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1. 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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2. 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


3. Andersen MK, Christiansen DH, Pedersen-Bjergaard J: Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML. Leukemia; 2005 Feb;19(2):197-200
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  • [Title] Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML.
  • Amplification or duplication of the AML1 gene at chromosome band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%).
  • All three patients were older, had previously received therapy with alkylating agents without topoisomerase II inhibitors, had complex karyotypes including abnormalities of chromosomes 5 or 7, and presented acquired point mutations of the TP53 gene.
  • The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics


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4. Asou N, Iwanaga E, Nanri T, Mitsuya H: Successful treatment with low-dose imatinib mesylate of therapy-related myeloid neoplasm harboring TEL-PDGFRB in a patient with acute promyelocytic leukemia. Haematologica; 2010 Sep;95(9):e1
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  • [Title] Successful treatment with low-dose imatinib mesylate of therapy-related myeloid neoplasm harboring TEL-PDGFRB in a patient with acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Neoplasms, Second Primary / drug therapy. Oncogene Proteins, Fusion / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage

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  • (PMID = 20807977.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / TEL-PDGFRbeta fusion protein, human; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC2930974
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5. 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


6. 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 gives about 60% overall survival rate (OS) after 5 years, a 30% of persistent complete remission and a 20% early death rate related to failure.
  • 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.
  • At diagnosis, 6% of AA had an abnormal karyotype using conventional cytogenetic not related to any time-to-event.
  • Two patients displayed a cytogenetic conversion related to the occurrence of secondary malignancies.
  • 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.
  • [MeSH-major] Androgens / administration & dosage. Anemia, Aplastic / drug therapy. Antilymphocyte Serum / administration & dosage. Immunosuppressive Agents / administration & dosage


7. 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).
  • However, it is unclear whether currently accepted cytogenetic risk groups, which were established for patients treated mostly with standard therapy, are optimally discriminating for patients undergoing HSCT.
  • Also, the impact of cytogenetics in the growing population of patients with therapy-related disease has not been completely elucidated.
  • In this study, we retrospectively analyzed data on 556 patients with AML or MDS transplanted at our institution.
  • We then applied this grouping scheme to the 80 patients with therapy-related disease.
  • Our proposed 3-group cytogenetic classification outperformed the established grouping schemes for both de novo and therapy-related disease.
  • After accounting for cytogenetics, patients with therapy-related AML or MDS had an equivalent outcome to those with de novo disease.
  • This study demonstrates the impact of cytogenetics on the risk of relapse and death for patients with both de novo and therapy-related disease undergoing transplantation; it also emphasizes the necessity of using cytogenetics to stratify patients entering clinical trials, and provides a system for doing so, which can be validated in a multi-institutional database.

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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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8. 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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9. Kim MK, Cho HS, Bae YK, Lee KH, Ki CS, Lee ST, Hyun MS: Therapy-related myeloid neoplasm in a patient with TP53 mutation: a dilemma in allogeneic stem cell transplant. Leuk Lymphoma; 2010 Jun;51(6):1144-7
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  • [Title] Therapy-related myeloid neoplasm in a patient with TP53 mutation: a dilemma in allogeneic stem cell transplant.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Mutation. Neoplasms, Second Primary / diagnosis. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Acute Disease. Adult. Base Sequence. Diagnosis, Differential. Female. Humans. Risk Assessment. Sequence Analysis, DNA. Stem Cell Transplantation / methods. Transplantation, Homologous

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  • (PMID = 20443677.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53
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10. Vardiman JW: The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasms. Chem Biol Interact; 2010 Mar 19;184(1-2):16-20
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  • [Title] The World Health Organization (WHO) classification of tumors of the hematopoietic and lymphoid tissues: an overview with emphasis on the myeloid neoplasms.
  • The World Health Organization (WHO) classification of myeloid and lymphoid neoplasms utilizes morphology, immunophenotype, genetics and clinical features to define disease entities of clinical significance.
  • In general, the classification stratifies neoplasms according to their lineage (myeloid, lymphoid, histiocytic/dendritic) and distinguishes neoplasms of precursor cells from those comprised of functionally mature cells.
  • Five major subgroups of myeloid neoplasms are recognized based mainly on their degree of maturation and biologic properties: myeloproliferative neoplasms (MPNs) which are comprised primarily of mature cells with effective proliferation; myeloid (and lymphoid) neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB and FGFR1, defined largely by the finding of significant eosinophilia and specific genetic abnormalities; myelodysplastic/myeloproliferative neoplasms (MDS/MPN), comprised mainly of mature cells with both effective and ineffective proliferation of various lineages; myelodysplastic syndromes (MDS), in which immature and mature cells are found with abnormal, dysplastic and ineffective maturation, and acute myeloid leukemia (AML), comprised of precursor cells with impaired maturation.
  • Genetic abnormalities play an important role as diagnostic criteria for further sub-classification of some myeloid neoplasms, particularly of AML.
  • Although therapy-related MDS and AML (t-MDS/AML) often have genetic defects identical to those found in de novo AML and de novo MDS, they are classified separately from de novo AML and MDS in order to emphasize their unique clinical and biologic properties.
  • [MeSH-major] Leukemia, Myeloid, Acute / classification. Lymphoma / classification. Myelodysplastic Syndromes / classification. Myelodysplastic-Myeloproliferative Diseases / classification. Myeloproliferative Disorders / classification


11. Alvarez S, Cigudosa JC: Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel. Hematol Oncol; 2005 Mar;23(1):18-25
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  • [Title] Gains, losses and complex karyotypes in myeloid disorders: a light at the end of the tunnel.
  • Complex karyotypes are seen in approximately 15% of de novo MDS/AML and in up to 50% of therapy-related MDS/AML.
  • On the basis of the available data from several studies of AML with complex karyotypes, similar findings on recurrent breakpoints and frequently lost and gained chromosomal regions have been observed.
  • Interestingly, this non-random pattern of DNA gains and losses, that characterizes AML cases with complex karyotypes, affects the gene expression pattern, and a specific expression profile, characterized by the upregulation of genes involved in the DNA repair and chromosome segregation pathways, has been recently reported.
  • Therefore, a comprehensive genome-wide analysis of patients with AML or MDS with complex karyotypes has led to a better characterization of chromosomal aberrations.
  • [MeSH-major] Chromosomes, Human / genetics. Gene Expression Regulation, Leukemic / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosome Segregation / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Core Binding Factor Alpha 2 Subunit / metabolism. DNA Repair / genetics. Gene Amplification / genetics. Gene Expression Profiling / methods. Genome, Human / genetics. Histone-Lysine N-Methyltransferase. Humans. Karyotyping. Myeloid-Lymphoid Leukemia Protein / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Neoplasm, Residual / genetics. Neoplasm, Residual / metabolism. Neoplasm, Residual / therapy. Risk Factors

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  • [Copyright] Copyright 2005 John Wiley & Sons, Ltd.
  • (PMID = 16142824.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / RUNX1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 53
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12. Herry A, Douet-Guilbert N, Morel F, Le Bris MJ, Morice P, Abgrall JF, Berthou C, De Braekeleer M: Evaluation of chromosome 5 aberrations in complex karyotypes of patients with myeloid disorders reveals their contribution to dicentric and tricentric chromosomes, resulting in the loss of critical 5q regions. Cancer Genet Cytogenet; 2007 Jun;175(2):125-31
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  • [Title] Evaluation of chromosome 5 aberrations in complex karyotypes of patients with myeloid disorders reveals their contribution to dicentric and tricentric chromosomes, resulting in the loss of critical 5q regions.
  • Dicentric chromosomes have often been observed in complex karyotypes in previously reported studies of therapy-related myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
  • Dicentric and tricentric chromosomes were identified in 21 patients (9 MDS and 12 AML) among the 133 consecutive MDS/AML patients (17%) who had a structural or numerical aberration of chromosome 5 using conventional cytogenetic analysis.
  • Dicentric and tricentric chromosomes involving chromosome 5 are frequently observed in complex karyotypes among patients with de novo or therapy-related MDS/AML.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Deletion. Female. Humans. Karyotyping. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged


13. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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14. Heller M, Provan D, Amess JA, Dixon-McIver A: Myelodysplastic syndrome associated with trisomy 2. Clin Lab Haematol; 2005 Aug;27(4):270-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Myelodysplastic syndrome associated with trisomy 2.
  • Clinical course and cytogenetic analysis suggest that myelodysplasia (MDS) is one step in a multistep model of malignant transformation of haematopoietic stem cells to acute myeloid leukaemia (AML).
  • We report a further case of MDS associated with trisomy 2, and comment on the significance of the cytogenetic abnormality, which as a sole abnormality only occurs in MDS, but is found in combination with other chromosomal abnormalities in AML.
  • Previous reports on balanced and unbalanced chromosomal abnormalities associated with therapy related MDS and therapy related AML suggest that trisomy 2 is an early chromosomal abnormality in leukaemogenesis.
  • [MeSH-major] Chromosomes, Human, Pair 2 / genetics. Myelodysplastic Syndromes / genetics. Trisomy


15. Ogasawara T, Yasuyama M, Kawauchi K: Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). Am J Hematol; 2005 Jun;79(2):136-41
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  • [Title] Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
  • We describe a patient who developed myelodysplastic syndrome over 2 years after achieving complete remission of acute myeloid leukemia (AML).
  • The patient was treated in July 1998 with anthracycline, etoposide, and behenoyl cytarabine chemotherapy for AML (French-American-British classification, M2; World Health Organization classification, AML with maturation) and achieved complete remission.
  • The patient was diagnosed with high-grade myelodysplastic syndrome (MDS)/refractory anemia with excess blasts (RAEB) subtype.
  • The pancytopenia progressed rapidly, and he died 2 months after the diagnosis of MDS.
  • Therapy-related MDS and AML (t-MDS/t-AML) developing after treatment for acute leukemia is unusual; the primary leukemia associated with most cases of t-MDS/t-AML is acute promyelocytic leukemia (APL).
  • This unusual case suggests that AML excluding APL should be considered a primary hematologic malignancy for t-MDS/t-AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 5. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / chemically induced. Monosomy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics


16. Lin P, Medeiros LJ, Yin CC, Abruzzo LV: Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia. Cancer Genet Cytogenet; 2006 Apr 1;166(1):82-5
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  • [Title] Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia.
  • We identified a reciprocal translocation between chromosomes 3 and 8, with breakpoints at bands 3q26 and 8q24, in five patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML).
  • In three patients, the AML or MDS developed 36, 52, and 57 months following chemotherapy for soft tissue sarcoma, mantle cell lymphoma, and diffuse large B-cell lymphoma, respectively; in these three patients, the neoplasms were considered to be therapy-related.
  • We conclude that the t(3;8)(q26;q24) is a recurrent translocation associated with therapy-related MDS/AML or de novo AML, and is frequently associated with monosomy 7.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 3 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasm Recurrence, Local / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Female. Humans. Karyotyping. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Male. Middle Aged. Sarcoma / drug therapy. Sarcoma / pathology


17. 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


18. Greco M, D'Alò F, Scardocci A, Criscuolo M, Fabiani E, Guidi F, Di Ruscio A, Migliara G, Pagano L, Fianchi L, Chiusolo P, Hohaus S, Leone G, Voso MT: Promoter methylation of DAPK1, E-cadherin and thrombospondin-1 in de novo and therapy-related myeloid neoplasms. Blood Cells Mol Dis; 2010 Oct 15;45(3):181-5
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  • [Title] Promoter methylation of DAPK1, E-cadherin and thrombospondin-1 in de novo and therapy-related myeloid neoplasms.
  • DNA methylation is one of the major epigenetic changes in human cancers, leading to silencing of tumor suppressor genes, with a pathogenetic role in tumor development and progression in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML).
  • Methylation of key promoter regions, induced by cytotoxic therapy together with complex genetic changes, is important in the biology of therapy-related myeloid neoplasms (t-MN).
  • We were interested in the characterization of the methylation pattern of AML and MDS de novo and therapy-related.
  • There were 105 MDS, 208 de novo AML and 72 t-MN (45 MDS and 27 AML).
  • In patients with MDS, there were no associations between hypermethylation and clinical characteristics, including IPSS score, WHO classification and cytogenetics.
  • DAPK1 was more frequently methylated in t-MDS/AML when compared to de novo MDS and AML (39% vs 15.3% and 24.4%, p=0.0001), while methylation of CDH1 was similar in t-MDS/AML and AML (51% and 53.4%), but less frequent in de novo MDS (29%) (p=0.003).
  • In the t-MDS/AML group, we found that the methylation pattern appeared to be related to the primary tumor, with DAPK1 more frequently methylated in patients with a previous lymphoproliferative disease (75% vs 32%, p=0.006).
  • TSP1 hypermethylation was rare and not characteristic of t-MDS/AML.
  • In 177 patients studied for concurrent methylation of several promoters, t-MN and AML de novo were significantly more frequently hypermethylated in 2 or more promoter regions than de novo MDS (20% vs 12.4%, p<0.001).
  • Chemotherapy and individual genetic predisposition have a role in t-MDS/AML development, the identification of specific epigenetic modifications may explain complexity and genomic instability of these diseases and give the basis for targeted-therapy.
  • The significant association with previous malignancy subtypes may underlie a likely susceptibility to methylation of specific targets and a role for constitutional epimutations as predisposing factors for the development of therapy-related myeloid neoplasm.
  • [MeSH-major] Apoptosis Regulatory Proteins. Cadherins. Calcium-Calmodulin-Dependent Protein Kinases. DNA Methylation. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Neoplasms, Second Primary / metabolism. Promoter Regions, Genetic. Thrombospondin 1

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20655775.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CDH1 protein, human; 0 / Cadherins; 0 / Thrombospondin 1; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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