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1. Kröger N, Brand R, van Biezen A, Zander A, Dierlamm J, Niederwieser D, Devergie A, Ruutu T, Cornish J, Ljungman P, Gratwohl A, Cordonnier C, Beelen D, Deconinck E, Symeonidis A, de Witte T, Myelodysplastic Syndromes Subcommittee of The Chronic Leukaemia Working Party of European Group for Blood and Marrow Transplantation (EBMT): Risk factors for therapy-related myelodysplastic syndrome and acute myeloid leukemia treated with allogeneic stem cell transplantation. Haematologica; 2009 Apr;94(4):542-9
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  • [Title] Risk factors for therapy-related myelodysplastic syndrome and acute myeloid leukemia treated with allogeneic stem cell transplantation.
  • BACKGROUND: After successful treatment of malignant diseases, therapy-related myelodysplastic syndrome and acute myeloid leukemia have emerged as significant problems.
  • DESIGN AND METHODS: The aim of this study was to investigate outcome and risk factors in patients with therapy-related myelodysplastic syndrome or acute myeloid leukemia who underwent allogeneic stem cell transplantation.
  • Between 1981 and 2006, 461 patients with therapy-related myelodysplastic syndrome or acute myeloid, a median age of 40 years and a history of solid tumor (n=163), malignant lymphoma (n=133), or other hematologic diseases (n=57) underwent stem cell transplantation and their data were reported to the European Group for Blood and Marrow Transplantation.
  • In a multivariate analysis significant factors for relapse were not being in complete remission at the time of transplantation (p=0.002), abnormal cytogenetics (p=0.005), higher patients' age (p=0.03) and therapy-related myelodysplastic syndrome (p=0.04), while higher non-relapse mortality was influenced by higher patients' age.
  • CONCLUSIONS: Allogeneic stem cell transplantation can cure patients with therapy-related myelodysplastic syndrome and acute myeloid leukemia and has markedly improved over time.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / therapy


2. 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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3. Lu GH: Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia. Beijing Da Xue Xue Bao; 2005 Feb 18;37(1):10-3
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  • [Title] Clinical cytogenetic diagnosis of therapy-related acute myeloid leukemia.
  • Therapy-related acute myeloid leukemia (tAML) is one of the two forms of secondary acute myeloid leukemia, with one derived from de novo myelodysplastic syndrome (MDS) and the other from exposure to environmental or therapeutic agents such as radiation and toxins.
  • There has been a marked increase in the number of incidences of therapy-related acute myeloid leukemia.
  • In this study, an interesting case with therapy-related myelodysplastic syndrome and acute myeloid leukemia (tMDS/tAML) will be presented.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / diagnosis. Lymphoma, B-Cell / drug therapy. Neoplasms, Second Primary / diagnosis

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  • (PMID = 15719033.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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4. Kwong YL: Azathioprine: association with therapy-related myelodysplastic syndrome and acute myeloid leukemia. J Rheumatol; 2010 Mar;37(3):485-90
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  • [Title] Azathioprine: association with therapy-related myelodysplastic syndrome and acute myeloid leukemia.
  • A recognized carcinogen, azathioprine is also associated with the development of therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/AML).
  • METHODS: In 56 reported cases, azathioprine had been administered for a median of 65 months (range 6-192) to a median cumulative dose of 146 g (range 19-750) before t-MDS/AML developed.
  • RESULTS: In 11 patients, repeated episodes of cytopenias developed during azathioprine therapy, ante-dating the development of t-MDS/AML.
  • These changes were cytogenetic hallmarks of MDS/AML secondary to known leukemogenic agents and radiotherapy.
  • It will be prudent to review the need for azathioprine therapy when unexpected cytopenias occur and prescription has been prolonged.
  • [MeSH-major] Azathioprine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Adult. Aged. Autoimmune Diseases / drug therapy. Female. Graft Rejection / prevention & control. Humans. Immunosuppressive Agents / adverse effects. Immunosuppressive Agents / therapeutic use. Karyotyping. Male. Middle Aged


5. 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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6. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


7. Litzow MR, Tarima S, Pérez WS, Bolwell BJ, Cairo MS, Camitta BM, Cutler CS, de Lima M, Dipersio JF, Gale RP, Keating A, Lazarus HM, Luger S, Marks DI, Maziarz RT, McCarthy PL, Pasquini MC, Phillips GL, Rizzo JD, Sierra J, Tallman MS, Weisdorf DJ: Allogeneic transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia. Blood; 2010 Mar 4;115(9):1850-7
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  • [Title] Allogeneic transplantation for therapy-related myelodysplastic syndrome and acute myeloid leukemia.
  • Therapy-related myelodysplastic syndromes (t-MDSs) and acute myeloid leukemia (t-AML) have a poor prognosis with conventional therapy.
  • We analyzed outcomes in 868 persons with t-AML (n = 545) or t-MDS (n = 323) receiving allogeneic transplants from 1990 to 2004.
  • Treatment-related mortality (TRM) and relapse were 41% (95% confidence interval [CI], 38-44) and 27% (24-30) at 1 year and 48% (44-51) and 31% (28-34) at 5 years, respectively.
  • (3) t-AML not in remission or advanced t-MDS; and (4) donor other than an HLA-identical sibling or a partially or well-matched unrelated donor.


8. Offman J, Gascoigne K, Bristow F, Macpherson P, Bignami M, Casorelli I, Leone G, Pagano L, Sica S, Halil O, Cummins D, Banner NR, Karran P: Repeated sequences in CASPASE-5 and FANCD2 but not NF1 are targets for mutation in microsatellite-unstable acute leukemia/myelodysplastic syndrome. Mol Cancer Res; 2005 May;3(5):251-60
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  • [Title] Repeated sequences in CASPASE-5 and FANCD2 but not NF1 are targets for mutation in microsatellite-unstable acute leukemia/myelodysplastic syndrome.
  • It is widespread among some tumor types, such as colorectal or endometrial carcinoma, but is rarely found in leukemia.
  • Therapy-related acute myeloid leukemia/myelodysplastic syndrome (tAML/MDS) is an exception, and MSI is frequent in tAML/MDS following cancer chemotherapy or organ transplantation.
  • We examined established MSI+ cell lines and tAML/MDS cases for frameshift-like mutations of repetitive sequences in several genes that have known, or suspected, relevance to leukemia.
  • CASPASE-5, an acknowledged frameshift target in MSI+ gastrointestinal tract tumors, was frequently mutated in MSI+ cell lines (67%) and in tAML/MDS (29%).
  • Frameshift-like mutations were also observed in the NF1 and FANCD2 genes that are associated with genetic conditions conferring a predisposition to leukemia.
  • FANCD2 mutations were also common in MSI+ tAML/MDS, although NF1 mutations were not observed.
  • [MeSH-major] Caspases / genetics. Leukemia, Myeloid, Acute / genetics. Microsatellite Repeats / genetics. Mutagenesis / genetics. Myelodysplastic Syndromes / genetics


9. 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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10. Aguilera DG, Vaklavas C, Tsimberidou AM, Wen S, Medeiros LJ, Corey SJ: Pediatric therapy-related myelodysplastic syndrome/acute myeloid leukemia: the MD Anderson Cancer Center experience. J Pediatr Hematol Oncol; 2009 Nov;31(11):803-11
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  • [Title] Pediatric therapy-related myelodysplastic syndrome/acute myeloid leukemia: the MD Anderson Cancer Center experience.
  • Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is a long-term complication of pediatric cancer.
  • We retrospectively studied pediatric t-MDS/AML patients treated at MD Anderson from 1975 to 2007.
  • We also compared those patients to pediatric patients with de novo MDS/AML during this time interval.
  • Among 2589 children with cancer treated at MD Anderson, we identified 22 patients with t-MDS/AML.
  • Patients with t-MDS/AML had a median age of 14 years.
  • Group 2 (n=5) patients received AML-type chemotherapy and a stem cell transplant postremission (n=5).
  • Group 3 (n=4) received a stem cell transplant as salvage therapy.
  • Patients with de novo AML were younger (P=0.001) and higher rates of complete remission (P=0.03), and survival (P<0.0001).
  • Independent factors predicting shorter survival were poor/intermediate-risk cytogenetics (P=0.01), lower hemoglobin level (P=0.0001), and t-MDS/AML (vs. de novo) (P=0.003).
  • Childhood t-MDS/AML has a poor prognosis.
  • Although patients benefited from AML-type induction chemotherapy followed by stem cell transplantation as postremission therapy, effective therapies, and prevention are needed.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Myelodysplastic Syndromes / mortality. Neoplasms, Second Primary / mortality
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Hodgkin Disease / mortality. Hodgkin Disease / therapy. Humans. Male. Osteosarcoma / mortality. Osteosarcoma / therapy. Retrospective Studies. Risk Factors. Sex Factors. Stem Cell Transplantation. Survival Rate. Transplantation, Homologous


11. Kim SJ, Park TS, Lee ST, Song J, Suh B, Kim SH, Jang SJ, Lee CH, Choi JR: Therapy-related myelodysplastic syndrome/acute myeloid leukemia after treatment with temozolomide in a patient with glioblastoma multiforme. Ann Clin Lab Sci; 2009;39(4):392-8
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  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia after treatment with temozolomide in a patient with glioblastoma multiforme.
  • Therapy-related myelodysplastic syndrome and acute leukemia after treatment with temozolomide have rarely been described in the literature.
  • The cases included anaplastic astrocytoma (4 cases), anaplastic oligodendroglioma (2 cases), low grade astrocytoma (2 cases), low grade oligodendroglioma (1 case), and one case of secondary Philadelphia-positive acute lymphoblastic leukemia in a patient with glioblastoma multiforme.
  • Here we report a novel case of therapy-related myelodysplastic syndrome/acute myeloid leukemia associated with der(1;7)(q10;p10) in a glioblastoma multiforme patient treated with temozolomide.
  • Results of bone marrow morphology, chromosome, and fluorescent in situ hybridization (FISH) analyses, as well as the clinical history, strongly suggest a treatment-related etiology in our case.
  • In past reports, karyotypes in cases of therapy-related myelodysplastic syndrome/acute myeloid leukemia mostly demonstrated abnormalities in chromosomes 5 and 7.
  • However, we report a case of temozolomide-related myelodysplastic syndrome/acute myeloid leukemia with der(1;7)(q10;p10), possibly the first reported case, to the authors' knowledge.
  • [MeSH-major] Dacarbazine / analogs & derivatives. Glioblastoma / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Adult. Aged. Biopsy. Bone Marrow Cells / pathology. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Magnetic Resonance Imaging. Male. Middle Aged. Skin / pathology


12. 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


13. 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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14. Arana-Yi C, Block AW, Sait SN, Ford LA, Barcos M, Baer MR: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine. Leuk Res; 2008 Jul;32(7):1043-8
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following treatment of acute myeloid leukemia: possible role of cytarabine.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) have been reported only rarely following treatment of AML.
  • We report five patients treated for de novo AML who developed t-MDS/t-AML, all with chromosome 7 abnormalities, including -7, del(7)(q22q36) and del(7)(p11.22p22).
  • These cases further document t-MDS/t-AML as a complication of therapy for AML.
  • Presence of chromosome 7 abnormalities in patients with and without prior alkylating agent therapy suggests possible association with the antimetabolite cytarabine.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytarabine / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / drug therapy


15. 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


16. Woodard P, Barfield R, Hale G, Horwitz E, Leung W, Ribeiro R, Rubnitz J, Srivistava DK, Tong X, Yusuf U, Raimondi S, Pui CH, Handgretinger R, Cunningham JM: Outcome of hematopoietic stem cell transplantation for pediatric patients with therapy-related acute myeloid leukemia or myelodysplastic syndrome. Pediatr Blood Cancer; 2006 Dec;47(7):931-5
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  • [Title] Outcome of hematopoietic stem cell transplantation for pediatric patients with therapy-related acute myeloid leukemia or myelodysplastic syndrome.
  • BACKGROUND: Therapy-related myelodysplastic syndrome (t-MDS) and acute myeloid leukemia (t-AML) carry a poor prognosis.
  • PROCEDURE: The effects of demographic, donor, and disease-related factors were analyzed to determine their effects on overall and disease-free survival (OS, DFS), relapse, and non-relapse mortality (NRM).
  • RESULTS: OS and DFS for t-AML and t-MDS were similar.
  • The 1-year cumulative risk of grade III-IV acute graft-versus-host disease (GVHD) and relapse were 23.7 +/- 7.0% and 18.7 +/- 6.5%, respectively.
  • The percentage of pre-transplant bone marrow (BM) blasts was positively associated with relapse (P = 0.05), while the percentage of BM blasts at diagnosis of therapy-related disease tended to associate with NRM (P = 0.07).
  • NRM was higher among patients who did not develop acute GVHD as compared to those with grade 1-2 acute GVHD (69.2 +/- 14.2% vs. +/- 12.7%, respectively), while NRM was 100% in patients with grade III-IV acute GVHD (P = 0.007).
  • High rates of NRM negatively impact the outcome of allogeneic HSCT for children with t-AML and t-MDS.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy


17. Orazi A: Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases. Pathobiology; 2007;74(2):97-114
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  • [Title] Histopathology in the diagnosis and classification of acute myeloid leukemia, myelodysplastic syndromes, and myelodysplastic/myeloproliferative diseases.
  • In spite of the impressive advances in the area of molecular pathology, bone marrow morphology remains the diagnosis cornerstone to identify the various subtypes of myeloid neoplasms.
  • Particular emphasis is being given to the correct identification of cases of myeloid neoplasms associated with myelofibrosis and for which the bone marrow biopsy represents the only available diagnostic mean.
  • Such cases include two subtypes of acute myeloid leukemia which typically cause diagnostic difficulties: acute megakaryoblastic leukemia and acute panmyelosis with myelofibrosis (acute myelosclerosis).
  • Acute myeloid leukemia with multilineage dysplasia, therapy-related myelodysplastic syndrome/therapy-related acute myeloid leukemia and de novo myelodysplastic syndromes (MDS) will also be discussed.
  • In MDS, in particular, bone marrow biopsy may help in confirming a suspected diagnosis by excluding reactive conditions in which dyshematopoietic changes may also be observed.
  • Among the alterations detected by bone marrow biopsy, a prognostically important finding is the presence of aggregates or clusters of immature myeloid precursor cells (myeloblasts and promyelocytes).
  • These can also be identified by immunohistochemistry with CD34, an antigen expressed in progenitor and early precursor marrow cells, which can be used to demonstrate pathological accumulations of blasts in aggressive subtypes of myeloid neoplasms.
  • Immunohistologic analysis is especially helpful in cases of MDS with fibrosis and cases with hypocellular marrows (hypoplastic MDS).
  • Finally, the important group of the myelodysplastic/myeloproliferative disorders can only be accurately categorized by a careful multiparametric approach in which the bone marrow biopsy exerts a pivotal role.
  • [MeSH-major] Bone Marrow / pathology. Leukemia, Myeloid / diagnosis. Myelodysplastic Syndromes / diagnosis. Myeloproliferative Disorders / diagnosis
  • [MeSH-minor] Acute Disease. Antigens, CD34 / analysis. Antineoplastic Agents / adverse effects. Biopsy / methods. Diagnosis, Differential. Humans. Immunohistochemistry. Leukemia, Megakaryoblastic, Acute / diagnosis. Leukemia, Megakaryoblastic, Acute / pathology. Primary Myelofibrosis / diagnosis. Primary Myelofibrosis / pathology. Prognosis. Reticulin / analysis


18. Carney DA, Westerman DA, Tam CS, Milner A, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Ritchie D, Came N, Seymour JF: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following fludarabine combination chemotherapy. Leukemia; 2010 Dec;24(12):2056-62
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following fludarabine combination chemotherapy.
  • Fludarabine combination chemotherapy achieves high response rates in chronic lymphocytic leukemia (CLL) and indolent lymphoma.
  • The aim of this study was to investigate the incidence and characteristics of treatment-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) after treatment with fludarabine in combination for lymphoproliferative disorders and identify risk factors for its development.
  • In all, 19 cases of t-MDS/AML have been identified for an overall rate of 10.8%.
  • Median overall survival post-t-MDS/AML diagnosis was 11 months.
  • Patients developing t-MDS/AML included 11/54 with follicular lymphoma (FL) (crude rate 20.4%), 5/82 with CLL (6.1%) and 3/24 with Waldenstrom macroglobulinemia or marginal zone lymphoma (12.5%).
  • Of the eleven patients (6.3%) who received mitoxantrone with their first fludarabine combination, four (36.4%) developed t-MDS/AML (P=0.007).
  • There was a trend toward prior cytotoxic therapy increasing the risk for t-MDS/AML (P=0.067).
  • Fludarabine combination chemotherapy is associated with a moderate risk of t-MDS/AML particularly when combined with mitoxantrone.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Vidarabine / analogs & derivatives


19. Roboz GJ, Bennett JM, Coleman M, Ritchie EK, Furman RR, Rossi A, Jhaveri K, Feldman EJ, Leonard JP: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following initial treatment with chemotherapy plus radioimmunotherapy for indolent non-Hodgkin lymphoma. Leuk Res; 2007 Aug;31(8):1141-4
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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following initial treatment with chemotherapy plus radioimmunotherapy for indolent non-Hodgkin lymphoma.
  • Radioimmunotherapy (RIT) has become an important part of treatment for relapsed patients and tositumomab/lodine I-131 tositumomab is a promising regimen currently being incorporated into first-line therapy.
  • While treatment-related myelodysplasia (tMDS) and acute myeloid leukemia (tAML) are well-known, poor-prognosis complications of conventional chemotherapy and radiation therapy, they have not been previously observed as a consequence of initial treatment with RIT-based regimens.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Lymphoma, Non-Hodgkin / drug therapy. Myelodysplastic Syndromes / chemically induced. Radioimmunotherapy / adverse effects
  • [MeSH-minor] Adult. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Iodine Radioisotopes. Male. Middle Aged


20. Czader M, Orazi A: Therapy-related myeloid neoplasms. Am J Clin Pathol; 2009 Sep;132(3):410-25
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  • [Title] Therapy-related myeloid neoplasms.
  • Session 5 of 2007 Workshop of the Society for Hematopathology/European Association for Haematopathology focused on therapy-related myeloid neoplasms.
  • We highlight common diagnostic issues such as the differentiation between therapy-related myelodysplastic syndrome and therapy-related acute erythroid leukemia.
  • As similar therapeutic interventions are frequently considered for patients with either of these diagnoses, in the current World Health Organization classification, regardless of morphologic presentation, therapy-related myeloid neoplasms are considered together as a unique clinicopathologic syndrome of therapy-related myelodysplastic syndrome/acute myeloid leukemia.
  • Nevertheless, recognition of the diverse morphologic features is crucial as bone marrow morphologic examination remains the first and important step of patient evaluation.
  • We also present examples of therapy-related acute myeloid leukemias with recurrent cytogenetic abnormalities.
  • [MeSH-major] Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary

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  • (PMID = 19687318.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 97
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21. 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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  • (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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22. 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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23. 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

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  • (PMID = 17556068.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. 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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25. 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


26. 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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27. Bolufer P, Collado M, Barragan E, Calasanz MJ, Colomer D, Tormo M, González M, Brunet S, Batlle M, Cervera J, Sanz MA: Profile of polymorphisms of drug-metabolising enzymes and the risk of therapy-related leukaemia. Br J Haematol; 2007 Feb;136(4):590-6
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  • [Title] Profile of polymorphisms of drug-metabolising enzymes and the risk of therapy-related leukaemia.
  • Therapy-related acute myeloid leukaemia/myelodysplastic syndrome (t-AML/t-MDS) results from an impaired ability to detoxify chemotherapeutic drugs or repair drug-induced genetic damage caused by genetic polymorphisms in enzymes involved in the metabolism of drugs.
  • We analysed the prevalence of genetic polymorphisms of CYP1A1*2A(T6235C), CYP2E1*5B(C-1019T), CYP3A4*1B(A-290G), del{GSTT1}, del{GSTM1}, NQO1*2(C609T), MTHFR(C677T) and TYMS 2R/3R in 78 t-AML/t-MDS and 458 normal individuals (control group, CG) using real-time and conventional polymerase chain reaction (PCR)-based methods.
  • The incidences of polymorphisms among t-AML/t-MDS patients and CG individuals were similar.
  • However, a polymorphism profile consisting of CYP1A1*2A, del{GSTT1} and NQO1*2 strongly modified the risk of t-AML/t-MDS.
  • The absence of all three polymorphisms decreased the risk of t-AML/t-MDS 18-fold (odds ratio (OR) = 0.054, 95% confidence interval (CI) = 0.005-0.63, P = 0.02), whereas the presence of only NQO1*2 or all three polymorphisms enhanced the risk of t-AML/t-MDS (OR = 2.09, 95% CI = 1.08-4.03, P = 0.03 and OR = 18.42, 95% CI = 1.59-212.76, P = 0.02 respectively).
  • Thus, the profiles of genetic polymorphisms of drug-metabolising enzymes might explain the increased risk to t-AML/t-MDS observed in some patients treated with polychemotherapy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytochrome P-450 CYP1A1 / genetics. Female. Genetic Predisposition to Disease. Genotype. Glutathione Transferase / genetics. Humans. Inactivation, Metabolic / genetics. Infant. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / enzymology. Myelodysplastic Syndromes / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasm Proteins / genetics. Retrospective Studies

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  • (PMID = 17367411.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
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28. Kröger N, Brand R, van Biezen A, Cahn JY, Slavin S, Blaise D, Sierra J, Zander A, Niederwieser D, de Witte T, Myelodysplastic Syndromes Subcommittee of The Chronic Leukaemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT): Autologous stem cell transplantation for therapy-related acute myeloid leukemia and myelodysplastic syndrome. Bone Marrow Transplant; 2006 Jan;37(2):183-9
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  • [Title] Autologous stem cell transplantation for therapy-related acute myeloid leukemia and myelodysplastic syndrome.
  • We report the results of 65 patients with treatment-related myelodysplastic syndrome (MDS)/acute myelogenous leukemia (AML) who were transplanted from an autograft and reported to the EBMT.
  • The primary disease was solid tumors (n = 37), Hodgkin's disease (n = 13), non-Hodgkin's lymphoma (n = 10), acute lymphoblastic leukemia (n = 2) or myeloproliferative syndromes (n = 3).
  • The types of MDS were as follows: RAEB (n = 1; 2%), RAEB-t (n = 3; 5%), or AML (n = 56; 87%).
  • The cumulative incidence of relapse was 58% (95% CI: 44-72%) and of treatment-related mortality 12% (95% CI: 6-38%).
  • Furthermore, age beyond 40 years resulted in a higher treatment-related mortality (47 vs 7%; P = 0.01).
  • Autologous transplantation may cure a substantial number of patients with treatment-related MDS/AML, especially if they are in CR1 and of younger age.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / mortality. Neoplasms, Second Primary / therapy. Stem Cell Transplantation


29. 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

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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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30. 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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  • [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


31. Leone G, Pagano L, Ben-Yehuda D, Voso MT: Therapy-related leukemia and myelodysplasia: susceptibility and incidence. Haematologica; 2007 Oct;92(10):1389-98
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  • [Title] Therapy-related leukemia and myelodysplasia: susceptibility and incidence.
  • Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is an increasingly recognized treatment complication in patients treated with radiotherapy or chemotherapy for previous hematologic malignancies or solid tumors.
  • Chromosome 7 and/or 5 losses or deletions are typical of alkylating agent-induced AML, while development of t-AML with balanced translocations involving chromosome bands 11q23 and 21q22 has been related to previous therapy with drugs targeting DNA-topoisomerase II.
  • Their combination may significantly increase the risk of t-MDS/AML.
  • Among patients with hematologic malignancies, long-term survivors of Hodgkin's lymphoma are exposed to an increased risk of t-MDS/AML, particularly when receiving MOPP-based, and escalated BEACOPP regimens, and when alkylators are combined with radiotherapy.
  • Patients with Hodgkin's and non-Hodgkin's lymphoma are at highest risk when total body irradiation followed by autologous stem cell transplantation is used as rescue or consolidation therapy.
  • The addition of granulocyte-colony-stimulating factor and radiotherapy plays a significant role in t-AML following treatment of children with acute lymphoblastic leukemia.
  • In non-hematologic malignancies, treatment for breast cancer and germ-cell tumors has been associated with a 1-5% lifetime risk of both lymphoid as well as myeloid leukemia.
  • In all cases the risk of t-MDS/AML drops sharply by 10 years after treatment.
  • [MeSH-major] Disease Susceptibility. Drug-Related Side Effects and Adverse Reactions. Leukemia / chemically induced. Leukemia / complications. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / complications. Radiotherapy / adverse effects


32. 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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33. 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


34. Godley LA, Larson RA: Therapy-related myeloid leukemia. Semin Oncol; 2008 Aug;35(4):418-29
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  • [Title] Therapy-related myeloid leukemia.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) are thought to be the direct consequence of mutational events induced by chemotherapy, radiation therapy, immunosuppressive therapy, or a combination of these modalities, given for a pre-existing condition.
  • The outcomes for these patients have been poor historically compared to people who develop de novo AML.
  • The spectrum of cytogenetic abnormalities in t-AML is similar to de novo AML, but the frequency of unfavorable cytogenetics, such as a complex karyotype or deletion or loss of chromosomes 5 and/or 7, is considerably higher in t-AML.
  • Survival varies according to cytogenetic risk group in t-AML patients, with better outcomes being observed in those with favorable-risk karyotypes.
  • A deeper understanding of the factors that predispose patients to the development of therapy-related myeloid leukemia would help clinicians monitor patients more carefully after treatment for a primary condition.

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  • (PMID = 18692692.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA 14599; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / P30 CA014599-30; United States / NCI NIH HHS / CA / CA 40046; United States / NCI NIH HHS / CA / CA014599-30; United States / NCI NIH HHS / CA / P01 CA040046-14; United States / NCI NIH HHS / CA / CA040046-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 51
  • [Other-IDs] NLM/ NIHMS66055; NLM/ PMC2600445
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35. Qian Z, Joslin JM, Tennant TR, Reshmi SC, Young DJ, Stoddart A, Larson RA, Le Beau MM: Cytogenetic and genetic pathways in therapy-related acute myeloid leukemia. Chem Biol Interact; 2010 Mar 19;184(1-2):50-7
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  • [Title] Cytogenetic and genetic pathways in therapy-related acute myeloid leukemia.
  • Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) are late complications of cytotoxic therapy used in the treatment of malignant diseases.
  • The most common subtype of t-AML ( approximately 75% of cases) develops after exposure to alkylating agents, and is characterized by loss or deletion of chromosome 5 and/or 7 [-5/del(5q), -7/del(7q)], and a poor outcome (median survival 8 months).
  • In the University of Chicago's series of 386 patients with t-MDS/t-AML, 79 (20%) patients had abnormalities of chromosome 5, 95 (25%) patients had abnormalities of chromosome 7, and 85 (22%) patients had abnormalities of both chromosomes 5 and 7. t-MDS/t-AML with a -5/del(5q) is associated with a complex karyotype, characterized by trisomy 8, as well as loss of 12p, 13q, 16q22, 17p (TP53 locus), chromosome 18, and 20q.
  • In addition, this subtype of t-AML is characterized by a unique expression profile (higher expression of genes) involved in cell cycle control (CCNA2, CCNE2, CDC2), checkpoints (BUB1), or growth (MYC), loss of expression of IRF8, and overexpression of FHL2.
  • Haploinsufficiency of the RPS14, EGR1, APC, NPM1, and CTNNA1 genes on 5q has been implicated in the pathogenesis of MDS/AML.
  • In previous studies, we determined that Egr1 acts by haploinsufficiency and cooperates with mutations induced by alkylating agents to induce myeloid leukemias in the mouse.
  • Identifying the genetic pathways leading to t-AML will provide new insights into the underlying biology of this disease, and may facilitate the identification of new therapeutic targets.

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 19958752.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / P30 CA014599; United States / NCI NIH HHS / CA / R01 CA140979; United States / NCI NIH HHS / CA / CA14599
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Ireland
  • [Number-of-references] 38
  • [Other-IDs] NLM/ NIHMS167239; NLM/ PMC4642715
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36. Shim H, Chi HS, Jang S, Seo EJ, Park CJ, Lee JH, Lee JH, Lee KH: Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor. Korean J Hematol; 2010 Sep;45(3):177-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related acute leukemia in breast cancer patients: twelve cases treated with a topoisomerase inhibitor.
  • BACKGROUND: Therapy-related myeloid neoplasm (t-MN) is a distinct class of acute myeloid leukemia (AML) in the World Health Organization (WHO) classification.
  • Both AML and acute lymphoblastic leukemia (ALL) may develop after treatment for primary cancer.
  • Topoisomerase inhibitors are commonly used to treat breast cancer patients and are well-known for their effect on leukemogenesis of therapy-related acute leukemias (t-AL).
  • METHODS: We retrospectively evaluated bone marrow test results, chromosomal findings, and clinical characteristics of 12 patients who received topoisomerase inhibitors for breast cancer treatment and later developed acute leukemia.
  • Among them, 9 patients (75%, 9/12) were diagnosed with therapy-related AML (t-AML) and 3 patients (25%, 3/12) with therapy-related ALL (t-ALL).
  • Translocation involving the MLL gene was frequently found in t-AL caused by a topoisomerase inhibitor and was related to poor prognosis.

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  • (PMID = 21120206.001).
  • [ISSN] 2092-9129
  • [Journal-full-title] The Korean journal of hematology
  • [ISO-abbreviation] Korean J Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2983048
  • [Keywords] NOTNLM ; 11q23 / Breast cancer / Therapy-related acute myeloid leukemia / Topoisomerase inhibitors
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37. Leone G, Fianchi L, Pagano L, Voso MT: Incidence and susceptibility to therapy-related myeloid neoplasms. Chem Biol Interact; 2010 Mar 19;184(1-2):39-45
Hazardous Substances Data Bank. BENZENE .

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  • [Title] Incidence and susceptibility to therapy-related myeloid neoplasms.
  • Therapy-related myeloid neoplasms (t-MN) include acute myeloid leukemias and myelodysplastic syndromes arising in patients who have been treated with chemotherapy, radiation therapy, immunosuppressive agents or after documented exposure to environmental carcinogen. t-MN are defined according to the primary treatment and the corresponding genetic and molecular lesions.
  • Chromosome(s) 7 and/or 5 monosomies or deletions are typical of alkylating agent-induced AML, while balanced translocations involving chromosome bands 11q23 and 21q22 are associated to preceeding therapy with DNA-topoisomerase II inhibitors.
  • Combination of polymorphisms impairing detoxification and DNA repair may significantly increase therapy-related myeloid neoplasm risk.
  • The addition of granulocyte-colony stimulating factor (G-CSF) and radiotherapy plays a significant role in t-MN following treatment of childhood acute lymphoblastic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / etiology. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / etiology

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  • [Copyright] Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20026017.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Topoisomerase II Inhibitors; J64922108F / Benzene
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38. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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39. Niparuck P, Kanoksil W, Chuncharunee S, Boonsakan P, Ungkanont A, Angchaisuksiri P, Karntisaviwat K, Apilugsanachit A, Rerkamnuatchoke B, Jootar S, Nitiyanant P, Atichartakarn V: Therapy-related myelodysplastic syndrome/acute myeloid leukemia following fludarabine therapy for non-Hodgkin lymphoma and chronic lymphocytic leukemia in Thai patients. Leuk Lymphoma; 2010 Nov;51(11):2120-5
Hazardous Substances Data Bank. VIDARABINE .

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  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia following fludarabine therapy for non-Hodgkin lymphoma and chronic lymphocytic leukemia in Thai patients.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / chemically induced. Lymphoma, Non-Hodgkin / drug therapy. Myelodysplastic Syndromes / chemically induced. Vidarabine / analogs & derivatives


40. 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
Hazardous Substances Data Bank. IMATINIB MESYLATE .

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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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41. Sill H, Olipitz W, Schimek MG: Therapy-related myelodysplastic syndrome and acute myeloid leukemia after autologous bone marrow transplantation: dosis facit venenum? J Clin Oncol; 2005 Nov 1;23(31):8120-1; author reply 8121-2
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

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  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia after autologous bone marrow transplantation: dosis facit venenum?
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Bone Marrow Transplantation. Cyclophosphamide / adverse effects. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary. Whole-Body Irradiation


42. Sill H, Zinke-Cerwenka W, Berghold A: Autologous stem cell transplantation for therapy-related acute myeloid leukemia and myelodysplastic syndrome. Bone Marrow Transplant; 2007 Apr;39(8):509; author reply 509-10
MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous stem cell transplantation for therapy-related acute myeloid leukemia and myelodysplastic syndrome.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Stem Cell Transplantation. Transplantation, Autologous






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