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


2. Gupta G, Singh R, Kotasthane DS, Kotasthane VD: Myelodysplastic syndromes/neoplasms: recent classification system based on World Health Organization Classification of Tumors - International Agency for Research on Cancer for Hematopoietic and Lymphoid Tissues. J Blood Med; 2010;1:171-82
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  • [Title] Myelodysplastic syndromes/neoplasms: recent classification system based on World Health Organization Classification of Tumors - International Agency for Research on Cancer for Hematopoietic and Lymphoid Tissues.
  • The myelodysplastic Syndromes (MDS) are a group of clonal hematopoietic stem cell diseases characterized by cytopenia(s), dysplasia in one or more of the major myeloid cell lines, ineffective hematopoiesis, and increased risk of development of acute myeloid leukemia.
  • The myelodysplastic syndromes are now classified into the following categories - refractory cytopenia with unilineage dysplasia, refractory anemia with ring sideroblasts, refractory cytopenia with multilineage dysplasia, refractory anemia with excess blasts, myelodysplastic syndrome associated with isolated del (5q), myelodysplastic syndrome - unclassifiable, and childhood myelodysplastic syndrome.

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  • (PMID = 22282696.001).
  • [ISSN] 1179-2736
  • [Journal-full-title] Journal of blood medicine
  • [ISO-abbreviation] J Blood Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3262332
  • [Keywords] NOTNLM ; leukemia / myelodysplastic syndromes
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3. Winer ES, Miller KB, Chan GW: GM-CSF and low-dose cytosine arabinoside in high-risk, elderly patients with AML or MDS. Oncology (Williston Park); 2005 Apr;19(4 Suppl 2):11-4
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  • [Title] GM-CSF and low-dose cytosine arabinoside in high-risk, elderly patients with AML or MDS.
  • In this study, we utilized these synergistic effects of granulocyte-macrophage colony-stimulating factor (GM-CSF, sargramostim [Leukine]), hydroxyurea, and low-dose cytosine arabinoside to treat elderly patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS).
  • In a single-institution, retrospective study, we evaluated 94 treatments with concomitant hydroxyurea, cytosine arabinoside, and GM-CSF between the years of 1997 and 2003 in high-risk elderly patients with AML or MDS.
  • Overall, our study showed that low-dose cytosine arabinoside given by continuous infusion together with continuous infusion GM-CSF and hydroxyurea was well-tolerated and effective in treating elderly AML and MDS patients who were not eligible for standard induction therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 15934494.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; 04079A1RDZ / Cytarabine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; X6Q56QN5QC / Hydroxyurea
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4. Broberg K, Höglund M, Gustafsson C, Björk J, Ingvar C, Albin M, Olsson H: Genetic variant of the human homologous recombination-associated gene RMI1 (S455N) impacts the risk of AML/MDS and malignant melanoma. Cancer Lett; 2007 Dec 8;258(1):38-44
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  • [Title] Genetic variant of the human homologous recombination-associated gene RMI1 (S455N) impacts the risk of AML/MDS and malignant melanoma.
  • Mutations altering BLM function are associated with highly elevated cancer susceptibility (Bloom's syndrome).
  • We have analyzed the common polymorphism Ser455Asn in RMI1 and its association with cancer risk in acute myeloid leukemia (AML, N=93), myelodysplatic syndromes (MDS, N=74), and malignant melanoma (MM, N=166).
  • The results showed a consistent pattern, where carriers of the Asn variant had a significantly increased risk of AML/MDS.
  • The risk of AML/MDS for SerAsn+AsnAsn subjects was odds ratio (OR)=1.7, 95% confidence interval (CI) 1.1-2.5 or MM was OR=1.5, 95% CI 1.0-2.2.
  • [MeSH-major] Carrier Proteins / genetics. Genetic Variation. Leukemia, Myeloid, Acute / genetics. Melanoma / genetics. Myelodysplastic Syndromes / genetics. Nuclear Proteins / genetics. Recombination, Genetic. Skin Neoplasms / genetics
  • [MeSH-minor] Adenosine Triphosphatases / genetics. Adult. Aged. Aged, 80 and over. Bloom Syndrome / genetics. Case-Control Studies. DNA Helicases / genetics. Female. Genotype. Humans. Male. Middle Aged. Polymerase Chain Reaction. Polymorphism, Genetic. RecQ Helicases

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  • (PMID = 17900800.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / RMI1 protein, human; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / Bloom syndrome protein; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / RecQ Helicases
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5. Watanabe-Okochi N, Kitaura J, Ono R, Harada H, Harada Y, Komeno Y, Nakajima H, Nosaka T, Inaba T, Kitamura T: AML1 mutations induced MDS and MDS/AML in a mouse BMT model. Blood; 2008 Apr 15;111(8):4297-308
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  • [Title] AML1 mutations induced MDS and MDS/AML in a mouse BMT model.
  • Myelodysplastic syndrome (MDS) is a hematopoietic stem-cell disorder characterized by trilineage dysplasia and susceptibility to acute myelogenous leukemia (AML).
  • Analysis of molecular basis of MDS has been hampered by the heterogeneity of the disease.
  • Recently, mutations of the transcription factor AML1/RUNX1 have been identified in 15% to 40% of MDS-refractory anemia with excess of blasts (RAEB) and MDS/AML.
  • Most mice developed MDS and MDS/AML-like symptoms within 4 to 13 months after BMT.
  • Interestingly, among integration sites identified, Evi1 seemed to collaborate with an AML1 mutant harboring a point mutation in the Runt homology domain (D171N) to induce MDS/AML with an identical phenotype characterized by marked hepatosplenomegaly, myeloid dysplasia, leukocytosis, and biphenotypic surface markers.
  • Collaboration between AML1-D171N and Evi1 was confirmed by a BMT model where coexpression of AML1-D171N and Evi1 induced acute leukemia of the same phenotype with much shorter latencies.
  • On the other hand, a C-terminal truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid dysplasia in transplanted mice, followed by progression to MDS-RAEB or MDS/AML.
  • Thus, we have developed a useful mouse model of MDS/AML that should help in the understanding of the molecular basis of MDS and the progression of MDS to overt leukemia.
  • [MeSH-major] Bone Marrow Transplantation. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics


6. Zatkova A, Merk S, Wendehack M, Bilban M, Muzik EM, Muradyan A, Haferlach C, Haferlach T, Wimmer K, Fonatsch C, Ullmann R: AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes. Genes Chromosomes Cancer; 2009 Jun;48(6):510-20
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  • [Title] AML/MDS with 11q/MLL amplification show characteristic gene expression signature and interplay of DNA copy number changes.
  • AML/MDS patients carrying 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are characterized by a complex aberrant karyotype (CAK) frequently including deletions within 5q, 17p, and 7q, older age and fast progression of the disease with extremely poor prognosis.
  • In this study, we investigated 19 patients with AML/MDS and MLL gain/amplification.
  • Furthermore, we demonstrate that the gene expression signature can be used to discriminate AML/MDS with MLL amplification from several other types of AML.
  • [MeSH-major] Gene Dosage. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 19306356.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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7. Armand P, Kim HT, Mayer E, Cutler CS, Ho VT, Koreth J, Alyea EP, Antin JH, Soiffer RJ: Outcome of allo-SCT for women with MDS or AML occurring after breast cancer therapy. Bone Marrow Transplant; 2010 Nov;45(11):1611-7
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  • [Title] Outcome of allo-SCT for women with MDS or AML occurring after breast cancer therapy.
  • Women with breast cancer who receive adjuvant therapy are at risk for developing therapy-related myelodysplastic syndrome (MDS) or AML (tMDS/AML).
  • Patients with tMDS/AML are often referred for consideration of allogeneic hematopoietic SCT (HSCT).
  • We report a retrospective study of all women who were treated with HSCT for MDS or AML at our institution between 1991 and 2008.
  • The cumulative incidences of tMDS/AML relapse and non-relapse mortality (NRM) were 38 and 17%, respectively.
  • A significant proportion of women with tAML/MDS after breast cancer treatment experience DFS after HSCT, similar to that of patients with de novo MDS or AML.

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  • (PMID = 20154738.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P01 AI 29350; United States / NIAID NIH HHS / AI / U19 AI029530-14; United States / NIAID NIH HHS / AI / AI029530-14; United States / NIAID NIH HHS / AI / U19 AI029530; United States / NCI NIH HHS / CA / P01 CA142106-06A1; United States / NCI NIH HHS / CA / P01 CA142106
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS180221; NLM/ PMC2889243
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8. Edlin R, Connock M, Tubeuf S, Round J, Fry-Smith A, Hyde C, Greenheld W: Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia. Health Technol Assess; 2010 May;14 Suppl 1:69-74
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  • [Title] Azacitidine for the treatment of myelodysplastic syndrome, chronic myelomonocytic leukaemia and acute myeloid leukaemia.
  • This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of azacitidine (aza) compared with conventional care regimes (CCR) for higher risk patients with myelodysplastic syndrome (MDS), chronic myelomonocytic leukaemia (CMML) and acute myeloid leukaemia (AML), based on the evidence submission from the manufacturer to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process.
  • The patient outcomes governing relative effectiveness and cost-effectiveness were defined as overall survival, time to progression (TTP) to AML, adverse events and health-related quality of life (HRQoL).
  • It compared aza with CCR in 358 patients with higher risk MDS, CMML and AML 20-30% blasts.
  • The outcomes reported in AZA-001 included overall survival, TTP to AML and adverse events.
  • The results showed that: the median overall survival was 24.5 months on aza, compared with 15.0 months in the CCR group (p = 0.0001); the response rates were low (complete remission 17% aza versus 8% CCR); the median time to transformation to AML was greater in the aza group (17.8 versus 11.5 months; p < 0.0001); and of patients who were red blood cell (RBC) transfusion-dependent at baseline, 45% of those on aza became RBC transfusion-independent during the treatment period, compared with 11.8% in the CCR group (p < 0.0001).
  • The AZA-001 study showed that, compared with CCR, those MDS patients receiving aza had prolonged median survival, had delayed progression to AML, had reduced dependence on transfusions and had a small improvement in response rate.
  • Given the general paucity of economic modelling work in MDS and the limitations of the submitted industry model there is an evident need for an independent cost-effectiveness analysis of aza in MDS.
  • At the time of writing, the guidance appraisal consultation document issued by NICE on 4 March 2010 states that azacitidine is not recommended as a treatment option for people not eligible for haemopoietic stem cell transplantation with the the following conditions: intermediate-2 and high-risk MDS according to the International Prognostic Scoring System, CMML with 10-29% marrow blasts without myeloproliferative disorder, or with AML with 20-30% blasts and multilineage dysplasia, according to World Health Organization classification.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Myelodysplastic Syndromes / drug therapy


9. Tabata R, Tabata C, Omori K, Nagai T: Disappearing myelodysplastic syndrome-associated hemolytic anemia in leukemic transformation. Int Arch Allergy Immunol; 2010;152(4):407-12
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  • [Title] Disappearing myelodysplastic syndrome-associated hemolytic anemia in leukemic transformation.
  • BACKGROUND: Here we report 2 rare cases of acute myeloid leukemia (AML) complicated with hemolytic anemia limited to the myelodysplastic syndrome (MDS) stage, and disappearing in leukemic transformation.
  • METHODS/RESULTS: A 66-year-old man with MDS-RAEB-2 was admitted to hospital for severe anemia with increased reticulocyte counts.
  • In another case, a 68-year-old man was admitted to hospital when laboratory findings showed a white blood cell count of 24,800/microl with increased myeloblasts (62.5%), leading to the diagnosis of AML with multilineage dysplasia.
  • Following a decrease in blasts due to anti-cancer drugs, supporting the MDS-RAEB-2 status, severe anemia with increased reticulocytes and positive direct antiglobulin test was diagnosed, suggesting the existence of autoimmune hemolytic anemia, which was then ameliorated by steroid therapy.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / diagnosis


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

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  • (PMID = 17589530.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] England
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11. Kremser A, Dressig J, Grabrucker C, Liepert A, Kroell T, Scholl N, Schmid C, Tischer J, Kufner S, Salih H, Kolb HJ, Schmetzer H: Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods. J Immunother; 2010 Feb-Mar;33(2):185-99
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  • [Title] Dendritic cells (DCs) can be successfully generated from leukemic blasts in individual patients with AML or MDS: an evaluation of different methods.
  • Myeloid-leukemic cells (AML, MDS, CML) can be differentiated to leukemia-derived dendritic cell [DC (DCleu)] potentially presenting the whole leukemic antigen repertoire without knowledge of distinct leukemia antigens and are regarded as promising candidates for a vaccination strategy.
  • We studied the capability of 6 serum-free DC culture methods, chosen according to different mechanisms, to induce DC differentiation in 137 cases of AML and 52 cases of MDS.
  • Comparing these methods on average 15% to 32% DC, depending on methods used, could be obtained from blast-containing mononuclear cells (MNC) in AML/MDS cases with a DC viability of more than 60%.
  • Average results of all culture methods tested were comparable, however not every given case of AML could be differentiated to DC with 1 selected method.
  • [MeSH-major] Cancer Vaccines. Cell Culture Techniques / methods. Dendritic Cells / pathology. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology

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  • (PMID = 20139775.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Culture Media, Serum-Free; 0 / Cytokines; 24939-03-5 / Poly I-C; 39325-01-4 / Picibanil
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12. Kokhno AV, Parovichnikova EN, Mikhaĭlova EA, Ustinova EN, Kaplanskaia IB, Dvirnyk VN, Ol'shanskaia IuV, Domracheva EV, Savchenko VG: [Efficiency of cyclosporin A therapy in patients with myelodysplastic syndrome]. Ter Arkh; 2010;82(8):48-53
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  • [Title] [Efficiency of cyclosporin A therapy in patients with myelodysplastic syndrome].
  • AIM: To evaluate the efficacy of cyclosporin A (CsA) in patients with myelodysplastic syndromes (MDS) and to identify determinants of a response to this therapy.
  • SUBJECTS AND METHODS: The efficacy of CsA was evaluated in 52 patients (30 men and 22 women aged 16 to 74 years) with MDS.
  • Its efficacy was evaluated following 3, 6, and 12 months.
  • Baseline refractory anemia (RA) transformed to RA with excess blasts (RAEB) in 31% of cases; baseline RAEB did to acute myeloid leukemia in 34%.
  • CONCLUSION: CsA is the drug of choice in treating patients with MDS, including RA, RA with ringed sideroblasts, refractory cytopenia with multilineage dysplasia, with hypoplasia of hematopoiesis, with nodular polyclonal lymphoid infiltration in the BM, a normal karyotype or changes corresponding to a low or moderate IPSS risk.
  • [MeSH-major] Cyclosporine / therapeutic use. Immunosuppressive Agents / therapeutic use. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 20873246.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine
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13. Paulsson K, Heidenblad M, Strömbeck B, Staaf J, Jönsson G, Borg A, Fioretos T, Johansson B: High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration. Leukemia; 2006 May;20(5):840-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberration.
  • Although trisomy 8 as the sole chromosome aberration is the most common numerical abnormality in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), little is known about its pathogenetic effects.
  • Considering that +8 is a frequent secondary change in AML/MDS, cryptic--possibly primary--genetic aberrations may occur in cases with trisomy 8 as the apparently single anomaly.
  • We performed a high-resolution genome-wide array-based comparative genome hybridization (array CGH) analysis of 10 AML/MDS cases with isolated +8, utilizing a 32K bacterial artificial chromosome array set, providing >98% coverage of the genome with a resolution of 100 kb.
  • A 1.8 Mb deletion at 7p14.1, which had occurred prior to the +8, was identified in MDS transforming to AML.
  • The present results show that cryptic genetic abnormalities are frequent in trisomy 8-positive AML/MDS cases and that +8 as the sole cytogenetic aberration is not always the primary genetic event.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Genome. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Nucleic Acid Hybridization / methods. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged


14. Inaba T: [Radiation-induced and therapy-related AML/MDS]. Nihon Rinsho; 2009 Oct;67(10):1880-3
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  • [Title] [Radiation-induced and therapy-related AML/MDS].
  • Radiation induced acute myeloid leukemia (AML) was recognized a century ago, soon after mankind found radiation.
  • Atomic bomb survivors developed de novo AML with relatively short latency with very high frequency.
  • By contrast, excess occurrence of myelodysplastic syndrome (MDS) as well as solid tumors was found decades late.
  • This difference may be due to etiology that many de novo AML patients harbor chimeric leukemogenic genes caused by chromosomal translocations, while MDS patients rarely carry chimeras.
  • Therapy related leukemia is mainly caused by topoisomerase II inhibitors that cause de novo AML with an 11q23 translocation or by alkyrating agents that induce MDS/AML with an AML1 point mutation and monosomy 7.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Leukemia, Radiation-Induced / etiology. Myelodysplastic Syndromes / etiology

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  • (PMID = 19860183.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 7
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15. Dutreix C, Huntsman Labed A, Roesel J, Lanza C, Wang Y: Midostaurin: Review of pharmacokinetics (PK) and PK/pharmacodynamic (PD) relationship in AML/MDS patients. J Clin Oncol; 2009 May 20;27(15_suppl):e14540

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

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  • (PMID = 27963644.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Jabbour E, Faderl S, Ravandi F, Konopleva M, Verstovsek S, Cortes J, Wierda W, Newsome WM, Yang H, Kantarjian H, Garcia-Manero G: Phase II study of vorinostat (V) in combination with idarubicin and high-dose cytarabine (IA) as front-line therapy in patients (pts) with high-risk myelodyplsatic syndrome (MDS) or acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7004

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

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  • (PMID = 27961376.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. 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.
  • To study this issue, we retrospectively analyzed a large cohort of patients with leukemia, who were evaluated at MD Anderson Cancer Center (MDACC), to determine the prevalence, timing, and characteristics of PEf in leukemia.
  • METHODS: We reviewed 3,327 patients with acute myeloid leukemia (AML, N = 1,809, 54%), acute lymphocytic leukemia (ALL, N = 494, 15%), or myelodysplastic syndrome (MDS, N =1,024, 31%), who were seen at MDACC from August 2003 to July 2008.
  • RESULTS: The overall prevalence of PEf was 21.7%, 21.1%, and 19.9% (p = 0.72) in patients with AML, ALL, and MDS, respectively.
  • CONCLUSIONS: PEf are relatively common in patients with leukemia at initial presentation and are usually asymptomatic.
  • Their incidence increases with therapy administration although it appears that this is not a process related to specific classes of treatment or type of leukemia.

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  • (PMID = 27961462.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Batty G, Kantarjian H, Issa JJ, Garcia-Manero G, Pierce S, O'Brien S, Jabbour E, Cortes J, Ravandi F: Feasibility of hypomethylating therapy in patients with renal insufficiency. J Clin Oncol; 2009 May 20;27(15_suppl):7089

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

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  • (PMID = 27961273.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Popat UR, Saliba R, Hosing C, Khouri I, Alousi AM, Giralt SA, de Lima MJ, Qazilbash MH, Champlin R, Anderlini P: Age at diagnosis does not adversely affect outcome in patients with Hodgkin's Disease (HD) after autologous transplantation. J Clin Oncol; 2009 May 20;27(15_suppl):e19507

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

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  • (PMID = 27960864.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Duhoux F, Libouton J, Bahloula K, Ameye G, Poirel HA: Identification by FISH of 4 novel partner loci of PRDM16 in myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):11037

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

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  • (PMID = 27964015.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Lyman GH, Dale DC, Culakova E, Poniewierski MS, Wolff D, Kuderer NM, Lambert K, Crawford J: Acute myeloid leukemia or myelodysplastic syndrome (AML/MDS) and overall mortality with chemotherapy (CT) and granulocyte colony-stimulating factor (G-CSF): A meta-analysis of randomized controlled trials (RCTs). J Clin Oncol; 2009 May 20;27(15_suppl):9524

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

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  • (PMID = 27964513.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Harada Y, Harada H: Molecular pathways mediating MDS/AML with focus on AML1/RUNX1 point mutations. J Cell Physiol; 2009 Jul;220(1):16-20
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  • [Title] Molecular pathways mediating MDS/AML with focus on AML1/RUNX1 point mutations.
  • AML1/RUNX1 point mutations have been identified in myelodysplastic syndrome (MDS) and MDS-related acute myeloid leukemia (AML), or MDS/AML, and are distributed throughout the full length of AML1/RUNX1.
  • Gene mutation is proposed to be one of the disease-defining genetic abnormalities of MDS/AML.
  • Most of the mutants lose trans-activation potential, which leads to a loss of normal function indicating that AML1/RUNX1 dysfunction is one of the major pathogenic mechanisms of MDS/AML.
  • Although biological analysis using a mouse bone marrow transplantation model transduced with Ni-type of D171N or Ct-type of S291fsX300 mutants has partially confirmed the oncogenic ability of AML1 mutants, it could not explain the mutant specific clinical features of MDS/AML.
  • Thus, AML1/RUNX1 mutants play a central role in the pathogenesis of MDS/AML.
  • Both AML1 mutants are initiating factors for MDS-genesis by inhibiting differentiation of hematopoietic stem cells, and Ni-type mutant requires acquisition of proliferation ability.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / metabolism. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Point Mutation

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  • (PMID = 19334039.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
  • [Number-of-references] 27
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28. Mackinnon RN, Campbell LJ: Dicentric chromosomes and 20q11.2 amplification in MDS/AML with apparent monosomy 20. Cytogenet Genome Res; 2007;119(3-4):211-20
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  • [Title] Dicentric chromosomes and 20q11.2 amplification in MDS/AML with apparent monosomy 20.
  • FISH analysis of 41 previously karyotyped cases of MDS and AML with apparent monosomy of chromosome 20 revealed a variety of dicentric abnormalities involving chromosome 20.
  • The retention and amplification of proximal 20q provides support for the hypothesis that there is an oncogene located in this region of 20q that is activated in cases of MDS/AML with del(20q).
  • Apparent monosomy 20 in MDS/AML should be treated as evidence of unidentified chromosome 20 abnormalities, and familiarity with the typical G-banded morphology of these derivatives can help with their identification.
  • The reported incidence of dicentric chromosomes is clearly an under-estimate but is increasing in myeloid disorders as more cases are studied with methods allowing their detection.
  • [MeSH-major] Chromosomes, Human, Pair 20 / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy / genetics. Myelodysplastic Syndromes / genetics

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  • [Copyright] Copyright (c) 2008 S. Karger AG, Basel.
  • (PMID = 18253031.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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29. Voso MT, D'Alò F, Greco M, Fabiani E, Criscuolo M, Migliara G, Pagano L, Fianchi L, Guidi F, Hohaus S, Leone G: Epigenetic changes in therapy-related MDS/AML. Chem Biol Interact; 2010 Mar 19;184(1-2):46-9
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  • [Title] Epigenetic changes in therapy-related MDS/AML.
  • Therapy-related Myelodysplastic Syndromes/Acute Myeloid Leukemias (t-MDS/AML) are one of the most compelling long term adverse events occurring in cancer survivors treated with chemo-radiotherapy regimes.
  • Gene promoter methylation is a common finding in t-MDS/AML and has been associated to a shorter latency period from the treatment of the primary tumor.
  • We found frequent methylation of DAPK in the t-MDS/AML group, especially in patients with a previous lymphoproliferative disease.
  • In patients studied for concurrent methylation of several promoters, t-MDS/AML were significantly more frequently hypermethylated in 2 or more promoter regions than de novo MDS or AML suggesting that promoter hypermethylation of genes involved in cell cycle control, apoptosis and DNA repair pathways is a frequent finding in t-MDS/AML and may contribute to secondary leukemogenesis.
  • [MeSH-major] Epigenesis, Genetic. Gene Expression Regulation, Neoplastic. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19874806.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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30. Herry A, Douet-Guilbert N, Morel F, Le Bris MJ, De Braekeleer M: Redefining monosomy 5 by molecular cytogenetics in 23 patients with MDS/AML. Eur J Haematol; 2007 Jun;78(6):457-67
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  • [Title] Redefining monosomy 5 by molecular cytogenetics in 23 patients with MDS/AML.
  • Deletion of the long arm of chromosome 5 [del(5q)] or loss of a whole chromosome 5 (-5) is a common finding, arising de novo in 10% of patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML) and in 40% of patients with therapy-related MDS or AML.
  • We investigated by molecular cytogenetics 23 MDS/AML patients for whom conventional cytogenetics detected a monosomy 5.
  • Sequential fluorescent in situ hybridization studies with whole chromosome paints and region-specific probes, used as a complement to conventional cytogenetic analysis, allow a better interpretation of karyotypes in MDS/AML patients.
  • [MeSH-major] Chromosomes, Human, Pair 5. Leukemia, Myeloid / genetics. Monosomy. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged

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  • (PMID = 17391336.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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31. Stone R, Sekeres M, Garcia-Manero G: Evolving strategies in the treatment of MDS and AML. Clin Adv Hematol Oncol; 2009 Aug;7(8):1-14; quiz 2 p following 14
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  • [Title] Evolving strategies in the treatment of MDS and AML.
  • Myelodysplastic syndrome (MDS) is a clonal hematopoietic disorder characterized by a hyperproliferative bone marrow, cellular dysplasia, and ineffective hematopoiesis.
  • The treatment of MDS involves improving patient survival and quality of life while decreasing the likelihood of progression to acute myelogenous leukemia (AML).
  • In addition to supportive care with transfusions and hematopoietic growth factors as well as stem cell transplantation, three chemotherapeutic agents have been approved to treat MDS--lenalidomide, azacitidine, and decitabine.
  • In addition, multiple agents and novel combinations are currently in development to treat both MDS AML.
  • Several clinical studies which have investigated these therapeutic approaches, as well as the incorporation of new tools used in the diagnosis of MDS, have been published since the 2008 American Society of Hematology (ASH) Annual Meeting and Exposition, and are discussed here.
  • [MeSH-major] Education, Medical, Continuing. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


32. Lübbert M, Bertz H, Rüter B, Marks R, Claus R, Wäsch R, Finke J: Non-intensive treatment with low-dose 5-aza-2'-deoxycytidine (DAC) prior to allogeneic blood SCT of older MDS/AML patients. Bone Marrow Transplant; 2009 Nov;44(9):585-8
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  • [Title] Non-intensive treatment with low-dose 5-aza-2'-deoxycytidine (DAC) prior to allogeneic blood SCT of older MDS/AML patients.
  • Novel, non-intensive treatment options in older MDS/AML patients planned for allografting, with the goal of down-staging the underlying disease and bridging time to transplantation, are presently being developed.
  • 5-azacytidine and decitabine (DAC) are of particular interest, as they can be given repetitively, with very limited non-hematologic toxicity and result in responses both in MDS and AML even at low doses.
  • We describe 15 consecutive patients (median age 69 years, range 60-75 years) with MDS (n=10) or AML (n=5) who all received first-line treatment with DAC and subsequent allografting (from sibling donor in four patients, unrelated donor in 11) after reduced-intensity conditioning with the FBM regimen.
  • We conclude that allografting after low-dose DAC and subsequent conditioning with FBM is feasible, with no unexpected toxicities and appears as a valid alternative to standard chemotherapy ('InDACtion instead of induction') in elderly patients with MDS/AML.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Azacitidine / analogs & derivatives. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy

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  • (PMID = 19363531.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
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33. van Besien K, Kunavakkam R, Rondon G, De Lima M, Artz A, Oran B, Giralt S: Fludarabine-melphalan conditioning for AML and MDS: alemtuzumab reduces acute and chronic GVHD without affecting long-term outcomes. Biol Blood Marrow Transplant; 2009 May;15(5):610-7
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  • [Title] Fludarabine-melphalan conditioning for AML and MDS: alemtuzumab reduces acute and chronic GVHD without affecting long-term outcomes.
  • The purpose of this study was to determine the effect of alemtuzumab on treatment-related mortality (TRM), relapse, overall survival (OS), and disease-free survival (DSF) in patients with acute myelogenous leukemia (AML) and myelodysplastic syndromes (MDS) undergoing reduced intensity conditioning (RIC).
  • The incidence of acute graft-versus-host disease (aGVHD) grade II-IV (relative risk [RR] 5.5, P < .01) and chronic GVHD (cGVHD) (RR 6.6, P < .01) were significantly lower in patients receiving alemtuzumab.
  • The addition of alemtuzumab to an RIC regimen dramatically reduces the incidence of aGVHD and cGVHD in patients with AML and MDS undergoing allogeneic transplantation.

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  • (PMID = 19361753.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K24 CA116471; United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / R21 CA101337; United States / NCI NIH HHS / CA / 1-R21 CA 101337-01
  • [Publication-type] Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 106XV160TZ / Vidarabine Phosphate; 1X9VK9O1SC / fludarabine phosphate; 3A189DH42V / alemtuzumab; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS589065; NLM/ PMC4348112
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34. Zatkova A, Schoch C, Speleman F, Poppe B, Mannhalter C, Fonatsch C, Wimmer K: GAB2 is a novel target of 11q amplification in AML/MDS. Genes Chromosomes Cancer; 2006 Sep;45(9):798-807
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GAB2 is a novel target of 11q amplification in AML/MDS.
  • Chromosome arm 11q amplifications involving the mixed lineage leukemia gene (MLL) locus are rare but recurrent aberrations in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Thus, the adaptor molecule GAB2 that has already been shown to enhance oncogenic signaling in other neoplasias appears as a novel target of 11q amplification in AML/MDS.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Chromosomes, Human, Pair 11. Gene Amplification / physiology. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


35. Armand P, Kim HT, DeAngelo DJ, Ho VT, Cutler CS, Stone RM, Ritz J, Alyea EP, Antin JH, Soiffer RJ: Impact of cytogenetics on outcome of de novo and therapy-related AML and MDS after allogeneic transplantation. Biol Blood Marrow Transplant; 2007 Jun;13(6):655-64
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  • [Title] Impact of cytogenetics on outcome of de novo and therapy-related AML and MDS after allogeneic transplantation.
  • Cytogenetics has an important impact on the prognosis of patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) for acute myelogenous leukemia (AML) or myelodysplastic syndromes (MDS).
  • In this study, we retrospectively analyzed data on 556 patients with AML or MDS transplanted at our institution.
  • After accounting for cytogenetics, patients with therapy-related AML or MDS had an equivalent outcome to those with de novo disease.

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  • (PMID = 17531775.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / U19 AI029530-14; United States / NIAID NIH HHS / AI / U19 AI 29530; United States / NHLBI NIH HHS / HL / P01 HL070149; United States / NCI NIH HHS / CA / T32 CA009172; United States / NIAID NIH HHS / AI / AI029530-14; United States / NHLBI NIH HHS / HL / P01 HL 070149; United States / NIAID NIH HHS / AI / U19 AI029530
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS25237; NLM/ PMC2743535
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36. Shimoni A, Hardan I, Shem-Tov N, Yeshurun M, Yerushalmi R, Avigdor A, Ben-Bassat I, Nagler A: Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: the role of dose intensity. Leukemia; 2006 Feb;20(2):322-8
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  • [Title] Allogeneic hematopoietic stem-cell transplantation in AML and MDS using myeloablative versus reduced-intensity conditioning: the role of dose intensity.
  • Allogeneic stem-cell transplantation (SCT) with both myeloablative and reduced-intensity conditioning (RIC) is an effective therapy in AML/MDS.
  • To define the role of dose intensity, we analyzed SCT outcomes of 112 consecutive patients with AML/MDS.
  • Myeloablative and RIC regimens had similar outcomes when leukemia was in remission at SCT; however, patients with active disease could only be salvaged by myeloablative conditioning.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myeloablative Agonists / therapeutic use. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Analysis. Transplantation, Homologous. Treatment Outcome


37. Christiansen DH, Desta F, Andersen MK, Pedersen-Bjergaard J: Mutations of the PTPN11 gene in therapy-related MDS and AML with rare balanced chromosome translocations. Genes Chromosomes Cancer; 2007 Jun;46(6):517-21
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  • [Title] Mutations of the PTPN11 gene in therapy-related MDS and AML with rare balanced chromosome translocations.
  • Activating mutations of the PTPN11 gene encoding the SHP2 tyrosine phosphatase is the most common genetic abnormality in juvenile myelomonocytic leukemia and is sporadically observed in myelodysplasia (MDS) and acute myeloid leukemia (AML).
  • An unselected series of 140 patients with therapy-related MDS or AML were investigated for mutations of PTPN11 in Exons 3, 4, 8, and 13.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Protein Tyrosine Phosphatases / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Aged. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Sequence Analysis, DNA

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17330262.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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38. Boehrer S, Adès L, Braun T, Galluzzi L, Grosjean J, Fabre C, Le Roux G, Gardin C, Martin A, de Botton S, Fenaux P, Kroemer G: Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study. Blood; 2008 Feb 15;111(4):2170-80
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  • [Title] Erlotinib exhibits antineoplastic off-target effects in AML and MDS: a preclinical study.
  • Erlotinib, an inhibitor of the epidermal growth factor receptor (EGFR), induces differentiation, cell-cycle arrest, and apoptosis of EGFR-negative myeloblasts of patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), as well as in EGFR-negative cell lines representing these diseases (P39, KG-1, and HL 60).
  • In apoptosis-sensitive AML cells, erlotinib caused a rapid (within less than 1 hour) nucleocytoplasmic translocation of nucleophosmin-1 (NPM-1) and p14(ARF).
  • Moreover, erlotinib reduced the growth of xenografted human AML cells in vivo.
  • Erlotinib also killed CD34(+) bone marrow blasts from MDS and AML patients while sparing normal CD34(+) progenitors.
  • One patient afflicted with both MDS and non-small cell lung cancer manifested hematologic improvement in response to erlotinib.
  • In summary, we here provide novel evidence in vitro, ex vivo, and in vivo for the potential therapeutic efficacy of erlotinib in the treatment of high-risk MDS and AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use


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

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  • (PMID = 20047095.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; 74KXF8I502 / Aclarubicin; ZRP63D75JW / Idarubicin
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40. 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.
  • 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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41. 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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42. Le Deley MC, Suzan F, Cutuli B, Delaloge S, Shamsaldin A, Linassier C, Clisant S, de Vathaire F, Fenaux P, Hill C: Anthracyclines, mitoxantrone, radiotherapy, and granulocyte colony-stimulating factor: risk factors for leukemia and myelodysplastic syndrome after breast cancer. J Clin Oncol; 2007 Jan 20;25(3):292-300
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  • [Title] Anthracyclines, mitoxantrone, radiotherapy, and granulocyte colony-stimulating factor: risk factors for leukemia and myelodysplastic syndrome after breast cancer.
  • PURPOSE: To determine the risk factors for acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) after breast cancer.
  • We included 182 AML and MDS patients and 534 matched controls.
  • RESULTS: The risk of AML/MDS was increased after topoisomerase-II inhibitor-based chemotherapy (P < 10-16) and was higher for mitoxantrone-based chemotherapy than for anthracycline-based chemotherapy (relative risk [RR] = 15.6; 95% CI, 7.1 to 34.2; and RR = 2.7; 95% CI, 1.7 to 4.5, respectively).
  • After adjustment for other treatment components, the risk of AML/MDS in patients who received radiotherapy was multiplied by 3.9 (95% CI, 1.4 to 10.8) but was not increased by alkylating agents.
  • Patients receiving granulocyte colony-stimulating factor (G-CSF) support had an increased risk of AML/MDS (RR = 6.3; 95% CI, 1.9 to 21), even when controlling for chemotherapy doses.
  • Similar results were obtained when AML and MDS were considered separately.
  • CONCLUSION: This large case-control study demonstrates that the risk of AML/MDS is much higher with mitoxantrone-based chemotherapy than with anthracyclines-based chemotherapy in a population of women recently treated for breast cancer.
  • The risk of AML/MDS associated with mitoxantrone must be kept in mind when using this drug to treat diseases other than breast cancer (eg, prostate cancer or multiple sclerosis).
  • [MeSH-major] Anthracyclines / adverse effects. Antineoplastic Agents / adverse effects. Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Leukemia, Myeloid / chemically induced. Mitoxantrone / adverse effects. Myelodysplastic Syndromes / chemically induced. Neoplasms, Radiation-Induced
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. France / epidemiology. Humans. Middle Aged. Risk Factors


43. 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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  • [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


44. Finazzi G, Caruso V, Marchioli R, Capnist G, Chisesi T, Finelli C, Gugliotta L, Landolfi R, Kutti J, Gisslinger H, Marilus R, Patrono C, Pogliani EM, Randi ML, Villegas A, Tognoni G, Barbui T, ECLAP Investigators: Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study. Blood; 2005 Apr 1;105(7):2664-70
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  • [Title] Acute leukemia in polycythemia vera: an analysis of 1638 patients enrolled in a prospective observational study.
  • Progression to acute myeloid leukemia/myelodysplastic syndromes (AML/MDS) is a possible evolution of polycythemia vera (PV), but whether some patients are at increased natural risk for this complication and how much the contribution of pharmacologic cytoreduction can affect the natural course of the disease remain uncertain.
  • AML/MDS was diagnosed in 22 patients after a median of 2.5 years from recruitment in the study and a median of 8.4 years from the diagnosis of PV.
  • Variables associated with progression to AML/MDS were assessed using different models of multivariate analysis.
  • Exposure to P32, busulphan, and pipobroman (HR, 5.46; 95% CI, 1.84-16.25; P = .0023), but not to hydroxyurea (HU) alone (HR, 0.86; 95% CI, 0.26-2.88; P = .8021), had an independent role in producing an excess risk for progression to AML/MDS compared with treatment with phlebotomy or interferon.
  • [MeSH-major] Leukemia, Myeloid / epidemiology. Polycythemia Vera / epidemiology
  • [MeSH-minor] Acute Disease. Adult. Aged. Aspirin / therapeutic use. Databases, Factual. Disease Progression. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multivariate Analysis. Platelet Aggregation Inhibitors / therapeutic use. Prospective Studies. Risk Factors

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  • [CommentIn] Curr Hematol Rep. 2005 May;4(3):211-2 [15865873.001]
  • (PMID = 15585653.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet Aggregation Inhibitors; R16CO5Y76E / Aspirin
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45. Grant S: New agents for AML and MDS. Best Pract Res Clin Haematol; 2009 Dec;22(4):501-7
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  • [Title] New agents for AML and MDS.
  • The heterogeneity of acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) has led to a multiplicity of treatments, from cytotoxic agents to signal transduction modulators, cell-cycle inhibitors and epigenetic therapies.
  • While some have shown promising initial results, the outlook for AML patients, particularly older and relapsed patients, as well as patients whose cells exhibit certain adverse chromosomal abnormalities or mutant oncoproteins, continues to be grim.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy

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  • (PMID = 19959100.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R21 CA115260-01; United States / NCI NIH HHS / CA / P50 CA130805-02; United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / RC2 CA148431-01; United States / NCI NIH HHS / CA / R01 CA063753-13; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA100866-04; United States / NCI NIH HHS / CA / P50CA130805; United States / NCI NIH HHS / CA / R01 CA093738; United States / CCR NIH HHS / RC / RC2 CA148431-01; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / RC2 CA148431; United States / NCI NIH HHS / CA / R01 CA093738-05A2; United States / NCI NIH HHS / CA / CA93738; United States / NCI NIH HHS / CA / R21 CA115260
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cytotoxins; 0 / Protein Kinase Inhibitors
  • [Number-of-references] 38
  • [Other-IDs] NLM/ NIHMS157911; NLM/ PMC2793080
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46. Drexler HG, Dirks WG, Macleod RA: Many are called MDS cell lines: one is chosen. Leuk Res; 2009 Aug;33(8):1011-6
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  • [Title] Many are called MDS cell lines: one is chosen.
  • Myelodysplastic syndromes (MDS) comprise a heterogenous group of clonal disorders of hematopoietic progenitors, showing genetic instability and in many cases progression to acute myeloid leukemia (AML).
  • When MDS progress towards AML (AML/MDS), additional genetic lesions cause a block in differentiation and an accumulation of blast cells.
  • Hence, both pathophysiologically and clinically the MDS and AML/MDS phases are distinguishable.
  • Leukemia cell lines are key resources for modelling hematological malignancies.
  • Some 31 cell lines have been described in the literature purportedly established from patients with MDS.
  • However, a significant minority of these has proved false after DNA profiling which revealed their cross-contamination with older established leukemia cell lines.
  • Most remaining ("authentic") MDS cell lines were established during the leukemic phase of the disease progression rather than during the MDS phase.
  • Based on these data we have assigned the 31 candidate MDS cell lines to one of the three categories:.
  • (2) malignant cell lines established in the AML/MDS leukemic phase; and (3) apparently legitimate MDS cell lines established during the MDS phase.
  • While MDS and AML/MDS cell lines both provide singular resources for modelling pathology, mining oncogenically modified macromolecules, and testing druggability, we contend these groups should be considered separately.
  • [MeSH-major] Cell Line, Tumor. Hematopoietic Stem Cells. Myelodysplastic Syndromes
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Genomic Instability. Humans. Leukemia, Myeloid, Acute. Models, Biological


47. Padmanabhan A, Baker JA, Zirpoli G, Sait SN, Ford LA, Moysich KB, Baer MR: Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members. Leuk Res; 2008 Dec;32(12):1820-3
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  • [Title] Acute myeloid leukemia and myelodysplastic syndrome following breast cancer: increased frequency of other cancers and of cancers in multiple family members.
  • Adjuvant chemotherapy and radiation therapy for breast cancer are associated with therapy-related acute myeloid leukemia (AML)/myelodysplastic syndromes (MDS), but little is known about additional risk factors.
  • Thirty-four patients with AML (n=26)/MDS (n=8) following breast cancer (cases) were compared with 2029 breast cancer patients without AML/MDS (controls).
  • Thus risk factors for AML/MDS following breast cancer include older age, other cancers and multiple first-degree relatives with cancer.
  • [MeSH-major] Breast Neoplasms / complications. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / epidemiology. Neoplasms / complications. Neoplasms, Second Primary / epidemiology


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

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  • (PMID = 20629097.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / TET2 protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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49. Ye Y, McDevitt MA, Guo M, Zhang W, Galm O, Gore SD, Karp JE, Maciejewski JP, Kowalski J, Tsai HL, Gondek LP, Tsai HC, Wang X, Hooker C, Smith BD, Carraway HE, Herman JG: Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies. Cancer Res; 2009 Nov 1;69(21):8482-90
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  • [Title] Progressive chromatin repression and promoter methylation of CTNNA1 associated with advanced myeloid malignancies.
  • Complete loss or deletion of the long arm of chromosome 5 is frequent in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).
  • This study is a comprehensive analysis of previously implicated and novel genes for epigenetic inactivation in AML and MDS.
  • In 146 AML cases, methylation of CTNNA1 was frequent, and more common in AML patients with 5q deletion (31%) than those without 5q deletion (14%), whereas no methylation of other 5q genes was observed.
  • In 31 MDS cases, CTNNA1 methylation was only found in high-risk MDS (>or=RAEB2), but not in low-risk MDS (<RAEB2), indicating that CTNNA1 methylation might be important in the transformation of MDS to AML.
  • CTNNA1 expression was lowest in AML/MDS patients with CTNNA1 methylation, although reduced expression was found in some patients without promoter methylation.
  • Repressive chromatin marks (H3K27me3) at the promoter were identified in CTNNA1-repressed AML cell lines and primary leukemias, with the most repressive state correlating with DNA methylation.
  • These results suggest progressive, acquired epigenetic inactivation at CTNNA1, including histone modifications and promoter CpG methylation, as a component of leukemia progression in patients with both 5q- and non-5q- myeloid malignancies.

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  • (PMID = 19826047.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA058184-090013; United States / NCI NIH HHS / CA / P50 CA058184; United States / NCI NIH HHS / CA / P50 CA058184-090013
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNA1 protein, human; 0 / Chromatin; 0 / RNA, Messenger; 0 / alpha Catenin; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ NIHMS142652; NLM/ PMC3081599
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50. Wong AK, Fang B, Zhang L, Guo X, Lee S, Schreck R: Loss of the Y chromosome: an age-related or clonal phenomenon in acute myelogenous leukemia/myelodysplastic syndrome? Arch Pathol Lab Med; 2008 Aug;132(8):1329-32
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  • [Title] Loss of the Y chromosome: an age-related or clonal phenomenon in acute myelogenous leukemia/myelodysplastic syndrome?
  • CONTEXT: The clinical association between loss of the Y chromosome and acute myelogenous leukemia and myelodysplastic syndrome (AML/MDS) has been debated because both phenomena are related to aging.
  • OBJECTIVE: To evaluate the relationship between loss of the Y chromosome and AML/MDS.
  • Of these, 16 patients demonstrated myeloid disease, with 2 cases of AML and 14 cases of MDS.
  • An increased incidence (P < .05) of AML/MDS was seen only in the group composed of 8 patients with complete loss of the Y chromosome in all karyotyped cells (1 case of AML and 7 cases of MDS).
  • However, in individuals in which all cells on cytogenetic analysis showed loss of the Y chromosome, there was a statistically significant increase in AML/MDS, suggesting that the absence of any normal-dividing cells in a bone marrow analysis may be indicative of AML/MDS.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Y. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


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


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


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


54. Babicka L, Ransdorfova S, Brezinova J, Zemanova Z, Sindelarova L, Siskova M, Maaloufova J, Cermak J, Michalova K: Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH. Leuk Res; 2007 Jan;31(1):39-47
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  • [Title] Analysis of complex chromosomal rearrangements in adult patients with MDS and AML by multicolor FISH.
  • We analyzed complex chromosomal aberrations in 37 adult patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) using classical cytogenetic method, FISH with locus-specific probes, multicolor FISH (mFISH) and multicolor banding (mBAND).
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Gene Rearrangement / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics


55. Nemoto N, Suzukawa K, Shimizu S, Shinagawa A, Takei N, Taki T, Hayashi Y, Kojima H, Kawakami Y, Nagasawa T: Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23). Genes Chromosomes Cancer; 2007 Sep;46(9):813-9
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  • [Title] Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23).
  • We have identified a novel fusion partner of MLL, namely the mastermind like 2 (MAML2 gene), in secondary acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with inv(11)(q21q23).
  • RT-PCR and sequencing revealed that exon 7 of MLL was fused to exon 2 of MAML2 in the AML and MDS cells.
  • MLL-MAML2 in secondary AML/MDS and MECT1-MAML2 in mucoepithelioid carcinoma, benign Wartin's tumor, and clear cell hidradenoma consist of the same COOH-terminal part of MAML2.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics


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

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20645416.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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57. Müller CI, Rüter B, Koeffler HP, Lübbert M: DNA hypermethylation of myeloid cells, a novel therapeutic target in MDS and AML. Curr Pharm Biotechnol; 2006 Oct;7(5):315-21
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  • [Title] DNA hypermethylation of myeloid cells, a novel therapeutic target in MDS and AML.
  • In vitro, inhibition of methylation using azanucleosides results in modest differentiation of transformed myeloid cell lines.
  • In vivo, low doses of these agents induce DNA demethylation of malignant myeloid cells.
  • Indeed, the first drug specifically approved for the treatment of myelodysplastic syndrome (MDS) was the azanucleoside 5-azacytidine (Vidaza).
  • FDA for treatment of MDS of all subtypes.
  • About 30 % of MDS patients with an abnormal karyotype have normalization of their karyotype after receiving the drug.
  • [MeSH-major] Amyotrophic Lateral Sclerosis / drug therapy. CpG Islands / drug effects. DNA Methylation / drug effects. Drug Delivery Systems / methods. Myelodysplastic Syndromes / drug therapy. Myeloid Cells / drug effects. Nucleosides / therapeutic use

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  • (PMID = 17076647.001).
  • [ISSN] 1873-4316
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nucleosides
  • [Number-of-references] 49
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58. Ciurea SO, Saliba R, Rondon G, Pesoa S, Cano P, Fernandez-Vina M, Qureshi S, Worth LL, McMannis J, Kebriaei P, Jones RB, Korbling M, Qazilbash M, Shpall EJ, Giralt S, de Lima M, Champlin RE, Gajewski J: Reduced-intensity conditioning using fludarabine, melphalan and thiotepa for adult patients undergoing haploidentical SCT. Bone Marrow Transplant; 2010 Mar;45(3):429-36
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  • A total of 21 out of 22 patients with AML/myelodysplastic syndrome (MDS) achieved remission after transplant (16 with relapsed/refractory AML).
  • Five out of the 12 patients (42%) with AML/MDS with <15% BM blasts survived long term as compared with none with more advanced disease (P=0.03).
  • HaploSCT with this fludarabine, melphalan and thiotepa and ATG RIC is an effective, well-tolerated conditioning regimen for patients with AML/MDS with low disease burden at the time of transplant and allowed a high rate of engraftment in patients without DSA.
  • [MeSH-minor] Adolescent. Adult. Antilymphocyte Serum / administration & dosage. Child. Female. Hematologic Neoplasms / therapy. Humans. Infection / etiology. Leukemia, Myeloid, Acute / therapy. Male. Melphalan / administration & dosage. Middle Aged. Myelodysplastic Syndromes / therapy. Survival Rate. T-Lymphocytes / immunology. Thiotepa / administration & dosage. Transplantation, Homologous. Treatment Outcome. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult

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


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

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  • (PMID = 18489993.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164-160020; United States / NCI NIH HHS / CA / 2P30CA16672-26; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Myeloablative Agonists; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ NIHMS52878; NLM/ PMC4230823
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61. Pollyea DA, Artz AS, Stock W, Daugherty C, Godley L, Odenike OM, Rich E, Smith SM, Zimmerman T, Zhang Y, Huo D, Larson R, van Besien K: Outcomes of patients with AML and MDS who relapse or progress after reduced intensity allogeneic hematopoietic cell transplantation. Bone Marrow Transplant; 2007 Dec;40(11):1027-32
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  • [Title] Outcomes of patients with AML and MDS who relapse or progress after reduced intensity allogeneic hematopoietic cell transplantation.
  • We describe treatment, outcomes and prognostic factors for patients who relapse following transplantation with a reduced intensity conditioning regimen.
  • Seventy consecutive patients with high-risk myeloid malignancies underwent transplant and 25 (36%) relapsed, a median of 120 days later.
  • Studies exploring the optimal treatment for relapse following reduced intensity HCT are warranted.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasm Recurrence, Local / therapy. Salvage Therapy / methods

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  • (PMID = 17846595.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q41OR9510P / Melphalan
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62. Strupp C, Knipp S, Hartmann J, Gattermann N, Haas R, Germing U: A pilot study of bendamustine in elderly patients with high-risk MDS and AML. Leuk Lymphoma; 2007 Jun;48(6):1161-6
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  • [Title] A pilot study of bendamustine in elderly patients with high-risk MDS and AML.
  • We examined the efficacy of bendamustine in 15 pretreated patients (12 men, 3 women, median age 69 years) with acute myeloid leukaemia (AML) or myelodysplastic syndromes (MDS) 3 AML, 5 sAML, 5 CMML II, 1 RAEB II.
  • Patients belonged to the following cytogenetic groups: 3 complex abnormal karyotypes, 7 normal karyotypes, 1 case with 20q- as sole anomaly and 4 single aberrations.
  • Three patients showed no response, one patient with AML died due to progressive disease.
  • In summary, treatment with bendamustine in patients with high-risk MDS or sAML with leukocytosis can result in a significant reduction of leukocytes, but fails to achieve hematological responses or improvement of transfusions dependency.
  • [MeSH-major] Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Nitrogen Mustard Compounds / therapeutic use
  • [MeSH-minor] Acute Disease. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Bendamustine Hydrochloride. Drug Evaluation. Female. Humans. Male. Pilot Projects

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  • [CommentIn] Leuk Lymphoma. 2007 Jun;48(6):1064-6 [17577766.001]
  • (PMID = 17577779.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrogen Mustard Compounds; 981Y8SX18M / Bendamustine Hydrochloride
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63. Shimoni A, Hardan I, Shem-Tov N, Rand A, Yerushalmi R, Nagler A: Fludarabine and treosulfan: a novel modified myeloablative regimen for allogeneic hematopoietic stem-cell transplantation with effective antileukemia activity in patients with acute myeloid leukemia and myelodysplastic syndromes. Leuk Lymphoma; 2007 Dec;48(12):2352-9
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  • [Title] Fludarabine and treosulfan: a novel modified myeloablative regimen for allogeneic hematopoietic stem-cell transplantation with effective antileukemia activity in patients with acute myeloid leukemia and myelodysplastic syndromes.
  • Allogeneic stem-cell transplantation (SCT) is potentially curative treatment for AML and MDS.
  • Treosulfan is an alkylating agent with in vitro cytotoxicity against leukemia as well as myeloablative and immunosuppressive properties when used in escalated doses.
  • We explored a regimen of fludarabine (30 mg/m(2) x 5) and treosulfan (12 gr/m(2) x 3) in 24 patients, median age 55 years (range, 30-69), with AML (n = 19) or MDS (n = 5), not eligible for standard myeloablation.
  • The incidence of acute and chronic GVHD was 15% and 47%, respectively.
  • The fludarabine/treosulfan regimen can be considered a fully intensive, modified myeloablative regimen with effective antileukemia activity and acceptable toxicity in patients with AML/MDS not eligible for standard myeloablation, and merits further study in larger scale studies.
  • [MeSH-major] Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives


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

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  • (PMID = 19561406.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P01 CA55164; United States / NCI NIH HHS / CA / 2P30CA16672-26
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS588342; NLM/ PMC4037323
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65. Leleu X, Terriou L, Duhamel A, Moreau AS, Andrieux J, Dupire S, Coiteux V, Berthon C, Micol JB, Guieze R, Facon T, Bauters F: Long-term outcome in acquired aplastic anemia treated with an intensified dose schedule of horse antilymphocyte globulin in combination with androgens. Ann Hematol; 2006 Oct;85(10):711-6
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  • ALG has been incriminated in the emergence of 10 to 20% therapy-related AML/MDS (t-AML/MDS) with the usual doses.
  • Questions remain whether higher doses of ALG could improve the response and OS rates and whether the combination with androgens is able to protect patients from t-AML/MDS.
  • The incidence of t-AML/MDS was 2.3% with an estimated 10-year cumulative incidence of 3.1.
  • Our results show that higher doses of ALG combined to androgens are feasible and give results close to those recently describe with the immunosuppressive treatments including ALG associated to cyclosporine, with a low SMD/AML incidence rate.

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  • (PMID = 16830141.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgens; 0 / Antilymphocyte Serum; 0 / Immunosuppressive Agents
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66. Reindl C, Quentmeier H, Petropoulos K, Greif PA, Benthaus T, Argiropoulos B, Mellert G, Vempati S, Duyster J, Buske C, Bohlander SK, Humphries KR, Hiddemann W, Spiekermann K: CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes. Clin Cancer Res; 2009 Apr 1;15(7):2238-47
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  • [Title] CBL exon 8/9 mutants activate the FLT3 pathway and cluster in core binding factor/11q deletion acute myeloid leukemia/myelodysplastic syndrome subtypes.
  • In this study, we determined the frequency of CBL mutations in acute leukemias and evaluated the oncogenic potential of mutant CBL.
  • EXPERIMENTAL DESIGN: The cDNA of 300 acute myeloid leukemia (AML)/myelodysplastic syndrome (MDS) and acute lymphoblastic leukemia (ALL) patients and 82 human leukemic cell lines was screened for aberrations in the linker and RING finger domain of CBL.
  • RESULTS: We identified 3 of 279 AML/MDS patients expressing CBL exon 8/9 deletion mutants.
  • One of 116 sequenced AML/MDS cases carried a R420G missense mutation.
  • All AML/MDS patients with identified CBL mutants belonged to the core binding factor and 11q deletion AML subtypes.
  • CONCLUSION: CBL exon8/9 mutants occur in genetically defined AML/MDS subtypes and transform hematopoietic cells by constitutively activating the FLT3 pathway.
  • This phenotype resembles the one of mutated RTKs and suggests that CBL mutant AML patients might benefit from treatment with FLT3 PTK inhibitors.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics. fms-Like Tyrosine Kinase 3 / metabolism


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


68. Meyers CA, Albitar M, Estey E: Cognitive impairment, fatigue, and cytokine levels in patients with acute myelogenous leukemia or myelodysplastic syndrome. Cancer; 2005 Aug 15;104(4):788-93
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  • [Title] Cognitive impairment, fatigue, and cytokine levels in patients with acute myelogenous leukemia or myelodysplastic syndrome.
  • BACKGROUND: The objective of the current study was to assess the correlations between cognitive function, fatigue, quality of life, and circulating cytokine levels in patients with acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS).
  • METHODS: Fifty-four patients with AML/MDS were seen for pretreatment evaluation of their cognitive function and symptoms.
  • CONCLUSIONS: Patients with AML/MDS are highly symptomatic and experience cognitive impairment and fatigue before the initiation of their treatment.
  • [MeSH-major] Cognition Disorders / etiology. Cytokines / blood. Fatigue / etiology. Leukemia, Myeloid, Acute / complications. Myelodysplastic Syndromes / complications


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

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  • (PMID = 17420284.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221; United States / NCI NIH HHS / CA / R01 CA101774; United States / NCI NIH HHS / CA / R01 CA101774-06; United States / NCI NIH HHS / CA / CA101774-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse
  • [Other-IDs] NLM/ PMC1924479
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70. Bunin N, Aplenc R, Leahey A, Magira E, Grupp S, Pierson G, Monos D: Outcomes of transplantation with partial T-cell depletion of matched or mismatched unrelated or partially matched related donor bone marrow in children and adolescents with leukemias. Bone Marrow Transplant; 2005 Jan;35(2):151-8
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  • Relapse occurred in 6% of ALL patients, and 22.8% of AML/MDS patients.
  • [MeSH-major] Bone Marrow Transplantation / methods. Histocompatibility. Leukemia / therapy. Lymphocyte Depletion / methods


71. Bellos F, Mahlknecht U: Valproic acid and all-trans retinoic acid: meta-analysis of a palliative treatment regimen in AML and MDS patients. Onkologie; 2008 Nov;31(11):629-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Valproic acid and all-trans retinoic acid: meta-analysis of a palliative treatment regimen in AML and MDS patients.
  • Currently, no standard treatment is available for elderly patients with de novo/secondary acute myeloid leukemia (AML) who are not eligible for intensive chemotherapy.
  • We treated 21 patients with de novo/secondary AML and 1 patient with myelodysplastic syndrome with ATRA (45 mg/m(2)/day in 2 doses, 14 days, q29 days) and VPA (150 mg/day 1 week, then 300 mg/day, continuously).
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / epidemiology. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / epidemiology. Palliative Care / statistics & numerical data. Tretinoin / administration & dosage. Valproic Acid / administration & dosage


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


73. Storb R: Reduced-intensity conditioning transplantation in myeloid malignancies. Curr Opin Oncol; 2009 Jun;21 Suppl 1:S3-5
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  • [Title] Reduced-intensity conditioning transplantation in myeloid malignancies.
  • The development of non-myeloablative and reduced-intensity conditioning regimens has enabled older or medically infirm patients with myeloid malignancies to be treated with allogeneic hematopoietic cell transplantation (HCT).
  • The regimens are sufficiently immunosuppressive to allow engraftment of allogeneic cells and they rely largely on graft-versus-leukemia effects rather than high-dose cytotoxic therapy to eliminate malignant cells.
  • Overall 2-5-year survivals after allogeneic HCT in older patients with acute myeloid leukemia (AML) or myelodysplastic syndromes (MDS) have ranged from 25% to 64%.
  • Despite still existing problems, early results in elderly patients with AML/MDS have been encouraging.

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  • (PMID = 19561410.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA015704; United States / NHLBI NIH HHS / HL / HL036444; United States / NCI NIH HHS / CA / CA078902; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA018029; United States / NCI NIH HHS / CA / P01 CA018029-36; United States / NCI NIH HHS / CA / P01 CA078902-13; United States / NHLBI NIH HHS / HL / P01 HL036444; United States / NCI NIH HHS / CA / P01 CA078902; United States / NHLBI NIH HHS / HL / P01 HL036444-30; United States / NCI NIH HHS / CA / P30 CA015704-37; United States / NCI NIH HHS / CA / CA078902-13
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 9
  • [Other-IDs] NLM/ NIHMS211792; NLM/ PMC2895692
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74. Clausen J, Wolf D, Petzer AL, Gunsilius E, Schumacher P, Kircher B, Gastl G, Nachbaur D: Impact of natural killer cell dose and donor killer-cell immunoglobulin-like receptor (KIR) genotype on outcome following human leucocyte antigen-identical haematopoietic stem cell transplantation. Clin Exp Immunol; 2007 Jun;148(3):520-8
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  • [Title] Impact of natural killer cell dose and donor killer-cell immunoglobulin-like receptor (KIR) genotype on outcome following human leucocyte antigen-identical haematopoietic stem cell transplantation.
  • To define the role of quantitative graft composition and donor killer-cell immunoglobulin-like receptor (KIR) genotype in clinical outcome following unmanipulated peripheral blood stem cell transplantation (PBSCT) from human leucocyte antigen (HLA)-identical siblings, 43 consecutive transplants for haematological malignancies were analysed retrospectively.
  • In patients with acute myelogenous leukaemia or myelodysplastic syndrome (AML/MDS; n = 18), no relapse occurred following transplants meeting both a high (above median) natural killer (NK) cell count and missing HLA-ligand(s) to donor's KIR(s), compared to all other AML/MDS patients (0% versus 44%; P = 0.049).
  • Moreover, in AML/MDS patients, this constellation predicted superior overall survival (OS) (P = 0.046).
  • [MeSH-minor] Acute Disease. Chronic Disease. Cytomegalovirus Infections / immunology. Female. Genotype. Graft vs Host Disease / immunology. Graft vs Host Disease / therapy. Graft vs Tumor Effect / genetics. Histocompatibility Testing. Humans. Ligands. Lymphocyte Count. Male. Opportunistic Infections / immunology. Receptors, KIR. Receptors, KIR3DL2. Recurrence. Retrospective Studies. Survival Analysis. Transplantation Conditioning / methods. Treatment Outcome

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  • (PMID = 17493020.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / KIR3DL2 protein, human; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR; 0 / Receptors, KIR3DL2
  • [Other-IDs] NLM/ PMC1941931
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75. Brakensiek K, Länger F, Kreipe H, Lehmann U: Absence of p21(CIP 1), p27(KIP 1) and p 57(KIP 2) methylation in MDS and AML. Leuk Res; 2005 Nov;29(11):1357-60
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  • [Title] Absence of p21(CIP 1), p27(KIP 1) and p 57(KIP 2) methylation in MDS and AML.
  • The three members of the KIP/CIP family of cyclin dependent kinase inhibitors (CDKIs), p21(CIP 1), p27(KIP 1), and p 57(KIP 2), play key roles in cell cycle regulation, but little is known about their methylation in myeloid neoplasia.
  • Therefore, we analysed 9 haematopoietic cell lines, 67 myelodysplastic syndrome (MDS) and 26 acute myeloid leukaemia (AML) cases as well as 11 controls. p 57(KIP 2) hypermethylation was found in 4/9 cell lines, but methylation of p21(CIP 1) and p27(KIP 1) was infrequent.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Cyclin-Dependent Kinase Inhibitor p57 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Cell Cycle / drug effects. Cell Line, Tumor. DNA Methylation. Female. Gene Silencing. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic

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  • (PMID = 15936816.001).
  • [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 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclin-Dependent Kinase Inhibitor p57; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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76. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML. Leukemia; 2005 Feb;19(2):197-200
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  • [Title] Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.
  • Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%).
  • The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 15618958.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors
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77. Cocco L, Manzoli L, Palka G, Martelli AM: Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia. Adv Enzyme Regul; 2005;45:126-35
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  • [Title] Nuclear phospholipase C beta1, regulation of the cell cycle and progression of acute myeloid leukemia.
  • Moreover, non-specific alterations in chromosome 20 have been found in patients affected by MDS and acute myeloid leukemia AML.
  • MDS is an adult hematological disease that evolves into AML in about 30% of the cases.
  • The availability of a highly specific probe gave an opportunity to perform in patients affected with MDS/AML, associated with normal karyotype, painting and FISH analysis aimed to check the PLC beta1 gene, given that this signaling molecule is a key player in the control of some checkpoints of the normal progression through the cell cycle.
  • FISH analysis disclosed in a small group of MDS/AML patients with normal karyotype the monoallelic deletion of the PLC beta1 gene.
  • In contrast, PLC beta4, another gene coding for a signaling molecule, located on 20pl2.3 at a distance as far as less than 1 Mb from PLC beta1, is unaffected in MDS patients with the deletion of PLC beta1 gene, hinting at an interstitial deletion.
  • The MDS patients, bearing the deletion, rapidly evolved to AML, whilst the normal karyotype MDS patients, showing non-deletion of PLC beta1 gene, are still alive at least 24 months after the diagnosis.
  • The immunocytochemical analysis using an anti PLC beta1 monoclonal antibody showed that all the AML/MDS patients who were normal at FISH analysis also had normal staining of the nucleus, which is a preferential site for PLC beta1.
  • The reported data strengthen the contention of a key role played by PLC beta1 in the nucleus, suggest a possible involvement of PLC beta1 in the progression of MDS to AML and pave the way for a larger investigation aimed at identifying a possible high risk group among MDS patients with a normal karyotype.
  • [MeSH-major] Cell Cycle / physiology. Cell Nucleus / enzymology. Isoenzymes / physiology. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / pathology. Type C Phospholipases / physiology
  • [MeSH-minor] Acute Disease. Gene Deletion. Humans. Phospholipase C beta. Signal Transduction / physiology


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

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  • (PMID = 16452126.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA32102
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / TRIB1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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79. Tefferi A, Gangat N, Wolanskyj AP, Schwager S, Pardanani A, Lasho TL, Mesa R, McClure RF, Li CY, Hanson CA: 20+ yr without leukemic or fibrotic transformation in essential thrombocythemia or polycythemia vera: predictors at diagnosis. Eur J Haematol; 2008 May;80(5):386-90
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  • OBJECTIVES: The current study identified patients with either essential thrombocythemia (ET) or polycythemia vera (PV) who have survived for at least 20 yr without the development of either acute myeloid leukemia/myelodysplastic syndrome (AML/MDS) or myelofibrosis (MF) and compared their presenting features with those in whom these complications occurred in the first 10 yr of disease.
  • In both instances, three distinct groups were delineated and their presenting features compared; group A included patients who have remained AML/MDS/MF free after a minimum follow-up of 20 yr; groups B and C included patients who developed either AML/MDS or MF, respectively, in the first decade of their disease.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Fibrosis / pathology. Humans. Leukemia / pathology. Male. Middle Aged. Time Factors


80. Nakamae H, Himuro K, Hagihara K, Terada Y, Sakamoto E, Takeoka Y, Nakane T, Nakamae M, Ohta K, Yamane T, Shimada H, Miki T, Hino M: [Chronic GVHD with polymyositis after non-myeloablative stem cell transplantation]. Rinsho Ketsueki; 2005 Nov;46(11):1213-7
Hazardous Substances Data Bank. PREDNISOLONE .

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  • He was diagnosed with further hematological examination as having acute myeloid leukemia with multilineage dysplasia following secondary myelodysplastic syndrome.
  • Prednisolone 50 mg/day as an initial dose was started for the polymyositis following which the prednisolone dose was gradually tapered off.

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  • (PMID = 16440806.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9PHQ9Y1OLM / Prednisolone
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81. Greiner RA, Meier Y, Papadopoulos G, O'Sullivan AK, Imhof A: Cost-effectiveness of posaconazole compared with standard azole therapy for prevention of invasive fungal infections in patients at high risk in Switzerland. Oncology; 2010;78(3-4):172-80
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  • METHODS: Decision tree models based on the results of two registration trials and subsequent Markov models over patient lifetimes were developed for patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) with neutropenia and for hematopoietic stem cell transplant recipients with graft-versus-host disease (GVHD).
  • RESULTS: By reducing IFIs in AML/MDS patients with posaconazole prophylaxis, the contained IFI-related treatment costs more than compensated for the incremental cost of posaconazole, resulting in savings of CHF 1,118 per patient.
  • [MeSH-minor] Cost-Benefit Analysis. Decision Support Techniques. Graft vs Host Disease / therapy. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Markov Chains. Models, Theoretical. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Neutropenia / complications. Neutropenia / drug therapy. Risk. Switzerland. Treatment Outcome

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20414005.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Triazoles; 6TK1G07BHZ / posaconazole
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82. Staber P, Langner S, Dornbusch HJ, Neumeister P: Antifungal management in cancer patients. Wien Med Wochenschr; 2007;157(19-20):503-10
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  • Established risk factors are previous fungal infection, neutropenia exceeding 10 days, older age, active cancer, corticosteroid therapy, administration of broad spectrum antibiotics, allogeneic HSCT, central venous catheter and organ dysfunction.
  • Benefit of antifungal prophylaxis has been proven for fluconazole (400 mg/d) in allogeneic transplant recipients, and for posaconazole (600 mg/d) in patients during AML/MDS induction chemotherapy as well as in patients with GvHD.

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  • (PMID = 18030555.001).
  • [ISSN] 0043-5341
  • [Journal-full-title] Wiener medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Wien Med Wochenschr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Antifungal Agents
  • [Number-of-references] 61
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83. Lim ZY, Pearce L, Ho AY, Barber L, Ingram W, Usai M, Tobal K, Devereux S, Pagliuca A, Mufti GJ: Delayed attainment of full donor chimaerism following alemtuzumab-based reduced-intensity conditioning haematopoeitic stem cell transplantation for acute myeloid leukaemia and myelodysplastic syndromes is associated with improved outcomes. Br J Haematol; 2007 Aug;138(4):517-26
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  • [Title] Delayed attainment of full donor chimaerism following alemtuzumab-based reduced-intensity conditioning haematopoeitic stem cell transplantation for acute myeloid leukaemia and myelodysplastic syndromes is associated with improved outcomes.
  • This prospective study evaluated the kinetics of lymphoid (CD3) engraftment in 110 patients with acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) after allogeneic transplantation and conditioning with fludarabine, busulphan and alemtuzumab, using ciclosporin for post-transplant immunosuppression.
  • In patients with AML/MDS undergoing alemetuzumab based-RIC HSCT, prolonged MDC beyond day+100 is associated with an improved OS.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods


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


85. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Centromeric breakage and highly rearranged chromosome derivatives associated with mutations of TP53 are common in therapy-related MDS and AML after therapy with alkylating agents: an M-FISH study. Genes Chromosomes Cancer; 2005 Apr;42(4):358-71
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  • [Title] Centromeric breakage and highly rearranged chromosome derivatives associated with mutations of TP53 are common in therapy-related MDS and AML after therapy with alkylating agents: an M-FISH study.
  • Multicolor fluorescence in situ hybridization (M-FISH) was performed on bone marrow cells of 116 unselected cases of therapy-related myelodysplasia (t-MDS) or acute myeloid leukemia (t-AML), and the results were compared with those of previously performed with G-banding.
  • A clustering of breakpoints was observed in the centromeric or pericentromeric region of chromosomes 1, 5, 7, 13, 17, 21, and 22 in 48 of 98 patients with t-MDS and t-AML and an abnormal karyotype, and was related to previous therapy with alkylating agents.
  • M-FISH had little impact on the prognostic classification of t-MDS and t-AML, as only three patients changed prognostic groups as a result of M-FISH.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Centromere. Chromosome Aberrations. Genes, p53. Leukemia, Myeloid / genetics. Mutation. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Translocation, Genetic

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15645489.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
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86. Keilholz U, Letsch A, Busse A, Asemissen AM, Bauer S, Blau IW, Hofmann WK, Uharek L, Thiel E, Scheibenbogen C: A clinical and immunologic phase 2 trial of Wilms tumor gene product 1 (WT1) peptide vaccination in patients with AML and MDS. Blood; 2009 Jun 25;113(26):6541-8
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  • [Title] A clinical and immunologic phase 2 trial of Wilms tumor gene product 1 (WT1) peptide vaccination in patients with AML and MDS.
  • This study investigated the immunogenicity of Wilms tumor gene product 1 (WT1)-peptide vaccination in WT1-expressing acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients without curative treatment option.
  • Seventeen AML patients and 2 refractory anemia with excess blasts patients received a median of 11 vaccinations.
  • Objective responses in AML patients were 10 stable diseases (SDs) including 4 SDs with more than 50% blast reduction and 2 with hematologic improvement.
  • This WT1 vaccination study provides immunologic, molecular, and preliminary evidence of potential clinical efficacy in AML patients, warranting further investigations.
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / therapy. Cancer Vaccines / therapeutic use. Immunotherapy, Active. Leukemia, Myeloid / therapy. Peptide Fragments / immunology. WT1 Proteins / immunology
  • [MeSH-minor] Acute Disease. Adjuvants, Immunologic / administration & dosage. Aged. Aged, 80 and over. CD8-Positive T-Lymphocytes / immunology. Erythema / etiology. Female. Genes, Wilms Tumor. Humans. Immunization Schedule. Injections, Intradermal. Injections, Subcutaneous. Male. Middle Aged. Neoplasm Proteins / immunology. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Salvage Therapy. T-Cell Antigen Receptor Specificity

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  • (PMID = 19389880.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Cancer Vaccines; 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 (126-134), human; 0 / WT1 Proteins
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87. Stam WB, O'Sullivan AK, Rijnders B, Lugtenburg E, Span LF, Janssen JJ, Jansen JP: Economic evaluation of posaconazole vs. standard azole prophylaxis in high risk neutropenic patients in the Netherlands. Eur J Haematol; 2008 Dec;81(6):467-74
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  • BACKGROUND: Acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients experience prolonged neutropenia after treatment with intensive chemotherapy, leading to a high risk of invasive fungal infections (IFI).
  • METHODS: A decision-tree model was developed using data from a randomized trial that compared posaconazole and standard azole (fluconazole or itraconazole) prophylaxis in neutropenic patients receiving remission-induction chemotherapy for AML/MDS (Cornely et al., N Engl J Med 2007;356:348-359).
  • Following initiation of prophylaxis, clinical events are modeled with chance nodes reflecting probabilities of IFIs, IFI-related death, and death from other causes.
  • CONCLUSION: Given the underlying data and assumptions, the economic evaluation demonstrated that posaconazole prophylaxis is expected to be cost-effective compared with fluconazole/itraconazole in neutropenic AML/MDS patients after intensive chemotherapy.
  • [MeSH-major] Antifungal Agents / economics. Fluconazole / economics. Itraconazole / economics. Leukemia, Myeloid, Acute / economics. Mycoses / economics. Myelodysplastic Syndromes / economics. Neutropenia / economics. Triazoles / economics

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  • (PMID = 18754857.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 304NUG5GF4 / Itraconazole; 6TK1G07BHZ / posaconazole; 8VZV102JFY / Fluconazole
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88. Klimek VM, Fircanis S, Maslak P, Guernah I, Baum M, Wu N, Panageas K, Wright JJ, Pandolfi PP, Nimer SD: Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes. Clin Cancer Res; 2008 Feb 1;14(3):826-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tolerability, pharmacodynamics, and pharmacokinetics studies of depsipeptide (romidepsin) in patients with acute myelogenous leukemia or advanced myelodysplastic syndromes.
  • PURPOSE: Epigenetic modulation of gene expression plays an important role in cancer, including leukemia.
  • The purpose of this study was to evaluate the toxicity, pharmacokinetic profile, and selected pharmacodynamic properties of the histone deacetylase inhibitor depsipeptide in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • EXPERIMENTAL DESIGN: Depsipeptide was administered to MDS or AML patients at a (solid tumor) phase I dose of 18 mg/m(2) i.v. on days 1 and 5 every 3 weeks.
  • RESULTS: Twelve patients (nine with AML, three with MDS) received one to five cycles of depsipeptide.
  • The best response of 11 assessed patients was one complete remission in a patient with AML, stable disease in six patients, and progression of disease in four patients.
  • Exploratory laboratory studies showed modest but rapid increases in apoptosis and changes in myeloid maturation marker expression.
  • Depsipeptide monotherapy has limited clinical activity in unselected AML/MDS patients.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Depsipeptides / pharmacokinetics. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy


89. Diehl V, Behringer K: Could BEACOPP be the new standard for the treatment of advanced Hodgkin's lymphoma? Cancer Invest; 2006 Jun-Jul;24(4):461-5
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  • These superior BEACOPP results are obtained inspite of a higher rate of secondary AML/MDS in the escalated BEACOPP arm.
  • To reduce acute and long-term toxicity, the GHSG started in the consecutive studies HD12 and HD15 for advanced stage HL to de-escalate BEACOPP by reducing the number of escalated BEACOPP cycles and by applying the baseline dose BEACOPP, a time dense regimen, called BEACOPP-14.

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  • (PMID = 16777701.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; BEACOPP protocol
  • [Number-of-references] 12
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90. Peinert S, Tam CS, Prince HM, Scarlett J, Wolf MM, Januszewicz EH, Westerman D, Seymour JF: Fludarabine based combinations are highly effective as first-line or salvage treatment in patients with Waldenström macroglobulinemia. Leuk Lymphoma; 2010 Dec;51(12):2188-97
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  • Three heavily pretreated patients subsequently developed AML/MDS (one fatal) at 56, 61, and 91 months post F-based treatment.
  • However, a possible contribution to the cumulative risk of treatment-related MDS/AML requires ongoing monitoring.

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

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  • (PMID = 17118782.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; BEACOPP protocol
  • [Number-of-references] 10
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92. Zharlyganova D, Harada H, Harada Y, Shinkarev S, Zhumadilov Z, Zhunusova A, Tchaizhunusova NJ, Apsalikov KN, Kemaikin V, Zhumadilov K, Kawano N, Kimura A, Hoshi M: High frequency of AML1/RUNX1 point mutations in radiation-associated myelodysplastic syndrome around Semipalatinsk nuclear test site. J Radiat Res; 2008 Sep;49(5):549-55
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  • [Title] High frequency of AML1/RUNX1 point mutations in radiation-associated myelodysplastic syndrome around Semipalatinsk nuclear test site.
  • It is known that bone marrow is a sensitive organ to ionizing radiation, and many patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) have been diagnosed in radiation-treated cases and atomic bomb survivors in Hiroshima and Nagasaki.
  • The AML1/RUNX1 gene has been known to be frequently mutated in MDS/AML patients among atomic bomb survivors and radiation therapy-related MDS/AML patients.
  • In this study, we investigated the AML1 mutations in radiation-exposed patients with MDS/AML among the residents near the Semipalatinsk Nuclear Test Site (SNTS), where the risk of solid cancers and leukemias was increased due to the radiation effects.
  • AML1 mutations were identified in 7 (39%) of 18 radiation-exposed MDS/AML patients.
  • In contrast, no AML1 mutation was found in 13 unexposed MDS/AML cases.
  • The frequency of AML1 mutations in radiation-exposed patients with MDS/AML was significantly higher compared with unexposed patients (p < 0.05).We also found a significant correlation between individual estimated doses and AML1 mutations (p < 0.05).
  • Considering these results, AML1 point mutations might be a useful biomarker that differentiates radio-induced MDS/AML from spontaneous MDS/AML.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Environmental Exposure / analysis. Environmental Exposure / statistics & numerical data. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / genetics. Nuclear Warfare. Radiation Injuries / epidemiology. Radiation Injuries / genetics


93. Chakraborty S, Sun CL, Francisco L, Sabado M, Li L, Chang KL, Forman S, Bhatia S, Bhatia R: Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma. J Clin Oncol; 2009 Feb 10;27(5):791-8
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  • [Title] Accelerated telomere shortening precedes development of therapy-related myelodysplasia or acute myelogenous leukemia after autologous transplantation for lymphoma.
  • PURPOSE: Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complication of autologous hematopoietic stem-cell transplantation (aHCT) for Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL).
  • Here, we investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the development of t-MDS/AML.
  • PATIENTS AND METHODS: A prospective longitudinal cohort was constructed to investigate the sequence of cellular and molecular abnormalities leading to development of t-MDS/AML after aHCT for HL/NHL.
  • This cohort formed the sampling frame for a nested case-control study to compare changes in telomere length in serial blood samples from patients who developed t-MDS/AML with matched controls who did not develop t-MDS/AML.
  • RESULTS: An initial increase in telomere length at day 100 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared with controls.
  • These telomere alterations preceded the onset of t-MDS and were independent of other known risk factors associated with development of t-MDS/AML on multivariate analysis.
  • Additionally, we observed reduced generation of committed progenitors in patients who developed t-MDS/AML, indicating that these telomere alterations were associated with reduced regenerative capacity of hematopoietic stem cells.
  • CONCLUSION: The development of t-MDS/AML after aHCT is associated with and preceded by markedly altered telomere dynamics in hematopoietic cells.
  • Accelerated telomere loss in patients developing t-MDS/AML may reflect increased clonal proliferation and/or altered telomere regulation in premalignant cells.
  • Genetic instability associated with shortened telomeres may contribute to leukemic transformation in t-MDS/AML.


94. Hu J, Shekhter-Levin S, Shaw PH, Bay C, Kochmar S, Surti U: A case of myelodysplastic syndrome with acquired monosomy 7 in a child with a constitutional t(1;19) and a mosaicism for trisomy 21. Cancer Genet Cytogenet; 2005 Jan 1;156(1):62-7
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  • [Title] A case of myelodysplastic syndrome with acquired monosomy 7 in a child with a constitutional t(1;19) and a mosaicism for trisomy 21.
  • A bone marrow aspirate revealed a myelodysplastic syndrome (MDS).
  • It is also possible that the t(1;19) played some role in the development of the MDS.
  • Because acute myelogenous leukemia (AML) and MDS with Down syndrome (DS) have distinct biologic and clinical features, the identification of DS patients with a mild or normal phenotype in the AML/MDS population is of fundamental importance for clinical diagnosis and management.
  • [MeSH-major] Down Syndrome / complications. Monosomy. Mosaicism. Myelodysplastic Syndromes / genetics. Translocation, Genetic


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

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  • (PMID = 20456363.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL079582; United States / NIAID NIH HHS / AI / R24 AI049393; United States / Intramural NIH HHS / / Z99 CA999999; United States / NIAID NIH HHS / AI / 2R24AI049393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS216450; NLM/ PMC2906693
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96. da Costa SV, Roela RA, Junqueira MS, Arantes C, Brentani MM: The role of p38 mitogen-activated protein kinase in serum-induced leukemia inhibitory factor secretion by bone marrow stromal cells from pediatric myelodysplastic syndromes. Leuk Res; 2010 Apr;34(4):507-12
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  • [Title] The role of p38 mitogen-activated protein kinase in serum-induced leukemia inhibitory factor secretion by bone marrow stromal cells from pediatric myelodysplastic syndromes.
  • Stromal cells from pediatric myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) associated with MDS (MDS-AML) present high expression of leukemia inhibitor factor (LIF).
  • We demonstrated using mitogen-activated protein kinase (MAPK) inhibitors that in stromal cells from pediatric MDS and MDS-AML, p38MAPK was critical in serum-induced secretion of LIF.
  • The serum induction of phosphorylated p38MAPK form was observed only in stromal cells from healthy children, whereas in MDS and MDS-AML basal levels were maintained suggesting constitutive p38MAPK activation.
  • Our study suggested the possible importance in pediatric MDS of p38MAPK signaling pathway which may be a future therapeutic target.
  • [MeSH-major] Bone Marrow Cells / secretion. Leukemia Inhibitory Factor / secretion. Myelodysplastic Syndromes / metabolism. Stromal Cells / secretion. p38 Mitogen-Activated Protein Kinases / physiology

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19913910.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Anthracenes; 0 / Flavonoids; 0 / Imidazoles; 0 / LIF protein, human; 0 / Leukemia Inhibitory Factor; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / SB 203580; 0 / anthra(1,9-cd)pyrazol-6(2H)-one; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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97. Guillem V, Tormo M: Influence of DNA damage and repair upon the risk of treatment related leukemia. Leuk Lymphoma; 2008 Feb;49(2):204-17
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  • [Title] Influence of DNA damage and repair upon the risk of treatment related leukemia.
  • Therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) are malignancies occurring after exposure to chemotherapy and/or radiotherapy.
  • Several studies have addressed cumulative dose, dose intensity and exposure to specific agents of preceding cytotoxic therapy in relation to the risk of developing such leukemia.
  • Since only a small percentage of patients exposed to cytotoxic therapy develop t-MDS/AML, it has been suggested that some genetic predisposition may be involved, specifically associated to polymorphisms in certain genes involved in chemotherapy/radiotherapy response - fundamentally genes intervening in drug detoxification and DNA synthesis and repair.
  • A review is made of the genetic studies related to t-MDS/AML predisposition, focusing on the mechanistic findings of how specific chemotherapeutic drug exposure produces DNA damage and induces the chromosomal abnormalities characteristic of t-MDS/AML, the molecular pathways involved in repairing such drug induced damage, and the way in which they influence t-MDS/AML genesis.
  • Specific issues are (a) the interaction of topoisomerase II inhibitors, alkylators and antimetabolite drugs with DNA repair mechanisms and their impact on t-MDS/AML leukemogenicity and (b) the influence of DNA polymorphisms in genes involved in DNA repair, drug metabolization and nucleotide synthesis, paying special attention to the relevance of folate metabolism.
  • Finally, we discuss some aspects relating to study design that are most suitable for characterizing associations between drug exposure and genotypes related to t-MDS/AML risk - stressing the importance of the inclusion of chemotherapy-exposed control groups.

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  • (PMID = 18231906.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 111
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98. Omidvar N, Kogan S, Beurlet S, le Pogam C, Janin A, West R, Noguera ME, Reboul M, Soulie A, Leboeuf C, Setterblad N, Felsher D, Lagasse E, Mohamedali A, Thomas NS, Fenaux P, Fontenay M, Pla M, Mufti GJ, Weissman I, Chomienne C, Padua RA: BCL-2 and mutant NRAS interact physically and functionally in a mouse model of progressive myelodysplasia. Cancer Res; 2007 Dec 15;67(24):11657-67
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  • Myelodysplastic syndromes (MDS) are clonal stem cell hematologic disorders that evolve to acute myeloid leukemia (AML) and thus model multistep leukemogenesis.
  • Activating RAS mutations and overexpression of BCL-2 are prognostic features of MDS/AML transformation.
  • Using NRASD12 and BCL-2, we created two distinct models of MDS and AML, where human (h)BCL-2 is conditionally or constitutively expressed.
  • Our novel transplantable in vivo models show that expression of hBCL-2 in a primitive compartment by mouse mammary tumor virus-long terminal repeat results in a disease resembling human MDS, whereas the myeloid MRP8 promoter induces a disease with characteristics of human AML.
  • Expanded leukemic stem cell (Lin(-)/Sca-1(+)/c-Kit(+)) populations and hBCL-2 in the increased RAS-GTP complex within the expanded Sca-1(+) compartment are described in both MDS/AML-like diseases.
  • When hBCL-2 is switched off with doxycycline in the MDS mice, partial reversal of the phenotype was observed with persistence of bone marrow blasts and tissue infiltration as RAS recruits endogenous mouse (m)BCL-2 to remain active, thus demonstrating the role of the complex in the disease.
  • This represents the first in vivo progression model of MDS/AML dependent on the formation of a BCL-2:RAS-GTP complex.
  • The colocalization of BCL-2 and RAS in the bone marrow of MDS/AML patients offers targeting either oncogene as a therapeutic strategy.
  • [MeSH-major] Genes, bcl-2. Genes, ras. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Animals. Bone Marrow Transplantation. Cell Transplantation. Colony-Forming Units Assay. Disease Models, Animal. Disease Progression. Immunophenotyping. Leukemia / genetics. Leukemia, Myeloid / genetics. Mice. Mice, Transgenic. Microscopy, Confocal. Spleen


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

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  • (PMID = 16467864.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ligands; 0 / RUNX1 protein, human; 62229-50-9 / Epidermal Growth Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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100. Tavernier E, Le QH, de Botton S, Dhédin N, Bulabois CE, Reman O, Vey N, Lhéritier V, Dombret H, Thomas X: Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials. Cancer; 2007 Dec 15;110(12):2747-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials.
  • BACKGROUND: Second malignant neoplasms are a serious complication after successful treatment of childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: By February 2005 secondary or concomitant neoplasms were documented in 23 patients, including 9 acute myeloid leukemias (AML) or myelodysplasias (MDS), 4 non-Hodgkin lymphomas (NHL), 5 skin tumors, and 5 other solid tumors (1 lung cancer, 1 tongue carcinoma, 1 thymoma, 1 condrosarcoma, 1 histiocytosis).
  • However, the median OS in patients developing AML/MDS was 5.7 months.
  • [MeSH-major] Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology






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