenylbutyrates - administration & dosage | Aged, 80 and over | Female | Myelodysplastic Syndromes - drug therapy | Azacitidine - administration & dosage | Promoter Regions, Genetic | Acute Disease | Azacitidine - pharmacokinetics | Myelodysplastic Syndromes - metabolism | Histone Deacetylases - genetics | Leukemia, Myeloid - enzymology | Treatment Outcome | DNA (Cytosine-5-)-Methyltransferases - genetics | Leukemia, Myeloid - drug therapy | Acetylation - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Leukemia, Myeloid - metabolism | Aged | Histone Deacetylase Inhibitors | Myelodysplastic Syndromes - genetics | Histones - metabolism | DNA Methylation - drug effects
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