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1. Harada H, Harada Y, Tanaka H, Kimura A, Inaba T: Implications of somatic mutations in the AML1 gene in radiation-associated and therapy-related myelodysplastic syndrome/acute myeloid leukemia. Blood; 2003 Jan 15;101(2):673-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Implications of somatic mutations in the AML1 gene in radiation-associated and therapy-related myelodysplastic syndrome/acute myeloid leukemia.
  • Somatically acquired point mutations of AML1/RUNX1 gene have been recently identified in rare cases of acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
  • Moreover, germ line mutations of AML1 were found in an autosomal dominant disease, familial platelet disorder with predisposition to AML (FPD/AML), suggesting that AML1 mutants, as well as AML1 chimeras, contribute to the transformation of hematopoietic progenitors.
  • In this report, we showed that AML1 point mutations were found in 6 (46%) of 13 MDS patients among atomic bomb (A-bomb) survivors in Hiroshima.
  • Unlike acute or chronic leukemia patients among A-bomb survivors, MDS patients exposed relatively low-dose radiation and developed the disease after a long latency period.
  • AML1 mutations also were found in 5 (38%) of 13 therapy-related AML/MDS patients who were treated with alkylating agents with or without local radiation therapy.
  • In contrast, frequency of AML1 mutation in sporadic MDS patients was 2.7% (2 of 74).
  • Among AML1 mutations identified in this study, truncated-type mutants lost DNA binding potential and trans-activation activity.
  • All missense mutations with one exception (Gly42Arg) lacked DNA binding ability and down-regulated the trans-activation potential of wild-type AML1 in a dominant-negative fashion.
  • The Gly42Arg mutation that was shared by 2 patients bound DNA even more avidly than wild-type AML1 and enhanced the trans-activation potential of normal AML1.
  • These results suggest that AML1 point mutations are related to low-dose radiation or alkylating agents and play a role distinct from that of leukemogenic chimeras as a result of chromosomal translocations caused by sublethal radiation or topoisomerase II inhibitors.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics. Neoplasms, Second Primary / genetics. Proto-Oncogene Proteins. Radioactive Fallout / adverse effects. Transcription Factors / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Case-Control Studies. Core Binding Factor Alpha 2 Subunit. DNA Mutational Analysis. Female. Humans. Japan. Male. Middle Aged. Point Mutation / genetics. Protein Binding / genetics. Radiation Dosage. Transcription Factor AP-2. Transcription, Genetic

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  • (PMID = 12393679.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Radioactive Fallout; 0 / Transcription Factor AP-2; 0 / Transcription Factors
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2. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • The majority of tAML resulting from the use of cytotoxic agents can be divided into two groups based on the drugs administered to the patient.
  • The first group includes the use of alkylating agents, and the second group includes agents that bind to the enzyme DNA-topoisomerase II.
  • Cytogenetic study can detect abnormalities most commonly associated with tAML and thus providing important diagnostic information.
  • In this study, an interesting case with therapy-related myelodysplastic syndrome and acute myeloid leukemia (tMDS/tAML) will be presented.
  • A laboratory diagnostic strategy for tAML laboratory diagnosis will also be proposed.
  • [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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3. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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
  • [MeSH-minor] Animals. DNA / genetics. DNA Repair / genetics. DNA Topoisomerases, Type II / metabolism. Humans. Incidence. Polymorphism, Genetic / genetics. Risk Factors. Topoisomerase II Inhibitors


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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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5. 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.
  • CONCLUSION: The observations implicate azathioprine as a leukemogenic agent.
  • 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


6. 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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7. Karran P, Offman J, Bignami M: Human mismatch repair, drug-induced DNA damage, and secondary cancer. Biochimie; 2003 Nov;85(11):1149-60
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  • [Title] Human mismatch repair, drug-induced DNA damage, and secondary cancer.
  • More recently, it has become apparent that MMR defects are common in acute myeloid leukaemia/myelodysplastic syndrome (AML/MDS) that follows successful chemotherapy for a primary malignancy.
  • Therapy-related haematological malignancies are often associated with treatment with alkylating agents.
  • Their frequency is increasing and they now account for at least 10% of all AML cases.
  • There is also evidence for an association between MMR deficient AML/MDS and immunosuppressive treatment with thiopurine drugs.
  • Here we review how MMR interacts with alkylating agent and thiopurine-induced DNA damage and suggest possible ways in which MMR defects may arise in therapy-related AML/MDS.
  • [MeSH-major] Base Pair Mismatch / genetics. DNA Damage / drug effects. DNA Repair / genetics. DNA Repair / physiology. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Humans

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  • (PMID = 14726020.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 98
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8. 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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  • [Cites] Blood. 2002 Feb 1;99(3):822-4 [11806982.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):481-7 [12181402.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1600-4 [12886249.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):129-41 [15710326.001]
  • [Cites] Blood. 2007 Jan 1;109(1):61-4 [16960151.001]
  • [Cites] Br J Haematol. 2009 Dec;147(5):681-5 [19735261.001]
  • [Cites] Blood. 2007 Jul 1;110(1):59-66 [17374742.001]
  • [Cites] Acta Haematol. 2008;119(1):57-9 [18268406.001]
  • [Cites] Haematologica. 2009 Mar;94(3):433-5 [19181784.001]
  • [Cites] Haematologica. 2009 Apr;94(4):454-9 [19336749.001]
  • [Cites] Int J Hematol. 2009 Jun;89(5):699-703 [19430863.001]
  • [Cites] Am J Hematol. 2007 Mar;82(3):248-9 [16924641.001]
  • (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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9. Clavio M, Gatto S, Beltrami G, Cerri R, Carrara P, Pierri I, Canepa L, Miglino M, Balleari E, Masoudi B, Damasio E, Ghio R, Sessarego M, Gobbi M: First line therapy with fludarabine combinations in 42 patients with either post myelodysplastic syndrome or therapy related acute myeloid leukaemia. Leuk Lymphoma; 2001 Jan;40(3-4):305-13
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  • [Title] First line therapy with fludarabine combinations in 42 patients with either post myelodysplastic syndrome or therapy related acute myeloid leukaemia.
  • Acute myeloid leukaemias (AML) evolving from a myelodysplastic syndrome (MDS) or secondary to chemoradiotherapy frequently display unfavorable biologic characteristics.
  • Recently, the association of Fludarabine with intermediate dose Ara-C has produced interesting results particularly in high risk AML patients.
  • Here, we report on 42 secondary AML patients treated with a combination of Fludarabine, intermediate dose Ara-C, G-CSF with or without an antracycline (FLANG, FLAG-IDA or FLAG).
  • Overall, complete remissions (CR) were documented in 14 patients (33%) and partial responses (PR) in 12 (29%), while 10 patients proved resistant (24%).
  • Taken together, these Fludarabine containing regimens proved to be an effective and tolerable treatment for patients with secondary AML.
  • Patients above 70 years of age may also benefit from this therapy, however the problem of treating patients with adverse chromosomal abnormalities still remains unresolved.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / pathology. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Cohort Studies. Cytarabine / administration & dosage. Cytarabine / toxicity. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Granulocyte Colony-Stimulating Factor / toxicity. Humans. Male. Middle Aged. Neoplasms, Second Primary / complications. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / mortality. Remission Induction. Survival Rate

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  • (PMID = 11426552.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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10. 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
  • [MeSH-minor] Alkylating Agents / adverse effects. Chimera / genetics. Enzyme Inhibitors / adverse effects. Epigenesis, Genetic. Humans. Nuclear Weapons. Topoisomerase II Inhibitors. Translocation, Genetic

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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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11. Sakugawa M, Kojima K, Kaneda K, Masuda K, Dansako H, Shinagawa K, Ishimaru F, Ikeda K, Niiya K, Harada M, Tanimoto M: Therapy-related myelodysplastic syndrome/acute myeloid leukemia M2 and translocation (8;21). Ann Hematol; 2001 Dec;80(12):763-6
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  • [Title] Therapy-related myelodysplastic syndrome/acute myeloid leukemia M2 and translocation (8;21).
  • An 80-year-old woman developed therapy-related myelodysplastic syndrome with translocation (8;21), which was successfully treated with an acute myeloid leukemia oriented chemotherapy.
  • The leukemia cell morphology alerted us to the possibility of the presence of t(8;21) before cytogenetic results were obtained, and AML1/ETO fusion transcript was detected by reverse transcription polymerase chain reaction.
  • Our experience suggests that recognition of typical morphological features for de novo M2 acute myeloid leukemia with t(8;21) would be important in diagnosis of therapy related myelodysplastic syndrome/acute myeloid leukemia with this translocation, which could respond to an intensive chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology. Translocation, Genetic
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Nucleus / pathology. Cytoplasm / pathology. Electrophoresis, Agar Gel. Endometrial Neoplasms / drug therapy. Erythroblasts / pathology. Female. Humans. Immunophenotyping. Megakaryocytes / pathology. Reverse Transcriptase Polymerase Chain Reaction


12. Dann EJ, Rowe JM: Biology and therapy of secondary leukaemias. Best Pract Res Clin Haematol; 2001 Mar;14(1):119-37
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  • [Title] Biology and therapy of secondary leukaemias.
  • Secondary leukaemias are common, accounting for more than 40% of all patients with acute myeloid leukaemia (AML) or myelodysplastic syndrome (MDS).
  • A clinical history of exposure to haematotoxins or radiation is helpful; however, many older patients are diagnosed with leukaemia with no antecedent history of exposure.
  • These patients' disease show a remarkably similar phenotype to classic therapy-related leukaemia.
  • The specific cytogenetic abnormalities common to MDS, alkylating-agent-related AML and poor-prognosis AML (3q-, -5, 5q-, -7, 7q-, +8, +9, 11q-, 12p-, -18, -19,20q-, +21, t(1;7), t(2;11)), probably reflect a common pathogenesis distinct from that of other de novo AMLs, although the pathogenetic pathway has yet to be elucidated.
  • Typically, these patients are either elderly or have a history of exposure to alkylating agents or environmental exposure 5-7 years prior to diagnosis.
  • Another distinct entity affects the mixed lineage leukaemia (MLL) gene located on 11q23.
  • These account for about 3% of patients with therapy-related leukaemia and have a short latency period from exposure, usually to an inhibitor of topoisomerase II.
  • Other therapy-related patients with t(8:21), inv16 or t(15;17) translocations should be treated as any other de novo AML with similar cytogenetics.
  • In summary, the major prognostic factor is related to the pathogenetic mechanisms of the leukaemia.
  • Cytogenetics and molecular features are a better predictor of outcome than patient history.
  • Patients should receive standard induction therapy.
  • [MeSH-major] Leukemia / chemically induced. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Cytogenetics. Humans. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / etiology. Myelodysplastic Syndromes / therapy. Risk Factors

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  • [Copyright] Copyright 2001 Harcourt Publishers Ltd.
  • (PMID = 11355927.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 102
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13. 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


14. Abrahamsen AF: [Acute myelogenous leukemia and myelodysplastic syndrome after treatment with cytostatic agents]. Tidsskr Nor Laegeforen; 2000 Sep 10;120(21):2542-5
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  • [Title] [Acute myelogenous leukemia and myelodysplastic syndrome after treatment with cytostatic agents].
  • INTRODUCTION: The introduction of high dose chemotherapy of cancer has been followed by an increased incidence of therapy-related acute myeloid leukaemia and myelodysplastic syndrome.
  • MATERIAL AND METHODS: A survey of the literature has shown that these complications have been attributed to a high accumulated dose of alkylating agents, antracyclins and epipodophyllotoxins.
  • RESULTS: After standard doses of leukaemogenic drugs the incidence of acute myeloid leukaemia and myelodysplastic syndrome is reported to be 0-4%, increasing to 8-10% after high dose therapy.
  • At diagnosis of acute myeloid leukaemia and myelodysplastic syndrome, most of the patients have chromosomal abnormalities.
  • INTERPRETATION: The prognosis of therapy-related acute myeloid leukaemia and myelodysplastic syndrome is poor compared to that in primary acute myeloid leukaemia and myelodysplastic syndrome.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced
  • [MeSH-minor] Dose-Response Relationship, Drug. Humans

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  • (PMID = 11070993.001).
  • [ISSN] 0029-2001
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] NORWAY
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 38
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15. 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.
  • Cytotoxic drugs and radiation have been shown to affect tissue DNA methylation profile.
  • 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.
  • Among the studied genes, p15 methylation correlated to monosomy/deletion of chromosome 7q, suggesting that it could be a relevant event in alkylating agent-induced leukemogenesis.
  • 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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16. 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).
  • All had been treated with cytarabine, topoisomerase 2 inhibitors and granulocyte or granulocyte-monocyte colony-stimulating factor and three with alkylating agents as part of autologous transplant regimens.
  • 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


17. de Witte T, Oosterveld M, Span B, Muus P, Schattenberg A: Stem cell transplantation for leukemias following myelodysplastic syndromes or secondary to cytotoxic therapy. Rev Clin Exp Hematol; 2002 Mar;6(1):72-85; discussion 86-7
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  • [Title] Stem cell transplantation for leukemias following myelodysplastic syndromes or secondary to cytotoxic therapy.
  • Two main forms of therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/AML) have been recognized.
  • The most frequent type, occurring after treatment with alkylating agents, is characterized by abnormalities of chromosomes 5 and/or 7 and t-MDS/AML following treatment with topoisomerase II inhibitors and is associated with molecular aberrations of MLL (11q23) and AML-1 (21q22).
  • Individuals with certain polymorphisms associated with impaired detoxification of cytotoxic agents have an increased risk of developing MDS or AML after treatment of unrelated cancers.
  • Multidrug chemotherapy is less effective for patients with MDS, or AML following MDS, or t-MDS/AML when compared with primary AML, and results in lower complete remission (CR) rates and lower long-term survival.
  • 21) and inversion 16 are an exception as their treatment outcome is comparable with primary AML patients.
  • Patients who attain a polyclonal and/or a cytogenetic CR may be candidates for autologous stem cell transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia / therapy. Myelodysplastic Syndromes / complications. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Leukemia, Radiation-Induced / therapy. Risk Factors


18. 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


19. 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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20. Andersen MK, Pedersen-Bjergaard J: Increased frequency of dicentric chromosomes in therapy-related MDS and AML compared to de novo disease is significantly related to previous treatment with alkylating agents and suggests a specific susceptibility to chromosome breakage at the centromere. Leukemia; 2000 Jan;14(1):105-11
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  • [Title] Increased frequency of dicentric chromosomes in therapy-related MDS and AML compared to de novo disease is significantly related to previous treatment with alkylating agents and suggests a specific susceptibility to chromosome breakage at the centromere.
  • Dicentric chromosomes are observed in many malignant diseases including myelodysplasia (MDS) and acute myeloid leukemia (AML) and have often been observed in a subset of these diseases, namely therapy-related MDS (t-MDS) and AML (t-AML).
  • Using fluorescence in situ hybridization (FISH) with centromere-specific probes, we investigated the frequency and type of dicentric chromosomes in 180 consecutive patients with t-MDS and t-AML and in 231 consecutive patients with de novo MDS and AML, whose karyotypes had been studied previously by conventional G-banding.
  • Twenty-seven out of 180 patients with t-MDS or t-AML presented dicentric chromosomes compared to only seven out of 231 patients with de novo disease (P = 0.00003).
  • Patients with dicentric chromosomes presented significantly more often as t-MDS compared to patients without dicentrics (P = 0.046), and the presence of a dicentric chromosome was significantly related to previous therapy with alkylating agents (P = 0.026).
  • Thus, only one out of 27 patients with a dicentric chromosome had not previously received an alkylating agent.
  • A specific susceptibility to breakage at the centromere after exposure to alkylating agents is suggested and may explain the frequent loss of whole chromosomes, in particular chromosomes 5 and 7 in t-MDS and t-AML, if the breaks are not followed by rejoining.
  • Leukemia (2000) 14, 105-111.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Centromere. Chromosome Aberrations. Leukemia, Myeloid / genetics. Myelodysplastic Syndromes / genetics

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  • (PMID = 10637484.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating
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21. Andersen MK, Christiansen DH, Kirchhoff M, Pedersen-Bjergaard J: Duplication or amplification of chromosome band 11q23, including the unrearranged MLL gene, is a recurrent abnormality in therapy-related MDS and AML, and is closely related to mutation of the TP53 gene and to previous therapy with alkylating agents. Genes Chromosomes Cancer; 2001 May;31(1):33-41
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  • [Title] Duplication or amplification of chromosome band 11q23, including the unrearranged MLL gene, is a recurrent abnormality in therapy-related MDS and AML, and is closely related to mutation of the TP53 gene and to previous therapy with alkylating agents.
  • Gene amplification is a rare phenomenon in acute leukemia, but recently amplification of specific chromosome bands containing genes rearranged in leukemia-specific balanced chromosome translocations has been reported in a few cases.
  • We detected duplication or amplification of chromosome band 11q23 with 3-7 copies of the MLL gene by fluorescence in situ hybridization in 12 out of 70 unselected patients with therapy-related myelodysplasia or acute myeloid leukemia (17%).
  • Patients with supernumerary copies of MLL were in general older (P = 0.007) and had a shorter survival (P < 0.001) compared to other patients.
  • Duplication or amplification of MLL was significantly associated with a complex karyotype (P = 0.002), with deletion or loss of 5q (P = 0.001), and with prior therapy with alkylating agents.
  • These results support the existence of a specific genetic pathway in t-MDS and t-AML with many previously unidentified chromosome aberrations demonstrated to represent extra copies of parts of 11q, including the unrearranged MLL gene.
  • [MeSH-major] Alkylating Agents / adverse effects. Chromosome Aberrations / genetics. Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Gene Amplification / genetics. Gene Duplication. Genes, p53 / genetics. Leukemia, Myeloid / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics. Proto-Oncogenes. Transcription Factors
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Chromosome Banding. Chromosome Disorders. Cytogenetic Analysis / methods. Female. Histone-Lysine N-Methyltransferase. Humans. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Nucleic Acid Hybridization / methods. Recurrence

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11284033.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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22. 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


23. 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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24. Arber DA, Slovak ML, Popplewell L, Bedell V, Ikle D, Rowley JD, International Workshop on Leukemia Karyotype and Prior Therapy: Therapy-related acute myeloid leukemia/myelodysplasia with balanced 21q22 translocations. Am J Clin Pathol; 2002 Feb;117(2):306-13
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  • [Title] Therapy-related acute myeloid leukemia/myelodysplasia with balanced 21q22 translocations.
  • The morphologic and immunophenotypic findings of 36 cases of 21q22 acute myeloid leukemia (AML) and myelodysplasia (MDS) were compared, including 14 de novo t(8;21) AMLs, 11 t(8;21) therapy-related AML/MDS cases, and 11 therapy-related AML/MDS cases with other 21q22 balanced translocations [t(n;21)].
  • Cases of de novo and therapy-related t(8;21) disease shared common morphologic features of chunky cytoplasmic granules, perinuclear hofs, and promyelocyte increases that were not seen consistently in the t(n;21) group of t-AML/MDS cases.
  • De novo and therapy-related t(8;21) disease, however, differed by the frequent presence of associated dysplasia in both t-AML/MDS groups, which was infrequent in the de novo t(8;21) group.
  • Therapy-related AMI/MDS with t(8;21) shares characteristic morphologic and immunophenotypic features with de novo t(8;21) AML, but frequently also occurs with associated myelodysplastic changes, similar to other therapy-related acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Drug-Related Side Effects and Adverse Reactions. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / pathology. Translocation, Genetic / genetics

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  • (PMID = 11863228.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-30206; United States / NCI NIH HHS / CA / CA-33572
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD34; 0 / Antigens, CD56
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25. 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.
  • One third (7/21) of the patients had received alkylating drugs for a previously diagnosed cancer or chronic myeloproliferative disease.
  • 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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26. 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
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Chromosome Aberrations. Disease-Free Survival. Female. Follow-Up Studies. Horses. Humans. Incidence. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies. Survival Rate. Time Factors

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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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27. Andersen MK, Larson RA, Mauritzson N, Schnittger S, Jhanwar SC, Pedersen-Bjergaard J: Balanced chromosome abnormalities inv(16) and t(15;17) in therapy-related myelodysplastic syndromes and acute leukemia: report from an international workshop. Genes Chromosomes Cancer; 2002 Apr;33(4):395-400
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  • [Title] Balanced chromosome abnormalities inv(16) and t(15;17) in therapy-related myelodysplastic syndromes and acute leukemia: report from an international workshop.
  • The Workshop identified 48 unselected patients with therapy-related myelodysplastic syndrome or acute myeloid leukemia (t-MDS/t-AML) and inv(16), and 41 patients with t(15;17) after chemotherapy (CT) and/or radiotherapy (RT) for a malignant or nonmalignant disease.
  • The general type of previous therapy was RT only in 10 patients with an inv(16) and in 12 patients with a t(15;17), alkylating agents plus topoisomerase II inhibitors in 24 patients with an inv(16) and in 18 patients with a t(15;17), topoisomerase II inhibitors only in 5 patients with an inv(16) and in 2 patients with a t(15;17), alkylating agents only in 6 patients in each subgroup, and other types of chemotherapy in 3 patients in each subgroup.
  • The latency period to development of t-MDS/t-AML was short: a median of 22 months in patients with inv(16) and 29 months in patients with t(15;17).
  • Trisomy of chromosomes 8, 21, and 22 and del(7q) were the most frequent additional abnormalities in the inv(16) subgroup, whereas +8, -5, and del(16q) were most frequent in the t(15;17) subgroup.
  • The disease was overt t-AML in 38/48 patients (79%) with an inv(16) and in 38/41 patients (93%) with a t(15;17).
  • The study supports the observation that t-MDS/t-AML with inv(16) and t(15;17) is often associated with prior therapy with topoisomerase II inhibitors; however, a notable finding was the high frequency of treatment with only radiotherapy, 29% of t(15;17) and 21% of inv(16).
  • Response rates to intensive chemotherapy in this study were comparable to those of de novo disease.
  • [MeSH-major] Chromosome Aberrations / chemically induced. Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 16 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Translocation, Genetic / genetics


28. Side LE, Curtiss NP, Teel K, Kratz C, Wang PW, Larson RA, Le Beau MM, Shannon KM: RAS, FLT3, and TP53 mutations in therapy-related myeloid malignancies with abnormalities of chromosomes 5 and 7. Genes Chromosomes Cancer; 2004 Mar;39(3):217-23
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  • [Title] RAS, FLT3, and TP53 mutations in therapy-related myeloid malignancies with abnormalities of chromosomes 5 and 7.
  • Oncogenic mutations in the KRAS2, NRAS, or FLT3 gene are detected in more than 50% of patients with de novo acute myeloid leukemia (AML).
  • RAS mutations are also prevalent in de novo myelodysplastic syndrome (MDS), especially chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia.
  • However, few studies have examined these genetic lesions in therapy-related myeloid malignancies.
  • Monosomy 7/del(7q) and monosomy 5/del(5q) represent the most common cytogenetic abnormalities in therapy-related MDS and AML (t-MDS/t-AML) and are strongly associated with prior exposure to alkylating agents.
  • Mutational analysis of bone marrow specimens from a well-characterized cohort of 26 t-MDS/t-AML patients with abnormalities of chromosomes 5 and/or 7 revealed 3 with RAS mutations.
  • RAS and FLT3 mutations, which are thought to stimulate the proliferation of leukemia cells, appear to be less common in t-MDS/t-AML than in de novo AML, whereas TP53 mutations are more frequent.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia, Myeloid / genetics. Neoplasms, Second Primary / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins p21(ras) / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Male. Middle Aged. fms-Like Tyrosine Kinase 3

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 14732923.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / HRAS protein, human; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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29. Seiter K, Feldman EJ, Sreekantaiah C, Pozzuoli M, Weisberger J, Liu D, Papageorgio C, Weiss M, Kancherla R, Ahmed T: Secondary acute myelogenous leukemia and myelodysplasia without abnormalities of chromosome 11q23 following treatment of acute leukemia with topoisomerase II-based chemotherapy. Leukemia; 2001 Jun;15(6):963-70
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  • [Title] Secondary acute myelogenous leukemia and myelodysplasia without abnormalities of chromosome 11q23 following treatment of acute leukemia with topoisomerase II-based chemotherapy.
  • Therapy-related MDS and AML are complications of intensive chemotherapy regimens.
  • Traditionally, patients exposed to topoisomerase II inhibitors are reported to develop secondary AML with abnormalities of chromosome 11q23.
  • We evaluated the long-term hematologic toxicity of topoisomerase II-intensive high-dose mitoxantrone-based chemotherapy in 163 newly diagnosed acute leukemia patients treated over an 8 year period.
  • Four patients developed MDS with progression to AML, three patients developed new abnormalities at the time of relapse, and three patients (including one of the former patients) had changes that were not associated with hematologic disease.
  • Despite the use of topoisomerase II-intensive treatment, no patient developed an abnormality involving chromosome 11q23.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11 / ultrastructure. Enzyme Inhibitors / adverse effects. Leukemia, Myeloid / chemically induced. Mitoxantrone / adverse effects. Myelodysplastic Syndromes / chemically induced. Neoplasm Proteins / antagonists & inhibitors. Neoplasms, Second Primary / chemically induced. Topoisomerase II Inhibitors
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Cytarabine / administration & dosage. Disease Progression. Disease-Free Survival. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Incidence. Karyotyping. Life Tables. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Randomized Controlled Trials as Topic. Remission Induction. Retrospective Studies. Treatment Outcome. Tretinoin / administration & dosage

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  • (PMID = 11417484.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Topoisomerase II Inhibitors; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
  • [Number-of-references] 37
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30. Blanco JG, Edick MJ, Hancock ML, Winick NJ, Dervieux T, Amylon MD, Bash RO, Behm FG, Camitta BM, Pui CH, Raimondi SC, Relling MV: Genetic polymorphisms in CYP3A5, CYP3A4 and NQO1 in children who developed therapy-related myeloid malignancies. Pharmacogenetics; 2002 Nov;12(8):605-11
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  • [Title] Genetic polymorphisms in CYP3A5, CYP3A4 and NQO1 in children who developed therapy-related myeloid malignancies.
  • Therapy-related acute myeloid leukemia and myelodysplastic syndrome (t-ML) are serious complications that affect some patients after acute lymphoblastic leukemia (ALL) treatment.
  • A polymorphism in CYP3A5 (CYP3A5*3) affects CYP3A activity and the wild-type allele (CYP3A5*1) is in partial linkage with the CYP3A4*1B allele.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cytochrome P-450 Enzyme System / genetics. Leukemia, Myeloid / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasms, Second Primary / genetics. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Base Sequence. Child. Child, Preschool. Cytochrome P-450 CYP3A. DNA Primers. Female. Humans. Infant. Infant, Newborn. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 12439220.001).
  • [ISSN] 0960-314X
  • [Journal-full-title] Pharmacogenetics
  • [ISO-abbreviation] Pharmacogenetics
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA13959; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA29139; United States / NCI NIH HHS / CA / CA30969; United States / NCI NIH HHS / CA / CA31566; United States / NCI NIH HHS / CA / CA32053; United States / NCI NIH HHS / CA / CA33606; United States / NCI NIH HHS / CA / CA33625; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / CA51001; United States / NIGMS NIH HHS / GM / U01 GM61393; United States / NIGMS NIH HHS / GM / U01GM61374
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Primers; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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31. 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
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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.
  • Antimetabolites, and in particular the immunosuppressive agents azathioprine and fludarabine, have also been recently associated to t-MN.
  • 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
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Benzene / adverse effects. Disease Susceptibility / etiology. Humans. Incidence. Radiotherapy / adverse effects. Topoisomerase II Inhibitors

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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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32. 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
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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
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Female. Humans. Male. Middle Aged. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / epidemiology. Prognosis. Retrospective Studies. Thailand / epidemiology. Young Adult


33. Andersen MK, Pedersen-Bjergaard J: Therapy-related MDS and AML in acute promyelocytic leukemia. Blood; 2002 Sep 1;100(5):1928-9; author reply 1929
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  • [Title] Therapy-related MDS and AML in acute promyelocytic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Myelodysplastic Syndromes / chemically induced






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