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1. Nguyen AN, Hollenbach PW, Richard N, Luna-Moran A, Brady H, Heise C, MacBeth KJ: Azacitidine and decitabine have different mechanisms of action in non-small cell lung cancer cell lines. Lung Cancer (Auckl); 2010;1:119-140
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  • Azacitidine (AZA) and decitabine (DAC) are cytidine azanucleoside analogs with clinical activity in myelodysplastic syndromes (MDS) and potential activity in solid tumors.

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  • (PMID = 28210112.001).
  • [Journal-full-title] Lung Cancer (Auckland, N.Z.)
  • [ISO-abbreviation] Lung Cancer (Auckl)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Keywords] NOTNLM ; apoptosis / azacitidine / decitabine / gene expression / non-small cell lung cancer
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2. Goyal R, Varma N, Marwaha RK: Myelodysplastic syndrome with erythroid hypoplasia. J Clin Pathol; 2005 Mar;58(3):320-1
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  • [Title] Myelodysplastic syndrome with erythroid hypoplasia.
  • The incidence of myelodysplastic syndrome (MDS) with erythroid hypoplasia/aplasia is probably underestimated because in most patients it is mistaken for acquired pure red blood cell aplasia.
  • This report describes three children who fulfilled the criteria for MDS with erythroid hypoplasia/aplasia.
  • [MeSH-major] Myelodysplastic Syndromes / diagnosis. Red-Cell Aplasia, Pure / diagnosis
  • [MeSH-minor] Blood Transfusion. Child. Child, Preschool. Diagnosis, Differential. Female. Humans. Infant. Male

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  • (PMID = 15735169.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1770594
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3. Mufti GJ, Bennett JM, Goasguen J, Bain BJ, Baumann I, Brunning R, Cazzola M, Fenaux P, Germing U, Hellström-Lindberg E, Jinnai I, Manabe A, Matsuda A, Niemeyer CM, Sanz G, Tomonaga M, Vallespi T, Yoshimi A, International Working Group on Morphology of Myelodysplastic Syndrome: Diagnosis and classification of myelodysplastic syndrome: International Working Group on Morphology of myelodysplastic syndrome (IWGM-MDS) consensus proposals for the definition and enumeration of myeloblasts and ring sideroblasts. Haematologica; 2008 Nov;93(11):1712-7
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  • [Title] Diagnosis and classification of myelodysplastic syndrome: International Working Group on Morphology of myelodysplastic syndrome (IWGM-MDS) consensus proposals for the definition and enumeration of myeloblasts and ring sideroblasts.
  • The classification of myelodysplastic syndromes is based on the morphological criteria proposed by the French-American-British (FAB) and World Health Organization (WHO) groups.
  • Accurate enumeration of blast cells, although essential for diagnosis of myelodysplastic syndrome and for assignment to prognostic groups, is often difficult, due to imprecise criteria for the morphological definition of blasts and promyelocytes.
  • An International Working Group on Morphology of Myelodysplastic Syndrome (IWGM-MDS) of hematopathologists and hematologists expert in the field of myelodysplastic syndrome reviewed the morphological features of bone marrows from all subtypes of myelodysplastic syndrome and agreed on a set of recommendations, including recommendations for the definition and enumeration of blast cells and ring sideroblasts.
  • It is recommended that (1) agranular or granular blast cells be defined (replacing the previous type I, II and III blasts), (2) dysplastic promyelocytes be distinguished from cytologically normal promyelocytes and from granular blast cells, (3) sufficient cells be counted to give a precise blast percentage, particularly at thresholds that are important for diagnosis or prognosis and (4) ring sideroblasts be defined as erythroblasts in which there are a minimum of 5 siderotic granules covering at least a third of the nuclear circumference.
  • Clear definitions and a differential count of a sufficient number of cells is likely to improve precision in the diagnosis and classification of myelodysplastic syndrome.
  • [MeSH-major] Granulocyte Precursor Cells / pathology. Myelodysplastic Syndromes / classification. Myelodysplastic Syndromes / diagnosis

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  • (PMID = 18838480.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Number-of-references] 16
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4. Issa JP: Epigenetic changes in the myelodysplastic syndrome. Hematol Oncol Clin North Am; 2010 Apr;24(2):317-30
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  • [Title] Epigenetic changes in the myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS) is characterized by frequent epigenetic abnormalities, including the hypermethylation of genes that control proliferation, adhesion, and other characteristic features of this leukemia.
  • Aberrant DNA hypermethylation is associated with a poor prognosis in MDS that can be accounted for by more rapid progression to acute myeloid leukemia.
  • In turn, treatment with drugs that modify epigenetic pathways (DNA methylation and histone deacetylation inhibitors) induces durable remissions and prolongs life in MDS, offering some hope and direction in the future management of this deadly disease.

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20359628.001).
  • [ISSN] 1558-1977
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA108631-050003; United States / NCI NIH HHS / CA / P50 CA100632-06S1; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / R01 CA121104-03; United States / NCI NIH HHS / CA / CA100632-060001; United States / NCI NIH HHS / CA / R01 CA121104; United States / NCI NIH HHS / CA / CA100632-06S1; United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / P50 CA100632-060001; United States / NCI NIH HHS / CA / CA108631-050003; United States / NCI NIH HHS / CA / R01 CA098006; United States / NCI NIH HHS / CA / CA121104-03; United States / NCI NIH HHS / CA / CA098006; United States / NCI NIH HHS / CA / P50 CA100632-010001; United States / NCI NIH HHS / CA / CA121104; United States / NCI NIH HHS / CA / CA100632-010001
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histone Deacetylase Inhibitors; 0 / Histones; 776B62CQ27 / decitabine; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Number-of-references] 107
  • [Other-IDs] NLM/ NIHMS177428; NLM/ PMC2848959
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5. Suzuki R, Irisawa A, Hikichi T, Takahashi Y, Kobayashi H, Kumakawa H, Ohira H: Cronkhite-Canada syndrome associated with myelodysplastic syndrome. World J Gastroenterol; 2009 Dec 14;15(46):5871-4
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  • [Title] Cronkhite-Canada syndrome associated with myelodysplastic syndrome.
  • We report a case of Cronkhite-Canada syndrome (CCS) associated with myelodysplastic syndrome (MDS).
  • A 54-year-old woman, diagnosed as MDS the prior year after evaluation of anemia, visited our hospital with the chief complaint of epigastric discomfort.
  • Her clinical manifestations and histology were consistent with CCS.
  • This is the first report of CCS in a patient with MDS.
  • [MeSH-major] Intestinal Polyposis / etiology. Myelodysplastic Syndromes / complications

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  • (PMID = 19998513.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2791285
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6. Sugimori C, List AF, Epling-Burnette PK: Immune dysregulation in myelodysplastic syndrome. Hematol Rep; 2010 Jan 26;2(1):e1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immune dysregulation in myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS) represents one of the most challenging health-related problems in the elderly.
  • Characterized by dysplastic morphology in the bone marrow in association with ineffective hematopoiesis, pathophysiological causes of this disease are diverse including genetic abnormalities within myeloid progenitors, altered epigenetics, and changes in the bone marrow microenvironment.
  • Currently, IST for MDS primarily involves anti-thymocyte globulin (ATG)-based regimens in which responsiveness is strongly associated with younger (under 60 years) age at disease onset.
  • Although most hematologists agree that IST can offer durable hematologic remission in younger patients with MDS, an international clinical study and a better understanding of the molecular mechanisms contributing to the expansion of self-reactive CTLs is crucial.

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  • (PMID = 22184512.001).
  • [ISSN] 2038-8330
  • [Journal-full-title] Hematology reports
  • [ISO-abbreviation] Hematol Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3222262
  • [Keywords] NOTNLM ; T lymphocytes / autoimmunity / myelodysplastic syndrome / treatment.
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7. Lavallée MC, Gingras L, Aubin S, Côté C, Larochelle M, Chrétien M, Beaulieu L: Poster - Thurs Eve-39: Full 3D dose calculation for total body irradiation: A comparison study between treatment planning systems in homogeneous and heterogeneous conditions. Med Phys; 2008 Jul;35(7Part3):3408
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  • [Title] Poster - Thurs Eve-39: Full 3D dose calculation for total body irradiation: A comparison study between treatment planning systems in homogeneous and heterogeneous conditions.
  • Dose distributions obtained with Pinnacle<sup>3</sup> v.7.9u (Philips Medical Systems) were compared with the ones calculated using our actual TBI planning system Theraplan Plus (TPP) by MDS Nordion/Nucletron.
  • Differences in patient extremities are attributed to the OFD contribution which is not correctly computed in TPP and std_Pinnacle<sup>3</sup> .

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28512892.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Biomedical modeling / Computer software / Lungs / Medical treatment planning / Statistical methods
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8. Malcovati L, Della Porta MG, Lunghi M, Pascutto C, Vanelli L, Travaglino E, Maffioli M, Bernasconi P, Lazzarino M, Invernizzi R, Cazzola M: Flow cytometry evaluation of erythroid and myeloid dysplasia in patients with myelodysplastic syndrome. Leukemia; 2005 May;19(5):776-83
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  • [Title] Flow cytometry evaluation of erythroid and myeloid dysplasia in patients with myelodysplastic syndrome.
  • The purpose of this study was to develop a flow cytometric approach to the evaluation of marrow dysplasia in myelodysplastic syndromes (MDS).
  • We first studied a cohort of 103 MDS patients as well as 46 pathological and healthy controls.
  • Analysis of erythroid cells showed higher proportions of immature cells (P < 0.001) and decreased levels of CD71 expression on nucleated red cells (P = 0.02) in MDS.
  • Analysis of myeloid cells showed lower proportions of CD10+ and higher proportions of CD56+ granulocytes (P < 0.001), and increased ratios of immature to mature cells (P = 0.007).
  • Since no single immunophenotype could accurately differentiate MDS from other conditions, we used discriminant analysis for generating erythroid and myeloid classification functions using combinations of immunophenotypic parameters.
  • These functions were prospectively validated in a testing cohort of 69 MDS patients and 46 pathological controls.
  • A diagnosis of MDS was obtained in 60/69 cases (87%).
  • Significant correlations between values of these functions and both degree of morphological dysplasia and the International Prognostic Scoring System were found.
  • These findings indicate that flow cytometry evaluation of marrow dysplasia is feasible and may be useful in the work-up of individual MDS patients.
  • [MeSH-major] Erythrocytes / pathology. Erythroid Cells / pathology. Flow Cytometry / methods. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology. Myeloid Cells / pathology

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  • (PMID = 15789068.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34
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9. Lukenda A, Bujger Z, Bajer-Feketić A, Kica S, Petricek I: [Haemosiderosis bulbi in a patient with myelodysplastic syndrome (MDS RAEB-1)]. Lijec Vjesn; 2010 Jul-Aug;132(7-8):232-4
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  • [Title] [Haemosiderosis bulbi in a patient with myelodysplastic syndrome (MDS RAEB-1)].
  • [Transliterated title] Haemosiderosis bulbi kod pacijenta s mijelodisplasticnim sindromom (MDS RAEB-1).
  • The cause of the haemophthalmus in our patient is protracted anaemia due to pre-existing myelodysplastic syndrome (MDS RAEB-1).
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / complications. Eye Diseases / complications. Hemosiderosis / complications. Myelodysplastic Syndromes / complications


10. Haimi M, Elhasid R, Gershoni-Baruch R, Izraeli S, Wanders RJ, Mandel H: Myeloid dysplasia in familial 3-methylglutaconic aciduria. J Pediatr Hematol Oncol; 2006 Feb;28(2):69-72
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  • [Title] Myeloid dysplasia in familial 3-methylglutaconic aciduria.
  • A kindred is reported with four members affected with neurodegenerative disorder and 3-methylglutaconic aciduria.
  • Two siblings developed thrombocytopenia heralding a myelodysplastic syndrome; in one patient it evolved into acute myeloid leukemia with monosomy 7 in the marrow.
  • The hematologic complications have hitherto not been previously reported in other cases of 3-methylglutaconic aciduria and are thus thought to represent a new disease entity.
  • This family adds additional evidence to the genetic heterogeneity of Mendelian disorders in which the primary mutation may have a mutator effect that could give origin to myelodysplastic syndrome and acute myeloid leukemia through acquired chromosomal changes.
  • [MeSH-major] Glutarates / urine. Metabolism, Inborn Errors / complications. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Child, Preschool. Chromosomes, Human, Pair 7 / genetics. Consanguinity. Ethnic Groups / genetics. Female. Humans. Infant. Intellectual Disability / genetics. Israel. Leukemia, Myeloid, Acute / genetics. Male. Monosomy. Pedigree. Thrombocytopenia / genetics

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  • [CommentIn] J Pediatr Hematol Oncol. 2006 Feb;28(2):62-3 [16462574.001]
  • (PMID = 16462576.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glutarates; 5746-90-7 / 3-methylglutaconic acid
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11. Chen BA, Gao C, Ding J, Ding JH, Sun YY, Zhao G, Cheng J, Wang J, Bao W, Song HH, Xia GH, Ma JL, Wu LL: [Analysis on laboratory and clinical characteristics in 65 cases of myelodysplastic syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Dec;17(6):1472-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis on laboratory and clinical characteristics in 65 cases of myelodysplastic syndrome].
  • The aim of this study was to gain more insight into the understanding of myelodysplastic syndrome in the clinical and laboratory features.
  • The clinical data of 65 patients with MDS were reviewed and analysed.
  • The median age of them was 66 years old (range 19-89 years), and 6 patients had a history of toxic exposure (secondary MDS).
  • The results showed that dysplasia was found in 64 patients examined with bone marrow smears (98.5%), among them trilineage dysplasia in 21 patients (32.3%), bilineage dysplasia in 33 patients (50.8%), only erythroid dysplasia in 8 cases (12.3%) and 2 patients (3.1%) only with myeloid dysplasia.
  • The abnormal chromosome was the major cytogenetic abnormality, which occurred more often in secondary MDS and the patients with RAEB or RAEB-T.
  • In conclusion, the incidence of MDS in our country is younger than that in Western countries, the rate of abnormal chromosome in high risk MDS is higher than that in low risk MDS.
  • Meanwhile, those who have the change of chromosome are related to the transformation of MDS into AML and have shorter survival time than those MDS patients with normal karyotypes.

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  • (PMID = 20030929.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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12. Tilak V, Sookmane DD, Gupta V, Shukla J: Myelodysplastic syndrome. Indian J Pediatr; 2008 Jul;75(7):729-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndrome.
  • Pediatric myelodysplastic syndrome (MDS), though rare, constitutes a distinct entity quite different from adult MDS.
  • They have unique clinical features, aggressive clinical course with an overall mean survival of only 9.9 months.
  • A pediatric approach to the WHO classification has become necessary since the WHO classification of MDS has failed to address the uniqueness of pediatric MDS.
  • A new prognostic system also needs to be evolved since the international prognostic system has limited prognostic impact in children.
  • Intensive chemotherapy such as the one used in de novo-acute myeloid leukemia (AML) leads to complete remission in some children and this may be the treatment of choice in pediatric MDS.
  • [MeSH-major] Myelodysplastic Syndromes / diagnosis
  • [MeSH-minor] Age Factors. Child. Diagnosis, Differential. Humans. Leukemia, Myeloid, Acute / diagnosis. Prognosis


13. Urabe A: [Myelodysplastic syndrome]. Gan To Kagaku Ryoho; 2005 Mar;32(3):287-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Myelodysplastic syndrome].
  • Myelodysplastic syndrome (MDS) is a heterogenous syndrome which has features of refractory anemia and preleukemic state due to the ineffective hematopoiesis of bone marrow cells.
  • MDS is classified by the FAB classification and/or WHO classification, and has an International Prognostic Scoring System (IPSS) for evaluation of the prognosis.
  • [MeSH-major] Myelodysplastic Syndromes
  • [MeSH-minor] Anemia, Refractory / diagnosis. Anemia, Refractory, with Excess of Blasts / diagnosis. Antilymphocyte Serum / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Immunosuppressive Agents / administration & dosage. Methylprednisolone / administration & dosage. Prognosis. World Health Organization

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  • (PMID = 15791810.001).
  • [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 / Antilymphocyte Serum; 0 / Immunosuppressive Agents; X4W7ZR7023 / Methylprednisolone
  • [Number-of-references] 12
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14. 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


15. Laursen SB, Nielsen MØ, Hasselbalch HC: [The myelodysplastic syndrome and autoimmunity]. Ugeskr Laeger; 2009 Sep 7;171(37):2639-42
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  • [Title] [The myelodysplastic syndrome and autoimmunity].
  • [Transliterated title] Det myelodysplastiske syndrom og autoimmunitet.
  • INTRODUCTION: An increased incidence of autoimmune diseases has been reported in patients with myelodysplastic syndrome (MDS).
  • The aim of the present study was to determine whether this association includes Danish MDS-patients.
  • A possible association between autoimmune comorbidity and French-American-British Classification of Myelodysplastic Syndrome (FAB) or karyotype was also investigated.
  • Patients diagnosed with MDS from 2001 to 2005 were included.
  • On the basis of their autoimmune status, patients were divided into two groups: One group with MDS and autoimmune comorbidity and one group with only MDS.
  • RESULTS: There was a significantly increased incidence of autoimmune disease in patients with MDS.
  • It was not possible to demonstrate an association between autoimmune comorbidity and age, sex, FAB- or karyotype.
  • CONCLUSION: The present study shows an increased incidence of autoimmune disease among Danish patients with MDS which is in accordance with the majority of previous studies on this issue.
  • Data suggests that treatment of autoimmune comorbidity may also improve some of the clinical and biochemical features of MDS.
  • [MeSH-major] Autoimmune Diseases / immunology. Myelodysplastic Syndromes / immunology


16. Duhoux F, Libouton J, Bahloula K, Ameye G, Poirel HA: Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):11037

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies.
  • : 11037 Background: PRDM16 is a gene located on 1p36.32 that encodes for a zinc finger transcription factor and contains an N-terminal PR domain.
  • It has been shown to be involved in the reciprocal translocation t(1;3)(p36;q21) and more rarely the t(1;21)(p36;q22) which both occur in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML).
  • These translocations result in the overexpression of a truncated version of the PRDM16 protein that lacks the PR domain.
  • This overexpression might play an important role in the pathogenesis of MDS and AML in blocking myeloid differentiation.
  • METHODS: We studied 35 myeloid malignancies, 12 lymphoid malignancies and 3 undifferentiated acute leukemias with 1p36 abnormalities by fluorescent in situ hybridization (FISH) with a bacterial artificial chromosomes (BAC) contig containing 50 BAC probes on 1p36.
  • RESULTS: In addition to the known t(1;3)(p36;q21) (11 cases) and t(1;21)(p36;q22) (1 case) involving RPN1 andAML1/RUNX1 respectively in myeloid malignancies, we specifically found PRDM16 to be rearranged in 4 additional translocations : a t(1;12)(p36;p13) in an AML-M4, a t(1;7)(p36;p12) in a MDS, an add(1)(p36) in an AML-M2 and a t(1;2)(p36;p12) in a relapsed AML-M4.
  • CONCLUSIONS: In our series of 50 cases of hematological malignancies with 1p36 abnormalities, PRDM16 was involved in about 45% of myeloid malignancies, and was never involved in lymphoid malignancies.
  • Interestingly, the shortest isoform of MDS/EVI-1, lacking the PR domain, is supposed to have an oncogenic effect due to its translocation-induced upregulation in AML.
  • Further characterization of these new partner genes and functional studies should give us more insight into the pathogenesis of AML and MDS mediated by PRDM16, and the role of its partner genes.

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  • (PMID = 27964015.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Cogle CR, Imanirad I, Scornik J, Wingard JR: Impact of azacytidine induction chemotherapies on post-transplant outcomes in patients with myelodysplastic syndromes. J Clin Oncol; 2009 May 20;27(15_suppl):7032

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impact of azacytidine induction chemotherapies on post-transplant outcomes in patients with myelodysplastic syndromes.
  • : 7032 Background: With the advent of azacytidines for treatment of MDS, disease remissions are achievable; however the disease nearly always relapses.
  • Whereas cytotoxic induction chemotherapy in patients with MDS provides no clear benefit after HCT, the effects of azacytidine therapy prior to HCT are unknown.
  • METHODS: To address this question, we analyzed post-transplant outcomes in 43 MDS patients, 9 who received an azacytidine before transplant and 34 who did not.
  • Azacytidine patients were marginally more likely to have higher disease burden at HCT (WPSS 4 vs 3, p = 0.08) and more likely to have received a graft from an unrelated donor (66% vs 33%, p = 0.07).
  • RESULTS: With a median follow-up of 7 months, the group that received azacytidine pre-transplant demonstrated higher donor chimerism at days 30, 60 and 100 (p < 0.01).
  • Rates of acute and chronic GVHD, and median overall survival (OS) did not differ significantly between groups.
  • The increased rate of relapse in the azacytidine group likely reflects the progressive nature of chemotherapy-insensitive disease at HCT.
  • Although only randomized controlled trials can establish a definite conclusion regarding use of azacytidines prior to HCT and duration of induction therapy before proceeding to HCT, the data presented support administration of azacytidines to MDS patients prior to HCT.

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  • (PMID = 27961394.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Spadaro P, Ingemi M, Pitini V, Arrigo C, Soto Parra H: Myelodysplastic syndromes developing after imatinib therapy for GIST. J Clin Oncol; 2009 May 20;27(15_suppl):10532

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndromes developing after imatinib therapy for GIST.
  • Previously, we had detected clonal chromosomal abnormalities in the bone marrow of GIST pts. who developed a myelodysplastic syndrome during treatment with imatinib, so we performed a systematic study in a series of male and female GIST pts. during treatment with imatinib.
  • METHODS: Between January 2007 and December 2008, bone marrow samples for morphologic analysis, FISH and classical cytogenetics were obtained from 49 pts. (30 male; 19 female, mean age 62) with unresectable or metastatic GIST before and during treatment with 400 mg/d of imatinib.
  • For pts. with progressive disease (15 pts.) or exon 9 mutant disease (5 pts.
  • All pathologic material was reviewed to identify pts. with MDS or AML according to the WHO classification.
  • A trisomy 8 was detectable in seven pts. even if, curiously, in four of these pts. this come and went on repeated sampling without any apparent clinical effect, three pts. developed an MDS (two refractory cytopenias with multilineage dysplasia, and one refractory cytopenia with multilineage dysplasia and ringed sideroblast).

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  • (PMID = 27963910.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Sampat KR, Garcia-Gutierrez V, Rossi A, Pierce S, Cortes J, Kantarjian H, Garcia-Manero G: Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7067

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia.
  • : 7067 Background: Little is known regarding the prevalence and natural history of pericardial disease in patients with leukemia.
  • Although a direct causal relationship has not been established yet, this complication may have a significant impact for the future development of this class of drugs.
  • To study this issue, we retrospectively analyzed a large cohort of patients with leukemia, who were evaluated at MD Anderson Cancer Center (MDACC), to determine the prevalence, timing, and characteristics of PEf in leukemia.
  • METHODS: We reviewed 3,327 patients with acute myeloid leukemia (AML, N = 1,809, 54%), acute lymphocytic leukemia (ALL, N = 494, 15%), or myelodysplastic syndrome (MDS, N =1,024, 31%), who were seen at MDACC from August 2003 to July 2008.
  • Data regarding diagnosis, timing, effusion size, and prior therapy was collected in the 401 patients (20.2%) that had echocardiographic evidence of PEf.
  • RESULTS: The overall prevalence of PEf was 21.7%, 21.1%, and 19.9% (p = 0.72) in patients with AML, ALL, and MDS, respectively.
  • In the 401 total patients with PEf, 22.8%, 25.0%, and 18.4% (p = 0.33) of these effusions were found before treatment in the three disease categories, respectively.
  • The rest occurred after some form of chemotherapy, accounting for 77.2%, 75.0%, and 81.6% (p = 0.73) of the total PEf by disease, respectively.
  • CONCLUSIONS: PEf are relatively common in patients with leukemia at initial presentation and are usually asymptomatic.
  • Their incidence increases with therapy administration although it appears that this is not a process related to specific classes of treatment or type of leukemia.

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  • (PMID = 27961462.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Braun E, Katz D, Venugopal P, Larson M, Shammo J, Fung H, Gregory S: Safety analysis of radioimmunotherapy (RIT) in patients with relapsed or refractory low grade, follicular or transformed non-Hodgkin's lymphoma and mantle cell lymphoma based on age at time of therapy. J Clin Oncol; 2009 May 20;27(15_suppl):e19529

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Incidence o myelodysplastic syndrome (MDS) was also compared between groups.
  • Groups characteristics such as sex, type of RIT, presence of disease in bone marrow, FLIPI/IPI and use of G-CSF were noted.
  • One patient in group 1 and three patients on group 2 were diagnosed with MDS but were also treated with different chemotherapy regimens.

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  • (PMID = 27960911.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Mukhopadhyay S, Basak J, Kar M, Mandal S, Mukhopadhyay A: The role of iron chelation activity of wheat grass juice in patients with myelodysplastic syndrome. J Clin Oncol; 2009 May 20;27(15_suppl):7012

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of iron chelation activity of wheat grass juice in patients with myelodysplastic syndrome.
  • The aim of our study was to see the effect of wheat grass juice in reducing Ferritin level in myelodysplastic syndrome and also do the biochemical analysis of the wheat grass juice.
  • METHODS: During period from January 2003 to December 2007 we selected 20 patients of transfusion dependent myelodysplastic syndrome in the oncology department of Netaji Subhash Chandra Bose Cancer Research Institute.
  • CONCLUSIONS: Wheat grass juice is an effective iron chelator and its use in reducing serum ferritin should be encouraged in myelodysplastic syndrome and other diseases where repeated blood transfusion is required.

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  • (PMID = 27961385.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Bhatnagar B, Tiu RV, Gondek LP, O'Keefe C, Huh J, Advani AS, Sekeres MA, Maciejewski JP: Use of SNP-array-based karyotyping for cytogenetic prognostication in unclassified cases of myelodysplasia and associated overlap disorders. J Clin Oncol; 2009 May 20;27(15_suppl):7016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of SNP-array-based karyotyping for cytogenetic prognostication in unclassified cases of myelodysplasia and associated overlap disorders.
  • : 7016 Background: Myeloproliferative disorders (MPD) and myelodysplastic syndromes (MDS) often have overlapping features resulting in unclassifiable cases (MDS-U and MDS/MPD-U).
  • Single nucleotide polymorphism arrays (SNP-A) are novel karyotyping tools with superior resolution and ability to detect copy neutral loss of heterozygosity, a defect not detected by MC.
  • METHODS: MDS-U (N = 17) and MDS/MPD-U (N = 61) patients were selected from an MDS database (N = 720, median age = 76, median follow-up = 42 mos).
  • 2) Micro-duplications/ deletions overlapping with copy number variants (CNV) were excluded.
  • Lesions not in CNV databases were confirmed by CD3 lymphocytes;.
  • International Prognostic Scoring System (IPSS) was used to assess routine risk.
  • Overall (OS) and event-free (EFS) survival defined by the MDS working group criteria were analyzed by Kaplan Meier analysis (log-rank or Wilcoxon and 2-sided significance).
  • MDS/MPD-U and MDS-U patients had similar OS and EFS (OS = 42 vs. 45 mos, p = 0.13; EFS = 42 vs. 45 mos p = 0.63).
  • SNP-A revealed a more complex karyotype in patients with advanced MDS.
  • CONCLUSIONS: SNP-A karyotyping complements MC in detecting chromosomal defects in MDS-U and MDS/MPD-U.
  • This technology will be helpful in refining diagnosis based on characteristic recurrent chromosomal lesions including UPD.

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  • (PMID = 27961389.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Chaubey R, Sazawal S, Mahapatra M, Saxena R: Low frequency of RAS and absence of FLT3-ITD gene mutations in patients with Myelodysplastic Syndromes in India: AIIMS experience. J Clin Oncol; 2009 May 20;27(15_suppl):e22231

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low frequency of RAS and absence of FLT3-ITD gene mutations in patients with Myelodysplastic Syndromes in India: AIIMS experience.
  • : e22231 Background: Chromosomal abnormalities and molecular detection has potential importance for diagnosis and prognosis of MDS, although the mechanisms underlying the development of MDS and their progressive evolution to AML are still largely unknown.
  • Since, no studies have been reported from India on the prevalence of N-RAS, K- RAS point mutation in codon 12 and FLT3-ITD mutations in patients with MDS, we undertook this study.
  • FLT3-ITD mutation was not observed in any of our cases, which is in contrast to 3% reported from the West.
  • CONCLUSIONS: Thus, it appears that the RAS and FLT3 mutations are uncommon in MDS patients in India.

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  • (PMID = 27964108.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Ritchie EK, Roboz G, Hinchcliff K, Curcio T, Scandura J, Feldman E: Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7054

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

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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized phase II study of sapacitabine, an oral nucleoside analogue, in elderly patients with AML previously untreated or in first relapse or previously treated MDS.
  • It is orally administered and has demonstrated promising anti-leukemic activity against relapsed or refractory AML and MDS in a phase 1 trial.
  • METHODS: Eligible patients must be ≥70 years with AML previously untreated or in first relapse or ≥60 years with MDS previously treated with hypomethylating agents.
  • The planned sample size is 60 AML patients and 60 MDS patients.
  • RESULTS: As of December 2008, 60 AML and 13 MDS patients were enrolled and had ≥ 30 days of follow-up.
  • Overall response rate is 31% (13% CR/CRp, 5% PR and 13% HI).

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  • (PMID = 27961383.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Lindquist K, Danese M, Knopf K, Mikhael J: Mortality and hospitalization in myelodysplastic syndromes (MDS) using the SEER-Medicare linked database. J Clin Oncol; 2009 May 20;27(15_suppl):7091

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mortality and hospitalization in myelodysplastic syndromes (MDS) using the SEER-Medicare linked database.
  • : 7091 Background: Mortality in patients with MDS is high, and most require transfusions, emergency department (ED) visits, and hospitalizations.
  • The relationship between these outcomes with the key complications of MDS (anemia, neutropenia, thrombocytopenia) has not been well studied.
  • METHODS: Patients who were ≥ 66 years at MDS diagnosis in 2001 or 2002 were identified from SEER registries.
  • The presence of complications was based on diagnosis codes, transfusions, and medication use.
  • RESULTS: In 1,863 MDS patients, the 3-month incidence of transfusion, ED and hospitalization was 45%, 41%, and 62%, and 3-year incidence was 75%, 87%, and 91% respectively.
  • CONCLUSIONS: Starting shortly after diagnosis, MDS patients have high rates of transfusions, ED visits, and hospitalizations.

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  • (PMID = 27961259.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Grinblatt DL, Narang M, Malone JM 3rd, Sweet DA, Dunne TS, Sullivan KA: Patients with secondary myelodysplastic syndromes (MDS) who are enrolled in AVIDA, a longitudinal registry for patients receiving azacitidine (AZA). J Clin Oncol; 2009 May 20;27(15_suppl):7094

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patients with secondary myelodysplastic syndromes (MDS) who are enrolled in AVIDA, a longitudinal registry for patients receiving azacitidine (AZA).
  • : 7094 Background: Prevalence of secondary MDS (sMDS) is increasing because of improved survival of patients treated with chemotherapy or radiotherapy and aging of the population.
  • AVIDA patients with sMDS were investigated and compared with registry patients with primary MDS (pMDS).
  • METHODS: Baseline demographics and disease characteristics were obtained at enrollment.
  • Median time since diagnosis was 1 month versus 4 months for pMDS patients (n = 203).
  • However, a higher proportion of patients with sMDS had a poor-risk karyotype (44% vs. 11%), 2 to 3 cytopenias (78% vs. 52%), and an International Prognostic Scoring System (IPSS) risk score of intermediate-2/high (57% vs. 23%) compared with pMDS patients.

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  • (PMID = 27961264.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Berg SL, Russell H, Cairo M, Ingle AM, Adamson PC, Blaney SM: Phase I and pharmacokinetic (PK) study of lenalidomide (LEN) in pediatric patients with relapsed/refractory solid tumors or myelodysplastic syndrome (MDS): A Children's Oncology Group Phase I Consortium study. J Clin Oncol; 2009 May 20;27(15_suppl):10023

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I and pharmacokinetic (PK) study of lenalidomide (LEN) in pediatric patients with relapsed/refractory solid tumors or myelodysplastic syndrome (MDS): A Children's Oncology Group Phase I Consortium study.
  • : 10023 Background: LEN, which has immunomodulatory, antiangiogenic, and antiproliferative effects, is indicated for the treatment of adults with MDS and multiple myeloma.
  • We report the final results of a phase 1 and PK study of LEN in children with recurrent or refractory solid tumors (ST) or MDS.
  • Children with MDS received a fixed dose of 5 mg/m2/d.
  • 39/46 ST patients and 3/3 MDS patients were fully evaluable for toxicity.
  • 0/3 patients with MDS had DLT.

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  • (PMID = 27962627.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Hollmig K, Waheed S, Nair B, Haessler J, Petty N, Pineda-Roman M, Alsayed Y, van Rhee F, Crowley J, Barlogie B: MDS-associated cytogenetic abnormalities (MDS-CA) after total therapy (TT) regimens for newly diagnosed multiple myeloma (MM): Apparent surge after introduction of post-transplant consolidation chemotherapy (CONS) in TT2 and TT3. J Clin Oncol; 2009 May 20;27(15_suppl):8595

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

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  • (PMID = 27962291.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Dutreix C, Huntsman Labed A, Roesel J, Lanza C, Wang Y: Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients. J Clin Oncol; 2009 May 20;27(15_suppl):e14540

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

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  • (PMID = 27963644.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Tsujimura H, Mimura N, Ise M, Sakai C, Shimada H, Nagata M, Kumagai K: Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e15663

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer.
  • RESULTS: Four patients, who achieved CR after CRT, developed leukemia.
  • Case1, 60-yo-male, developed overt acute myeloid leukemia (AML) from myelodysplastic syndrome 48 months after CRT.
  • Case3, 72-yo-male, developed Burkitt leukemia with t(8;14)(q24;q32) 19 months after CRT.
  • Case4, 65-yo-male, developed myeloid crisis of chronic myelogenous leukemia with complicated abnormalities including t(9;22)(q34;q11) 48 months after CRT.
  • Case 1 and 3 had localized disease and received single course of neoadjuvant CRT.
  • Case 2 and 4 had advance disease and received 2 courses of CRT.
  • All patients eventually died of leukemia.
  • CONCLUSIONS: Since platinum and fluorouracil have shown relatively low chance of secondary neoplasm, our data demonstrates that the concurrent radiotherapy which involves massive bone marrow tissue may increase the risk of leukomogenesis.
  • To this end, atypical cytogenetic abnormalities seen in the present cases give a new insight into the biology of therapy-related leukemia.
  • Notably, this is the first report presenting the incidence of secondary leukemia by nedaplatin.

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  • (PMID = 27962759.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Mohty M, Balere M, Socie G, Milpied N, Ifrah N, Harousseau JL, Michallet M, Blaise D, Esperou H, Yakoub-Agha I, SFGM-TC: Effect of antithymocyte globulins (ATG) as part of the myeloablative conditioning (MAC) regimen on the risk of severe graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT) from matched-unrelated donors (MUD). J Clin Oncol; 2009 May 20;27(15_suppl):7025

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of antithymocyte globulins (ATG) as part of the myeloablative conditioning (MAC) regimen on the risk of severe graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT) from matched-unrelated donors (MUD).
  • 171 adult patients with acute leukemia and MDS, for whom detailed allelic HLA typing (4 digits) was available, were included.
  • 120 patients (70%) did not receive ATG (no-ATG group), while 51 patients received ATG (ATG group; thymoglobuline* in all cases) as part of the MAC regimen.
  • Finally, LFS and OS at 2 years were not significantly different between the no-ATG and ATG group (48.8% vs. 41.3%, p = NS; and 53.6% vs. 54.3%, p = NS; respectively).

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  • (PMID = 27961398.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Popat UR, Saliba R, Hosing C, Khouri I, Alousi AM, Giralt SA, de Lima MJ, Qazilbash MH, Champlin R, Anderlini P: Age at diagnosis does not adversely affect outcome in patients with Hodgkin's Disease (HD) after autologous transplantation. J Clin Oncol; 2009 May 20;27(15_suppl):e19507

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Age at diagnosis does not adversely affect outcome in patients with Hodgkin's Disease (HD) after autologous transplantation.
  • : e19507 Background: Age at diagnosis is a poor prognostic factor for overall survival after standard therapy for HD.
  • Whether older age is a prognostic factor for outcome after autologous transplantation is not known.
  • We sought to evaluate the effect of older age at diagnosis on transplant outcome.
  • Seventy two patients (29%) were older than 40 years of age at the time of initial diagnosis.
  • At transplantation, 63 (25%) were in complete remission (CR); 148 (60%) were in partial remission (PR); and 37 (15%) had stable (SD) or progressive disease (PD).
  • The cumulative incidence of secondary MDS or AML was 8%.
  • In univariate analysis, disease status (p<0.001) and number of prior chemotherapy regimens (p=0.007) were the only factors significantly predicting OS.
  • Disease status was the only factor significant (p<0.01) in a multivariate analysis with a hazard ratio of 2.7 (1.1-6.9) and 9.2 (3.4-25) for patients in PR, and SD/PD respectively (CR reference group).
  • Age at diagnosis was not a significant factor (see table ).
  • CONCLUSIONS: High-dose chemotherapy and autologous transplantation abrogate the adverse impact of age at diagnosis in patients with HD.

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  • (PMID = 27960864.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Tagawa ST, Parmar S, Pena J, Petrillo K, Matulich D, Selzer J, Vallabhajosula S, Goldsmith SJ, Bander NH, Nanus DM: Bone marrow recovery and subsequent chemotherapy following radiolabeled anti-prostate-specific membrane antigen (PSMA) monoclonal antibody J591 in patients (pts) with metastatic castration-resistant prostate cancer (metCRPC). J Clin Oncol; 2009 May 20;27(15_suppl):e16004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cases of marrow damage, including myelodysplasia and acute leukemia have been reported with the RIT most used to date (that targeting CD20 in Non- Hodgkin's lymphoma), though no statistically significant association exists.
  • Administration of pre- and post-RIT chemo was analyzed.
  • Specific searches for subsequent myelodysplasia and/or leukemia were performed.
  • 43% received at least 1 line of pre-RIT chemo, 53% received at least 1 line of post-RIT chemo, and 20% have never received chemo to date.
  • No cases of post-RIT myelodysplasia and/or leukemia were discovered.

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  • (PMID = 27962929.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Galili N, Ravandi F, Palermo G, Bubis J, Illingworth A, Castro-Malaspina H, Raza A: Prevalence of paroxysmal nocturnal hemoglobinuria (PNH) cells in patients with myelodysplastic syndromes (MDS), aplastic anemia (AA), or other bone marrow failure (BMF) syndromes: Interim results from the EXPLORE trial. J Clin Oncol; 2009 May 20;27(15_suppl):7082

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of paroxysmal nocturnal hemoglobinuria (PNH) cells in patients with myelodysplastic syndromes (MDS), aplastic anemia (AA), or other bone marrow failure (BMF) syndromes: Interim results from the EXPLORE trial.
  • Presence of even minor populations of PNH cells in AA or MDS patients is medically important as it may indicate a higher likelihood of response to immunosuppressive therapy.
  • We conducted the first large multicenter, point-prevalence study (EXamination of PNH, by Level Of CD59 on REd and white blood cells [EXPLORE]) of PNH cells in patients with AA, MDS, or other BMF syndromes.
  • RESULTS: Among 5,212 patients screened, 4,500 (86.3%) were MDS patients, 413 (7.9%) were AA patients, and 356 (6.8%) had other BMF syndromes.
  • Approximately 1/4 (24.5%) of patients with AA, 1.2% with MDS, and 4.6% with other BMF were newly found to have a significant PNH clone ≥ 1%.
  • Many of the newly identified clones were of clinical significance as the median PNH clone size was 11.1% in AA patients, 16.3% in MDS patients, and 32.6% in patients with other BMF.
  • Presence of PNH cells (≥ 0.01%) was common in all examined BMF types: 70% of AA patients, 55% of MDS patients and 55% of patients with other BMF.
  • PNH cells were identified in all MDS subtypes represented in the trial.
  • CONCLUSIONS: Interim analysis from this first large multicenter study demonstrates that PNH cells are present in a majority of patients with AA, MDS, and other BMF.
  • The EXPLORE trial continues to enroll patients with AA. (EXPLORE Clinical Study Abstract 1/6/2009) [Table: see text].

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  • (PMID = 27961475.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Laille E, Ward R, Nasser A, Stoltz M, Cogle C, Gore S, Skikne BS, Garcia-Manero G: The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • : 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.
  • Few studies have evaluated the pharmacokinetics (PK) of AZA and the renal elimination of AZA has not been previously published to our knowledge.
  • METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m<sup>2</sup> AZA during their first treatment cycle.
  • The apparent total clearance (CL/F) and volume of distribution (Vd/F) were 143 L/hr and 318 L, respectively.
  • After SC dosing, CL/F exceeded hepatic blood flow indicating extra-hepatic metabolism.

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  • (PMID = 27961481.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Li EC, Hinkel JM, Gallagher L, DeVader SR, Vandergrift JL, Lepisto EM: NCCN Chemotherapy Order Templates: Enhancing patient safety through standardization. J Clin Oncol; 2009 May 20;27(15_suppl):e17537

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e17537 Background: NCCN Chemotherapy Order Templates (COT), which delineate antineoplastics and associated supportive care agents, monitoring and safety parameters, and instructions for self-administered agents, were launched in 2008 to complement the NCCN Clinical Practice Guidelines in Oncology and NCCN Drugs and Biologics Compendium for nine cancers.
  • The survey was emailed on December 18, 2008 to a convenience sample of 10,183 registered users of NCCN.org who had clicked at least once to the COT; 110 (1%) survey emails were undeliverable.
  • RESULTS: 476 (64%) respondents were providers, including MDs (47%), mid-level (8%) and nurses (10%); 11% were pharmacists.
  • 292 users (63%) agreed that COT impacted patient safety; with MDs more likely to agree (p = 0.001) compared to other providers.
  • Among providers, MDs were more likely to agree (p = 0.002).
  • CONCLUSIONS: Adding NCCN Chemotherapy Order Templates to the core NCCN content was done to make the NCCN Clinical Practice Guidelines in Oncology more accessible to providers.

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  • (PMID = 27963786.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Shabbir M, Daniels L, Shirai K, Cole S, Willey J, Iovino L, Labarre K, Green MR: Prescribing plans (PP) of American Oncologists for first-line therapy (Rx) for patients with stage III (wet)/IV non-small cell lung cancer (NSCLC) and PS 2: Overall selection and impact of gender and smoking status. J Clin Oncol; 2009 May 20;27(15_suppl):e19046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Between February '07 and October '08, we used a core case scenario of stage IV mucin positive adenocarcinoma (Adeno ca) of lung in a 68-year-old former smoker (FS; stopped 6 years ago) with PS 2, to study patient related variations in PP of almost 800 American medical oncologists during 10 live research events [393 MDs/5 events during 2008].
  • RESULTS: In 2007-08, 97%/97%% MDs planned anti-tumor Rx: 53%/63% combination; 44%/34% single agent.
  • For a female NS with Adeno ca /PS2, ≥2/3 of MDs plan erlotinib 1<sup>st</sup>-line.
  • In the absence of testing results for EGFR expression by IHC, EGFR gene copy number by FISH, EGFR gene mutation testing, or kras mutation testing, our data show a direct correlation of patient "phenotype" and PP for erlotinib as 1<sup>st</sup>-line Rx, a setting not specifically an approved indications for this agent.
  • The impact of recently reported progression free survival data from an Asian phase III trial (IPASS: gefitinib or chemotherapy or as 1<sup>st</sup>-line therapy in non or former light-smoking patients with lung adenoca) on future prescribing plans in this clinical setting will be of great interest.

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  • (PMID = 27962104.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Bello CM, Yu D, Zhu W, Wetzstein GA, Lancet JE: Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors. J Clin Oncol; 2009 May 20;27(15_suppl):7088

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors.
  • : 7088 Background: Secondary acute myeloid leukemia (sAML) arising from myelodysplasia (MDS) or a myeloproliferative neoplasm (MPN) has a poor prognosis.
  • METHODS: Retrospective chart review of patients with untreated AML from MDS/MPN treated with standard induction therapy from January 2004 to September 2008.
  • Age, IPSS, ECOG PS, cytogenetics, duration of MDS, and prior MDS treatment were evaluated for their impact on obtaining complete remission (CR) or CR with low platelets (CRp) and overall survival (OS).
  • RESULTS: Sixty-one patients with sAML who received induction therapy were evaluated: median age (range) = 66 (36-82) years; M = 67%, ECOG PS 0 or 1 = 86%; poor-risk (PR) cytogenetics = 33%; IPSS > 1 = 43%; prior therapy for MDS with decitabine or azacitidine (DM) or lenalidomide (L) = 41% (25 pts).
  • Multivariable analysis indicated that the same three factors were significantly negatively associated with CR/CRp as well as OS: PR cytogenetics, prior treatment with DM/L, and long transformation to AML on log scale.
  • The CR/CRp rate for those with intermediate risk (IR) cytogenetics was 70% compared to only 35% for those with PR cytogenetics (OR = 4.33, 95% CI: 1.38-13.6).
  • Those with PR cytogenetics had a median OS of 2.8 mo compared to 7.5 mo for IR (p = 0.01).
  • CONCLUSIONS: Prior MDS treatment with a DM/L, PR cytogenetics and long transformation to AML are independent negative prognostic factors for response and OS in patients with sAML following induction therapy, suggesting that such patients may be better served by novel approaches, and that stratification for these risk factors should be considered in future clinical trials.

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  • (PMID = 27961482.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Villano JL, Letarte N, Yu JM, Shakir AR, Bressler L: Hematologic adverse events associated with temozolomide (TMZ). J Clin Oncol; 2009 May 20;27(15_suppl):2053

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

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  • (PMID = 27964671.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Jabbour E, Faderl S, Ravandi F, Konopleva M, Verstovsek S, Cortes J, Wierda W, Newsome WM, Yang H, Kantarjian H, Garcia-Manero G: Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML).
  • : 7004 Background: Standard induction therapy for pts with AML has not changed over the last 2 decades nor has the outcome of these pts.
  • We designed a phase II study of V with IA as front-line therapy for MDS/AML.
  • METHODS: Pts with untreated int-2/high-risk MDS or AML ages 15-65 with adequate liver and renal functions and PS, and EF ≥ 50% were eligible.
  • 8 (47%) had secondary disease.
  • The median PFS has not been reached.
  • CONCLUSIONS: The combination of IA and V is safe and active in AML/MDS.

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  • (PMID = 27961376.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • There was no correlation of the chromosomal abnormalities in CLL MSC with clinical stage.

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  • (PMID = 27963169.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Naik SG, Negrin R, Laport G, Miklos D, Shizuru J, Arai S, Blume K, Wong R, Lowsky R, Johnston L: Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies.
  • : 7033 Patients (pts) with high risk (HR) or advanced myeloid malignancies have limited effective treatment options.
  • All pts were treated with a uniform preparatory regimen: busulfan 16.0 mg/kg (d-8 to-5), etoposide 60mg/kg (d-4), cyclophosphamide 60mg/kg (d-2), and graft-versus-host-disease (GVHD) prophylaxis of cyclosporine and prednisone.
  • Disease status at transplantation was induction failure (IF) acute myeloid leukemia (AML) (n = 10), HR AML in 1st complete remission (CR1) n = 11, in CR2 (n = 5), in CR3 (n = 2), relapsed refractory (RR) AML (n = 14), chronic myeloid leukemia (CML) in second chronic phase (n = 6), blast crisis (n = 2), myelofibrosis (n = 6), myeloproliferative disorders (n = 2), and MDS (n = 38).
  • These results confirm that pts with high-risk or advanced myeloid malignancies can achieve long-term survival following myeloablative allogeneic HCT with aggressive conditioning.

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  • (PMID = 27961395.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A phase I study in patients (pts) with solid tumors revealed clinical activity, defined MTD as 30 mg/m<sup>2</sup>/d administered on daily x 3 schedule, and confirmed manageable toxicity.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.
  • Edema and other vascular leak syndromes are characteristic toxicities of the agent at higher dose levels.

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Naqvi K, Oh J, Garcia-Manero G, Pierce S, Suarez-Almazor ME: Comorbidities and prognosis of myelodysplastic syndromes. J Clin Oncol; 2009 May 20;27(15_suppl):7086

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comorbidities and prognosis of myelodysplastic syndromes.
  • Few studies have evaluated comorbidities in myelodysplastic syndromes (MDS).
  • The aim of our study was to determine the effect of comorbidity on the survival of patients with MDS.
  • METHODS: We reviewed the medical records of consecutive adult MDS patients who presented to our comprehensive cancer center in 2002.
  • For each patient, we obtained demographic data and specific staging information based on the International Prognostic Scoring System (IPSS).
  • The three most common comorbidities were hypertension, diabetes mellitus, and coronary artery disease.
  • Median survival according to ACE-27 scores was: 22 months for patients with no comorbidity, 11 months for patients with mild or moderate comorbidity, and 8 months for those with severe comorbidity; this trend did not reach statistical significance (p = 0.42).
  • Further studies are needed to evaluate the effects of comorbidities on the prognosis and therapeutic options of patients with early-stage MDS.

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  • (PMID = 27961479.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Fowler NH, McLaughlin P, Kwak L, Hagemeister F, Fanale M, Fayad L, Pro B, Samaniego F: Lenalidomide and rituximab for untreated indolent non-Hodgkin's lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8548

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 8548 Background: Despite advances in therapy and a better understanding of the natural history of indolent non-Hodgkins lymphomas (NHL), the optimal treatment for newly diagnosed patients (pts) has not been determined.
  • Lenalidomide has been shown to have single agent activity in indolent NHL, and is approved for the treatment of multiple myeloma and myelodysplastic syndrome.
  • METHODS: Pts with indolent NHL who were previously untreated, with measurable disease (>1.5 cm), were eligible for enrollment.
  • In the 5 pts eligible for response assessment, 4 pts (80%) attained a complete response (CR), 1 patient (20%) had stable disease (SD).
  • After 3 cycles, one patient had unconfirmed stable disease who also was previously treated with combination chemotherapy for Hodgkin's lymphoma.

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  • (PMID = 27960963.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. Lyman GH, Dale DC, Culakova E, Poniewierski MS, Wolff D, Kuderer NM, Lambert K, Crawford J: Acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) and overall mortality with chemotherapy (CT) and granulocyte colony-stimulating factor (G-CSF): A meta-analysis of randomized controlled trials (RCTs). J Clin Oncol; 2009 May 20;27(15_suppl):9524

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

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  • (PMID = 27964513.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Chamberlain MC, Raizer J: Extended exposure to alkylator chemotherapy: Delayed appearance of myelodysplasia. J Clin Oncol; 2009 May 20;27(15_suppl):e13030

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extended exposure to alkylator chemotherapy: Delayed appearance of myelodysplasia.
  • OBJECTIVE: A case series of gliomas treated with alkylator-based chemotherapy who subsequently developed myelodysplastic syndrome (tMDS) or acute myelocytic leukemia (AML).
  • The diagnosis of tMDS was determined by bone marrow biopsy in seven patients.
  • Seven patients showed chromosomal abnormalities consistent with chemotherapy induced MDS.
  • Interval from last chemotherapy exposure to diagnosis of tMDS/AML ranged from 3 months to 31 months (median 24 months).

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  • (PMID = 27962878.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Ramanarayanan J, Pahuja S, Elefante AN, Hernandez-Ilizaliturri FJ: Abrogation of tumor necrosis alpha (TNF-alpha) pathway by anti-TNF therapy in hematological malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7093

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • While the incidence of malignancies with TNF alpha inhibitors (infliximab, adalimumab, etanercept) are not significantly higher than the untreated control population, their role in cancer treatment itself is unclear.
  • METHODS: We reviewed the English literature by conducting systematic MEDLINE using the terms TNF-, infliximab, adalimumab, etanercept, cancer therapy, hematologic malignancies, myelodysplastic syndrome (MDS), multiple myeloma (MM), myeloproliferative disease (MPD), chronic lymphocytic leukemia (CLL), and lymphoma from January 2001 to August 2008.
  • We also performed a complete literature search of American Society of Hematology (ASH) and American Society of Clinical Oncology (ASCO) published abstracts.
  • RESULTS: Overall 11 phase I and II studies (n = 237; CLL n = 44, MM n = 10, MDS n = 109, MPD n = 51, HCL n = 3, TCL 13, FL 7) that involved anti-TNF- therapy in hematological malignancies were identified.
  • As a single agent, etanercept did not yield significant responses.
  • In conjunction with ATG or azacitidine in low-/intermediate-risk MDS, TNF inhibitors resulted in improvement in cytopenia.
  • No significant clinical benefit was seen among lymphoproliferative disorders, but treatment was well tolerated.
  • CONCLUSIONS: Existing data suggests that anti-TNF therapy by itself does not induce a therapeutic response in hematologic malignancies.

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  • (PMID = 27961263.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. Steensma D, Kantarjian H, Wijermans P: Clinical experience with different dosing schedules of decitabine in patients with myelodysplastic syndromes (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7011

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

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  • (PMID = 27961372.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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51. Batty G, Kantarjian H, Issa JJ, Garcia-Manero G, Pierce S, O'Brien S, Jabbour E, Cortes J, Ravandi F: Feasibility of hypomethylating therapy in patients with renal insufficiency. J Clin Oncol; 2009 May 20;27(15_suppl):7089

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7089 Background: Epigenetic therapy with hypomethylating agents (HA) is the standard of care in patients (pts) with myelodysplastic syndrome (MDS).
  • Moreover, there are no reports of use of these agents in pts with renal insufficiency (RI) commonly seen in pts with MDS.
  • METHODS: We investigated the outcomes of pts with RI and MDS, chronic myelomonocytic leukemia (CMML), or acute myeloid leukemia (AML) receiving therapy with HA.
  • RESULTS: Forty-two pts with sCr ≥ 1.5 mg/dL (including 17 with MDS, 16 with AML, and 9 with CMML) were treated with DAC or 5AZA alone or in combination with other agents (primarily histone deacetylase inhibitors).
  • The incidence of complications, DA, and the response rate were not significantly different for pts with sCr > 2.0 mg/dL.
  • CONCLUSIONS: The use of HA is well tolerated in pts with MDS and AML and RI who achieved comparable OR rates to those without RI.

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  • (PMID = 27961273.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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52. Helft PR, Terry C, Chamness AR, Uhrich MM: Oncology nurses' views of oncologists' prognosis-related communication (PRC). J Clin Oncol; 2009 May 20;27(15_suppl):6602

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Deficits in oncologists' (MDs) PRC have previously been identified.
  • The role oncology nurses (RNs) play in PRC and their views and experiences of PRC among MDs with whom they work is unknown.
  • 46% of RNs always/often cared for ACPs who did not appear to understand their prognosis, and 58.6% of RNs always/often encountered questions that suggested pts wanted more prognosis related information (PRI).
  • 26.1% disagreed that the MDs they worked with were skilled at PRC.
  • 54.9% of RNs always/often/sometimes felt pressured not to provide pts PRI because they did not want to contradict what MDs had said.
  • 25.1% of RNs felt that MDs rarely or never kept them informed about their PRC with pts (frequency positively associated with yrs as an RN, yrs working with cancer pts, education level).
  • RNs with at least an MSN were more likely to report that MDs more frequently kept them informed about their PRC.
  • 30.2% of RNs felt that MDs rarely or never addressed end of life issues early in the course of their illness.
  • 32.8% of RNs agreed that, when pts did not appear to understand their prognosis, it was because MDs had not discussed it fully (positively associated with working in an inpt setting).
  • CONCLUSIONS: Oncology RNs identify several deficits in MDs' PRC with ACPs, including provision of information early in the course of illness, gaps in sharing content of PRC with RNs, and communicative aspects of team-based pt care.

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  • (PMID = 27961728.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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53. Sekeres M, Kantarjian H, Fenaux P, Becker P, Boruchov A, Guerci-Bresler A, Hu K, Franklin J, Berger D: Subcutaneous or intravenous administration of romiplostim in thrombocytopenic patients with myelodysplastic syndrome (MDS). J Clin Oncol; 2009 May 20;27(15_suppl):7009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcutaneous or intravenous administration of romiplostim in thrombocytopenic patients with myelodysplastic syndrome (MDS).
  • : 7009 Background: Thrombocytopenia is common in patients (pts) with MDS, and treatment options are currently limited to platelet (plt) transfusions.
  • Eligibility criteria included IPSS low or intermediate-1 risk MDS and a mean baseline plt count ≤50x10<sup>9</sup>/L.
  • Five pts experienced serious AEs, and there were 2 cases of disease progression to AML: one pt in the QWSC cohort who received romiplostim for 4 weeks and one in the Q2WSC cohort who received romiplostim for 20 weeks.
  • For pts who completed 8 weeks treatment, 15/23 (65%) achieved a plt response, defined by IWG 2006 criteria, and 14/23 (61%) did not require a plt transfusion during this period.
  • CONCLUSIONS: IV and SC romiplostim appeared well-tolerated and effective in raising plt counts and avoiding plt transfusions in low and intermediate-1 risk MDS pts.

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  • (PMID = 27961381.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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54. Bakanay SM, Karakiliç E, Civriz-Bozdag S, Arat M, Ozcan M, Gurman G, Ilhan O, Beksac M, Konuk N, Arslan O: 5-azacytidine treatment results in myelodysplastic syndrome. J Clin Oncol; 2009 May 20;27(15_suppl):e18003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 5-azacytidine treatment results in myelodysplastic syndrome.
  • : e18003 Background: Myelodysplastic syndrome (MDS) is a clonal disease of hematopoiesis characterized by dysplasia in one or more series.
  • 5-azacytidine (5-AZA) which is one of the methyl transferase inhibitors, targets the epigenetic changes in MDS and has been used for the last few years.
  • METHODS: In this study the aim was to retrospectively analyze the response rates of 26 MDS patients who were treated with 5-AZA between years 2002-2008.
  • The patients were; median age 58 (21-84); male/female = 16/10; RAEB-I (7 patients); RAEB-II (18 patients); ve CMML (1 patient); secondary MDS (2 patients).
  • According to an international prognostic scoring system, 6 patients were intermediate-1; 9 patients were intermediate-2; and 11 patients were high risk.
  • RESULTS: Seven patient were not elligible for response evaluation.
  • Nine patients (47%) did not respond to the therapy and 8 of them were lost.

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  • (PMID = 27963997.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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55. Whitworth PW, Presant CA, Rutledge J, Hallquist A, Perree M, Agapitos D: Chemosensitivity (CS) of patient (pt) breast cancer (BrCa) cells in vitro: Correlation with prior chemotherapy (CT) and implications for personalized treatment planning. J Clin Oncol; 2009 May 20;27(15_suppl):e11563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Tumor excisions or biopsies were sent to a central laboratory, prepared using our previously described MiCK technology (Lab Invest 74: 557, 1996) and tc apoptosis was measured over 48 hours with various drugs.
  • In vitro results were compared to clinical status.
  • Physicians (MDs) decided on CT without knowledge of MiCK results.
  • These data may be useful to MDs in selecting CT for individual pts.
  • For clinical trials that began accrual on or after April 29, 2004, ASCO's Policy places some restrictions on the financial relationships of principal investigators (J Clin Oncol.
  • (2) is the inventor of a unique technology or treatment being evaluated in the clinical trial; or (3) is involved in international clinical oncology research and has acted consistently with recognized international standards of ethics in the conduct of clinical research.

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  • (PMID = 27964068.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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56. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • OBJECTIVES: This study analyzes changes in the degree of global methylationlevel in myelodysplastic syndrome during progression of the disease.
  • METHODS: Methylation status was analyzed in 127 patients with histologically confirmed MDS and 26 reactive controls.
  • RESULTS: We detected an increase of methylation level of LINE-1 sequences using pyrosequencing and an increase of methylation in the HpaII recognition site employing LUMA during the progression of MDS.
  • The genome wide hypermethylation of MDS is a distinct feature of this disease.
  • It discriminates MDS from other neoplasia and may explains the success of hypomethylation inducing reagents like azadeoxycytidine in MDS therapy.
  • [MeSH-major] DNA Methylation. Long Interspersed Nucleotide Elements / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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57. Bartholomeyczik S, Halek M, Hunstein D, Isfort M, Roser JM, Hebart-Herrmann M, Bernhard F, Schreier MM, Cramer H, Wagner A: [Comment about the policy statement of the MDS. A position statement of the assessment group of the University Witten/Herdecke with regard to nursing documentation]. Pflege Z; 2007 Mar;60(3):145-9
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  • [Title] [Comment about the policy statement of the MDS. A position statement of the assessment group of the University Witten/Herdecke with regard to nursing documentation].
  • [Transliterated title] Kommentar zur Grundsatzstellungnahme "Pflegeprozess und Dokumentation" des MDS. Positionspapier der Assessmentgruppe, Universität Witten/Herdecke, zur Pflegedokumentation.
  • In 2005 the Medical Advisory Service of Social Health Insurance (MDS) in Germany published a policy statement with regard to the nursing process and documentation.
  • [MeSH-minor] Forecasting. Germany. Health Policy / trends. Health Services Needs and Demand / standards. Humans. National Health Programs / standards. Nursing Assessment / standards. Nursing Diagnosis / standards. Quality Assurance, Health Care / standards

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  • (PMID = 17416183.001).
  • [ISSN] 0945-1129
  • [Journal-full-title] Pflege Zeitschrift
  • [ISO-abbreviation] Pflege Z
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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58. Samúelsson O, Bjartmarz S, Jensdóttir AB, Jónsson PV: [Comparison of MDS-AC registration and conventional medical records in Iceland and other Nordic countries. A part of a Nordic study]. Laeknabladid; 2005 Apr;91(4):335-41
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  • [Title] [Comparison of MDS-AC registration and conventional medical records in Iceland and other Nordic countries. A part of a Nordic study].
  • [Transliterated title] Samanburdur á MDS-AC skráningu og hefdbundinni sjúkraskrá á brádadeild á Islandi og ödrum Nordurlöndum. Hluti samnorraennar rannsóknar.
  • The MDS-AC is an evaluation system for geriatric acute care patients that records functional impairment and co-morbid states.
  • The object of this study was to compare the MDS-AC registration with the traditional nurses and doctors records for chosen variables important to older patient care in Iceland and other Nordic countries.
  • The results presented here show data from selected variables collected with the MDS-AC instrument version 1,1 in the first 24 hours of admission, compared with hospital notes for the first 48 hours.
  • RESULTS: For ADL and IADL impairments the medical record missed between 20 to 96% of items registered with the MDS-AC and between 33 to 100% when there is no impairment detected.
  • CONCLUSION: The MDS-AC documents better than traditional medical records several important variables relating to function among the elderly.
  • It may be possible to improve documentation with a standardized instrument such as the MDS-AC.
  • [MeSH-minor] Activities of Daily Living. Aged. Comorbidity. Denmark. Finland. Forms and Records Control. Humans. Iceland. Medical Records Systems, Computerized. Norway. Nursing Records / standards. Nursing Records / statistics & numerical data. Prospective Studies. Sweden

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  • (PMID = 16155327.001).
  • [ISSN] 0023-7213
  • [Journal-full-title] Læknablađiđ
  • [ISO-abbreviation] Laeknabladid
  • [Language] ice
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Iceland
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59. Melchert M, List A: Targeted therapies in myelodysplastic syndrome. Semin Hematol; 2008 Jan;45(1):31-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapies in myelodysplastic syndrome.
  • Therapeutic alternatives for patients with myelodysplastic syndrome (MDS) have expanded in recent years but remain limited.
  • While agents approved by the US Food and Drug Administration (FDA), including azacitidine, decitabine, and lenalidomide, have yielded hematologic and cytogenetic responses in a substantial portion of patients, these therapies are not curative.
  • Active investigation of novel targets with biological relevance in myelopoiesis has stimulated the pharmacologic development of a multitude of agents that show promise in the treatment of MDS.
  • Many of these drugs have entered or completed early phase clinical testing in MDS and include immunomodulatory agents, immunosuppressive therapies, survival signal inhibitors, thrombopoiesis-stimulating agents, pharmacologic differentiators, and anti-angiogenic and apoptotic agents.
  • As we continue to collect clinical experience with these agents, the repertoire of available therapeutics for the treatment of MDS will expand and provide a foundation for novel therapeutic combinations.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Growth Inhibitors / therapeutic use. Immunologic Factors / therapeutic use. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 18179967.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Growth Inhibitors; 0 / Immunologic Factors; 0 / Immunosuppressive Agents; 0 / Receptors, Thrombopoietin; EC 2.5.1.29 / Farnesyltranstransferase
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60. Farmakis D, Polymeropoulos E, Polonifi A, Deftereos S, Giakoumi X, Floudas H, Grapsa A, Aessopos A: Myelodysplastic syndrome associated with multiple autoimmune disorders. Clin Rheumatol; 2005 Aug;24(4):428-30
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  • [Title] Myelodysplastic syndrome associated with multiple autoimmune disorders.
  • The association between myelodysplastic syndromes (MDS) and autoimmune manifestations is not uncommon.
  • As a rule, autoimmune abnormalities follow the diagnosis of MDS.
  • We describe here a patient with MDS who developed a striking spectrum of diverse autoimmune disorders, including dermatitis, polyarthritis, and vasculitis, which preceded the clinical appearance of MDS.
  • [MeSH-major] Autoimmune Diseases / diagnosis. Autoimmune Diseases / therapy. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Arthritis / complications. Arthritis / diagnosis. Blood Transfusion / methods. Combined Modality Therapy. Dermatitis / complications. Dermatitis / diagnosis. Drug Therapy, Combination. Epoetin Alfa. Erythropoietin / therapeutic use. Filgrastim. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Male. Methylprednisolone / therapeutic use. Recombinant Proteins. Risk Assessment. Severity of Illness Index. Treatment Outcome. Vasculitis / complications. Vasculitis / diagnosis


61. Ingram W, Lim ZY, Mufti GJ: Allogeneic transplantation for myelodysplastic syndrome (MDS). Blood Rev; 2007 Mar;21(2):61-71
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  • [Title] Allogeneic transplantation for myelodysplastic syndrome (MDS).
  • Haematopoietic stem cell transplantation (HSCT) remains the only curative option for patients with myelodysplastic syndrome (MDS).
  • Developing conditioning regimens with low toxicity, at the same time as preserving an effective graft versus tumour response, is pivotal to expanding the scope for allogeneic transplantation in older patients with MDS.
  • With the introduction of reduced intensity conditioned regimens, transplant centres worldwide are able to offer allogeneic HSCT to a much larger cohort of patients.
  • Graft versus host disease (GvHD) remains a significant cause of morbidity and mortality, however with the use of T-cell depletion, centres have been able to utilise volunteer unrelated donors with an increasing degree of HLA disparity.
  • The graft versus dysplasia effect resulting from allogeneic HSCT and the infusion of donor leukocytes has led to a greater understanding of the immunological mechanisms that govern outcome following transplantation in MDS.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Donor Selection. Graft vs Host Disease / immunology. Graft vs Leukemia Effect. Humans. Immunotherapy. Leukocyte Transfusion. Transplantation Conditioning. Transplantation, Autologous


62. Wang YY, Cen JN, He J, Shen HJ, Liu DD, Yao L, Qi XF, Chen ZX: Accelerated cellular senescence in myelodysplastic syndrome. Exp Hematol; 2009 Nov;37(11):1310-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Accelerated cellular senescence in myelodysplastic syndrome.
  • OBJECTIVE: To investigate the contribution of cellular senescence to the progression and prognosis of myelodysplastic syndrome (MDS).
  • MATERIALS AND METHODS: We have analyzed the expression of p16INK4a in bone marrow mononuclear cells or CD34(+) cells from 53 patients with MDS, 12 acute myeloid leukemia (AML), and 11 healthy controls.
  • Additionally, We have assessed quantitatively senescence-associated beta-galactosidase (SA-beta-gal) staining on bone marrow mononuclear cells from MDS and AML patients, HL60 and SHI-1 leukemia cell lines, and healthy control cells.
  • RESULTS: An upregulated expression of senescence-associated molecular marker p16INK4a was found in MDS compared with healthy controls, while a lower expression of p16INK4a was observed in AML compared with healthy controls.
  • International Prognostic Scoring System score was negatively correlated with the percentage of p16INK4a-positive cells.
  • The SA-beta-gal activity measured by mean percentage of positive cells was significantly higher in MDS cases when compared with controls.
  • Meanwhile, percentage of SA-beta-gal-positive cells was also remarkably higher in dysplastic cells of MDS when compared to nondysplastic cells from MDS.
  • CONCLUSIONS: These results of our present study suggested an accelerated cellular senescence occurred in MDS, and the cellular senescence may be involved in the progression and prognosis of MDS.
  • [MeSH-major] Cell Aging. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Anemia, Refractory / metabolism. Anemia, Refractory / pathology. Anemia, Refractory, with Excess of Blasts / metabolism. Anemia, Refractory, with Excess of Blasts / pathology. Biomarkers. Cell Line, Tumor / chemistry. Cell Line, Tumor / pathology. Cyclin-Dependent Kinase Inhibitor p16 / analysis. Female. Genes, p16. Humans. Male. Middle Aged. Neoplasm Proteins / analysis. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Severity of Illness Index. Young Adult. beta-Galactosidase / analysis

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  • (PMID = 19748549.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 3.2.1.23 / beta-Galactosidase
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63. Angotti LB, Post GR, Robinson NS, Lewis JA, Hudspeth MP, Lazarchick J: Pancytopenia with myelodysplasia due to copper deficiency. Pediatr Blood Cancer; 2008 Nov;51(5):693-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancytopenia with myelodysplasia due to copper deficiency.
  • We present a case of pancytopenia in a 9-month-old infant with total parenteral nutrition (TPN) dependence due to short bowel syndrome.
  • Bone marrow examination revealed left-shifted myeloid maturation, erythroid and myeloid dysplasia with normal iron stores.
  • Copper deficiency should be considered in the differential diagnosis of cytopenias and myelodsyplasia, particularly in the growing number of pediatric patients with TPN dependency or malabsorption.
  • [MeSH-minor] Enterocolitis, Necrotizing / surgery. Humans. Infant. Male. Parenteral Nutrition, Total. Short Bowel Syndrome / physiopathology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18623212.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 789U1901C5 / Copper
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64. Xu J, Guo YX, Zhao H, Hui WH, Wan SG, Sun XJ: [Abnormality of immunophenotyping in patients with myelodysplastic syndrome]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Aug;17(4):894-7
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  • [Title] [Abnormality of immunophenotyping in patients with myelodysplastic syndrome].
  • The study was aimed to investigate the abnormality of immunophenotypes in patients with myelodysplastic syndrome (MDS) and its role in the identification of MDS.
  • The cell immunophenotypes of 136 patients with hypocytosis accompanied by abnormal hematopoiesis of bone marrow were detected by flow cytometry, the detected results were evaluated by flow cytometric scoring system (FCSS), and the sensitivity and specificity of positive results were determined by FCSS also.
  • The correlation of results detected by FCSS to traditional diagnosis method was analysed.
  • The results indicated that 111 out of 136 cases were diagnosed as MDS, and 25 were diagnosed as non-MDS.
  • Among 111 MDS cases, 85 cases were FCSS positive, 18 cases were FCSS intermediate and 8 cases were FCSS negative, whereas in 25 non-MDS cases 24 cases were FCSS negative, 1 case was FCSS intermediate and no case was FCSS positive.
  • The sensitivity of FCSS in identification of MDS was 76.6%, and the specificity of FCSS was 100%.
  • It is concluded that the various abnormalities of immunophenotyping are found in patients with MDS, in which the main immunophenotype abnormality and the abnormality involving two cell lineages are key points to distinguish MDS from non-MDS.


65. Feldman EJ: Farnesyltransferase inhibitors in myelodysplastic syndrome. Curr Hematol Malig Rep; 2006 Mar;1(1):20-4
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  • [Title] Farnesyltransferase inhibitors in myelodysplastic syndrome.
  • The farnesyltransferase inhibitors (FTIs) are in active clinical development in a variety of human malignancies.
  • The most promising activity to date has been demonstrated in patients with hematologic malignancies, in particular acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • In patients with MDS, two nonpeptidomimetic agents, tipifarnib (Zarnestra, Johnson & Johnson, New Brunswick, NJ) and lonafarnib (Sarasar, Schering-Plough, Kenilworth, NJ) have been the most extensively studied.
  • Lonafarnib in patients with MDS has also resulted in clinical responses in approximately 30%, including significant improvements in platelet counts.
  • Clinical response correlation with documentation of inhibition of farnesyltransferase and/or evidence of decreased farnesylation of downstream protein targets has not been demonstrated with either agent.
  • In addition, the presence of an activating Ras mutation has not predicted response to therapy with FTIs in MDS and AML.
  • Despite this lack of evidence, significant clinical efficacy of the FTIs has been observed in MDS, on a par with the efficacy of currently available chemotherapeutic agents, leading to further development of this new class of drugs in MDS and AML.
  • [MeSH-major] Farnesyltranstransferase / antagonists & inhibitors. Myelodysplastic Syndromes / drug therapy. Piperidines / therapeutic use. Pyridines / therapeutic use. Quinolones / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Bone Marrow Diseases / chemically induced. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Disease Progression. Gastrointestinal Diseases / chemically induced. Genes, ras. Hematologic Neoplasms / drug therapy. Humans. Middle Aged. Prenylation / drug effects. Protein Processing, Post-Translational / drug effects. Treatment Outcome

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  • (PMID = 20425327.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Piperidines; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 193275-84-2 / lonafarnib; EC 2.5.1.29 / Farnesyltranstransferase
  • [Number-of-references] 37
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66. Larson RA: Myelodysplasia: when to treat and how. Best Pract Res Clin Haematol; 2006;19(2):293-300
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplasia: when to treat and how.
  • Myelodysplastic syndrome (MDS) is a disorder of hematopoietic stem cells characterized by ineffective hematopoiesis.
  • The result is pancytopenia leading to transfusion-dependent anemia, an increased risk of infection or bleeding, and a potential to progress to acute myeloid leukemia (AML).
  • MDS is most prevalent among older individuals, many of whom also suffer from other medical conditions.
  • MDS is classified according to World Health Organization criteria and the International Prognostic Scoring System.
  • Those with low-risk MDS can often be monitored for an extended period of time without specific therapy, whereas those with intermediate- or high-risk MDS benefit from treatment.
  • Currently, only azacitidine is approved for the treatment of MDS.
  • Lenalidomide appears particularly effective in patients with low-risk MDS with the deletion of chromosome 5q31.
  • Allogeneic stem cell transplantation is an alternative for high-risk MDS.
  • However, it is necessary to assess each patient's disease individually and to evaluate prognostic factors, other treatment options, and the appropriateness and timing of transplantation.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Enzyme Inhibitors / therapeutic use. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation
  • [MeSH-minor] Anemia / etiology. Anemia / therapy. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Humans. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / genetics. Prognosis. Transplantation, Homologous

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  • (PMID = 16516126.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Enzyme Inhibitors
  • [Number-of-references] 15
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67. Ol'shanskaia IuV, Domracheva EV, Udovichenko AI, Vodinskaia LA, Zakharova AV, Parovichnikova EN, Tsvetaeva NV, Mikhaĭlova EA, Glasko EN, Kolosova LIu, Kokhno AN, Tikhonova LIu, Shitareva TV, Smirnova EA, Alimova GA, Shirin AD, Vinogradova OIu, Khoroshko ND, Savchenko VG: [Chromosomal aberrations in myelodysplastic syndrome]. Ter Arkh; 2005;77(7):27-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chromosomal aberrations in myelodysplastic syndrome].
  • AIM: To analyse incidence rate of chromosomal aberrations in myelodysplastic syndromes (MDS), specification of clinicomorphological features of some cytogenetic variants.
  • MATERIAL AND METHODS: Chromosomal analysis by the method of G-differential staining of chromosomes was made in 209 patients with different variants of MDS.
  • Chromosomal aberrations determined not only clinical and morphological features but also the prognosis of the disease.
  • CONCLUSION: Cytogenetic examination is an essential component of MDS patients examination.
  • It allows more precise classification of MDS variant and prognostification of the disease course.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, X / genetics. Chromosomes, Human, Y / genetics. Myelodysplastic Syndromes / genetics


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


69. Sekeres MA: Are we nearer to curing patients with MDS? Best Pract Res Clin Haematol; 2010 Dec;23(4):481-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Are we nearer to curing patients with MDS?
  • Myelodysplastic syndromes (MDS) are a heterogeneous collection of clonal hematopoietic disorders derived from abnormal multipotent progenitor cells.
  • They have been classified by the World Health Organization as myeloid neoplasms with several different subtypes based on morphology and cytogenetics.
  • Because MDS was only recently recognized as a cancer, epidemiological data is tentative and incidence and prevalence will probably increase as reporting improves.
  • Prognosis for MDS patients is calculated using the International Prognostic Scoring System, though this system is currently being revised by several groups.
  • Therapy for MDS varies based on pathobiology, prognosis, and cytogenetics, such as the deletion of 5q.
  • Treatment options range from supportive care, to disease-modifying chemotherapeutic agents, to stem cell transplantation, to therapies that may affect quality of life, improve survival, or even cure the disease.
  • [MeSH-major] Myelodysplastic Syndromes
  • [MeSH-minor] Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Cytogenetics / methods. Disease-Free Survival. Humans. Multipotent Stem Cells / pathology. Prevalence. Stem Cell Transplantation. Survival Rate

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21130411.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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70. Kerbauy DB, Deeg HJ: Apoptosis and antiapoptotic mechanisms in the progression of myelodysplastic syndrome. Exp Hematol; 2007 Nov;35(11):1739-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis and antiapoptotic mechanisms in the progression of myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS), previously known as preleukemia, comprises a spectrum of heterogeneous, clonal disorders of hematopoiesis.
  • Recent studies provide some insight into the pathophysiology of MDS.
  • Tumor necrosis factor (TNF)-alpha, Fas ligand, TNF-related apoptosis-inducing ligand, and other proapoptotic cytokines are upregulated in early-stage/low-risk MDS, and neutralization of these signals can improve hematopoiesis.
  • In a proportion of patients, MDS will eventually evolve to acute leukemia.
  • The role of the microenvironment in the pathophysiology and progression of MDS has remained controversial, although there is evidence that stroma and matrix components, and their interactions with clonal cells, play an important role.
  • Microarray gene-expression studies are consistent with dysregulation of apoptosis, but not all data are in agreement.

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  • (PMID = 17976524.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL082941-03; United States / NHLBI NIH HHS / HL / HL036444-270016; United States / NHLBI NIH HHS / HL / HL36444; United States / NCI NIH HHS / CA / CA119599-02; United States / NHLBI NIH HHS / HL / R01 HL082941-03; United States / NHLBI NIH HHS / HL / R01 HL082941; United States / NCI NIH HHS / CA / R21 CA119599; United States / NHLBI NIH HHS / HL / HL082941; United States / NHLBI NIH HHS / HL / P01 HL036444-270016; United States / NCI NIH HHS / CA / R21 CA119599-02; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / CA119599
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 68
  • [Other-IDs] NLM/ NIHMS34139; NLM/ PMC2131709
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71. Gyulai Z, Balog A, Borbényi Z, Mándi Y: Genetic polymorphisms in patients with myelodysplastic syndrome. Acta Microbiol Immunol Hung; 2005;52(3-4):463-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in patients with myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS) is a family of clonal disorders characterized by dyshematopoiesis and susceptibility to acute myelogenous leukemia.
  • Tumor necrosis factor-a (TNF-alpha) and transforming growth factor-beta (TGF-beta) are cytokines that play key roles in the pathogenesis of MDS.
  • The association between TNF-alpha and TGF-beta1 gene polymorphism and the susceptibility to MDS and the progression of the disease was investigated.
  • As compared with healthy control subjects (n = 74), patients with MDS (n = 55) showed no significant deviations in genotype or allele frequencies of TNF-alpha.
  • Similarly, there were no differences in the distribution of TNF-alpha genotypes between the MDS patients with only anemia (mild group) and those with bi- or pancytopenia (severe group).
  • These findings suggest that the investigated genetic polymorphisms do not predispose to the development of MDS, but that TGF-beta1 gene polymorphism may affect the disease progression.
  • [MeSH-major] Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / physiopathology. Polymorphism, Genetic. Transforming Growth Factor beta / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Gene Frequency. Genotype. Humans. Male. Middle Aged. Transforming Growth Factor beta1

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  • (PMID = 16400883.001).
  • [ISSN] 1217-8950
  • [Journal-full-title] Acta microbiologica et immunologica Hungarica
  • [ISO-abbreviation] Acta Microbiol Immunol Hung
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / TGFB1 protein, human; 0 / TNF protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha
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72. Mihara K, Takihara Y, Kimura A: Genetic and epigenetic alterations in myelodysplastic syndrome. Cytogenet Genome Res; 2007;118(2-4):297-303
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic and epigenetic alterations in myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS) is a clonal disorder characterized by dyshematopoiesis and high susceptibility to acute myeloid leukemia (AML).
  • As patients with MDS have widely variable prognosis, we need to stratify them according to chromosomal abnormalities, genetic alterations, and epigenetic deregulations associated with progression to AML in order to treat these patients appropriately.
  • We have reported that the expression of BMI1, a member of PcG, in hematopoietic stem cells or progenitor cells predicts the prognosis of patients with MDS and progression to acute leukemia.
  • Thus PcG not only provides a molecular marker for monitoring disease progression of MDS, but also provides a clue for elucidating a molecular mechanism underlying the disease progression, which may help in the development of a new therapeutic strategy against MDS.
  • Herein, we describe cytogenetic, genetic and molecular aberrations in MDS, focusing on epigenetic alterations through PcG.
  • [MeSH-major] Chromosome Aberrations. Epigenesis, Genetic. Myelodysplastic Syndromes / genetics

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 18000383.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers
  • [Number-of-references] 66
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73. Ebert BL: Genetic deletions in AML and MDS. Best Pract Res Clin Haematol; 2010 Dec;23(4):457-61
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  • [Title] Genetic deletions in AML and MDS.
  • Chromosomal deletions are common molecular events in myeloid malignancies.
  • Heterozygous deletions may contain a tumor suppressor gene that undergoes homozygous inactivation or may contain one or more genes that alter the disease phenotype through haploinsufficiency.
  • The most common karyotypic abnormality in myelodysplastic syndrome (MDS) is deletion of chromosome 5q.
  • A subset of patients with del(5q) as a sole cytogenetic abnormality has a consistent set of clinical features, termed the 5q- syndrome.
  • While no tumor suppressor genes have been identified on 5q that are homozygously inactivated, recent studies have highlighted several genes and micro RNAs (miRNAs) that cause the phenotype of the 5q- syndrome through allelic insufficiency.
  • For example, deletion of one allele of the RPS14 gene causes a severe defect in erythropoiesis, analogous to the congenital syndrome Diamond Blackfan anemia, which is itself caused by mutations that inactivate one allele of a ribosomal gene.
  • The functional approaches used to dissect the molecular basis of the 5q deletion in MDS have the potential to identify key genes and therapeutic targets within other chromosomal deletions in hematologic malignancies.

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 21130407.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL082945-06; United States / NHLBI NIH HHS / HL / R01 HL082945; United States / NHLBI NIH HHS / HL / R01 HL082945-06
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / MIRN145 microRNA, human; 0 / MIRN146 microRNA, human; 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm; 0 / RPS14 protein, human; 0 / Ribosomal Proteins
  • [Other-IDs] NLM/ NIHMS251639; NLM/ PMC3032259
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74. Niemeyer CM, Baumann I: Myelodysplastic syndrome in children and adolescents. Semin Hematol; 2008 Jan;45(1):60-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndrome in children and adolescents.
  • Myelodysplastic syndromes (MDS) are clonal disorders characterized by ineffective hematopoiesis and subsequent frequent development of acute myeloid leukemia (AML).
  • In children and adolescents, MDS are uncommon disorders, accounting for less than 5% of hematopoietic malignancy, with great heterogeneity in presentation and clinical course.
  • The genetic changes predisposing children to MDS are largely obscure.
  • Monosomy 7 is the most common chromosomal abnormality, often occurring as a sole abnormality.
  • Refractory cytopenia (RC) is the most common MDS subtype in children, occurring in about half of all MDS cases.
  • There is consensus that the relationship between MDS with increased blast count and de novo AML is better defined by biological and clinical features than by blast count.
  • Because monosomy 7 is the only chromosomal abnormality strongly suggestive of MDS, children presenting with a low blast count and other chromosomal aberrations or normal karyotype must be closely observed before a diagnosis of MDS can be established.
  • With an increasing number of children surviving primary cancer with chemotherapy or radiation therapy, the incidence of secondary therapy-related MDS is rising.
  • The MDS risk is also increased in patients with inherited bone marrow failure disorders; this relationship provides valuable insights into MDS biology.
  • Allogeneic hematopoietic stem cell transplantation (HSCT) from a matched related or suitable unrelated donor is the choice for most children with MDS and can rescue a large proportion of patients.
  • [MeSH-major] Anemia, Refractory. Immunosuppressive Agents / therapeutic use. Myelodysplastic Syndromes
  • [MeSH-minor] Adolescent. Child. Chromosomes, Human, Pair 7. Diagnosis, Differential. Hematopoietic Stem Cell Transplantation. Humans. Monosomy. Transplantation, Homologous


75. Kindwall-Keller T, Isola LM: The evolution of hematopoietic SCT in myelodysplastic syndrome. Bone Marrow Transplant; 2009 Apr;43(8):597-609
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  • [Title] The evolution of hematopoietic SCT in myelodysplastic syndrome.
  • Allogeneic hematopoietic SCT (allo-HCT) is the only curative therapy for myelodysplastic syndrome (MDS).
  • Numerous myeloablative (MA), nonmyeloablative SCT (NST) and reduced conditioning transplant (RIC) studies have included MDS patients.
  • Twenty-four MA HCT studies published from 2000 and 2008 reported OS and disease-free survival (DFS) ranging from 25 and 16% at 2 years to 52 and 50% at 4 years.
  • Until recently, the International Prognostic Scoring System (IPSS) dictated the use and timing of HCT.
  • The WHO classification and WHO Prognostic Scoring System (WPSS) may be better suited in predicting the outcomes and should probably be incorporated in transplant algorithms.
  • Most published MDS transplant series combine matched related donors (MRD) and matched unrelated donors (MUD).
  • Umbilical cord blood (UCB) grafts will likely broaden the population of MDS patients eligible for allografting, but outcome data for MDS are scant.
  • At this time, it is reasonable to consider the availability of an MRD or MUD as separate from an UCB graft in the decision of transplantation for MDS.
  • The development of RIC, improvements in supportive therapy and alternative donor selection will provide better OS for MDS patients undergoing transplantation.
  • Simultaneously, better understanding and medical therapy of MDS are leading us to re-examine patient selection and the timing of HCT.
  • The results of HCT for MDS continue to improve together with the outlook of patients afflicted with myelodysplasia.
  • [MeSH-major] Hematopoietic Stem Cells / cytology. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation / methods
  • [MeSH-minor] Adult. Aged. Cell Transplantation. Fetal Blood / cytology. Graft vs Host Disease / therapy. Humans. Middle Aged. Prognosis. Recurrence. Risk. Transplantation Conditioning. Treatment Outcome


76. Feldman EJ: Farnesyltransferase inhibitors in myelodysplastic syndrome. Curr Hematol Rep; 2005 May;4(3):186-90
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  • [Title] Farnesyltransferase inhibitors in myelodysplastic syndrome.
  • The farnesyltransferase inhibitors (FTIs) are in active clinical development in a variety of human malignancies.
  • The most promising activity to date has been demonstrated in patients with hematological malignancies, in particular acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • In patients with MDS, two non-peptidomimetic agents, tipifarnib (Zarnestra, Johnson & Johnson, New Brunswick, NJ) and lonafarnib (Sarasar, Schering-Plough, Kenilworth, NJ) have been the most extensively studied.
  • Lonafarnib in patients with MDS has also resulted in clinical responses in approximately 30%, including significant improvements in platelet counts.
  • Clinical response correlation with documentation of inhibition of farnesyltransferase and/or evidence of decreased farnesylation of downstream protein targets has not been demonstrated with either agent.
  • In addition, the presence of an activating Ras mutation has not predicted response to therapy with FTIs in MDS and AML.
  • Despite this, significant clinical efficacy of the FTIs in MDS, on par with that of currently available chemotherapeutic agents, has been observed, leading to further development of this new class of drugs in MDS and AML.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Myelodysplastic Syndromes / drug therapy. Piperidines / therapeutic use. Pyridines / therapeutic use. Quinolones / therapeutic use
  • [MeSH-minor] Acute Disease. Aged. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Disease Progression. Farnesyltranstransferase. Genes, ras. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / enzymology. Humans. Leukemia, Myeloid / etiology. Leukemia, Myeloid / genetics. Middle Aged. Protein Prenylation / drug effects. Protein Processing, Post-Translational / drug effects. Proto-Oncogene Proteins p21(ras) / chemistry. Proto-Oncogene Proteins p21(ras) / metabolism. Remission Induction. Signal Transduction / drug effects. Treatment Outcome

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  • (PMID = 15865870.001).
  • [ISSN] 1541-0714
  • [Journal-full-title] Current hematology reports
  • [ISO-abbreviation] Curr. Hematol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Piperidines; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 193275-84-2 / lonafarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Number-of-references] 37
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77. Nolte F, Hofmann WK: Molecular mechanisms involved in the progression of myelodysplastic syndrome. Future Oncol; 2010 Mar;6(3):445-55
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  • [Title] Molecular mechanisms involved in the progression of myelodysplastic syndrome.
  • Myelodysplastic syndromes (MDS) are a heterogeneous group of diseases characterized by ineffective hematopoiesis presenting with peripheral cytopenias in combination with a hyperplastic bone marrow.
  • MDS patients have an increased risk of disease evolution to acute leukemia.
  • Strong efforts have been made to gain further insights into the pathobiology of MDS.
  • Development and progression of MDS to acute myeloid leukemia is suggested to be a multistep alteration to hematopoietic stem cells consisting of class I and class II alterations: the former targeting genes that are involved in signal transduction (e.g., FLT3, RAS and KIT), whereas the latter affect transcription factors (e.g., RUNX, RARA, EVI1 and WT1).
  • These alterations consist of not only genomic mutations but also epigenetic aberrations, which can lead to reversible gene silencing.
  • Accumulation of such defects may finally cause the leukemic transformation of MDS.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Myelodysplastic Syndromes / genetics. Precancerous Conditions / genetics
  • [MeSH-minor] Animals. Disease Progression. Humans


78. Vidal DO, Paixão VA, Brait M, Souto EX, Caballero OL, Lopes LF, Vettore AL: Aberrant methylation in pediatric myelodysplastic syndrome. Leuk Res; 2007 Feb;31(2):175-81
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  • [Title] Aberrant methylation in pediatric myelodysplastic syndrome.
  • Aberrant promoter methylation is frequently observed in adult patients with myelodysplastic syndrome (MDS), but in pediatric patients it has been poorly investigated.
  • METHODS: We examined the promoter methylation status of 13 genes in bone marrow cells collected at diagnosis of 21 pediatric patients with MDS (subtype RAEB or RAEB-t).
  • RESULTS: In pediatric MDS samples, we observed two genes frequently methylated: CALCA was methylated in 85.7% (18/21) of the analyzed samples and CDKN2B in 50% (6/12).
  • CONCLUSIONS: Our findings indicate that CALCA and CDKN2B are frequently methylated in pediatric MDS.
  • It suggests that aberrant methylation in pediatric MDS seems to be similar to adult MDS, thus pediatric patients could be also benefited with treatment using demethylating agents.
  • [MeSH-major] Calcitonin / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. DNA Methylation. Myelodysplastic Syndromes / genetics. Protein Precursors / genetics

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  • (PMID = 16890288.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Protein Precursors; 56645-65-9 / procalcitonin; 9007-12-9 / Calcitonin; 9007-49-2 / DNA
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79. Douet-Guilbert N, Laï JL, Basinko A, Gueganic N, Andrieux J, Pollet B, Plantier I, Delattre C, Crépin O, Corm S, Le Bris MJ, Morel F, De Braekeleer M: Fluorescence in situ hybridization characterization of ider(20q) in myelodysplastic syndrome. Br J Haematol; 2008 Dec;143(5):716-20
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  • [Title] Fluorescence in situ hybridization characterization of ider(20q) in myelodysplastic syndrome.
  • Isochromosome of the long arm of chromosome 20 with loss of interstitial material [ider(20q)] is a variant of deletion of chromosome 20q and a rare abnormality in myelodysplastic syndrome (MDS).
  • We studied seven cases with an ider(20q) in MDS.
  • [MeSH-major] Chromosomes, Human, Pair 20. Isochromosomes. Myelodysplastic Syndromes / genetics

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  • (PMID = 19036015.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DIDO1 protein, human; 0 / DNA-Binding Proteins; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / TNFRSF6B protein, human; EC 2.7.10.2 / HCK protein, human; EC 2.7.10.2 / Proto-Oncogene Proteins c-hck
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80. Li YQ, DU X: [Clonal expanded T-cell repertoire in MDS]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Jun;18(3):793-7
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  • [Title] [Clonal expanded T-cell repertoire in MDS].
  • The myelodysplastic syndromes (MDS) comprises a heterogeneous group of clonal hematopoietic stem cell disorders, while immunological abnormalities are frequently observed in such patients.
  • T-cell mediated suppression of hematopoietic precursors contributes to the cytopenia and is related to the initiation and development of myelodysplastic syndromes (MDS).
  • In this review, current knowledge concerning the feature of T-cell clonal expansion in MDS based on the analysis of T-cell receptor repertoire is summarized, including following issues: autoimmunity in MDS patients associated with T-cell mediated suppression of hematopoiesis, characteristics of T-cell clonal expansion in MDS patients, change of T-cell repertoire and recent thymus output function in MDS patients, efficiency of immunosuppressive treatment associated with T-cell clonal expansion in MDS patients and significance of T-cell clonal analysis in clinical application.

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  • (PMID = 20561453.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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81. Tabata R, Tabata C, Okamoto T, Omori K, Terada M, Nagai T: Autoimmune pancreatitis associated with myelodysplastic syndrome. Int Arch Allergy Immunol; 2010;151(2):168-72
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  • [Title] Autoimmune pancreatitis associated with myelodysplastic syndrome.
  • A 65-year-old man with myelodysplastic syndrome (MDS) was admitted for progressive jaundice.
  • Diffuse pancreatic swelling and stricture of the main pancreatic duct were observed with elevated serum levels of direct bilirubin, aspartate transaminase, alanine transaminase, alkaline phosphatase, gammaGTP and amylase, and impaired glucose tolerance.
  • He was diagnosed with autoimmune pancreatitis associated with MDS, and biliary drainage followed by immunosuppressive therapy ameliorated the jaundice and laboratory findings.
  • In addition to diffuse pancreatic FDG accumulation, fine incorporations of FDG to the lachrymal and submandibular glands were demonstrated, suggesting the recently proposed IgG4+ multiorgan lymphoproliferative syndrome (MOLPS).
  • The etiology of IgG4+ MOLPS is still unknown; however, autoantibodies to blood cells in this case suggested that the autoimmune mechanism, which is caused by abnormal immune functions in MDS patients, might be involved in the pathogenesis of IgG4+ MOLPS.
  • [MeSH-major] Autoimmune Diseases / etiology. Myelodysplastic Syndromes / complications. Pancreatitis / etiology


82. Shah SR, Tran TM: Lenalidomide in myelodysplastic syndrome and multiple myeloma. Drugs; 2007;67(13):1869-81
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  • [Title] Lenalidomide in myelodysplastic syndrome and multiple myeloma.
  • Lenalidomide is approved by the US FDA for the treatment of patients with low-risk myelodysplastic syndrome (MDS) with deletion 5q cytogenetic abnormality.
  • Two studies and a case report have evaluated lenalidomide in these MDS patients and showed significantly higher cytogenetic responses and durable red blood cell transfusion independence.
  • Lenalidomide should be the drug of choice for patients with low and intermediate-1 risk MDS (based on the International Prognostic Scoring System) with chromosome 5q31 deletion with or without other karyotype abnormalities.
  • Lenalidomide does not produce significant sedation, constipation or neuropathy, but does lead to significant myelosuppression, unlike thalidomide.
  • Administration of lenalidomide is recommended at a starting dose of 10 mg/day orally for deletion 5q in MDS patients.
  • Clinical trials of relapsed and refractory MM have shown that lenalidomide is clinically efficacious at a dosage of 25 mg/day when administered in combination with dexamethasone.
  • Lenalidomide should be continued until disease progression in both MDS and MM patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / drug therapy. Myelodysplastic Syndromes / drug therapy. Thalidomide / analogs & derivatives


83. Huang J, Jin J, Xu WL: [WT1 gene expression in myelodysplastic syndrome and its clinical implication]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2006 Mar;35(2):132-5
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  • [Title] [WT1 gene expression in myelodysplastic syndrome and its clinical implication].
  • OBJECTIVE: To investigate the expression of WT1 gene in myelodysplastic syndrome (MDS) and to explore its clinical implications.
  • METHODS: Expression of WT1 mRNA was detected in 53 patients with myelodysplastic syndrome and 10 healthy subjects by reverse transcriptase polymerase chain reaction (RT-PCR).
  • RESULT: WT1 gene was expressed in all MDS patients.
  • The positive rate and expression level in MDS patients were higher than those in healthy subjects.
  • The positive rates of WT1 expression in MDS-RAEB and MDS-RAEB-t groups were higher than those in MDS-RA and MDS-RAS groups.
  • The expression level was gradually increased from MDS-RA and MDS-RAS groups to MDS-RAEB and MDS-RAEB-t groups.
  • CONCLUSION: The expression of WT1 gene might be associated with the development of MDS, and it can be used for risk assessment and monitor of disease progression and therapeutic effects in MDS patients.
  • [MeSH-major] Myelodysplastic Syndromes / genetics. WT1 Proteins / biosynthesis

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  • (PMID = 16610077.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / WT1 Proteins
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84. Look AT: Molecular Pathogenesis of MDS. Hematology Am Soc Hematol Educ Program; 2005;:156-60
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  • [Title] Molecular Pathogenesis of MDS.
  • Clonal disorders of hematopoiesis, such as myelodysplastic syndromes (MDS) and myeloproliferative diseases (MPD), affect both hematopoietic stem cells and progenitor cells within the erythroid, platelet and granulocytic lineages and can have devastating consequences in children and adults.
  • The genetic features of these diseases often include clonal, nonrandom chromosomal deletions (e.g., 7q-, 5q-, 20q-, 6q-, 11q- and 13q-) that appear to inactivate tumor suppressor genes required for the normal development of myeloid cells (reviewed in Bench and Fenaux).
  • These putative tumor suppressors have proved to be much more difficult to identify than oncogenes activated by chromosomal translocations, the other major class of chromosomal lesions in MDS and MPD.
  • Although MDS and MPD are almost certainly caused by mutations in stem/progenitor cells, the role of inactivated tumor suppressor genes in this process remains poorly understood.
  • In a small portion of myeloid diseases, mutations have been identified in genes encoding factors known to be required for normal hematopoiesis, such as PU.1, RUNX1, CTNNA1 (alpha-catenin) and c/EBPalpha, and implicating these genes as tumor suppressors.
  • In general MDS have proved surprisingly resistant to conventional treatments.
  • Targeted therapeutic advances in MDS will likely depend on a full comprehension of underlying molecular mechanisms, in particular the tumor suppressor genes lost through clonal, nonrandom chromosomal deletions, such as the 7q- and (del)5q.

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  • (PMID = 16304374.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
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85. Graubert T: AML1 and Evi1: coconspirators in MDS/AML? Blood; 2008 Apr 15;111(8):3916-7
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  • [Title] AML1 and Evi1: coconspirators in MDS/AML?
  • In this issue of Blood, Watanabe-Okochi and colleagues use a mouse bone marrow transplantation model to demonstrate that mutant alleles of AML1 (RUNX1) can initiate a myelodysplastic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpression of Evi1.

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  • [CommentOn] Blood. 2008 Apr 15;111(8):4297-308 [18192504.001]
  • (PMID = 18434965.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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86. Sternberg A, Killick S, Littlewood T, Hatton C, Peniket A, Seidl T, Soneji S, Leach J, Bowen D, Chapman C, Standen G, Massey E, Robinson L, Vadher B, Kaczmarski R, Janmohammed R, Clipsham K, Carr A, Vyas P: Evidence for reduced B-cell progenitors in early (low-risk) myelodysplastic syndrome. Blood; 2005 Nov 1;106(9):2982-91
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  • [Title] Evidence for reduced B-cell progenitors in early (low-risk) myelodysplastic syndrome.
  • Early, low-risk International Prognostic Scoring System (IPSS) myelodysplastic syndrome (MDS) is a heterogeneous disorder where the molecular and cellular hematopoietic defects are poorly understood.
  • To gain insight into this condition, we analyzed gene expression profiles of marrow CD34+ progenitor cells from normal-karyotype, low-blast-count MDS patients, age-matched controls, and patients with non-MDS anemia.
  • Given the heterogeneity of early MDS, a surprisingly consistent finding was decreased expression of B-cell lineage-affiliated genes in MDS patients compared with healthy controls and 3 of 5 samples with non-MDS anemia.
  • Both patients with non-MDS anemia with reduced B-cell gene expression were on chemotherapy.
  • In 25 of 27 of the original samples and 9 further MDS samples, Taqman real-time polymerase chain reaction (PCR) confirmed these data.
  • Flow cytometry on unfractionated marrow from independent samples also demonstrated reduced B-cell progenitors in MDS patients compared with healthy controls.
  • These novel findings suggest a common perturbation in early MDS hematopoiesis.
  • They also provide the rationale for a larger study to evaluate the diagnostic utility of reduced B-cell progenitor number as a diagnostic biomarker of early low-risk MDS, which can pose a diagnostic challenge.
  • [MeSH-major] B-Lymphocytes / pathology. Myelodysplastic Syndromes / pathology

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  • (PMID = 16076868.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Complementary; 0 / RNA, Messenger
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87. Hamblin TJ: The management of anemia in the myelodysplastic syndrome. Leuk Res; 2005 Oct;29(10):1101-2
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  • [Title] The management of anemia in the myelodysplastic syndrome.
  • How to treat anemia in the myelodysplastic syndrome (MDS) is controversial.
  • Many health care systems refuse to fund erythropoietin on grounds of health economics.
  • A new paper on the effect of anemia in MDS on cardiac remodeling has suggested that a higher treatment threshold level for hemoglobin should be introduced.
  • [MeSH-major] Anemia / therapy. Erythropoietin / therapeutic use. Myelodysplastic Syndromes / complications


88. Schiffer CA: Myelodysplasia: the good, the fair and the ugly. Best Pract Res Clin Haematol; 2007 Mar;20(1):49-55
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  • [Title] Myelodysplasia: the good, the fair and the ugly.
  • The myelodysplastic syndromes (MDS) are a heterogeneous group of hematopoietic disorders.
  • The molecular pathogenesis of the disease is poorly understood and a large number of fundamental biologic questions remain.
  • Only a small number of randomized clinical trials have been conducted, although three new drugs (azacitidine, lenalidomide, and decitabine) have been approved for use in the last few years.
  • The response rates for most drugs used or studied for MDS range from <10%-20%.
  • The DNA hypomethylating agents, azacitidine and decitabine, can be of significant benefit for a fraction of patients and further investigation is needed to determine whether higher response rates occur in particular subgroups of MDS patients.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Agents / therapeutic use. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / therapeutic use. Bone Marrow Transplantation. Clinical Trials as Topic. Hematopoietic Stem Cell Transplantation. Humans. Immunosuppression / methods. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use

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  • (PMID = 17336254.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide; 776B62CQ27 / decitabine; F0P408N6V4 / lenalidomide; M801H13NRU / Azacitidine
  • [Number-of-references] 16
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89. Zainina S, Cheong SK: Myelodysplastic syndrome transformed into Acute Lymphoblastic Leukaemia (FAB:L3). Clin Lab Haematol; 2006 Aug;28(4):282-3
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  • [Title] Myelodysplastic syndrome transformed into Acute Lymphoblastic Leukaemia (FAB:L3).
  • Myelodysplastic syndrome (MDS) is recognized as a preleukaemic disorder with a variable risk of transformation to acute myeloid leukaemia.
  • Usually the blast cells in leukaemia are transformed after MDS displays a myeloid phenotype.
  • Even though lymphoid progression had been reported previously, most displayed myeloid-lymphoid hybrid or early B phenotype.
  • We report a case of an elderly man who had MDS transformed into Acute Lymphoblastic Leukaemia (ALL:L3) which is a rare lymphoid transformation.

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  • (PMID = 16898972.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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90. Cataldo VD, Cortes J, Quintás-Cardama A: Azacitidine for the treatment of myelodysplastic syndrome. Expert Rev Anticancer Ther; 2009 Jul;9(7):875-84
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome.
  • The myelodysplastic syndromes (MDS) encompass a heterogeneous group of malignant hematologic disorders characterized by ineffective hematopoiesis, peripheral cytopenias, frequent karyotypic abnormalities and significant risk for transformation to acute myeloid leukemia (AML).
  • The prognosis of patients with intermediate- or high-risk MDS is very poor.
  • Neither autologous stem cell transplantation (SCT) nor chemotherapeutic regimens have been shown to prolong survival in patients with MDS.
  • Allogeneic SCT, while potentially curative, is only available to a selected group of patients and is associated with high morbidity and mortality in elderly patients, which constitute the majority of patients with MDS.
  • Hypermethylation of tumor-suppressor genes has been invoked as an important pathogenetic mechanism in MDS.
  • The pyrimidine nucleoside analog azacitidine, which inhibits DNA methyltransferases, has recently become the first therapeutic to prolong survival in patients with MDS, thus changing the natural history of these malignancies.
  • The activity of azacitidine in MDS has spurred the development of combinations of this agent with other epigenetic modifiers for the treatment of MDS and AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 19589026.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
  • [Number-of-references] 55
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91. Epling-Burnette PK, Bai F, Painter JS, Rollison DE, Salih HR, Krusch M, Zou J, Ku E, Zhong B, Boulware D, Moscinski L, Wei S, Djeu JY, List AF: Reduced natural killer (NK) function associated with high-risk myelodysplastic syndrome (MDS) and reduced expression of activating NK receptors. Blood; 2007 Jun 1;109(11):4816-24
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  • [Title] Reduced natural killer (NK) function associated with high-risk myelodysplastic syndrome (MDS) and reduced expression of activating NK receptors.
  • Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis with potential for progression to acute myeloid leukemia (AML).
  • We compared natural killer (NK) cytolytic function in 48 MDS patients with 37 healthy donors and found reduced activity in the patient population (K562 cytolysis, 19% +/- 21% SD versus 40% +/- 17%) (P < .001).
  • NK cytotoxicity in MDS patients was reduced against 3 disparate tumor targets with differential activating receptor requirement, suggesting global defects in NK function.
  • Reduced NK function in MDS was significantly associated with higher International Prognostic Score (P = .01), abnormal karyotype (P = .05), the presence of excess blasts (P = .01), and age-adjusted bone marrow hypercellularity (P = .04).
  • MDS patients had a display of the activating receptor NKp30, and NKG2D down-regulation closely correlated with impaired NK function (P = .001).
  • NKG2D ligands (MICA and MICB) were expressed on CD34(+) cells from bone marrow of 30% of MDS patients and a leukemic cell line derived from an MDS patient (MDS1).
  • Collectively, these findings suggest that impairment of NK cytolytic function derives in part from reduced activating NK receptors such as NKG2D in association with disease progression.
  • Evasion of NK immunosurveillance may have importance for MDS disease progression.

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  • (PMID = 17341666.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 112112-01; United States / NCI NIH HHS / CA / R01 CA112112; United States / NIAID NIH HHS / AI / AI 056213; United States / NCI NIH HHS / CA / CA 098080; United States / NCI NIH HHS / CA / R01 CA098080; United States / NIAID NIH HHS / AI / R01 AI056213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34
  • [Other-IDs] NLM/ PMC1885518
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92. Mano H: DNA micro-array analysis of myelodysplastic syndrome. Leuk Lymphoma; 2006 Jan;47(1):9-14
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  • [Title] DNA micro-array analysis of myelodysplastic syndrome.
  • Myelodysplastic syndrome (MDS) is an enigmatic disorder characterized by ineffective hematopoiesis and dysplastic morphology of blood cells.
  • The clinical course of MDS consists of distinct stages, with early stages often progressing to advanced ones or to acute myeloid leukemia (AML).
  • Little is known of the molecular pathogenesis of MDS or of the mechanism of its stage progression.
  • DNA micro-array analysis, which allows simultaneous monitoring of the expression levels of tens of thousands of genes, has the potential to provide insight into the pathophysiology of MDS.
  • Several studies have applied this new technology to compare gene expression profiles either between MDS and the healthy condition, among the different stages of MDS or between MDS-derived AML and de novo AML.
  • These studies have revealed that each stage of MDS has its own 'molecular signature', indicating the feasibility of differential diagnosis of MDS based on gene expression profile.
  • They have also demonstrated that the current clinical diagnosis of MDS results in the misclassification of patients with regard to these molecular signatures.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Acute Disease. Humans. Sensitivity and Specificity


93. Kasner MT, Luger SM: Update on the therapy for myelodysplastic syndrome. Am J Hematol; 2009 Mar;84(3):177-86
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  • [Title] Update on the therapy for myelodysplastic syndrome.
  • The myelodysplastic syndromes (MDS) are a diverse group of clonal hematopoietic stem cell disorders characterized by cytopenias.
  • Patients have a risk of developing acute leukemia though most succumb to complications of low blood counts.
  • In this article, we discuss the classification and prognostic systems that are used in MDS, the agents available for treatment of MDS as well as review supportive and palliative care options for patients who are not candidates for, or opt against, newer treatment strategies.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Drug Design. Myelodysplastic Syndromes / drug therapy
  • [MeSH-minor] Aged. Clinical Trials as Topic. Hematopoietic Stem Cell Transplantation. Humans. Middle Aged. Risk Factors


94. Sokol L, Caceres G, Rocha K, Stockero KJ, Dewald DW, List AF: JAK2(V617F) mutation in myelodysplastic syndrome (MDS) with del(5q) arises in genetically discordant clones. Leuk Res; 2010 Jun;34(6):821-3
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  • [Title] JAK2(V617F) mutation in myelodysplastic syndrome (MDS) with del(5q) arises in genetically discordant clones.
  • The 2008 World Health Organization (WHO) proposed revision of the classification of MDS recognizes a deletion (5q) subtype with mutation of Janus kinase-2 (JAK2(V617F)).
  • We investigated the clonal origin of this gene mutation in a patient with del(5q) MDS presenting with thrombocytosis and normal hemoglobin.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 5. Clone Cells / pathology. Janus Kinase 2 / genetics. Myelodysplastic Syndromes / genetics


95. Köksal D, Mutluay N, Boyac E, Basay N, Bayiz H, Berktas MB, Aydn M, Kaya S, Berkoglu M: Waxing and waning pulmonary nodules and myelodysplastic syndrome. South Med J; 2009 Jul;102(7):741-3
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  • [Title] Waxing and waning pulmonary nodules and myelodysplastic syndrome.
  • A 53-year-old diabetic woman with the diagnosis of myelodysplastic syndrome was admitted to our hospital with symptoms of anorexia, malaise, fatigue, night sweats, and weight loss.
  • A diagnosis of pulmonary tuberculosis was reached by pathologic examination of a wedge biopsy.
  • We did not find a similar case in the literature.
  • [MeSH-major] Myelodysplastic Syndromes / complications. Tuberculosis, Pulmonary / complications. Tuberculosis, Pulmonary / diagnosis

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  • (PMID = 19488012.001).
  • [ISSN] 1541-8243
  • [Journal-full-title] Southern medical journal
  • [ISO-abbreviation] South. Med. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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96. Vundinti BR, Kerketta L, Jijina F, Ghosh K: Cytogenetic study of myelodysplastic syndrome from India. Indian J Med Res; 2009 Aug;130(2):155-9
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  • [Title] Cytogenetic study of myelodysplastic syndrome from India.
  • BACKGROUND & OBJECTIVE: Myelodysplastic syndrome (MDS) represents a group of clonal haematological disorders characterized by progressive cytopenia reflecting defects in erythroid, myeloid and megakaryocytic maturation.
  • The incidence of MDS is more in older age groups and frequent chromosome abnormalities reported to be monosomies 5 and 7.
  • However, the data on cytogenetic changes in Indian MDS patients are scanty.
  • The present study was therefore undertaken to study the aetiology and frequency of chromosomal changes in MDS patients, attending a tertiary care hospital in Maharashtra, India.
  • METHODS: The study was carried out in 145 MDS patients for six years (2001-2006) at National Institute of Immunohaematology (ICMR), and KEM Hospital, Mumbai, India.
  • RESULTS: Chromosomal abnormalities, including novel chromosome aberrations were detected in 54.48 per cent MDS patients and frequency of chromosomal aberrations increased with increase in age (> or = 30 yr).
  • INTERPRETATION & CONCLUSION: Our findings showed 54.48 per cent chromosome abnormalities including novel chromosome aberrations in MDS patients and these chromosome aberrations were increased with advancing age.
  • In our series a high frequency of younger population (53%) developed MDS, a detailed molecular genetics and aetiological factors need to be studied.
  • [MeSH-major] Chromosome Aberrations. Cytogenetics. Myelodysplastic Syndromes / genetics


97. Marcondes AM, Bair S, Rabinovitch PS, Gooley T, Deeg HJ, Risques R: No telomere shortening in marrow stroma from patients with MDS. Ann Hematol; 2009 Jul;88(7):623-8
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  • [Title] No telomere shortening in marrow stroma from patients with MDS.
  • Given the role of the microenvironment in the pathophysiology of the myelodysplastic syndrome (MDS), primarily a disease of older age, we determined telomere length in primary cultured marrow stroma cells using quantitative fluorescent in situ hybridization (qFISH) and quantitative polymerase chain reaction (qPCR).
  • qFISH showed comparable rates of decrease in telomere length with age in MDS patients and age-matched healthy controls.
  • These findings suggest a lack of significant differences between MDS patients and healthy controls in terms of telomere stability in marrow stroma in contrast to that observed in hematopoietic cells.
  • In conclusion, this demonstrates that, although MDS stroma cells and hematopoietic cells share the same microenvironment, the stromal cells do not share the processes that contribute to accelerated telomere attrition, suggesting that stromal cell proliferative potential is not limiting in MDS.

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  • (PMID = 19050887.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL36444; United States / NHLBI NIH HHS / HL / R01 HL082941; United States / NIA NIH HHS / AG / AG13280; United States / NHLBI NIH HHS / HL / HL082941; United States / NIA NIH HHS / AG / AG013280-14; United States / NHLBI NIH HHS / HL / R01 HL082941-04; United States / NHLBI NIH HHS / HL / HL036444-28; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NHLBI NIH HHS / HL / P01 HL036444-28; United States / NIA NIH HHS / AG / P30 AG013280-14; United States / NIA NIH HHS / AG / P30 AG013280; United States / NHLBI NIH HHS / HL / HL082941-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Other-IDs] NLM/ NIHMS79334; NLM/ PMC2693355
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98. Deeg HJ: Optimization of transplant regimens for patients with myelodysplastic syndrome (MDS). Hematology Am Soc Hematol Educ Program; 2005;:167-73
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  • [Title] Optimization of transplant regimens for patients with myelodysplastic syndrome (MDS).
  • Myelodysplastic syndrome (MDS) is a hemopoietic stem cell disorder that is potentially curable by transplantation of normal hemopoietic stem cells.
  • Among selected patients with less advanced/low-risk MDS (< 5% marrow myeloblasts), 3-year survivals of 65% to 75% are achievable with HLA-matched related and unrelated donors.
  • Among patients with more advanced/ high-risk disease (> or = 5% marrow blasts; high International Prognostic Scoring System [IPSS] scores), the probability of post-transplant relapse ranges from 10% to 40%, and, as a result, relapse-free survival is inferior.
  • In addition to disease stage, co-morbid conditions, pre-transplant chemotherapy, conditioning regimen, source of stem cells, and post-transplant immunosuppression affect transplant outcome.
  • Graft-versus-host disease, both acute and chronic, and post-transplant relapse remain challenging problems.

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  • (PMID = 16304376.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA87948; United States / NHLBI NIH HHS / HL / HL36444
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antilymphocyte Serum; 0 / HLA Antigens; 0 / thymoglobulin
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99. Hwang Y, Huh JW, Mun YC, Seong CM, Chung WS: [Myelodysplastic syndrome mimicking idiopathic thrombocytopenic purpura]. Korean J Lab Med; 2010 Apr;30(2):105-10
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  • [Title] [Myelodysplastic syndrome mimicking idiopathic thrombocytopenic purpura].
  • BACKGROUND: In patients with isolated thrombocytopenia, but without significant dysplasia, diagnosis of idiopathic thrombocytopenic purpura (ITP) rather than myelodysplastic syndrome (MDS) may be taken into account.
  • It is important to make an accurate diagnosis because different treatments are used for ITP and MDS.
  • The purpose of this study was to investigate the clinical and hematologic features of patients who were initially diagnosed as ITP but had cytogenetic abnormalities.
  • METHODS: We retrospectively reviewed cytogenetic studies of 100 patients who were diagnosed as ITP from 2004 to 2009 at Mokdong Hospital of Ewha Womans University based on clinical features and hematologic studies.
  • The numbers of megakaryocytes in bone marrow were increased and dysplasia was not found in megakaryocyte, erythroid, and myeloid cell lineages.
  • Presumptive diagnosis of MDS or diagnosis of idiopathic cytopenia of undetermined significance (ICUS) was made according to 2008 WHO classification.
  • During the follow up, disease progression was not found.
  • If specific clonal chromosomal abnormality is found, presumptive diagnosis of MDS has to be considered and close follow up is needed.
  • [MeSH-major] Myelodysplastic Syndromes / diagnosis. Purpura, Thrombocytopenic, Idiopathic / diagnosis
  • [MeSH-minor] Adult. Bone Marrow Cells / cytology. Cell Lineage. Chromosome Aberrations. Diagnosis, Differential. Female. Humans. Male. Megakaryocytes / immunology. Megakaryocytes / pathology. Middle Aged. Retrospective Studies


100. 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






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